ANCC CVN Review Course Day 1 (1) - CCRN … CVN Review Course ... • Dorthea Orem: Self Care •...

6/20/2012

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ANCC CVN Review Course

Karen Marzlin DNP, RN, CCNS, CCRN‐CMC

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Opening Thought

Link your roots deeply into whatever task you are doing, for commitment and enthusiasm transform monotony into freshness; and routine into joy and discovery.

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ETHICAL AND LEGAL PRINCIPLES CVN Review Course

Definitions

• Morality: social consensus regarding norms of right and wrong

• Ethics

• Bioethics

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Moral Virtues for Health Care

Compassion

TrustworthinessConscientiousness

Integrity Discernment

Ethical Principles

• Beneficence • Nonmalficence• Autonomy • Justice • Veracity • Privacy / Confidentiality • Fidelity

ANA Code of Ethics for Nurses

HIPPA

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Informed Consent

• Decision making capacity – Surrogate decision makers

• Disclosure • Voluntariness • Consent

Special Issues

• Advanced Directives

• Withdrawal or withholding of treatment

• Access to Care

• Patient rights

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Ethical Reasoning

• Review both facts and assumptions

• Define specific dilemma

• List options in course of action

• Consider the context

• Choose the course

• Evaluate the course

Professional Standards of Practice

• Standards of care versus standards of professional performance

• 1980 Social Policy Statement defining nursing – The diagnosis and treatment of human responses to actual or potential health problems

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Professional Standards of Practice

• Professional licensure – Advanced practice

• Professional certification

• Nurse Practice Acts – Law– Interpretation – Rules

Legal Aspects

Accountability • Personal accountability

• Employer accountability

Torts • Unintentional (negligence)

– Duty – Breach of duty – Injury – Causation

• Intentional – Assault and battery – Defamation – Invasion of privacy

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THEORY TO GUIDE PRACTICE CVN Review Course

The Importance of Theory

• The relationship between theory – practice –and research

• What is theory?– Set of concepts, definitions, and propositions that provide a view (explanation for understanding) of a specific phenomena.

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More on theory

Concept • Clear description of an

abstract concept

• Bui lding blocks for theory

• Concept analyses

Propositions • Statements about

relationships between concepts

Grand Theories

• Patient

• Nursing

• Environment

• Heatlh

• Dorthea Orem: Self Care• Sister Callisata Roy: Adaptation• Betty Neuman: Systems Model • Martha Rogers: Unitary Man • Jean Watson: Caring • Margaret Newman: Expanding Consciousness

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Health as Primary Focus of Nursing

• Difference between focus on health and illness

• Difference between illness and disease

• Definitions of health within nursing theory

Theories Related to Human Behavior

Maslow’s Hierarchy of Needs – Physiological – Safety – Belonging – Self actualization

Erickson’s Stages of Human Development

• Trust versus mistrust • Autonomy versus shame and

doubt • Initiative versus guilt • Industry versus inferiority • Identity versus role confusion • Intimacy versus isolation • Generosity versus absorption• Integrity versus despair

Social Cognitive Theory and the Importance of Self

Efficacy

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Theories Related to Human Behavior

Health Belief Model • Individual perceptions

• Modifying factors

• Cues to action

Health Promotion Model • Individual characteristics,

expectations, and experiences

• Behavior specific thoughts and feelings

Human Behavior Theory: TranstheoreticalModel

• Pre‐contemplation • Contemplation • Preparation • Action • Maintenance • Termination

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Theory Related to Community Change

• Social Ecology Theory – Responsibility for health is shared between individual and the community

– Health promotion goes beyond individual to include community action and public policy.

Theories Related to Organizational Change

• Lewin’s Planned Change– Unfreezing existing structures – Introducing change – Moving to a new level – Refreezing structures – Strengthen driving forces – Reduce restraining forces

• Roger’s Theory of Adoption of Innovation– Process of diffusion– Innovators – Early adopters – Early majority – Late majority – Laggards

• Strategies – Empirical rationale – Normative re‐educative

(Social Cognitive Theory) – Power‐coercive strategies

• Barriers

• Drivers

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Theory Related to Family Dynamics

• Family Systems Theory– Functional whole– Contact with environment – Transmission of culture – Roles and functions – Social support – Problems reflect adaptation

– On time events create less strain than off time events

• Family Life Cycle – Unattached young adult – Newly married – Family with young children – Family with adolescent children

– Family launching – Later life family

Crisis Theory

• Loss and threat can precipitate situational crisis • Developmental crisis can occur at predictabepoints

• Usual coping is insufficient • All energy and resources are directed at crisis • Crisis is self limited (4 to 10 weeks) • Those is crisis more open to help

– Minimal help may yield meaningful results

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Crisis Intervention

• Goals:– Safety – Restore to previous level of function or higher – Enhance coping / self esteem

• Strategies – Reassurance– Suggestion – Support – Environmental manipulation – Pharmacotherapy

LEADERSHIPCVN Review Course

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Leadership Styles

• Autocratic • Participative • Laissez‐faire • Situational • Transactional • Transformational

– Articulates vision– Empowers

Team Building Models Traditional Model of Team Effectiveness • Examines the symptoms of

team effectiveness rather than causes

• Assumes team is passive and stable

• Team processes include communication, social integration, role clarification, and goal setting

• Team effectiveness is measured by process and perception indicators

Cognitive Motivational Model of Team Effectiveness • Assumes team is active,

dynamic, and cognitively motivated

• Team purpose includes self evaluation and ability to redesign interventions

• Team effectiveness i s measured by results

• Team building: Redesigning cognitive functioning by analyzing team effectiveness

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Case Management

• Case Management Society of America: Process

• ANCC: Defines nursing case management

• Nursing case management models– Coordination of care – Trans itions of care – Interdisciplinary

• Community based case management

• Long term healthcare models

• Rehabilitation models • Insurance based models • Managed care and HMO models

• Private models

Quality Total Quality Management • Emphasizes empowerment

of employees– Person at point of service as

most information

• Customers are internal and external

• Qual ity problems more related to systems problems rather than people problems

• Qual ity is cost effective

Continuous Quality Improvement • Focus is more on processes

than people • Complex processes require

an interdisciplinary team • Also empowers workers to

reduce cost and improve quality

• Synonymous with Performance Improvement

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ShewhartCycle

• Also known as Deming Cycle • 4 Steps in the Cycle (PDCA)

–Plan (based on assessment and measurements)

–Do (trial)

–Check (assesses results) –Act (full implementation) – Back to Plan

Outcomes Evaluation

• Process Indicators versus Outcome Indicators– Compliance with VAP protocol (versus) – Infection rates __________________________________________

• Patient Outcomes • Provider Outcomes • System Outcomes

– Often incudes financial outcomes

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Benchmark Data and Recognition

• Magnet Designation – NDNQI (nurse sensitive indicators)

• Joint Commission

• Specialty Organizations – ACC – AHA

• Program Certifications – JC Disease Specific

• Heart Failure

– Chest Pain Center Accreditation

– Cardiopulmonary Rehab • AACVPR

PATIENT EDUCATION AND COUNSELING

CVN Review Course

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Therapeutic Communication

• Empathy • Unconditional acceptance

• Acknowledging patient worth

• Listen thoroughly before concluding

• Non verbal skills – Mindful approach – Same level – No interruptions / dis tractions

Therapeutic Communication: Techniques

• Offering leads • Restating • Reflecting • Focusing• Clarifying • Sequencing

• Encourage participation

• Encourage evaluation

• Make observations

• Summarize

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Communication No Nos!

Why Questions

Give Advice

False Reassurance

Use Leading Questions

Use Jargon

Defensive Response

Use Clichés

Barriers

• Language • Vision • Hearing • Culture

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Learning

Adult Learners

• Self directed •Need to know

• Life Experiences

Domains of Learning

•Cognitive •Affective •Psychomotor

Conditions for Learning

•Motivation to learn

•Ability to learn

• Learning environment

More on Healthcare Literacy

• REALM tool• National Institute for Literacy • Signs of low literacy • Interventions

– Simple language – Teach back – Open ended questions – Repeat information

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Patient Education Process

Assessment Diagnostic

Statement and Objectives

Teaching / Learning

Interventions

Education and Reteaching Documentation

Strategies for Patient Education

• Include expected effects of interventions• Small changes rather than large changes • Be specific! • Focus on addition of positive behaviors • Link new behavior to existing behavior • Power of the profession • Interdisciplinary / multifaceted • Ask patient for a commitment

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Health and Self Management

Health Maintenance/ Improvement

Maintenance or improvement

Perception of health, Motivation to

Change, Adherence to Prescribed Interventions

Population Based Initiatives

Disease Prevention:

Health Promotion

Self Care

Maintenance

Management

Discharge Planning

Levels • Bas ic

– Patient Education

• Simple – Referral to community

resources

• Complex – Interdisciplinary – Sub‐acute – Long term

Transitions of Care • Hand offs• Medication reconciliation• Coordination / facilitation of

care • Negotiation• High risk populations

– Elderly – Chronic disease states

• Models for transitions of Care – Coleman

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NURSING RESEARCH CVN Review Course

Problem Identification

• All research starts here!• Questions stem from observationClinical Inquiry

• Has the question been answered? • To what degree? Review the Evidence

• Frequency and magnitude of problem? • Would answers change practice? • Can interest sustain the effort?

Does the question warrant a research initiative?

• Qualitative • QuantatativeWhat research method

will answer the question?

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Qualitative

• Inductive • Broad research question

• Used when little is known about subject

• To generate hypothesis for further testing

• Can be used with quantitative research – Triangulation

• Discover meaning • Explore complexities • Data collection and analysis occur concurrently

• Purposeful sampling is used

• Trustworthiness is key issue with qualitative studies

Qualitative Research Methods

Phenomenology

Grounded theory

Ethnography

Historiography

Content Analysis

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Quantitative Research

• Variables– Independent – Dependent – Demographic

• Causality versus correlation

• Validity – Internal – External – Construct – Type 1 Error – Type 2 Error

Quantitative Design

• Descriptive

• Correlational – Cross sectional – Longitudinal

• Experimental – Control – Randomization

• Quasi‐experimental – Control

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Concepts in Quantitative Research

Sampling • Population / accessible

population • Sampling criteria

– Inclusion – Exclusion

• Representativeness • Sampling error

– Systematic variation • Adequacy of size

– Effect size – Power – Statistical significance

Measurement • Process of assigning

numbers according to a rule – Interval scale – Ratio scale

• Error – Random error – Systematic error

• Rel iability • Val idity • Sensitivity

Concepts in Quantitative Research

Data Collection • Observation

• Sel f Report

• Exis ting Data

• Phys iological Measures

Data Analysis • Descriptive statistics

– Measures of central tendency – Shape of distribution – Measures of dispersion – Measures of association

• Inferential statistics – Tests of difference

• t‐test, ANOVA (parametric)• Mann‐Whitney U test, sign test (non

parametric) – Tests of association

• Pearson correlation coefficients (parametric)

• Spearman and Kendall correlation coefficients (nonparametric )

• Meta‐analysis – Pooled statistics from multiple studies – Helpful when study outcomes varied

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Evaluation of Research

Qualitative QuantitativeCredibility (truth value) Internal validity Transferability External validity Dependability Reliability Confirmability Objectivity

Additional Research Concepts

Epidemiology • Population based research • Prevalence: total number of

cases in given period • Incidence: number of new

cases in a given period • Relative risk • Framingham Study

Protection of Human Rights • Historical abuses

• Role of IRB / HRRB

• Informed consent

• Vulnerable populations

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RISK FACTORS CVN Review Course

Disease Paradigm

Atherosclerosis is a diffuse inflammatory process. We need to treat the systemic disease and not just the symptomatic stenosis.

Class Summary: Hyperlipidemia, hypertension, and diabetes impair endothelial function.

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Risk Factor

A characteristic found in a healthy personindependently related to the future

development of coronary heart disease.

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Non Modifiable Risk Factors

– Age – Gender – Family History – Previous CHD event

– Socioeconomic Status – Ethnicity

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Age

• Eighty five percent of people who die from CHD are > 65 years of age

• Mortality for those < age 65– 80% related to first MI

• Lifetime risk of developing CHD after the age of 40

• 49% men • 32% women

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Gender • In general men (35‐65) have

a higher ri sk of CHD than women

• The average age for fi rst myocardial infarction in men i s 64.5 years and 70.3 years in women– The incidence of CHD in

women generally lags behind men by about 10 years (American Heart Association Statistics, 2009).

• Presentation differences between men and women

• More women than men die each year from cardiovascular disease . – Women have a higher

mortality rate than men after a heart attack (American Heart Association Statistics, 2009)

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Family History

Development of CHD in a first degree relative: Males < 55 years of ageFemales < 65 years of age

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Previous CHD • Single greatest risk factor

for having a future cardiac event

• 20% ri sk of having a cardiac event over ten years

• A ri sk equivalent puts the person at the same risk as someone with a prior CHD event

• Approximately 90% of those who present with CHD have at least one major risk factor from among hyperlipidemia, hypertension, cigarette smoking, or diabetes (American Heart Association Statistics, 2009).

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Risk Equivalents

• There are three CHD Risk Equivalent Groups:

• Persons with 2 or more CHD Risk Factors who score at the equivalent ri sk on the Framingham tool

• Persons with other forms of atherosclerotic vascular disease (PVD, AAA, symptomatic carotid disease)

• Type I I Diabetes

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Modifiable Risk Factors – Diabetes Mellitus

• ./(Metabolic Syndrome) – Tobacco Use – Obesity – Hypertension – Dyslipidemia

• Hypercholesterolemia – Elevated total cholesterol – Elevated low density lipoprotein cholesterol (LDL‐C) – Elevated triglycerides

• Low high density l ipoprotein cholesterol (HDL‐C)

– Physical Inactivity, Stress, Alcohol

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DIABETES, METABOLIC SYNDROME, OBESITY

CVN Review Course

Diabetes Mellitus

• Diabetes and CHD Risk – Age adjusted rates for CHD are 2‐3 times higher for men and 3‐7 times higher for women with diabetes than their nondiabetic counterparts

• Diabetes and Mortality and Morbidity – 75% of all diabetic deaths results from CHD – Mortality and morbidity with an MI

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Diabetes Mellitus

Diabetes Mellitus is associated with an acceleratedatheromatous process resulting in increased risk forCAD.

►Incidence of Type I I Diabetes – 18 million (90% of al l diabetes)

►Underlying Causes (obesity, physical inactivity, genetic)

►Uncontrolled Diabetes (Hemoglobin A1C > 6%)

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Metabolic Syndrome

• Metabolic Syndrome – Represents a grouping of lipid and non lipid risk factors of metabolic origin

– Prevalence • 22% of population (48 million people)

– Closely linked to the generalized disorder of insulin resistance

• Excess body fat and physical inactivity promote the development of insulin resistance

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Metabolic Syndrome

• Metabolic syndrome abnormalities – Defective glucose uptake by skeletal muscle – Increased release of free fatty acids by adipose tissue

– Over production of glucose by the liver – Hyper‐secretion of insulin by beta cells in pancreas

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Diagnostic Criteria for Metabolic Syndrome

• Metabolic Syndrome diagnosis is made when three or more of the following are present:

• Waist circumference > 40 inches for men and > 35 inches for women

• Triglycerides > 150 mg/dl• HDL‐C < 40 mg/dl for men and < 45 mg/dl for women

• BP > 135 mmHg systolic or > 85 mmHg diastolic

• Fasting glucose > 110‐125 mg/dl

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ACC / AHA Secondary Prevention Guidelines

• Goal: HbA1c < 7%

– Exercise – Diet – Medication– Collaboration with Endocrinologist

Blood Pressure Control more important than glycemic control in reducing risk of death: Macrovascular risk reduction 32-44%.

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Intensive Glycemic Control

• “the lack of significant reduction in CVD events with intensive glycemic control in the ADVANCE trial (and also ACCORD and VADT) should not result in abandoning the target of an A1c < 7.0%– Benefit of good control on serious microvascularcomplications.”.

– .ACC / AHA 2009

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Intensive Glycemic Control • Subset analyses of ADVANCE (and VADT and ACCORD)

– Shorter duration of type 2 diabetes and without established atherosclerosis might reap cardiovascular benefit from intensive glycemiccontrol.

– Risks of intensive glycemic control may outweigh benefits in patients with a very long duration of diabetes, known history of severe hypoglycemia, advanced atherosclerosis, and advanced age/frailty

» ACC / AHA 2009

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Obesity

√Obes ity adversely affects most other ri sk factors

√Obesity and LVH

√Abdominal obesity (determined by waist / hip ratio) is an independent ri sk factor for vascular disease in women and older men.

√BMI independently predicts coronary atherosclerosis in whites

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Obesity and CABG

• Independent risk factor for: – Perioperative respiratory failure – Sternal and leg wound complications – Perioperative MI – Arrhythmias

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Obesity and Prevention

• Body Mass Index (BMI) used to define obesity and overweight

• Limitations of BMI – Does not take distribution of fat into account

• BMI measurements – Healthy 18.5 to 24.9 – Overweight 25.0 to 29.99 – Obes ity > 30

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• Waist to hip ratio

– Waist circumference < 35 inches for women and < 40 inches for men

– Waist to hip ratio < 0.8 for women and < 1.0 for men

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• Weight loss: – Improves lipid levels – Improves insulin res istance

– Lowers blood pressure

– Weight loss is especially important for those with high lipids, HTN and elevated blood glucose levels

• Prevention of obesity is high priority to reduce CVD ri sk

• Heredity and environmental factors play a role in obesity

• Obes ity is associated with many co‐morbidities

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• BMI 18.5 to 24.9 kg/m2

• Waist circumference – Men < 40 inches – Women < 35 inches

Initial goal: Decrease 10% from baseline

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Barriers to Effectiveness of Dietary Counseling

• lack of assessment of the patient’s interest in making dietary change,

• primary care providers have low estimate of self efficacy with regard to nutrition counseling,

• providers are unwilling to confront patients on weight issues, and

• time restrictions on reimbursement impose limitations on traditional medical office visits.

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Nutrition Guidelines

• Providers should deliver simple positive messages– Eat breakfast– Eat fruits, vegetables, and whole grains– Limit snacks to once a day– Eat smaller portions– Limit intake of sugar containing beverages to less than 12 oz./day

– Weigh yourself regularly and adjust dietary intake based on your weight.

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TOBACCOISMCVN Review Course

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Tobacco Use

– Tobacco use should be approached as a chronic disease itself as opposed to a mere risk factor

– Approximately 21% of adult Americans smoke resulting in approximately 45 million adult American smokers (Fiore, et al., 2008).

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Tobacco Use

• Most important modifiable risk factor – > 20 cigarettes per day results in a 2 to 3 fold increase in CHD risk

• 50% reduction in CV risk with smoking cessation including reduction in reinfarction rates and mortality

• After 15 years of smoking cessation, the CHD risk for a former smoker approaches that of a nonsmoker

• (Sohn, et al., 2010).

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Effects of Tobacco • Increased arterial wall s tiffness with impaired coronary

vasodilitation • Decreases the threshold for ventricular ectopy • Enhances the oxidation of LDL‐C• Lowers HDL‐C• Increases C‐reactive protein and fibrinogen • Increases platelet aggregation • Increases hematocrit • Increases monocyte adhesion to endothelial cells• Destabilizes coronary plaque and promotes plaque rupture

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Nicotine Addiction

• Nicotine and carbon monoxide are the two most important chemicals in cigarette smoke. – Nicotine creates physical addiction

• Smoking creates physiological and psychological addiction – Peaks within 1stweek – Subsides 2‐4 weeks – Physical withdrawal during hospitalization

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Understanding Addiction

Physical • Withdrawal cravings lessen

over time and are less severe than situational cravings

Behavioral • Si tuational cravings – levels

remain high but become more sporadic

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Cessation Counseling

• Cessation techniques – Pharmacologic agents– Behavior modification

– Important point: ASK PERMISSION !!

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Smoking Cessation Counseling

• Minimal interventions of less than 3 minutes by a wide variety of clinicians has been proven effective in reducing tobacco use.

• Physician advice to stop smoking adds to the success of cessation efforts.

– Fiore et al., 2008

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Cessation Counseling

• Ask the patient if he or she uses tobacco. • Assess the patient’s interest in quitting.• Advise (Inform) the patient about the importance of quitting.

• Assist the patient by helping him or her pick to resources that can provide counseling and pharmacotherapy.

• Arrange a follow‐up phone call with the patient and referral to a smoking cessation resources

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Counseling Specifics

• Interventions including 4 or more sessions are particularly effective – Individual counseling,– Group counseling– Telephone follow up.

• Therapies with the highest success – Practical counseling coupled

with support – (Fiore et al., 2008).

• Structured programs can also be part of a comprehensive cardiac rehabilitation program.

• Referral to a formal nurse‐led smoking cessation program can improve the effectiveness of smoking cessation counseling by up to 61% (Gibbons et al., 2002).

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Pharmacological Agents:Nicotine Replacement

– Patch (OTC), gum (OTC), inhaler, and nasal spray – Improves cessation rates – Caution with very recent MI, worsening angina, and serious arrhythmias – not contraindicated in CAD

– Cardiovascular effects no worse than smoking• The use of nicotine‐replacement therapy can substantially improve smoking cessation success rates (Fiore et al., 2008).

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Pharmacological Agents:Nicotine Replacement

Benefits of maintenance and bolus dosing – Two combinations very effective

• Patch with the use of either gum or nasal spray• Patch with the inhaler (Fiore et al., 2008).

– Patch and lozenges

• NRT is not recommended– People who smoke less than 10 cigarettes per day– Those who use smokeless tobacco– Pregnant women, and adolescents.

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Pharmacological Agents:Bupropion

(Zyban and Wellbutrin)

• Can double rate of cessation compared to placebo – Started while smoking; quit date set for during 2nd week of therapy (1 week till therapeutic level).

– Therapy continued for 7 to 12 weeks • May be continued for up to six months

– Bupropion may also be used in conjunction with a nicotine patch (Fiore et al., 2008). 94

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Pharmacological Agents:Bupropion

(Zyban and Wellbutrin)

• Neuronal blockade of the re‐uptake of norepinephrine and dopamine

• Blockade of the nicotinic acetylcholinergicreceptors.

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Pharmacological Agents: Varenicline (Chantix)

• Selectively binds to nicotine acetycholine receptors in the brain – Binds to and partially stimulates the receptors without full nicotine effect on release of dopamine

– Blocks ability of nicotine to stimulate the central nervous mesolimbic dopamine system (system that reinforces smoking)

• Superior to Bupropion and placebo in achieving smoking cessation – FDA recommends that patients disclose any psychiatric history to their provider before the starting the medication, and that providers monitor for any behavior ore mood changes after starting a patient on the medication (Fiore, et al., 2008).

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Pharmacological Therapy: Varenicline (Chantix)

• 5 days to achieve steady state; set quit date 1 week from starting

• Started with low dose to prevent nausea • 12 weeks of initial therapy (starting month pack x 1 and continuing month pack x 2)

• Additional benefit with an additional 12 weeks of therapy

• Not used with nicotine replacement therapy

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ACC / AHA Guidelines for Secondary Prevention

• Complete smoking cessation – Ask – Advise – Assess – Assist – Arrange

• Avoidance of exposure to environmental smoke

• Pharmacotherapy

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Tips for Effectiveness

• Ask Permission – worth saying twice

• Congratulations on committing to QUIT

• A failed attempt at cessation should be viewed as practice for future successful cessation

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• Preparing patients for post discharge triggers

• Develop strategies for cravings

• Action plan for any slips or relapses

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• Involving significant others

• Address depression and weight gain

• Quit dates for women

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Referrals and Resources

• Inform patient of available quit line support 1‐800‐QUITNOW for access to all state quit lines. (Fiore et al., 2008).

• Additional on‐line resources available for patients can be found at http://smokefree.gov/

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Stages of Change

Assessing Readiness • Pre‐contemplation

• Contemplation

• Action

• Maintenance

After the Change • Sl ip

• Relapse

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Motivational Interviewing

• Accept ambivalence –The Importance Ruler –The Confidence Ruler

• Ask patient to elaborate • Use open ended questions

–Ask – don’t tell –The patient must own the idea to change

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Motivational Interviewing

• Focus on priorities • Listen reflectively • Support and encourage • Be a barrier remover • If committed – guide the patient in formulating a plan

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DYSLIPIDEMIA CVN Review Course

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Dyslipidemia • Hypercholesterolemia: Elevated total cholesterol – 50% of adults have cholesterol > 200 mg/d

– 20% of adults have cholesterol > 240 mg/dl

– There is a 20% to 30% increase in CHD ri sk for each 10% increase in serum cholesterol

• Elevated Low Density Lipoprotein Cholesterol (LDL‐C)

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LDL Cholesterol Treatment Goals

– For CHD or CHD risk equivalent: • Goal is < 100 mg/dl

– For 2 or > risk factors but not a risk equivalent : Goal is < 130 mg/dl

– For < than or equal to 1 major risk factor• Goal i s < 160 mg/dl *

New Optimal < 70

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Dyslipidemia

• Elevated Triglycerides – Borderline high or high triglycerides now cons idered an independent risk of CHD

– Borderline high to high levels: 150 mg/dl to 500 mg/dl

• Low High Density Cholesterol (HDL‐C)– The lower the concentration of HDL‐C the increased risk of CHD

– 2‐4% ri sk reduction for 1% increase in HDL

– HDL‐C < 40 = low – HDL‐C> 60 = high

• Associated with decreased risk of CHD

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Dyslipidemia

• Screening fasting lipid profile q 5 years • 50% of adult population and 10% of teenage children have are affected

• Primary Treatment Goal – Preventing and Treating Dyslipidemia – LDL primary goal for CAD and risk equivalents

• Secondary Treatment Goal –Treating Metabolic Syndrome

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Lipid Levels

Total LDL HDL Triglycerides< 200 desirable

< 100 (<70) optimal

< 40 low < 150 Normal

200-239 borderline

100-129 above optimal

> 60 desirable

> 240High

130-159 borderline high

160-189 high > 190 very high

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More on Lipids

• The size of LDL‐C particles is also important (small dense particles)

• VLDL: Very low density lipoprotein

• Combination of low LDL‐C and normal systolic BP very important to optimal outcomes!

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Cholesterol

• The cholesterol content of the liver is derived predominantly from three sources. – Synthesis of cholesterol by the liver – Uptake of cholesterol from the blood from circulating lipoproteins

– Uptake of cholesterol absorbed by the small intestine.

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% ReductionHMG CoA RI (statins) 20-50%

Bile acid resins 15-25%Nicotinic acid 15-30%

Gemfibrozil 10-15%FenofibrateIntestinal Absorption Inhibitors

10-25%18%

Effect of Drugs on LDL‐C Levels

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Effect of Drugs on Triglyceride and HDL‐C Levels

HDL-C TriglycerideNicotinic acid 10-25% 20-50%

Fibrates 10-25% 20-50%

HMG CoA RI 5-10% 10-25%

Bile acid resinsIntestinal Absorption Inhibitors

3-5%1%

0-20%8%

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New AHA Nutrition Guidelines

• Balance caloric intake and physical activity to maintain normal weight

• Eat diet rich in fruits and vegetables • Eat whole grain high fiber foods • Eat fish (oily) 2 x per week minimum • Limit saturated fat, trans fat, and cholesterol • Minimize food and beverages high in sugar • Use little or no salt • Consume alcohol only in moderation

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• LDL‐C < 100 mg/dL all patients • Further reduction LDL‐C< 70 mg/dL• If triglycerides > 200 mg/dL then non‐HDL‐C< 130mg/dL• If triglycerides > 500 mg/dL: treat before LDL‐C to prevent

pancreatitis

– Assess within 24 hours – Start therapy prior to discharge – Plant sterols and stanols

• 2 grams per day can decrease cholesterol by 15% – Omega 3 fatty acids

• 1 gram of EPA and DHA daily (fish preferred / supplements as alternative) • 2 to 4 grams daily for elevated triglycerides

– LDL – Lowering (Statins) – Non HDL‐C additional options Niacin and Fibrates117

HMG CoA Reductase Inhibitors (Statins)

• Agents – Atorvastatin (Lipitor) – Provastatin (Pravachol) – Fluvostatin (Lescol) – Simvastatin (Zocor) – Lovastatin (Mevacor) – Rosuvastin (Crestor)

• Mechanism of Action – Inhibition of HMG‐CoA reductase

– HMG –CoA reductase cata lyzes an early step in cholesterol biosynthesis

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• Decrease mortality• Reduce risk of major coronary events by 30%• Stimulate plaque regression

• Decrease LDL‐C (18‐55%); increase HDL (5 to 15%) and decrease triglycerides (7 to 30%)

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• Some agents most effective at bedtime (not all) – Highest rate of cholesterol synthesis between 12 midnight and 5 am

• Can be combined with nicotinic acid, fibric acid and bile acid sequestrants if necessary

• Best tolerated and overall most effective agents

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• Contraindicated in acute or chronic liver disease – Liver enzymes at 6 weeks and q 6 months

• Can cause myopathy and rhabdomyolysis • Patients must report muscle aching / weakness• Grapefruit juice interferes with metabolism and cause increased levels

• Can also cause cataracts

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Bile Acid Sequestrants (Resins)

• Used to treat elevated LDL‐C

• Agents – Cholestyramine (Questran)

– Colestipol (Colestid) – Covesevelam (Welchol)

• Mechanism of Action – Form insoluble complex with bile salts

– Stimulates production of more bile acid

– More LDL‐C receptors to remove LDL‐C from ci rculation

– Oxidation of cholesterol from LDL to form more bile salts

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Bile Acid Sequestrants (Resins)• Decrease LDL‐C (15 to 30%) and increase HDL‐C (3 to 5%)

without affecting triglycerides • Can be used with statins – but single drug therapy should

always be tried first • Do not give powder in dry form –mix with fluids • Tablets should not be cut, chewed, or crushed (needs to break

down in GI track)• SE: GI distress, constipation, malabsorption of vi tamins A, D, K • Contra indicated with biliary obstruction or abnormal

intestinal function; also contraindicated with elevated triglycerides

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Niacin

• Used to treat elevated LDL levels

• Agents: – Nicotinic Acid– Nicobid– Niaspan – Note: Niacin found in vitamin

supplements does not provide high enough dose

• Mechanism of Action – Decreases lipolysis of

triglycerides in adipose tissue

– Decreases hepatic triglyceride synthesis

– Reduces VLDL‐C production

– Lower LDL – C

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Niacin

• Decreases LDL‐C (5 to 25%); triglycerides (20 to 50%); and increases HDL‐C (15 to 35%)

• SE: flushing, hyperglycemia, gout, GI distress, and hepatotoxicity

• Flushing and dyspepsia are common limiting compliance

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Intestinal Absorption Inhibitors

• Selectively inhibits the intestinal absorption (small intestine) of cholesterol and related phytosterols

• Intestinal cholesterol is derived primarily from cholesterol secreted in the bile and from dietary cholesterol.

• Ezetimibe (Zetia) reduces total‐C, LDL‐C, Apo B, and TG, and increases HDL‐C in patients with hypercholesterolemia.

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Fibric Acids

• Indicated for hyperlipidemia with Hypertriglyceridemia.

• Agents – Clofibrate (Atromid‐S) – Fenofibrate (Tricor) – Gemfibrozil (Lopid)

• Mechanism of Action – Unclear – Decreases VLDL‐C synthesis

– Reduces triglycerides by s timulating lipoprotein l ipase activity

– Decreases hepatic TG production

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Fibric Acids Decreases TG 25‐50%

LDL decreases, remains the same, orincreasesIncreases HDL 15‐25% in hypertriglyceridemia

Tend to normalize LDL‐C particle composition, changing the atherogenic small, dense LDL particles to a larger, less dense, less atherogenic type.

This increase in LDL particle size may contribute to an increase in LDL‐C level while still reducing the risk for coronary atherosclerosis

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Fibric Acids

• SE: dyspepsia, rash, alopecia, fatigue, HA, impotence, anemia; myositis flu like syndrome, cholelithiasis, abnornal liver function studies

• Contraindicated in severe renal (renally excreted)and hepatic disease, pre‐existing gall bladder disease

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Statin plus Fibrate Combination Therapy• May be associated with a greater risk of myopathyand rhabdomyolysis

• The myopathy risk is enhanced under these situations:

‐ High doses of statins‐ Renal insufficiency (Cr > 2.0)‐ Concomitant medications:

Itraconazole, KetoconazoleCyclosporin AErythromycin

‐ Age > 70 years

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HYPERTENSION CVN Review Course

Hypertension • 1 in every 3 adults has hypertension (American Heart

Association Statistics, 2009).

• Almost 79% are aware that they have high blood pressure

• About 69% are under active treatment • Only 45% have their blood pressure under control• Each increase in 20 mm Hg for systolic blood pressure (SBP) or 10 mm Hg diastolic blood pressure (DBP) doubles the risk for a fatal coronary event (Rosendorff et al., 2007).

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Hypertension• Effective antihypertensive therapy reduces CHD risk but not back to baseline

• Blood pressure goals should be lower in patients who are diabetics or have renal disease

• Prevalence of hypertension is higher in African‐Americans– Other ri sk factors for the development of hypertension include family history, genetics, lower socioeconomic status, obesity, physical inactivity, psychological stress, dietary factors of high fat and sodium, high alcohol intake, and s leep apnea (American Heart Association Statistics, 2009).

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Joint National Committee

• Joint National committee on the prevention, detection, evaluation and treatment of high blood pressure

• Coalition of leaders from 46 agencies• Establish guidelines for treating hypertension• JNC 7 in May, 2003• Since that time the American Heart Association released a scientific statement in 2007: Treatment of Hypertension in the Prevention and Management of Ischemic Heart Disease.

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Joint National Committee: 7 Key Points

• People over age 50: SBP>140 a more important cardiovascular risk factor than high DBP

• People with normal blood pressure at age 55 have a 90% life time risk of developing hypertension

• Stricter guidelines of blood pressure classification• Thiazide diuretics are often first line treatment

– Note: Updated information • Two agents usually required• Patient motivation

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CLASSIFICATION OF BLOOD PRESSURE

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Hypertension

• Primary (essential) hypertension– Without known cause – 90 to 95% of hypertension in adults

• Secondary hypertension – Identifiable cause that can be corrected – More than 80% of hypertension in children

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Pathophysiology Primary Hypertension

– Excessive salt and water retention – Increased SNS activity– Increased vasoconstrictive response to circulating cathecholamines

– At any age HTN impairs endothelial function • Decreased production of nitric oxide

– Co‐existing Risk Factors • Vascular dysfunction predicts diabetes in patients with HTN • HTN and diabetes incrementally worsen endothelial function

– Complications: • Structural and functional changes

– Impaired coronary vasodilation – Impaired endothelial function – Inward remodeling and hypertrophy of vessels

» Increased risk cerebral bleed 138

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Identifiable Causes of Secondary Hypertension

• Adults • Chronic renal disease • Renovascular disease • Primary aldosteronism• Oral contraceptive use• Drug induced • Chronic steroid therapy and Cushing’s syndrome

• Pheochromocytoma• Coarctation of the aorta • Thyroid or parathyroid disease

– Children • Renal disease • Vascular problems

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Hypertension

• Clinical findings associated with secondary hypertension – Unexplained hypokalemia (primary aldosteronism) – Abdominal or renal bruits (renovascular disease) – Decreased BP in legs compared to arms (aortic coarctation)

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Systolic Hypertension

• Isolated systolic hypertension accounts for 70% in the elderly

• Systolic hypertension correlates with cardiovascular disorders more than diastolic hypertension

• Pulse pressure as predictor or coronary events • Clinical Application: The coronary arteries are perfused during diastole so it is important to maintain an adequate diastolic blood pressure.

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Hypertension Management

• Weight reduction

• Physical Activity

• Sodium restriction

• Alcohol intake reduction

• DASH Diet

Lifestyle Interventions

5 – 20 mmHg / 10 kg

4-9 mmHg

2-8 mmHg

2-4 mmHg

8-14 mmHg

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Pharmacological Management – Diuretics (Thiazide)– Thiazide diuretics are cost effective and have a relatively low risk of side

effects. The one concern about thiazide diuretics is the impact of thiazideinduced hyperglycemia and diabetes mellitus on long term CHD risk (Rosendorff, et al., 2007).

– ACE Inhibitors – Angiotensin II receptor blockers – Calcium Channel Blockers – Beta Blockers – Alpha Blockers – Centrally Acting Drugs – Direct Vasodilators – Many combination medications available for dual therapy

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Stage II Hypertension = 2 Drug Therapy

Thiazide diuretic plus another agent based on specific disease process or

other risks.

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Special Consideration Heart Failure

• LV dysfunction – asymptomatic – ACE Inhibitors – Beta Blockers

• Symptomatic ventricular dysfunction – ACE Inhibitors – Angiotensin Receptor Blockers – Beta Blockers – Aldosterone antagonists – Loop Diuretics

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Special Consideration Ischemic Heart Disease

• HTN and Stable Angina – Beta Blocker (alternative: long acting calcium channel blocker)

• HTN and ACS – Beta Blocker and Ace Inhibitor

• Post Myocardial Infarction – Beta Blocker– ACE Inhibitor – Aldosterone Antagonist – Lipid management – ASA therapy

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Special ConsiderationsElderly

• Target BP same as for younger adults • Systolic rather than diastolic is a better predictor of events

• Pseudo hypertension may occur due to excessive vascular stiffness

• Thiazide diuretics are preferred first line treatment• Long acting dihydropyridine calcium channel blockers also used

• Risk of orthostatic BP is high (always assess)

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Special ConsiderationAfrican Americans

• Highest prevalence and severity• Produce less renin and are not as receptive to ACE‐I, ARBs, or beta blockers as monotherapy

• Develops earlier in life with a higher blood pressure

• 80% higher stroke mortality rate• 50% higher heart disease mortality rate

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Special ConsiderationDiabetes

• HTN with insulin dependent diabetes mellitus and proteinuria– ACE Inhibitors (or ARB therapy)

• Often need two or more drugs to keep blood pressure under 130/80 to prevent vascular events

• Micro vascular complications:Type 1 Vis ion loss, nephropathy, neuropathyamputation

• Macrovascular complication:Type 2Coronary artery disease, stroke

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Special ConsiderationsRenal Disease

Three or more drugs needed to keep blood pressure less than 130/80 to reduce renal function deterioration

ACE‐I and ARBs effective in decreasing diabetic and non diabetic renal disease

Serum creatinine can be 35% above baseline without stopping the drug

Need for loop diuretics

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Special ConsiderationsCerebral Vascular Disease

• CVA: Control of blood pressure to about 160/100 to maintain adequate blood flow– Do not induce hypotension

• Use of ACE‐I and thiazide diuretics reduce rate of recurrent stroke

• Low dose aspirin should be considered in patients with history of uncontrolled HTN to reduce risk of cerebral hemorrhage

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Resistant Hypertension • Definition: A patient is considered to have resistant hypertension if he or she is on 3 or more medications at full‐dose therapy, including a diuretic and still unable to achieve target blood pressure.

• A patient is also considered to have resistant hypertension if it takes 4 medications to achieve goal (Calhoun et al., 2008).

Consultation withhypertension specialist

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Resistant Hypertension • Before the diagnosis of resistant hypertension is made, pseudo resistance must be ruled out.

• Common causes of pseudo resistance include the white coat effect, poor technique in taking blood pressure, or poor adherence by the patient to the prescribed regime. – Proper technique for blood assessment includes using a proper sized cuff that encircles 80% of the patient’s arm. Use of a cuff that is too small is one of the most causes of inaccurate readings, resulting a recorded measurement that is falsely high.

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Resistant Hypertension Causes • Lifestyle Related • High dietary sodium • Obesity • Heavy alcohol intake • Medication Related

– Non narcotic analgesics especially NSAIDs – Sympathomimetics (decongestants / diet pills) – Stimulants – Oral contraceptives – Glucocorticoids and mineralcorticoids– Herbals (ephedra / ma huang) – Natural licorice (found in smokeless tobacco)

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Resistant Hypertension Causes

• Secondary Diagnoses (Most Common)

• Obstructive sleep apnea • Chronic kidney disease • Primary aldosteronism• Renal artery stenosis

• Secondary Diagnoses (Less Common)

• Pheochromocytoma• Cushing’s disease • Hyperparathyroindism• Coarctation of the aorta • Intracranial tumor (Calhoun

et al., 2008)

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Treatment for Resistant Hypertension

• Focus on lifestyle interventions to reduce sodium intake, alcohol intake, and reduce body weight.

• Discontinue or decrease doses of drugs that are contributing to hypertension. Non‐steroidal anti‐inflammatory agents (NSAIDS) are one of the more common culprits.

• Screen for secondary diagnoses

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Treatment for Resistant Hypertension • Maximize pharmacological therapy:

– Maximize diuretic therapy with long acting thiazidediuretic. • Chlorthalidone is preferred agent in resistance.

– Consider addition of mineral corticoid antagonist such as spironolactone or eplerenone.

– Use loop diuretic if chronic kidney disease is present. – Combine medications that have different modes of actions.

• Recent research has shown favorable results when an ACE inhibitor or angiotensin receptor blocker is combined with a calcium channel blocker.

• Consider giving at least one antihypertensive at bedtime to achieve better overall control. (Calhoun et al., 2008).

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Nursing Considerations for Hypertension

• Dose reduction should be attempted after one year of controlled therapy

• Compliance– Cost – Side Effects

• Self Monitoring of BP • OTC Medications may

increase BP • Aggressive Risk Factor

Modification

Monthly follow up BP checks and medication adjustments until goal

More frequent for Stage 2 or co morbid conditions

Three – s ix month follow up after goal i s met

Serum K+ and creatinine twice annually

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• All hypertensive patients < 140/90 mmHg

• Diabetes and kidney disease < 130/80

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SLEEP APNEA AND CARDIOVASCULAR DISEASE

American Heart Association / American College of Cardiology July 2008

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Sleep Apnea

Obstructive Central• Repetitive interruption of

venti lation during sleep caused by collapse of pharyngeal airway.

• > 10 second pause in respiration associated with ongoing ventilatory effort

• Repetitive cessation of ventilation during sleep resulting from loss of ventilatory drive

• > 10 second pause with no associated ventilatory effort

• > 5 events per hour considered abnormal

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Sleep Apnea Syndromes

Obstructive Central • Apnea / hypoapnea index

(Number per hour of sleep)– > 5 and – Symptoms of excessive day

time sleepiness

• > 5 centra l apneas per hour of s leep and– Associated symptoms of

disruption of sleep (frequent arousals) and / or

– Hypersomnolence during the day

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Hypoapnea

• Decrease in but not complete cessation

• Fall in oxygen saturation or arousal from sleep– Fall in > 4% might be clinically significant

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Obstructive Sleep Apnea

Higher prevalence of following with OSA • HTN (resistant) • Type 2 diabetes • CV disease (nocturnal angina) • Atrial fib • Stroke

Difficult to tease out causative effect of these overlapping disorders • Overlapping risk factors for CV disease and OSA

Male gender and obesity are ri sk factors Not uncommon in women and non obeseAge is more associated than obesity with women

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Approximately 1 in 5 adults: mild Approximately 1 in 15 adults: moderate / severe15 million Americans > 85% have not been diagnosed Adverse consequences may be greater in those < 50 years. High prevalence of pathological daytime sleepiness in OSA Almost all with OSA snore but not all snorers have OSA

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OSA

• Pharyngeal airway from posterior nasal septum to epiglottis dependent on muscle activity for patency

• Collapse usually occurs posterior to tongue, uvula, or soft palate (or some combination)

• Etiology: anatomically small pharyngeal airway – Obesity – Bone and soft tissue structure – Tonsils / adenoids in children

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Compensation when Awake

Increase airway resistance

Increase negative pressure during inspiration

Mechanoreceptors in larynx respond:

Increase activity of pharyngeal dilator muscles

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During Sleep

• Airway narrowing or collapse

Reflex muscle activity is

reduced / lost

• Hypoxia and hypercapnea stimulate ventilatory effort and arousal occurs

Apnea or hypoapnea occurs

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Severe intermittent hypoxemia •Saturations < 60%

CO2 retention •Both interfere with normal autonomic and hemodynamic response to sleep

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Physiological Impact of Obstruction

Increased negative

intrathoracic pressure

Increased transmural gradient Ventricular

Dysfunction

Autonomic Instability

Hemodynamic Instability

Increased Afterload

Increased atrial size

Diastolic dysfucntion

Aortic dilation

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Physiological Consequences of Apnea

Endothelial Dysfunction

Systemic Inflammation

PrresssorSurges

Oxidative stress

SNS Activation

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Other Possible Physiological Consequences

1.

InsulinResistance

Platelet Activation

Increased Fibrinogen

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Central Sleep Apnea

• Crescendo – decrescendo pattern with central apnea or hypoapnea at the nadir

Associated with Cheyne Stokes

• Thought to be due to increased hypercapnic responsiveness combined with prolonged circulatory time

In Heart Failure: Unstable Ventilatory Control

• Idiopathic CSA can lead to obstructive events

Idiopathic central sleep apnea: Due to very steep ventilatory response

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Central Sleep Apnea

• May not be clinically recognized

• Requires full night polysomnogram

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Treatment for OSA General

Special Circumstances Weight loss Avoid alcohol and sedatives Behavior techniques if apnea is positional Oral appliance (2nd line) Uvulopalatopharyngealplasty

Limited efficacy CPAP as primary therapy

Pneumatic splint for pharyngeal airway Adherence to therapy is problem

Humidification Appropriate mask Addition of pressure ramp

• Aggressively treat HF – Fluid retention can

exacerbate obstruction

• Manage ischemia • Nocturnal diuresis or

more aggressive dia lysis in ESRD

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177

Treatment for CSA • Optimize management of heart failure

– Diuresis – Beta blockers may help modulate ventilatory response in HF

– ACE inhibitors potentially helpful • Caution side effect can exacerbate obstruction

• Nocturnal O2

• Potential other medications • CRT Therapy ? • Role of CPAP Unclear

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Other Modifiable Risk Factors

Physical Inactivity:

Inactivity associatedwith other risk factors

Fit but overweightpeople have risk similar to those without CHD risk

factors.

Stress:

Can cause coronary Vasoconstriction.

Catecholamine promote alterations in thrombosis

and coagulation to favor clot formation.

Alcohol:

Protective effects mediated through: Increase in HDL‐C, lower platelets and

fibrinolysis.

Alcohol abuse leads to hypertension and increased cardiac sudden death.

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• 30 (to 60) minutes: 7 days per week (aerobic) – Minimum 5 days per week

• Resistance training 2 days per week • Medically supervised rehab for high risk patients

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Alcohol and Prevention

• Light drinkers have lower blood pressure than both non drinkers and those who drink heavily

• The AHA recommends moderate alcohol consumption in appropriate individuals– No more than one alcoholic beverage per day for women – No more than two alcoholic beverages per day for men

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Additional Emerging Risk • Hyperhomocysteinemia • Hypercoagulability • Estrogen deficiency • Lipoprotein (a)• Oxidative Stress • LVH • Carotid intimal medial thickness; ankle‐brachial index • Coronary ca lcification score • Inflammatory Process

– hs‐CRP

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183

Hyperhomocysteinemia

• Increased homocysteine levels are independently associated with increased risk for cardiovascular disease – Produces endothelial toxicity – Accelerates oxidation of LDL‐C– Impairs endothelial derived relaxation factor – Causes decreased flow mediated arterial vasodilitation

The folate and B vitamin connection.

184

Hypercoagulability

• Fibrinogen is positively associated with:• Age• Obes ity • Smoking• Diabetes • LDL‐C

• Fibrinogen is inversely associated with: • HDL‐C• Alcohol abuse • Phys ical activity and exercise

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Hormone Replacement Therapy

• Estrogen + Progestin– Stopped in July 2002 – Risks > benefits

• Increased risk heart disease• Increased risk stroke • Increased risk breast cancer

• Increased risk dementia in greater than 65

• Decreased risk hip fracture

• Estrogen alone – Stopped March 2 2004 – Prel iminary ri sks > benefits

• Neutral heart disease• Neutral breast cancer • Increased risk stroke • Increased risk dementia in greater than 65

• Decreased risk hip fracture

Women’s Health Initiative

186

Hormone Replacement Therapy

The results of the Women’s Health Initiative have been challenged because the mean age of women enrolled in the study was 63 years.

There was a difference in response to HRT between younger and older women in the study.

The KEEPS (Kronos Early Estrogen Prevention Study) is currently in process to evaluate the potential HRT benefits in women aged 45 to 54.

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187

Left Ventricular Hypertrophy

• LVH increases with age, obesity and hypertension

• Independently associated with increased risk of cardiovascular disease

• Reduction of LV mass effective in reducing risk when accompanied by a decrease in BP

188

Apolipoprotein B and Lipoprotein(a)

• Apolipoprotein B (Apo B), the major protein constituent of LDL

• Lipoprotein (a) – Studies suggest + relationship between LP (a ) and vascular ri sk

• Limitations – Levels are elevated with acute ischemia– Lack of testing standardization – Unclear predictive value

LDL‐C and Lipoprotein (a)

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189

Oxidative Stress

• AHA recommendations include no use of supplements

• Antioxidants via fruits and vegetables

190

Inflammatory Process

• Inflammatory markers are released during acute phase of CHD – hs – CRP (high sensitivity C‐reactive protein)

– ICAM‐1 (adhesion molecules)

– IL‐6 (cytokine) – Tumor necrosis factor (cytokine)

• hs – CRP is a marker of risk

– Elevated hs‐CRP increases the relative ri sk for vascular events 3 to 4 times

– Elevated levels found in smokers and in healthy men with other risk factors

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Inflammatory Process

• Many infectious agents are thought to be possible culprits in vascular injury and inflammation

• Extravascular sources of chronic infection might be the culprit

Recent Results / Current Issues • Sodium reduction

– 70% of population – 1 gram reduction (800,000 l ife years 2010‐2019)

• Aspirin recommendations for primary prevention– Men > 45 years – Women > 55 years

• Power of low LDL‐C plus normal systolic • Non HDL as target • Benefits of exercise not sustained past 4 weeks • Neck thickness versus waist circumference • Endothelial vasomotor function • Short sleepers / nappers 192

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CVN Review Course

194194

Cerebrovascular Disease Approximately 780,000 strokes per year 600,000 are new strokes

> 160,000 deaths3rd leading cause of death Number one cause of disability. 15 – 30% of stroke survivors are left wit a permanent disability.

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195195

Stroke Risk Factors

• Hypertension• Cigarette smoking• Diabetes • Hyperlipidemia• Physical inactivity • Increased body weight /

abdominal fat • Excessive alcohol use• Oral contraceptive use

• Age

• Gender

• Race ethnicity

• Heredity

196196

Other Condition with Increased Risk for Stroke

• Previous TIA • Vascular bed disease • Migraine HA • Sleep apnea • Hypercoagulability • Sickle cell disease

• Atrial fibrillation • Dilated myopathy • Extensive MI • Valvular heart disease (endocarditis)

• Cardiac surgical procedures

• Congenital heart defects

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197197

Conditions with Increased Risk for Stroke

• Previous TIA • Vascular bed disease • Migraine HA • Sleep apnea • Hypercoagulability • Sickle cell disease

• Atrial fibrillation • Dilated myopathy • Extensive MI • Valvular heart disease (endocarditis)

• Cardiac surgical procedures

• Congenital heart defects

Risk f actors for CVA similar for those f or CAD: Hypertension most important risk factor!

198198

Prevention of Stroke

Gorelick PB. Stroke. 1994;25:220-224.

~23,5004.71.687.2Heavy alcohol consumption

~47,0009.43.603.98Atrial fibrillation

~61,50012.31.5227.0Cigarette smoking

~246,50049.32.7356.2Hypertension

Projected No. of Strokes Prevented

Estimated Population‐attributable Risk, %

EstimatedRelativeRisk

EstimatedPercent Exposed

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199199

Prevention of Stroke

• Antiplatelet therapy – Aspirin – Clopidogrel

• Carotid endarterectomy / stenting • HRT (not indicated)

200

Risk Factors for PAD

• Cigarette smoking – 80% of PAD patients

• Diabetes • Dyslipidemia • Hypertension • Hyperhomocysteinemia

– 30‐40% PAD patients

• Increased C reactive protein • Age

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201

Medical Conditions and Symptoms for High Risk

• CAD • Carotid / cerebrovascular disease • Renal artery stenosis

• Leg pain (claudication or rest) • Abnormal pulse assessment

ANATOMY / PHYSIOLOGY / AND ASSESSMENT

CVN Review Course

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203 203

Neuro Anatomy

• Cerebral hemispheres • Diencephalon

– Thalamus – Hypothalamus – Limbic system

• Bra instem – Midbrain – Pons – Medulla

• Cerebellum

204204

Cerebral Hemisphere Key Functions

• Left – Analysis – Problem solving – Language – Mathematics – Abstract reasoning

• Right – Spatial relationships – Non verbal communication

– Music – Artis tic ability

Corpus Callosum

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205205

206206

Cerebral Lobes: Key Functions

• Frontal: Voluntary motor function, intellectual function, personality

• Temporal: Memory function and emotion • Parietal: Sensory function, object recognition and position sense, body awareness and image

• Occipital: Visual reception

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207 207

Cerebral Circulation • Two internal common carotid arteries anteriorly

– Provide the major blood supply to the brain– Arise from the common carotids– Supply optic nerves, retina, and the majority of the

cerebral hemispheres– Divides into: Anterior cerebral artery and middle

cerebral artery• Two vertebral arteries posteriorly

– Arise from right and left subclavian arteries.– Merge to form basilar artery; basilar artery divides

into two posterior cerebral arteries.– Supplies the cervical cord, brainstem,medulla,

cerebellum, caudal part of diencephalons, medial and posterior temporal lobes, and the occipital lobes

208 208

Cerebral Circulation

• Circle of Willis ‐ an anatomical ring of vessels joining the carotid artery system and the vertebrobasilar system.

• Posterior communicating artery.

• Posterior cerebral artery.• Anterior communicating artery.

• Anterior cerebral artery.

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209209

Anatomy Application

Middle Cerebral Artery Most common intracerebral

vessel affected by stroke

210 210

Cerebral Circulation • Two internal common carotid arteries anteriorly

– Provide the major blood supply to the brain– Arise from the common carotids– Supply optic nerves, retina, and the majority of the

cerebral hemispheres– Divides into: Anterior cerebral artery and middle

cerebral artery• Two vertebral arteries posteriorly

– Arise from right and left subclavian arteries.– Merge to form basilar artery; basilar artery divides

into two posterior cerebral arteries.– Supplies the cervical cord, brainstem,medulla,

cerebellum, caudal part of diencephalons, medial and posterior temporal lobes, and the occipital lobes

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211 211

Cerebral Circulation

• Circle of Willis ‐ an anatomical ring of vessels joining the carotid artery system and the vertebrobasilar system.

• Posterior communicating artery.

• Posterior cerebral artery.• Anterior communicating artery.

• Anterior cerebral artery.

212212

Anatomy Application

Middle Cerebral Artery Most common intracerebral

vessel affected by stroke

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213

Heart Anatomy

• Muscular organ• 4 Chambers• Blunt Cone‐shaped

• Located between the sternum and spine – Mediastinum

214

Heart Anatomy

• Base– 2nd intercostal space– Behind Sternum

• Apex – 5th intercostal space – mid‐clavicular l ine.

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215

Chambers Of The Heart

• 4 chambers • Atria

– Right Atria– Left Atria

• Ventricles– Right ventricle– Left Ventricle

• Divided by:– Interatrial septum– Interventricular septum

216

Ventricles Of The HeartRight ventricle

– thin‐walled• 3‐5 mm

– Low pressure pump– Pumps blood to the

lungs

Left ventricle– thick‐walled

• 8‐15 mm– High pressure pump– Pumps blood to all

other parts of the body

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217

Cardiac Anatomy – Structure

(Visceral Layer of Pericardium)

218

Layers Of The Heart Wall

• Pericardium – Layered sac – Surrounds and protects the heart

– Serous Pericardium• Visceral layer• Parietal layer

– Fibrous Pericardium

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219

Layers Of The Heart Wall

• Pericardial Space– Pericardial Fluid

• Serous fluid • 10‐30 ml• Reduces friction as the heart moves

• Sac in which to move during contraction

220

Blood Flow Through the Heart

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221

Right Sided vs.

Left Side System

222

The Coronary Arteries • Layers of Arteries –Intima–Media–AdventitiaPlaque forms between the intima and media (donut analogy)

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223

Veins

• Layers of Veins– Intima–Media–Adventitia–Valves

224

The Coronary Arteries • Left Main Coronary Artery (LM)

– Left Anterior Descending Artery (LAD)– Diagonal Branch

– Left Circumflex Artery (LCA)– Obtuse Marginal (OM)

• Right Coronary Artery– Marginal Branch – Posterior Descending Artery

• (PDA)– Concept of dominance

• 80% of hearts RCA dominant

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The Coronary Arteries • LAD

– Anterior LV– Septum (anterior 2/3)– Apex of LV

• LCA– Lateral LV (OM)– Posterior LV (OM)

• RCA– Inferior LV (marginal)– Septum (posterior 1/3)– Right Ventricle (marginal)– Posterior LV (PDA)

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The Coronary Arteries

Anterior LV LADLateral LV LCA (OM)Posterior LV RCA (PDA)

LCA (OM)Inferior LV RCA (marginal)Septum LAD

RCA (PDA) Right ventricle RCA

(marginal/ PDA)

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The Coronary ArteriesConduction System Supply

• SA node RCA in 55% (LCA in 45%)

• AV node RCA in 90% (LCA in 10%)

• Bundle Branches LAD

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Pathophysiology of Coronary Arteries

• Ischemia starts in the endocardium, moves outward, then laterally

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The ElectronicsAction Potential of Cardiac Cells • Phase 0: Rapid depolarization• Phase 1: Brief, rapid initiation of repolarization

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The Electronics Action Potential of Cardiac Cells • Phase 2: Slowing of the repolarization• Phase 3: Sudden acceleration in the rate of repolarization• Phase 4: Resting membrane potential

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The Electronics Conduction System

• Sinoatrial Node (SA)

• Internodal atrial conduction tracts

• Interatrial conduction tract • Atrioventricular node (AV) • Bundle of His• Atrioventricular (AV) junction

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The ElectronicsConduction System

• Left Bundle Branch

• Right Bundle Branch

• Purkinje Network

• Purkinje Fibers

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The Valves

• Purpose –Permit Antegrade Flow

–Prevent Retrograde Flow

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Heart Valves

• 4 Valves in the heart. • AV Valves

– Tricuspid– Mitra l (bicuspid)

• Semilunar Valves– Pulmonic– Aortic

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AV (Atrioventricular) Valves

• Tricuspid– Between right atrium and right ventricle

– Larger, but thinner– 3 cusps

• Mitral– Smaller– 2 cusps– Between left atrium and left ventricle

• Both have fibrous rings• Both have Cordae Tendineae• Both have papillary muscles

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AV Valves

• Chordae Tendineae– Tendon like fibrous cords that connect the pointed ends of the va lves to the papillary muscles that are located on the inner surface of the ventricles.

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Semilunar Valves

• Semilunar valves:– Pulmonic

• Between the right ventricle and pulmonary trunk

– Aortic• Between the left ventricle and aorta

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Semilunar Valves

• Three cusps • Leaflets are smaller and thicker than the AV valves

• Openings are smaller than the AV valves

• The velocity of ejected blood is higher than AV valves.

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Neurologic Control of the Heart

• Autonomic Nervous System– SNS– PNS

• Chemoreceptors• Baroreceptors

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Neurologic Control of the HeartAutonomic Nervous System

• Both divisions of the autonomic nervous system extend into the heart

• The atria are innervated by both parasympathetic and sympathetic fibers

• The ventricles are almost entirely innervated by sympathetic fibers only

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Autonomic Nervous System

• Sympathetic Nervous System– Fight or flight– + chronotropic– + dromotropic– + inotropic – Alpha, Beta1, Beta2 and Dopamanergic responses

Sympathetic Nervous System Adrenergic Receptors and Effects

Alpha Receptors (Alpha1) Located in VesselsVasoconstriction of most vessels especially the arterioles

• β1 Receptors– Located in the heart– Increases heart rate

(chronotropic)– Increases conductivity

(dromotropic)– Increase contractility

(inotropic)– Increase automaticity– Increase conduction velocity

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Sympathetic Nervous System Adrenergic Receptors and Effects

• β 2 Receptors– Located in bronchial and

vascular smooth muscle– Causes bronchial dilatation– Causes arterial vasodilatation

to skeletal muscle – Causes renin release and

therefore activation of the RAAS

• Dopaminergic Receptors (D1) – Located in renal and

mesenteric artery bed– Dilation of renal and

mesenteric arteries


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Autonomic Nervous System

• Parasympathetic (Vagal) nervous system– Maintains a steady state– Causes – chronotropic, ‐dromotropic effects– Causes minimal decrease in inotropic effects– Primarily slow heart rate and conduction– Cardiovascular effects of PNS generally undesirable

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Chemoreceptors

• Located in carotid and aortic bodies• Sensitive to changes in PaO2, PaCO2, and pH.• in pH or O2 or in CO2 SNS response• in pH or in CO2 PNS response

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Baroreceptors

• Located in the carotid sinus and aortic arch• Sensitive to arterial wall tension• Cause reflex response in either SNS or PNS• Decrease BP SNS (adrenergic) response• Increase BP PNS (cholinergic) response• Vagal Maneuvers slow heart rate

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Contraction of the Myocardium(Ability to shorten and to develop force)

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Hemodynamic Principles for Practice

Cynthia Webner DNP, RN, CCNS, CCRN, CMCKaren Marzlin DNP, RN, CCNS, CCRN, CMC

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Paradigm Shift

• Hemodynamics does not equalinvasive monitoring

One must be comfortable with shades of grey!!

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Flow is determined by:

√Pressure √ Resistance √ Volume

The Heart as a PumpGoal: Forward propulsion of blood to perfuse the body.

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Right Sided versus Left Sided System

CNEA / Key Choice

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Basic Hemodynamic Formula

Cardiac Output

Heart Rate X Stroke Volume

Preload Afterload Contractility

Same four components also determine myocardial oxygen demand

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Preload

The ventricle is preloaded for ejection.


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Preload • End‐diastolic stretch on myocardial muscles

fibers• Determined by:

– Volume of blood filling the ventricle at end of diastole

– Greater the volume the greater the stretch (muscle fiber length)

– Greater the stretch the greater the contraction

– Greater the contraction the greater cardiac output

TO A POINT

CNEA / Key Choice

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Non Invasive Assessment of Preload

Right Ventricular • JVD• Hepatojugular reflux

• Peripheral edema *• Weight*

Left Ventricular • Orthopnea / PND/ Dyspnea • Rales/crackles

– Consider role of lymph drainage • S3 Gallop• Frothy sputum• Hypoxemia from decreased

diffusion of oxygen

• Weight*


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Measuring JVD• Raise HOB 30 – 45 degrees

• Internal preferred • May use external • Use tangential light• Use centimeter ruler• Difficult to assess if HR>100

CNEA / Key Choice

• Normal JVP level is < 3 cm above the sternal angle

• Sternal angle is 5cm above right atrium

• JVP of 3 cm + 5cm = estimated CVP of 8cm H2O

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Estimated CVP> 8 cmH2OIncreased blood volumeUsually RV failureTricuspid valve regurgitationPulmonary hypertension

CNEA / Key Choice

JVD (Jugular Venous Distension)

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Additional assessment tip: Sitting or standing patient up to see top of column.

CNEA / Key Choice

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Jugular Vein Carotid Artery No pulsations palpable. Palpable pulsations.Pulsations obliterated by pressure above the clavicle.

Pulsations not obliterated by pressure above the clavicle.

Level of pulse wave decreased on inspiration; increased on expiration.

No effects of respiration on pulse.

Usually two pulsations per systole (x and y descents).

One pulsation per systole.

Prominent descents. Descents not prominent.Pulsations sometimes more prominent with abdominal pressure.

No effect of abdominal pressure on pulsations.

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Factors Influencing Preload• Body Position• Venous Tone• Intrathoracic pressure• Intrapericardialpressure

• Dysrhythmias • Atrial Kick• LV Function

• Circulating blood volume – Hypervolemia– Hypovolemia– Third spacing

• Distribution of blood volume– Sepsis– Anaphylaxis– Venous vasodilators

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Afterload

After the ventricle is loaded, it must work!


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Afterload

• Pressure ventricle needs to overcome to eject blood volume

• Left ventricle: – Systemic vascular resistance – Other components

• Valve compliance• Viscosity of blood• Arterial wall compliance

– Aortic compliance

• Right ventricle: – Pulmonary vascular resistance

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BP and Afterload

• Blood pressure does not equal afterload

•Blood Pressure (MAP) = •Cardiac Output x Systemic Vascular Resistance (Afterload)


BP = CO x SVR• Low BP could be due to:

–Low CO• HR too slow or too fast• Preload too low or too high• Contractility low

–Low SVR• Vasodilation due to sepsis, anaphylaxis, altered neurological function, drugs


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Blood Pressure Monitoring

• Definitions:–BP = CO X SVR

• Always determine etiology of hypotension

– Systolic: Maximum pressure when blood is expelled from the left ventricle

– Diastolic: Measures rate of flow of ejected blood and vessel elasticity

– Pulse Pressure: Difference between systolic and diastolic pressure

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Cardiac Assessment

• Blood Pressure

– Variation of up to 15mm Hg between arms is normal– BP in legs ‐10 mm Hg higher than arms

– Narrowed pulse pressure –vasoconstriction• Innervation of sympathetic nervous system

– Hypovolemic shock– Widened pulse pressure –vasodilitation

• Excessive vasodilatory mediator release– Septic shock

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More on Vascular Tone

• Increased vascular tone is usually associated with compensation for low SV – Acute Cardiogenic shock – Hypovolemic shock

• Decreased vascular tone is usually due to abnormally pathology – Sepsis – Anaphylaxis – Altered neurological control


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Causes of Increased LV Afterload

– Arterial vasoconstrictors– Hypertension – Aortic va lve stenosis – Increased blood viscosity – Hypothermia – Compensatory vasoconstriction from hypotension in shock

– Arterial vasodilators – Hyperthermia– Vasogenic shock states (sepsis and anaphylactic) where the body cannot compensate with vasoconstriction

– Aortic Regurgitation –hyperdynamiccardiac output therefore lowering systemic vascular resistance

Causes of Decreased LV Afterload

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Increased Right Sided Afterload • Pulmonary hypertension

– mPAP > 25 mmHg or > 30 mmHg with exercise – PVR > 250 dynes/sec/cm‐5

• Causes – Hypoxemia – Acidosis – Inflammation– Hypothermia – Excess sympathetic s timulation – Pulmonary endothelial dysfunction

• Impaired nitric oxide and prostacyclin (PGI2) release – Primary pulmonary hypertension

CNEA / Key Choice

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Contractility

• Ability of myocardium to contract independent of preload or afterload

–Velocity and extent of myocardial fiber shortening

–Inotropic state

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Contractility

• Related to degree of myocardial fiber stretch (preload) and wall tension (afterload).

• Influences myocardial oxygen consumption• contractility

myocardial workload myocardial oxygen consumption

CNEA / Key Choice

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Important Points about Contractility • No accurate way to measure contractility

• Low cardiac output does not necessarily mean diminished contractility (i .e. hypovolemia)

• Correct preload and afterload problems first in a patient with a low ejection fraction.

• Increasing contractility with medications will also increase myocardial oxygen demand.

CNEA / Key Choice

Noninvasive Assessment: Ejection Fraction

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Factors Altering Contractility• Decreased contractility

– Excessive preload or afterload

– Drugs –negative inotropes– Myocardial damage– Ischemia– Cardiomyopathy– Hypothyroidism– Changes in ionic

environment:hypoxia, acidosis or electrolyte imbalance

• Increased contractility– Drugs

• Positive inotropes

– Hyperthyroidism– Adrenal Medulla Tumor

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Contractility • Low cardiac output does not necessarily mean diminished contractility

• Correct preload and afterload problems first

Medications which increase

contractility impact not only

cardiac output but also myocardial oxygen demand.

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Heart Rate

• Mathematically heart rate increases cardiac output

• Physiological limit where increased heart rate will decrease cardiac output due to decreased filling time (decreased preload)

• Consider as first line strategy to increase cardiac output when temporary pacemaker in place

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The Art of Auscultation

• Quiet room• Quiet patient• Quiet visitors• Stethoscope• Bell vs. diaphragm• Systematic Approach

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Rules to Consider – Left‐sided vs Right‐sided events

Left‐sided heart events• Precede right‐sided events• Are normally louder than

right‐sided events• Normally loudest during

expiration (right‐sided events loudest during inspiration)

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Auscultatory Areas

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• Diastole

– Passive Ventricular Filling• S3

– Active Ventricular Filling• Atrial Kick –S4

– Valves Open• Mitral • Tricuspid• Don’t open well

– Stenosis

– Valves Closed• Aortic • Pulmonic• Don’t close well

– Regurgitation

• Systole– Isovolumiccontraction– Ejection of LV Contents

– Valves Open:• Aortic• Pulmonic• Don’t open well

– Stenosis– Valves Closed

• Mitral• Tricuspid• Don’t close well

– Regurgitation

Heart Sounds – the Basis for the sounds

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Basic Heart SoundsS1

• Closure of the Mitral (M1) valve and the Tricuspid (T1) valve

• Beginning of Ventricular Systole and Atrial Diastole

• Location: Mitral area • Intensity: Directly related to force of contraction

• Duration: Short• Quality: Dull• Pitch: High

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Basic Heart SoundsS2

• Closure of Aortic (A2) and Pulmonic (P2) Valve

• End of Ventricular Systole• Location: Pulmonic area• Intensity: Directly related to closing pressure in the aorta and pulmonary artery

• Duration: Shorter than S1• Quality: Booming• Pitch: High

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Diastolic Filling Sounds S3 ‐ Ventricular Gallop

• Early diastolic filling sound • Caused by increased pressure and

resistance to filling.• Most frequently associated with systolic

dysfunction• Associated with:

– Fluid overload state– Right or left ventricular failure– Ischemia– Aortic regurgitation– Mitral regurgitation

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Diastolic Filling Sounds S3 ‐ Ventricular Gallop

• Patient position: left lateral decubitus position

• Location:– Left‐sided S3 – mitral area.– Right‐sided S3 – tricuspid area.

• Intensity– Left‐sided heard best during

expiration.– Right‐sided heard best during

inspiration.• Duration: short.• Quality: dull, thud like.• Pitch: low.• May be normal in children, young

adults (up to 35‐40) and in the 3rd trimester of pregnancy.

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Diastolic Filling Sounds S4 ‐ Atrial Gallop

• Late diastolic filling sound • Caused by atrial contraction and the

propulsion of blood into a noncompliant (stiff) ventricle.

• Most frequently associated with diastolic dysfunction

• Associated with: – Fluid overload state– Systemic hypertension– Restrictive cardiomyopathy– Ischemia– Aortic stenosis– Hypertrophic cardiomyopathy

• May be normal in athletes286

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Diastolic Filling Sounds S4 ‐ Atrial Gallop

• Patient position: left lateral decubitus position.

• Location– Left‐sided S4 –mitral area.– Right‐sided S4 –tricuspid area.

• Intensity– Left‐sided louder on expiration.

– Right‐sided louder on inspiration.

• Duration: Short• Quality: Thud like• Pitch: Low

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MURMURS

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Murmur FundamentalsTurbulence

• Murmur: If turbulence is intracardiac

• Bruit: If turbulence is extracardiac

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Murmur FundamentalsCauses of Turbulence

Forward flow through a stenotic valve

Backward flow through an incompetent valve

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Murmur FundamentalsCauses of Turbulence

• Flow through a septaldefect or an AV fistula

• Flow into a dilated chamber or a portion of a vessel

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Murmur Fundamentals

• Stenotic Murmurs– Valve does not open appropriately– Heard during the part of the cardiac cycle when the valve is open

• Regurgitant Murmurs– Valve does not close appropriately– Heard during the part of the cardiac cycle when the valve is to be closed

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Murmur Fundamentals

• Timing– Systolic

• Holosystolic• Ejection (midsystolic)• Late

– Diastolic• Early• Middiastolic• Late

• Location– Place heard the loudest

• Radiation– Direction in which murmur radiates

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Murmur Fundamentals

• Configuration– Crescendo

• Gets louder– Decrescendo

• Gets softer– Crescendo –Decrescendo

• Louder then softer– Plateau

• Even intensity throughout

• Pitch– High Pitched ‐diaphragm– Low Pitched –bell

• Quality– Soft– Harsh– Blowing– Musical– Rumbling– Rough

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Systolic Murmurs

• Tricuspid and Mitral Valve Closed– Tricuspid Regurgitation– Mitra l Regurgitation

• Pulmonic and Aortic Valve Open– Pulmonic Stenosis– Aortic Stenosis

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Aortic StenosisSystolic Ejection Murmur

• Timing: Midsystolic• Location: Best heard over

aortic area• Radiation:Toward right

side of neck• Configuration:Crescendo‐

decrescendo• Pitch: Medium to high • Quality: Harsh

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Pulmonic StenosisSystolic Ejection Murmur

• Timing: Midsystolic• Location: Best heard over pulmonic area

• Radiation: Left neck of left shoulder

• Configuration:Crescendo‐decrescendo

• Pitch: Medium • Quality: Harsh

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Systolic MurmursMitral Regurgitation

• Timing: Holosystolic• Location: Mitral area• Radiation: To the left axilla

• Configuration: Plateau• Pitch: High• Quality: Blowing, harsh or musical

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Systolic MurmursTricuspid Regurgitation

• Timing: Holosystolic• Location: Tricuspid area• Radiation: To the right of

sternum• Configuration: Plateau• Pitch: High• Qual ity: Scratchy or

blowing

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Diastolic Murmurs

• Diastolic regurgitant murmurs– Retrograde flow across an incompetent semilunar valve

• Diastolic filling murmurs– Forward flow across stenotic or obstructed AV valves

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Diastolic Murmurs

• Tricuspid and Mitral Valves Open– Tricuspid Stenosis– Mitra l Stenosis

• Pulmonic and Aortic Valves Close– Pulmonic Regurgitation– Aortic Regurgitation

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Diastolic MurmursAortic Regurgitation

• Timing: Early diastole• Location: Aortic area• Radiation: Toward apex• Configuration:Decrescendo

• Pitch: High • Quality: Blowing

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Diastolic MurmursPulmonic Regurgitation

• Timing: Early diastole• Location: Pulmonic area Erb’s Point

• Radiation: Toward apex• Configuration:Decrescendo

• Pitch: High • Quality: Blowing

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Diastolic MurmursMitral Stenosis

• Timing: Mid to Late diastole

• Location: Mitral area• Radiation: None• Configuration:Crescendo

• Pitch: Low • Quality: Rumbling

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Diastolic MurmurTricuspid Stenosis

• Timing: Mid to Late diastole

• Location: Tricuspid area• Radiation:None• Configuration:

Decrescendo• Pitch: Low • Quality: Rumbling• Increases during

inspiration and decreases during expiration

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Other SoundsPericardial Friction Rub

• Timing: Systolic, Early diastolic and late diastolic• Location: Tricuspid area and Xyphoid area• Radiation:None• Configuration: Plateau• May get louder during inspiration• Pitch: High• Quality: Grating, scratching

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Other SoundsVentricular Septal Defect or Rupture

• Timing: Continuous• Location: 3‐4 LSB• Radiation: Widely throughout the precordium

• Configuration: Plateau• Pitch: High• Quality: Harsh

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Systolic vs Diastolic Dysfunction

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Systolic Dysfunction

• Impaired wall motion and ejection

• Dilated chamber • 2/3 of HF Population• Hallmark: Decreased LV Ejection Fraction< 40%

• Coronary artery disease is cause in 2/3 of patients

• Remainder –other causes of LV dysfunction

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Cardiomyopathy not synonymous with HF

Diastolic Dysfunction

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• Filling impairment • Normal chamber size• 20 to 40% of patients with HF have preserved LV function

• Normal EF or elevated• Caused by

– Hypertension– Restrictive myopathy– Ischemic heart disease– Ventricular hypertrophy– Valve disease– Idiopathic

Primarily disease of elderly women with HTN

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Diastolic Dysfunction

• Diagnosis is made when rate of ventricular filling is slow

• Elevated left ventricular filling pressures when volume and contractility are normal

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In practice: the diagnosis is made when

a patient has typical signs and symptoms of heart failureand has a normal or elevated ejection fraction with

no valve disease.

Left and Right Sided Heart Failure • Two sides of the heart form a circuit, neither side can pump significantly

more blood than the other for long• Signs/symptoms of failure reflect each respective ventricle

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Left‐Sided Heart Failure• Decrease in CO/stroke volume• Pressure rises in the LV, LA,

and pulmonary vasculature• Hydrostatic forces can cause

intracellular fluid to accumulate in the pulmonary capillary bed (pulmonary congestion)

• Signs/symptoms result from elevated pulmonary pressures (SOB/paroxysmal nocturnal dyspnea)

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Right‐Sided Heart Failure• Typically follows LS failure• Isolated RV failure (COPD, pulmonary hypertension)

• Pressure increases in the RS of heart• Hydrostatic pressures force more blood into the systemic venous circulation

• Causing neck vein distention, peripheral edema, weight gain, engorgement of hepatic and gastric vessels

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Backwards Failure: Pulmonary Congestion

Forwards Failure: Hypoperfusion


Ventricular Remodeling• Process of pathological growth

• Can occur from prolonged activation of SNS/RAAS

• InvolvesHypertrophy of myocytes

Pressure – thicken (concentric)Volume – elongate (eccentric)

Genetically abnormal – inefficient contractionIncreased ventricular muscle mass, change in ventricular shapeCollagen matrix becomes fibrotic

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Apoptosis (a component of remodeling)

Preprogrammed cell death without inflammation/scarring (necrosis)Process is accelerated in HF but in a random patternCell slippageBricks –myocytes Morter – collagen Degredation (slippage) or Fibrotic 317

Key Assessment Considerations in PAD

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Assessment: History

• Walking impairment • Classic claudication • Rest pain (recumbent position) • Poor healing of lower extremity wounds • Abdominal discomfort after eating • Family history of 1st degree relative with AAA

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Physical Assessment

• Bilateral arm pressure • Carotid pulse assessment • Palpation of abdomen

– Pulsatile mass

• Auscultation for bruits • Peripheral pulse assessment (0 to 3) • Inspection of feet / nails

– Distal hair loss – Hypertrophic nails

Check capillary refill in non dependent position

Verify pulses with Doppler

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Ankle Brachial Index • Most objective measure of lower extremity PAD • Does not correlate strongly with walking impairment

• Systolic in brachial arteries, posterior tibial, and dorsalis pedis arteries – Supine resting position fro 10 minutes

• Ankle pressure should be 10 to 15mmHg higher than brachial pressure

• Normal ABI> I.0

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Indications for Resting ABI

• Exertional leg symptoms• Non healing wounds • > 70 years • > 50 years with history of smoking or diabetes

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Ankle Brachial Index • Above 0.9 = Normal • 0.71 – 0.9 = Mild disease • 0.41 – 0.7 = Moderate disease • < 0.40 = Severe disease • Patients with ABI > 0.5 are not likely to progress to critical limb ischemia

• Toe Brachial Index – Non compressible arteries

• Exercise Ankle Brachial Index – Normal ABI

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Other Diagnostic Studies • Continuous Wave Doppler Ultrasound

– Velocity waveforms and systolic blood pressure at sequential segments– Location and severity of disease, quantitative improvement

• Lower extremity duplex ultrasound – Peak systolic velocity ratios – Location and degree of stenosis – Follow up after surgical revascularization – Aneurysms and dissections

• Abdominal ultrasound – Aortic and abdominal aneurysms

• MRA / CTA – Aortic and abdominal aneurysms– Lower extremity PAD

• Contrast angiography – Gold standard – Contrast induced nephropathy

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Claudication • Definition

– Ischemic pain during exercise– Speci fic leg muscle groups – Rel ieved in 2 to 3 minutes– Reproducible, stable

• Prevalence – Most common symptom – Symptoms only in 20% of patients with PAD

• Location – Gastrocnemius muscle – Relation of pain to location of disease

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Claudication: Differential Diagnosis

• Lumbar disc disease (sciatica) • Spinal stenosis • Osteoarthritis • Muscle pain • Neuropathy • Chronic compartment syndrome • Venous obstructive disease

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Key Assessment Considerations in Ischemic Stroke

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328328

Key Signs and Symptoms

• Numbness • Confusion • Slurred speech / difficulty speaking

• Sudden visual problems • Loss of balance / coordination

• Severe dizziness • Sudden severe HA

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FAST

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Sample Face Arm Speech Test

Facial palsy affected sideArm weakness affected side

Speech impairmentTime of onset

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Symptoms: Left (dominant hemisphere)

• Left gaze preference• Right visual field deficit• Right hemiparesis• Right hemisensory loss

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Symptoms: Right (nondominanthemisphere)

• Right gaze preference• Left visual field deficit• Left hemiparesis• Left hemisensory loss neglect (left hemi‐inattention)

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Symptoms: Brainstem

• Nausea and/or vomiting• Diplopia, dysconjugate gaze, gaze palsy• Dysarthria, dysphagia• Vertigo, tinnitus• Hemiparesis or quadriplegia• Sensory loss in hemibody or all 4 limbs• Decreased consciousness• Hiccups, abnormal respirations

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Symptoms: Cerebellum

• Truncal/gait ataxia• Limb ataxia, neck stiffness

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Symptoms: Hemorrhage

• Focal neurological deficits as in AIS• Headache (especially in SAH)• Neck pain• Light intolerance• Nausea, vomiting• Decreased level of consciousness

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Questions in Expected Stroke • Time patient last known well (will be used as presumed time of onset)• Time symptoms were first observed (if different from time last known

well)• Was anyone with patient when symptoms began? If so, who?• History of diabetes?• History of hypertension?• History of seizures?• History of trauma related to current event?• History of myocardial infarction or angina?• History of cardiac arrhythmias? Atrial fibrillation?• History of prior stroke or TIA?• What medications is patient currently taking? Is patient receiving

anticoagulation therapy with warfarin?

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PHARMACOLOGY CVN Review Course

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Antiarrhythmic Medications Effecting the Action Potential

• Class I – Fast sodium channel blockers– IA:Quinidine, Procainamide, Disopyramide– IB: Lidocaine, Mexiletine, Tocainide – IC: Flecainide, Propafenone

• Class III – Potassium channel blockers – Amiodarone, Ibutalide, Dofetalide, Sotalol

• Class IV – Calcium channel blockers– Verapamil, Diltiazem

Class II ???

Effects of Class 1 Antiarrhythmics

• All Class 1 antiarrhythmics by definition block the fast sodium channel – Different drugs do this to a di fferent degree

– IC > IA > IB

• Blocking of the fast sodium channel interferes with rapid depolarization and decreases conduction velocity – This will increases the duration of the cardiac action potential

– Note: This effect is seen in the action potential of the purkingefibers but not in the action potential of the nodal tissue

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Benefits of Reducing Rate and Degree of Depolarization

• Decrease in conduction velocity in non‐nodal tissue is called negative dromotropy.

• This is suppress reentrant tachycardiasbecause reentrant tachycardias are caused by abnormal conduction.

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Effects of Class 1 Antiarrhythmics • In addition to blocking the fast sodium channel (Phase 0) –

some class I agents also block the potassium channel (Phase 3)

• Potassium channel blockade directly affects the duration of the cardiac action potential and the effective refractory period.

• Benefits and disadvantages of effecting refractory period – Beneficial in reentrant tachycardias– Can increase risk for Torsades

• Different drugs do this to a different degree– IA (increase refractory period) > IC (no effect) >

IB (decrease refractory period)

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Effects of Class 1 Antiarrhythmics

Depression of Automaticity

• Can suppress abnormal automaticity

• Not related to sodium channel effect

• Mechanism not fully understood

Anticholinergic Effect

• Strong inhibitors of vagal activi ty

• Offsets some of benefit (i.e. an increase ventricular rate during the treatment of atrial arrhythmias)

• Can increase SA rate and conduction through the AV node

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Class I A AntiarrhythmicsAction Potential

Depresses Phase O of Action Potential; Inhibits influx of sodium in the f ast channel of the cardiac cell membrane

Also blocks Phase 3 of the Action Potential (blocks potassium ef f lux)

Actions Slows conduction v elocity (including over accessory pathways) Increases the recov ery period af ter repolarization; Effective ref ractory period prolonged; slightly prolongs QT (greatest ef f ect of all Class 1 antiarrhythmics) Can hav e anticholinergic effect Decreases automaticity, excitabilityCan hav e a negativ e inotropic effect

Cautions See indiv idual drugs

Uses Atrial f ib / f lutter Ventricular tachy cardia

Drugs Quinidine Procainamide (Pronesty l) Disopy ramide (Norpace)

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Class I A AntiarrhythmicsQuinidine Effective antimalarial agent (S.E. cinchonism (blurred vision,

tinnitus, headache, psychosis); cramping and nausea)Anticholinergic effects - increase ventricular rate in A fib / flutter Enhances digoxin toxicity

Procainamide (Pronesty l)

Anticholinergic effects less pronounced Indications: Stable monomorphic or polymorphic VT with preserved ventricular function Can be used along with class IC drugs in WPW tachycardiasS.E. – Lupus like syndrome

Disopy ramide(Norpace)

Significant anticholinergic effects (l imits uses) Significant negative inotropic effect IV form not approved in US. (Has been used to convert atrial arrhythmias). Only used for suppression of life threatening v entricular arrhythmias

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Class I B AntiarrhythmicsAction Potential

Blocks Phase O of Action Potential; inhibits influx of sodium the f ast channel of cardiac cell membrane (least suppression of the sodium channel of all three groups of Class 1 drugs). Does not block Phase III of the cardiac action potential

Actions Slows conduction v elocity (the least of class I antiarrhythmics) Actually decreases refractory period Suppresses automaticity but not in the SA nodeSuppresses spontaneous depolarization in the v entricle Acts pref erentially on ischemic tissueNo anticholinergic properties

Cautions Heav ily metabolized in liv er; toxicity manifested neurologically

Uses Acceptable f or stable monomorphic or poly morphic VT (Acceptable f or impaired v entricular function)Not f or prophy laxis of arrhythmias post infarction

Drugs Lidocaine; Mexiletine (Mexitil); Tocainide (Tonocard)

Chart based on Lidocaine:

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Class I B AntiarrhythmicsLidocaine Parenteral administration only; Can give via E-Tube

during code Amiodorone considered first for pulseless ventricular tachycardia or ventricular fibrillationGood efficacy in ischemic tissueCNS: Effects confusion, numbness or tingling of l ips or tongue, blurred vision

Mexiletine (Mexitil)

Orally active lidocaine analogUsed in treatment of l ife threatening ventricular arrhythmias (good efficacy in ischemic tissue) Also used to treat diabetic neuropathy pain

Tocainide (Tonocard)

Orally active lidocaine analogTablets were discontinued in US 12/31/2003Potential fatal hematological side effect of agranulocytosis; can also cause pulmonary fibrosis

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Class I C Antiarrhythmics

Action Potential

Potent inhibition of fast sodium channel; decrease in maximal rate of phase 0 depolarization

Actions Slow His-Purkinge conduction and cause QRS widening; QT interv als are also usually prolongedNo ef f ect on refractory period

Cautions Proarrhy thmic effects

Uses Lif e threatening v entricular arrhythmias Conv ersion to SR (Flecainide)

Drugs Flecainide (Tambocor) Moricizine (Ethomozine) Propof enone (Rhy thmol)

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Class I C AntiarrhythmicsFlecainide(Tambocor)

Not a first l ine agent for ventricular arrhythmias Will slow conduction over accessory pathways in WPW tachycardiasUsed in atrial fibril lation (pil l in the pocket) CAST Trial: propensity for fatal proarrhythmic effects Not used post MI or with depressed LV function

Moricizine(Ethmozine)

CAST studies: Reserved for l ife threatening ventricular arrhythmias Has properties of class I B also

Propafenone(Rhythmol)

Used in supraventricular arrhythmias and life threatening ventricular arrhythmias Also has small beta blocking actions and calcium channel blocking effects that can worsen HF Must be initiated in hospital setting to monitor ECG

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A Closer Look at Antiarrhythmics

– Beta blockers– Depresses SA node automaticity– Increases refractory period of atrial and AV junctional tissue to slow conduction

– Inhibits sympathetic activity– “lol” medications – Sotalol (Class II and III)

Class II

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Cardiovascular Indications for Beta Blockers

• Hypertension • Angina • AMI • Post Infarction • Supraventricular

arrhythmias • Ventricular arrhythmias

• Aortic Dissection • Hypertrophic cardiomyopathy

(actually increase C.O.) • Mitral valve prolapse• Prolonged QT syndrome • Heart failure • Digitalis induced ventricular

arrhythmias


Beta Blockers

• Nonselective: Block both Beta 1 and Beta 2

– Propranolol (Inderal)– Timilol (Blocadren)– Nandolol (Corgard)– Sotolol (Betapace)– Carvedilol (Coreg)

(also alpha blockade)

• Cardio selective: Block Beta 1– Acebutolol (Sectral)– Metoprolol (Lopressor)– Atenolol (Tenormin)– Esmolol (Breviblock)– Bisoprolol (Z Beta) – Nebivolol (Bystol)

(also nitric oxide vasodilatory properties)


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Class III Antiarrhythmics

Action Potential

Inhibits potassium ion f luxes during phase II and III of the action potential

Actions Directly on myocardium to delay repolarization (prolongs QT); prolongs ef fective refractory period in all cardiac tissue; By definition act only on repolarization phase and should not impact conduction

Cautions Proarrhy thmic Effects (amiodarone less)

Uses Drug dependent

Drugs Amiodarone (Pacerone, Cordorone) Ibutilide (Corv ert) – pure class III Dof etilide (Tikosyn) – pure class III Sotalol (Betapace)

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Class III AntiarrhythmicsAmiodarone (ARRESTTrial)

Approved for l ife threatening refractory ventricular arrhythmias; considered before lidocaine in pulseless VT or V fib; considered ahead of l idocaine for stable VT with impaired cardiac function; expanded to atrial and ventricular arrhythmias, conversion and maintenance of atrial fib Slows conduction in accessory pathways Originally marketed as anti-anginal (potent vasodilator) Relaxes smooth and cardiac muscle, reduces afterload and preload (well tolerated in heart failure and cardiomyoapthy) Proarrhythmias less frequentIs also a weak sodium channel blocker, also has effects similar to class II and IV, also has anticholinergic properties

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Amiodarone Dosing • Life‐threatening ventricular arrhythmias

– Rapid loading infusion 150 mg administered at a rate of 15 mg/minute (over 10 minutes); initial infusion rate should not exceed 30 mg/minute

– The slow loading phase is 360 mg at a rate of 1 mg/minute (over 6 hours)– First maintenance phase of the infusion is 540 mg at a rate of 0.5 mg/minute

(over 18 hours).– After the first 24 hours, maintenance infusion rate of 0.5 mg/minute should be

continued; the rate of the maintenance infusion may be increased to achieve effective arrhythmia suppression.

– In the event of breakthrough episodes supplemental infusions of 150 mg administered at a rate of 15 mg/minute (over 10 minutes) may be given.

• For cardiac arrest secondary to pulseless ventricular tachycardia or ventricular fibrillation– Initial adult loading dose is 300 mg (diluted in 20–30 mL of a compatible IV

solution) given as a single dose, rapid IV

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More on Amiodarone

• Nursing Considerations– Peripheral IV concentration not to exceed 2mg/ml – Oral administration / GI symptoms – Severe adverse reactions (potentially lethal interstial pneumonitis –

CXR q 3 ‐6 mos); less common in lower doses; Thyroid dysfunction is also a side effect (by weight amiodarone is 37% iodine)

• Toxic side effects increase with length of use

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Ibutilide (Corvert)

Indicated for rapid conversion of atrial fib or flutter to sinus rhythm; IV use only; also facil itated cardioversion (Don’t convert atrial fib or flutter of duration without anticoagulation) Rather than blocking outward potassium currents –promotes influx of sodium through slow inward sodium channel

Dofetilide (Tykosin)

More “pure” class III agent Conversion to and maintenance of SR in A fib and flutter Reserved for very symptomatic patients, monitored 3 days in hospital Widens the QT; cannot be given with many other drugs (prolong QT or inhibit metabolism or elimination); no negative inotropic effects, neutral effect on mortality from arrhythmias post MI and in in HF, can be used in this population to prevent worsening HF from atrial fib

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Sotalol (BetapaceR) (Betapace AF)

Used in atrial arrhythmias and life threatening ventricular arrhythmias Indicated for stable monomorphic VT or Polymorphic VT with normal QT in ACLS protocolNon selective beta blocking agent with class III properties Significant class III effects are only seen at doses >160 mg Proarrhythmic potential (prolonged QT) More effective in preventing reoccurring arrhythmias than several other drugs

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Newer Antiarrhythmic

• Dronedarone (Multaq)– Rejected by FDA 2006 – Approved by FDA 2009– Decreases hospitalizations in atrial fibrillation

• Not permanent atrial fibrillation – Proposed safer alternative to amiodarone in terms of extra cardiac side effects

• Iodine content – Black box warning for HF – FDA warning regarding hepatic injury

More on Dronederone

• PALLAS Trial – Dronederone in permanent atrial fibrillation – Stopped early due to adverse outcomes in dronederone arm

– Adverse outcomes were cardiovascular in nature and not hepatic in nature

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Class IV Antiarrhythmics – Phase II of Action Potential– Depresses automaticity in the SA and AV Junction – Increases the refractory period at the AV junction– Decreases contractility– Calcium Channel Blockers– Verapamil (SA Node), Cardizem (AV Node)

A Closer Look at Calcium Channel Channel Blockers


Decrease HR

Decrease Contractility

Decrease Afterload

Note: Not all calcium channel blockers are created equal: theref ore not all calcium channel blockers hav e the same actions

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A Closer Look at Calcium Channel Channel Blockers

• Three potential effects of Calcium Channel Blockers– Cardiac Muscle Contractility

• Blocks inward flow of calcium in Phase II of action potential and decreases force of contraction

– Cardiac Conduction• Depresses automaticity and velocity and decreases HR

– Vascular Smooth Muscle Relaxant• Coronary artery dilatation and increases blood flow to coronary arteries (except nifedipine)


A Closer Look at Calcium Channel Blockers

Verapamil Dihydropyridines Diltiazem

Heart Rate ▼▼ ▼

AV Nodal Conduction

▼▼ ------ ▼

Contractility ▼▼ ▼ ▼

Arterial Vasodilatation

2011CNEA / Key Choice 362

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Calcium Channel Blockers: Indications

• Atria l Fibrillation / Flutter and PSV– Diltiazem and Verapamil

• Treatment of angina in combination with beta blockers and nitrates – Diltiazem and Verapamil with

Nitrates – “Ines” with Beta Blockers

• Hypertension (decreases SVR) – “ines”

• Adjunct treatment for diastolic not systolic heart fa i lure

• Hypertrophic cardiomyopathy (verapamil)

• Prevention of coronary spasm for patients undergoing PCI


A Closer Look at “Ine” Calcium Channel Blockers

• Newer DihydropyridinesCalcium Channel Blockers– Amlodipine (Norvasc)– Effects vascular smooth muscle with minimal to no effect on heart rate or conductivity

– Good decrease in total peripheral vascular resistance– Directly dilates coronary arteries (nitric oxide release)


Caution with Nifedipine

Amlodipine in Heart Failure

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Adenosine (Adenocard)

• Slows conduction through the AV Node• Vasodilator • Interrupts reentry pathways through the AV node and restores sinus rhythm

• Uses: Paroxsysmal SVT, AVNRT, Drug stress testing

• Side Effects: Headache, arrhythmias (blocks), SOB, chest pressure

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Adenosine• Nursing Considerations:

– Use cautiously in patients with asthma – could cause bronchospasm

– Onset IV: Immediate– Peak: 10 sec– Duration 20‐30 seconds– Dosing for conversion of arrhythmia:

• 6mg IV rapid push• If no change within 1‐2 minutes repeat with 12mg rapid push• Not indicated in WPW

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Digoxin

• Inhibits the NA+ and K+ membrane pump▼

• Increase in intracellular Na+▼

• Enhances the Na+ and Ca++ exchange▼

• Leads to ▲in intracellular Ca++▼

• ▲inotropic activity

3672011 CNEA / Key Choice

Digoxin

• Increases vagal activi ty • Digoxin decreases conduction velocity through the AV node

(sympathetic stimulation easily overrides the inhibitory effects of digoxin on AV node conduction)

• The conduction velocity increases in the atria, but decreases in the AV node.

• Automaticity i s also increased, in the atria, AV node, Purkinje fibers and ventricles.– Calcium channel blockers are replacing digoxin as agent for rate

control in atrial arrhythmias – Digoxin no better than placebo in converting atrial fib to SR

• Digoxin decreases sympathetic outflow and decreases renin production – Beneficial in heart failure


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Digoxin • Indications

– HF – Atria l arrhythmias (older indication)

• Still an option when BP is a concern

• Contraindication / cautions– Acute MI – Ventricular arrhythmias, HB, Sick Sinus Syndrome – Obstructive Hypertrophic Cardiomyopathy – Electrolyte abnormalities (decreased K+, Ca++ and Mg++)


Digoxin

• Has a narrow therapeutic range • Toxicity may occur at therapeutic levels • Lower doses now routinely used 0.125 mg daily• Amiodorone increases serum digoxin concentration (digoxin doses must be reduced if starting amiodarone)

• Multiple other medication interactions • Dialysis is not effective with digoxin toxicity because of high tissue binding of digoxin


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More About Digoxin Toxicity

• EKG Changes with Toxicity – Increased automaticity with with impaired conduction is common (example: PAT with AV Block)

• Other Signs and Symptoms of Toxicity – N & V, HA, Confusion– Visual disturbances: halos, change in color perception


Thiazide Diuretics

– Inhibit reabsorption of Na+ and Cl‐• In the distal tubule.

– Delayed onset but longer duration of action than loop diuretics

– Low ceiling diuretics – Less potent diuretic than loop diuretics– Diminished effectiveness in presence of renal failure


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Thiazide Diuretics Bendrofluazide (Naturetin) General side ef fects of

thiazide diuretics:

Blood Chemistry changes:Hypokalemia (↓ K+)Hyperglycemia (↑ blood sugar)Hyperuricemia (↑ uric acid)Hypercalcemia (↑ Ca++)Decreased glomerular filtration in kidneys (↑ BUN, creatinine)↑ cholesterol↑ triglycerides↓ HDL cholesterol

Other side effects:Impaired glucose toleranceGoutImpotenceVentricular arrhythmias (↓ K+)Nausea, dizziness, headache

Benthiazide (Aquatag, Exna)

Chlorothiazide (Diuril)

Chlorthalidone (Hygroton)

Cyclothiazide (Anhydron)

Hydrochlorothiazide (HCTZ) (HydroDiuril, Esidrix)

Hydroflumethazide (Saluron, Diucardin)

Indapamide (Lozol)

Metolazone (Zaroxolyn)

Polythiazide (Renese)

Trichlormethiazide (Metahydrin, Naqua)

2011CNEA / Key Choice 373

Loop Diuretics

• Work in ascending loop of Henle • Loss of H2O, K+, Na+, Cl‐, H+• More loss of H2O and less K+ and Na+ than thiazides• Promotes venous vasodilatation • Rapid onset and short duration • Can be effective in presence of renal failure• High ceiling diuretic


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Loop Diuretics


Bumetanide (Bumex) General side effects of loop diuretics:

Blood Chemistry changes (less severe than with thiazides):

Hypokalemia (↓ K+)Hyperglycemia (↑ blood sugar)Hyperuricemia (↑ uric acid)↑ cholesterol↑ triglycerides↓ HDL cholesterol

Other side effects:GoutDiabetesOtotoxicity (deafness, reversible)

Furosemide (Lasix)

Torsemide (Demadex)

A Closer Look at ACE Inhibitors and Angiotensin II Receptor Blockers


Afterload and preload reduction

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A Closer Look at ACE Inhibitors

• ACE Inhibitors impact afterload and preload because they block the vasoconstrictive effects of angiotensin II – Very important in reducing workload of left ventricle in systolic dysfunction

• ACE Inhibitors additionally assist with preload reduction by blocking the effects of aldosterone release


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A Closer Look at ACE Inhibitors and

Angiotensin II Receptor Blockers

• Angiotensin‐converting enzyme inhibitors (“pri l ” medications)

– Captopril, Enalapril, Lisinopril, Quinapril, Ramipril, Benazepril, Fosinopril

• Angiotensin II Receptor Blockers (“sartan” medications)

– Losartan, Irbesartan, Candesartan,Telmisartan,Valsartan, Eprosartan


A Closer Look at ACE Inhibitors• The effects of blocking the Renin Angiotensin Aldosterone system are complex: – Overa ll cardioprotective and vasculoprotective effect – Improved balance of myocardial oxygen supply and demand by decreasing left ventricular preload and afterload

– Reduction of left ventricular mass in LV hypertrophy – Can decrease the progression rate of kidney failure especially in insulin dependent diabetics

– Kinins and Prostaglandins


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A Closer Look at ACE Inhibitors

• Influences bradykinin and can produce cough • Cough is side effect in 10‐20% of patients • Need to assure cough is not sign of worsening heart failure

• Patient may need changed to ARB


Absolute Contraindication!

A Closer Look at ACE Inhibitors • Can cause acute renal failure in patients with bilateral renal artery stenosis – Di lating efferent glomerular arterioles which result in decreased glomerular filtration

• Renal function – Evaluated prior to and 1‐2 weeks after initiation of ACE inhibitors in high ri sk patients

• If acute kidney injury develops from ACE – I, then hydralazine in combination with isosorbide dinitrate should be used– Combination achieves venous and arterial vasodilitation)


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Clinical Effects of Aldosterone

• Promotes retention of sodium • Promoted loss of potassium and magnesium • Potentiates catecholamines • Inhibits the parasympathetic nervous system • Decreases arterial compliance • Promotes direct remodeling • Has prothrombotic properties • Causes vascular inflammation and injury


Spironolactone (Aldactone) • Non selective aldosterone blocker

– Blocks aldosterone and androgen; stimulates progesterone

• Side effect of hyperkalemia when used with ACE Inhibitor or ARB

• Morta l ity reduction


Major side ef f ect: gynecomastia, sexual dysfunction and menstrual problems due to non selectiv ity

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Eplerenone (Inspra) • Selective aldosterone receptor antagonist

• Side effect of hyperkalemia when used with ACE Inhibitor or ARB

• Indicated in MI with LV Dsyfunction – Prevent progression of heart failure – Prevent sudden cardiac death – Prevent recurrent MI


Eliminates most gy necomastia and sexual side effects associated with aldactone

Anticoagulants

• Unfractionated Heparin

• Low Molecular Weight Heparin

• Direct Thrombin Inhibitors

• Factor Xa Inhibitors

• Warfarin (Coumadin)

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A Closer Look at Heparin • Prevents conversion of prothrombin to thrombin by binding to

anti thrombin I II• Anti thrombin I II naturally inhibits thrombin; when heparin

binds with it the inhibition i s increased 1000 times • Neutra lizes the clotting capabilities of thrombin• Works in the intrinsic and common pathway• Also Inhibits platelets (thrombin is most potent platelet

stimulator) • Anticoagulation is almost instant• ½ l i fe relatively short • Antidote: Protamine 1 mg per 100 units

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More About Heparin • aPTT (activated partial thromboplastin time) is used to monitor effectiveness and safety

• Goal is aPTT 1.5 Xs the control • Weight based heparin dosing reaches goal 90% of time compared to 77% with standard therapy

• Baseline aPTT, PT/INR, platelets and CBC• Increased bleeding can occur with renal failure

– Heparin has dual clearance mechanism but greater effect on platelet function than LMWH

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Complications of Heparin • Bleeding• Mild thrombocytopenia

– Mild thrombocytopenia occurs in 10‐20% of patients• Severe thrombocytopenia occurs in 1‐2% of patients

– Platelet aggregation resulting in venous or arterial thrombosis

– Determining patients at ri sk is unpredictable – Generally occurs 5 to 10 days after initiation of heparin– DC heparin i f platelets fall below 100,000– Severe thrombocytopenia is due to an immune response (HITTS)

• No additional heparin including line flushes

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More on HIT

• Heparin – dependent platelet activating antibodies – Recognize a self protein (platelet factor 4: PF4) that is bound to heparin

• This results in platelet activation and increased thrombin generation

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A Closer Look at Low Molecular Weight Heparin

• Low Molecular Weight Heparin (Lovenox) – Enoxaprin, dalteparin, tinzaparin, and nadroparin– Smaller in size – Anti thrombin by inhibiting factor Xa– Causes less inactivation of thrombin and less inhibition of platelets and less bleeding than standard heparin

– Does not significantly influence bleeding time– Anti Xa levels can be drawn 4 hours after SQ dose – Renal failure results in increased ri sk of bleeding because LMWH i s renally cleared

• Special dosing for chronic renal insufficiency with enoxaparin

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Benefit of Low Molecular Weight Heparinover Unfractionated Heparin

• More predictable anticoagulant response• Lower incidence of heparin induced thrombocytopenia

• Lower incidence of osteoporosis • No need to monitor APTT• Less platelet activation• Can be self administered with Sub – Q administration• ½ life 4‐6 hours • Protamine reverses 60% of drug effect

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Administration of Enoxaparin • Full length of 27 gauge ½

needle (prepackaged) should be injected

• Skin fold held until needle withdrawn

• Use anterolateral or posterorlateral walls of abdomen

• Rotate sites frequently • Do not massage site

• Prevention of DVT – 30 mg BID or 40 mg daily– 40 mg daily in most situations

• Venous thrombosis / DVT – 1mg/kg BID or 1.5 mg/kg daily

depending of specific circumstances • Unstable Angina / NSTEMI (or as

adjunct in STEMI) – 1 mg/kg BID – IV dosing can be used in STEMI

• Embolism with Atrial Fib – 1 mg/kg BID

• Dosing adjustments are required in several renal impairment

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Direct Thrombin Inhibitor

• Indicated for patients with HITTS• Approved in Non STEMI guidelines and for PCI • Ability to inactivate fibrin bound thrombin• Less binding to plasma proteins, therefore more reliable anticoagulation effect

• Examples– Lipi rudin and desirudin (hirudin)– Argatroban– Biva lirudin* (Angiomax)

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Synthetic Factor Xa Inhibitor• Fondaparinux (Arixtra)

– Used for venous thromboembolism and PE – Approved for DVT prophylaxis in certain surgical patients– Recently approved and added to NonSTEMI Guidelines – Cannot be used as sole anticoagulant during PCI

• Neutra lizes Factor Xa and interrupts the clotting cascade• Does not inhibit thrombin• No reported HIT • Sub Q injection• Once daily dosing (fixed dose can cover a range of body

weights – lower dose for low body weight) • Contra indicated in severe renal dysfunction • No laboratory monitoring• No antidote (Recombinant factor VIIa can help reverse

anticoagulation effect)395

A Closer Look at Coumadin

– Inhibits the synthesis of prothrombin.– Acts indirectly through the liver by altering the synthesis of vitamin K dependent factors in the extrinsic pathway. The vitamin K dependent factors are left biologically inactive.

– It takes 4‐5 days to reach a therapeutic level.• Can have initial transient hypercoagulable s tate • Must be overlapped with heparin

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More About Coumadin • PT (prothrombin time

monitored to evaluate effectiveness and safety)

• PT – problems with standardization of anticoagulation intensity

• INR (International Normalized Ratio) –relates the patients PT to the intensity of actual coagulation.

• Dosing– Start with 5mg per day– Loading doses not recommended – PT / INR daily until therapeutic

level reached – Dosage may need adjusted after

4‐6 days due to individual sensitivity

– PT / INR twice weekly for 2 weeks and weekly for two months

– PT / INR every 4‐6 weeks after dose stable

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More About Coumadin

• Goal for INR of 2.0 – 3.0 is adequate in most situations

• INR of 2.5 – 3.5 is goal for mechanical prosthetic valves and prevention of recurrent MI

• Chronic condition require lifelong therapy • Acute conditions (PE, DVT) usually require at least six months of therapy

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Nursing Considerations with Coumadin

• Many many drugs interact with coumadin to alter PT

• Consistency in diet is important especially with known high vitamin K foods (green vegetables)

• Patient compliance is critical

• Antidote: Vitamin K • Fresh frozen plasma if

severe hemorrhage • Recombinant factor VIIa is

also an option for l ife threatening bleeding

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Dabigatran

• Oral direct thrombin (factor I Ia) inhibitor– Is a prodrug (dabigatran etexilate) that i s converted in l iver to active form

– Peak plasma levels in 1.5 hours; half‐life 14‐17 hours– El iminated mostly by kidneys (reduced dose for moderate renal

failure, not recommended in severe renal failure)

– No known reversal agent• Predictable dose‐response relationship so no lab monitoring of coagulation status needed

• Dose:– 110 mg PO bid (shown not inferior to warfarin) or 150 mg PO bid (shown superior to warfarin)

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Dabigatran• Study results compared to warfarin:

– Rate of bleeding less than warfarin with 110 mg dose and about the same with 150 mg dose of dabigatran

• One area of concern GI Bleed

– Hemorrhagic stroke significantly lower with dabigatran

• Indicated for reduction of stroke in patients with AF at intermediate or high risk of stroke.

• Specific patient considerations– Can’t or won’t comply with warfarin monitoring requirements– Have inconsistent response to warfarin– Take multiple medications that can interact with warfarin

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Rivaroxaban• Oral direct factor Xa inhibitor

– Maximum plasma level in 3 hours– Half‐l ife 4‐9 hours (up to 12 hrs if > 75 years old)– Dose 10 mg PO daily– Few drug interactions– Excreted by kidneys (contraindicated in severe renal failure)

• Predictable dose‐response relationship so no lab monitoring needed

• Approved firstly in Europe and Canada for prevention of VTE after hip and knee surgery

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Rivaroxaban• ROCKET AF

– Double‐blind randomized trial– 14,264 patients with nonvalvular atrial fibrillation (at increased risk for stroke)

– Rivaroxaban(at a daily dose of 20 mg) or dose‐adjusted warfarin.

– P<0.001 for noninferiority of rivaroxaban– no significant between‐group difference in the risk of major bleeding, although intracranial and fatal bleeding occurred less frequently in the rivaroxabangroup.

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Antiplatelet Drugs

• GP IIb/ IIIa Inhibitors

• ADP Antagonists

• Thromboxane A2 Inhibitor

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A Closer Look at Antiplatelet Drugs: GP IIb/IIIa Inhibitors

• GP IIb/IIIa Inhibitors– Eptifibitide (Integrelin)– Tirofiban (Aggrastat)– Abciximab (Repro)– Inhibit the glycoprotein protein IIb/IIIa receptors which platelets and fibrinogen bind with to form the fibrin mesh

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More about GP IIb / IIIa Inhibitors

• Glycoprotein 2b / 3a receptors are most abundant protein on the platelet surface. It is tightly packed on the platelet surface with about 80,000 receptors per platelet. Primary receptor for platelet aggregation.

• Fibrinogen links to these receptors and simultaneously binds receptors on two separate platelets. Platelet cross‐linking occurs leading to platelet aggregation.

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A Closer Look at ADP Inhibitors: A Type of Thienopyridine

Clopidogrel (Plavix)

– Inhibit ADP which is released by platelets.

• ADP enhances adhesiveness and aggregation of platelets by activating GPIIb/ IIIa receptors.

– Concern with Proton Pump Inhibitors

– Res istance concern

Prasugrel (Effient)

– Inhibit ADP which is released by platelets.

• ADP enhances adhesiveness and aggregation of platelets by activating GPIIb/ IIIa receptors.

– Greater anti‐ischemic protection (compared to clopidogrel)

– Increased bleeding risk – Not able to use with prior

stroke or TIA, small body size, or advanced age

– Able to give with PPIs

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Triton TIMI 38

Ticagrelor (Brillinta) • Better anti‐ischemic effect compared to clopidogrel

• No significant increase in major bleeding• PLATO trial • Faster onset and shorter duration than clopidogrel (known as reversible mode of action)

• BID dosing is a potential concern for compliance • Although shorter ½ life – recommendation to be held 5 days before surgery.

• Cannot be given with more than 100 mg ASA daily.

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A Closer Look at Aspirin

• ASA– Inhibits Thromboxane A2 which is released with vascular injury. Platelet reactivity is diminished.

– Also inhibits the endothelium’s production of prostaglandin I2 which decreases platelet aggregation and induces vasodilation.

– Caution with asthma

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