Cardio Function 2015

ASSESSMENT OF CARDIOVASCULAR FUNCTION

Nelia B Perez RN, MSPCU - MJCN

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LECTURE OBJECTIVES

1. Review anatomy & physiology of the cardiovascular system.

2. Discuss relevant aspects of the patient history.

3. Describe physical assessment of cardiovascular status.

4. Review diagnostic procedures, tests and medications relative to the cardiovascular system.

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Anatomy & Physiology

Functions of the heart & CV system

• Pumps blood to tissues to supply O2 & nutrients

• Remove CO2 & metabolic wastes

(What makes it “tick”!)


CARDIAC CELLS HAVE UNIQUE PROPERTIES

• AUTOMATICITY CELLS CONTRACT INDEPENDENTLY (THEY INITIATE THEIR OWN IMPULSE)

• EXCITABILITY ION SHIFT• CONDUCTIVITY TRANSMIT

IMPULSE TO ANOTHER CARDIAC CELL

• CONTRACTILITY HOW WELL THE CELL CONTRACTS



PERICARDIUM / PERICARDIAL SAC

• Protects heart from trauma• Serous fluid lubricates and prevents friction• Prevents heart from over filling



CORONARY ARTERIES

Right & Left arteries encircle the heart and supply blood to the myocardium

during ventricular relaxation( diastole)LEFT MAIN CORONARY ARTERY

L ANTERIOR DESCENDING (LAD)

L CIRCUMFLEX (LCX)RIGHT CORONARY ARTERY

POSTERIORMARGINAL


CORONARY ARTERIES

(R) ARTERY

(L) ARTERY

LAD

CIRCUMFLEX


CONTRACTION OF CARDIAC MUSCLE

The heart can’t pump unless an electrical stimulus occurs

Action Potential (AP) – electrical change

(depolarization = contraction)

Brought about by release of calcium

(+ charge) into cells- mechanical change

Intrinsic Pacemakers – depolarize and generate the AP


CONTRACTION OF CARDIAC MUSCLE

The pacemaker with the fastest rate of depolarization stimulates the AP

• SA node (60-100 bpm)- Upper R atrium- capable of initiating electrical impulse

• AV node (40-60 bpm)- Lower R atrium• Other pacemakers ( 40 bpm)

-what can affect SA/AV node function ?


1. Cardiac Innervation: ■ Sympathetic NS excitability.

■ Parasympathetic NS (vagus) excitability.

2. Effect of ions concentration in ECF: ■ Ca2+ excitability.

■ K+ excitability.

3. Physical factors:

■ temperature excitability.

■ temperature excitability.

Factors affecting myocardial excitability

4. Blood flow:

■ Insufficient bl flow to cardiac ms excitability &

myocardial metabolism for 3 reasons: (1) lack of O2,

(2) excess accumulation of CO2, &

(3) lack of sufficient food nutrients. 5. Chemical factors (drugs):

■ Digitalis excitability.

Factors affecting myocardial excitability (continued)

1. Cardiac innervation.

2. Effect of ions concentration in ECF.

3. Physical factors.

4. Blood flow.

5. Chemical factors (drugs).

Factors affecting myocardial conductivity:

1. Cardiac Innervation: ■ Sympathetic NS conductivity.

■ Parasympathetic NS (vagus) conductivity.

2. Effect of ions concentration in ECF: ■ Ca2+ conductivity.

■ K+ conductivity.


■ temperature conductivity.

■ temperature conductivity.

Factors affecting myocardial conductivity (continued)

4. Blood flow:

■ Insufficient bl flow to cardiac ms conductivity &

myocardial metabolism for 3 reasons: (1) lack of O2,

(2) excess accumulation of CO2, &

(3) lack of sufficient food nutrients.

5. Chemical factors (drugs): ■ Digitalis conductivity.

Factors affecting myocardial conductivity (continued)


2. Oxygen supply.

3. Calcium & potassium ions concentration in ECF.


5. Hormonal & chemical factors (drugs).

6. Mechanical factors.

Factors affecting myocardial contractility: (Inotropic effectors)

1. Cardiac Innervation: ■ Sympathetic NS force of contraction.

■ Parasympathetic NS (vagus) atrial force of contraction w no significant effect on ventricular ms.

Factors affecting myocardial contractility (continued)

2. Oxygen supply: ■ Hypoxia contractility.

3. Calcium & potassium ions concentration in ECF:

■ Ca2+ contractility. ■ K+ contractility.

4. Physical factors: ■ Warming contractility. ■ Cooling contractility.


5. Hormonal & chemical factors (drugs):

■ +ve inotropics: (Adrenaline, noradrenaline,

alkalosis, digitalis, Ca2+, caffeine,…)

■ -ve inotropics: (Acetylcholine, acidosis, ether,

chloroform, some bacterial toxins (e.g. diphtheria toxins), K+, …)


6. Mechanical factors:

a. Cardiac ms. obeys ‘all or none law’:

i.e. minimal or threshold stimuli lead to maximal cardiac contraction, because cardiac ms. behaves as a syncytium.


b. Cardiac ms. can’t be stimulated while it is contracted, because its excitability during contraction is zero due to long ARP, so it can’t be tetanized.

c. Cardiac ms. can perform both isometric & isotonic types of contractions.


d. Starling’s law of the heart:

■ “Length-tension relationship” ‘Within limits, the greater the initial length of the

fiber, the stronger will be the force of its contraction; However, overstretching the fiber as in heart

failure its power of contractility decreases’ i.e. within limits, the power of contraction is directly proportional to the initial length of the ms.

■ Cardiac ms accommodates itself (up to certain limit) to the changes in venous return.


e. Cardiac ms shows staircase phenomenon (gradation), if providing all other conditions kept constant.

i.e. if an isolated heart is stimulated by successive equal & effective stimuli, the 1st few contractions show a gradual in the magnitude of contraction.



2. Effect of ions concentration in ECF.


4. Chemical factors (drugs).

Factors affecting myocardial rhythmicity

(chronotropic effectors):

a. Sympathetic stimuli:

Tachycardia, by spontaneous depolarization of SA- node.

How? ■ SA- node membrane permeability to K+ less K+

efflux. ■ membrane permeability to Ca2+ more Ca2+ influx.

■ As a result, the slope of depolarization , causing rate of SA- node firing & HR.

Factors affecting myocardial rhythmicity:

1. Cardiac Innervation:

b. Parasympathetic stimuli (vagus):

Bradycardia, by spontaneous depolarization of SA- node.

How? ■ SA- node membrane permeability to K+ more K+

efflux. ■ membrane permeability to Ca2+ less Ca2+ influx.

■ As a result, the prepotential slope , causing rate of SA- node firing & HR.

Factors affecting myocardial rhythmicity:1. Cardiac Innervation (continued)

a. Warming: rhythmicity.

b. Cooling: rhythmicity.

c. Exercise: HR as a result of sympathetic n. stimulation & vagal inhibition to SA- node.

d. Endurance-trained athletes: Resting bradycardia due to high vagal activity.



a. Thyroid hormones & catecholamines:

rhythmicity.

b. Ach:

rhythmicity.

c. Hypoxia:

rhythmicity.


4. Chemical factors (drugs):

DISRUPTION IN SERUM ELECTROLYES CAN RESULT IN ALTERATION IN CARDIAC CYCLE

• Potassium

• Calcium

• Sodium

• Magnesiumnhelzki-2014 ncm-103

MONITORING MOVEMENT OF THE CARDIAC ACTION POTENTIAL (AP)

• EKG – monitors the movement of the AP, in other words, the electrical changes.

• How are the mechanical changes ( cardiac output ) monitored ?


CARDIAC CYCLE CARDIAC CYCLE – all the

activities occurring in the heart during one contraction, and subsequent period of relaxation. Graphically represented on an EKG (ECG).


CARDIAC CYCLE

EKG – A 12 lead EKG is a graphic record of the electrical forces produced by the heart


CARDIAC CYCLEPolarized (resting) cell – represented on

EKG as baseline or isoelectric line

Depolarization – impulse over specialized cardiac cells (not neuromuscular impulse)

Repolarized cell – returns to normal. Na moves out of cell, K moves in – requires ATP

How will ischemic tissue change the cardiac cycle ?


ELECTRODE POSITIONS

“LEADS”

• Leads measure electrical activity between 2 points

• Movement toward electrode causes positive deflection

• Movement away from electrode causes negative deflection


ELECTRODE POSITIONS

A 12 Lead EKG shows electrical activity from 12 different positions in the heart, concentrating on (L) ventricle

A 14 Lead EKG includes (R) ventricle activity


Cardiac output

• SV-• CO-• Preload-• Afterload-• Ejection fraction • GOAL is to maintain adequate MAP so

perfusion of oxygenated blood to vital organs occurs


Regulation of cardiac function & BP

• Autonomic nervous system• Sympathetic norepinephrine• Parasympathetic – acetylcholine• Stimulation of adrenals by SNS –

norepinephrine• Peripheral baro receptors• Stretch receptors• chemorecptors• hormones


STROKE VOLUME (SV) & CARDIAC OUTPUT (CO)

• SV – amount of blood ejected by 1 ventricle in 1 beat

• CO – volume ejected in 1 min

Control of SV and HR = SV&HR are continually adjusted by the body, and are affected by the return of blood from the tissues (think of exercise)

CO = SVxHR



Extrinsic control of HR is a more powerful way of controlling CO than changing SV

11 CVP causes stretching of (R) atrial muscle which stimulates SNS & HR (to help pump all the blood returned to it)

Remember “Starling’s Law”



2. Stretch baroreceptors (aorta & carotid) detect in pressure which stimulates SNS & HR (to ensure adequate blood supply to heart/ brain)

3. If pressure detected, then PSNS is stimulated & HR is slowed (vagus nerve) (prevents excess arterial pressure which can damage organs)


CARDIAC LOAD

Preload = degree of myocardial fiber stretch at the end of diastole and just before contraction

Afterload = pressure against which ventricles must eject blood. This pressure is affected by systemic vascular resistance (SVR)


Blood Pressure

• Reflects the driving pressures produced by the ventricles

• Because arterial pressure is pulsatile, a single value is used to represent the overall driving pressure. This is called the mean arterial pressure.

MAP = diastolic P + 1/3(systolic P-diastolic P)

Why does diastolic pressure account for a greater proportion of the overall value?

SVR = systemic vascular resistance

CO = cardiac output

SV = stroke volume

MAP = Q x Rarterioles

Explain how these two equations are equivalent

What factors influence blood pressure?

•Blood volume

•Vascular resistance

•Autoregulation

•Autonomic influences

Regulation of Blood Pressure

• Main coordinating center is in the medulla oblongata of the brain; medullary cardiovascular control center

• Reflex control of blood pressure

•Baroreceptor reflex

Age related changes

• Decreased myocardial contractility• Thickening of endocardium & valves• Coronary arteries rigid & thickened• Decreased elasticity of vessel walls• Decreased internal diameter of vessels


CARDIAC ASSESSMENT

Cardiac status of all patients should be routinely assessed. Everyone has a

1. Objective2. Subjective CP Dyspnea FatigueWhat else ?


IMMEDIATE NURSING INTERVENTIONS FOR ACUTE CARDIAC EVENT MOVIE Acronym

M- Monitor for painO- O2 and pulse oxV- Vital signs I- Intravenous fluidsE- EKG monitoring

Anything else??


Pain Assessment

SLIDA or

Precipitating/alleviating factors

Quality

Radiation

Severity

Timing


OTHER ELEMENTS OF CARDIAC ASSESSMENT

• Previous cardiac hx• Other medical conditions that may

affect heart function• Chest injury• Previous heart surgery• Past medical hx• Medications: prescribed, OTC, herbals• Activity tolerance• Health habits• Family hx


EXAMINATION

• Inspection• Palpation• Percussion-?

• Auscultation = S1, S2 at PMI

Aortic

Pulmonic

Tricuspid

Mitral


Heart RhythmRegular, Irregular, Regular Irregular

Abnormal Sounds: Gallops

Murmurs

Bruits

S3 ventricular gallop – heard in early diastole

S4 atrial gallop – generally abnormal


Assessment of MurmursTurbulent blood flow in valvular disorders

and septal defects

Timing of murmurs is a must!

Systolic murmurs occur between S1 & S2

Diastolic murmurs occur between

S2 & S1

Grade 1 – 6 identifies intensity of murmur


Other assessments• Jugular vein pressure – assess JVD

which reflects increased filling volume and pressure on (R) side of heart

JVD associated with (R) HF, SVC obstruction (Normal is 3-10cm H20)

• Pulse deficit – the difference between apical HR and peripheral pulse-associated with Afib, and heart blocks

• Pulse pressure – the difference between systolic & diastolic pressure


Other assessments

• Respiratory: Lung sounds = rate, rhythm, quality, sputum

• GI-Abdomen• Peripheral Vascular:Lower extremities


Diagnostic Procedures

1. EKG 12 Lead

continuous cardiac monitoring

holter monitor

2. Chest x-ray – detects enlargement of heart & pulmonary congestion


Diagnostic procedures

3. Echocardiography – ultrasound that reveals size, shape and motion of cardiac structuresEvaluates heart wall thickness, valve structure, differentiates murmurs

4. TEE – transesophageal echocardiography provides a clearer image because less tissue for sound waves to pass through


Diagnostic procedures

5. Angiography / cardiac catherization

determines coronary lesion size, location, evaluate (L) ventricular function, measures heart pressures

6. Exercise tolerance test

7. Radionuclide Imaging


1. Cardiac enzymes = enzymes are released when cells are damaged (MI). Enzymes are found in many tissues/muscles, and some are specific to cardiac tissue.

Serial measurement can aid in dx, and monitor course of MI

Cardiac enzymes = CPK – MB (CK-MB),myoglobin, Troponin

In general, the greater the rise in the serum level of an enzyme, the greater the degree or extent of damage to the muscle.

LDH

Lab Studies


LAB studies CONT

2. Electrolytes

3. Lipid panel

4. CBC

5. C – Reactive Protein

6. BNP- Human B-Natriuretic Peptide

7. Blood coags-PT/PTT/INRnhelzki-2014 ncm-103

REVALIDATION TIME

Mary is attending a sophomore level nursing class on anatomy and physiology. Which statement, if made by Mary, demonstrates a good understanding of the anatomy and physiology of the heart?

A."The heart is encapsulated by a protective coating called the endocardium.“

B."The SA node is considered the main regulator of heart rate.“

C."The left atrium receives deoxygenated venous blood from all peripheral tissues.“

D."Stroke volume is the amount of blood ejected by the right ventricle during each diastole


Kirsten is completing her graduate clinical rotation in a large urban teaching hospital in a medical coronary care unit (CCU). Which observation demonstrates a good understanding of completing a thorough cardiac examination?

• A. In an obese client, an adult cuff size of 12 to 14 cm is preferable.

• B.The carotid artery on the neck is auscultated to assess for the presence of a bruit.

• C.The apical impulse is auscultated over the fifth intercostal space in the midclavicular line.

• D.Palpation is used to determine cardiac size.


Edward is a 40-year-old white male. He is an accountant who works on average 11 hours per day. He reports feeling stressed each day, even with mundane things such as a traffic jam. His father had a massive myocardial infarction at the age of 48. His mother has a history of congestive heart failure. He seldom has time to exercise, but does eat balanced meals when possible, although he does not get to eat three meals a day. Select all factors that place Edward at risk for heart disease.

• A.Family history• B.Age• C.Coping-stress tolerance• D.Race• E.Occupation


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Cardio Function 2015

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