Cardiology Review Craig Ernst MHS, PA-C Lock Haven University.
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Transcript of Cardiology Review Craig Ernst MHS, PA-C Lock Haven University.
![Page 1: Cardiology Review Craig Ernst MHS, PA-C Lock Haven University.](https://reader033.fdocuments.in/reader033/viewer/2022051316/56649e115503460f94afda2a/html5/thumbnails/1.jpg)
Cardiology Review
Craig Ernst MHS, PA-C
Lock Haven University
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Heart Function Heart: A blood pump which sends oxygen
rich blood to every living cell in the body. William Harvey (1578-1657) “On the Motion
of Heart and Blood” -First physician who accurately described heart function, systemic, and pulmonary circulation. "...I found the task so truly arduous... that I was almost tempted to
think... that the movement of the heart was only to be comprehended by God. For I could neither rightly perceive at first when the systole and when the diastole took place by reason of the rapidity of the movement..."
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The Burden of CV Disease 1900: CV disease < 10 % all deaths worldwide
rheumatic valvular & nutritional cardiomyopathies infectious disease & malnutrition
2000: CV disease ~ 50% all deaths in developed countries and 25 % in developing world
by 2020: CAD disease will surpass infectious disease as world’s # 1 cause of death and disability
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US Epidemiology of CV Disease
#1 cause of death in the United States 10 % of acute complaints in medical clinic 8 % of ER visits 60 % of a provider’s time treating CV disease
hypertension heart failure arrhythmias coronary artery disease valvular heart disease
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Physician Assistant Certification
Cardiology: up to 30-40 % of your
certification exam!
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Scope of this review Hypertension Ischemic disease MI CHF Cardiomyopathy
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Hypertension
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EPIDEMIOLOGY Hypertension affects ~50 million individuals in USA
Affects ~1billion world wide.
As the population ages, the prevalence of hypertension is expected to increase.
Most common reason for office visits and medications in the USA.
35 million office visits as primary diagnosis.
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EPIDEMIOLOGY Both genetic predisposition and environmental
factors (increased salt intake, obesity, smoking, ETOH)
African Americans affected at higher rates.
Lowest BP control rates are seen in Mexican Americans and Native Americans.
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Prevalence Variable by race and criteria Framingham data in predominately white
population revealed incidence of 1:5 Higher prevalence in:
Males African Americans Smokers Sedentary lifestyle
Female prevalence closely related to age > 50 y.o. = increased incidence
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Why Hypertension? Major contributing factor in:
CAD CHF Renal failure Bigest risk factor for stroke
Only 50% of patients with hypertension are treated
Only 30% treated achieve goals
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Hypertension Essential or Primary Hypertension
Hypertension without an identifiable cause Secondary Hypertension
Hypertension secondary to a known underlying cause
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Hypertension Hypertensive emergency
BP greater than 180/120 plus hypertensive encephalopathy, nephropathy, intracranial hemorrhage, aortic dissection, eclampsia, pulm edema, UA, MI
Malignant Hypertension Requires the presence of papilledema
Refractory Hypertension BP of greater than 140/90 despite maximal doses
of two or more medications
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Primary HTN >90% of all hypertension is primary Diagnosis made on basis of average blood
pressure determination on two or more properly measured, seated BP readings on each of two or more office visits. Unless end organ damage already exists
Standards for blood pressure follow-up set by Joint National Commission Seventh Annual Report
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Taking a BP Patient seated for 5 min in a chair, arm
supported at heart level Appropriate sized cuff for arm Two meaurements Provide readings verbally and in writing to
the patient
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JNC 7 BP ClassificationBP Classification SBP (mmHg) DBP (mmHg)
Normal < 120 And < 80
Prehypertension 120 – 139 Or 80 – 89
Stage 1 Hypertension 140 – 159 Or 90 – 99
Stage 2 Hypertension ≥ 160 Or ≥ 100
New classification of “prehypertension” recognizes risk of progressing to HTN and signals a need for increased education of health care professionals and the public to reduce BP levels and prevent the
development of hypertension in general populations.
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JNC 7 Key Messages
For persons over age 50, SBP >140 is a much more important CVD risk factor than DBP.
Starting at 115/75 mmHg, CVD risk doubles with each increment of 20/10 mmHg throughout the BP range.
Persons who are normotensive at age 55 have a 90% lifetime risk for developing HTN.
Those with SBP 120–139 mmHg or DBP 80–89 mmHg should be considered prehypertensive and require health-promoting lifestyle modifications to prevent CVD.
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JNC 7 Key Messages
Thiazide-type diuretics should be initial drug therapy for most with uncomplicated HTN, either alone or combined with other drug classes.
Certain high-risk conditions are compelling indications for other drug classes.
Most patients will require two or more antihypertensive drugs to achieve goal BP (<140/90 or <130/80 if DM or CKD).
If BP is >20/10 mmHg above goal, initiate therapy with two agents, one usually should be a thiazide-type diuretic.
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JNC 7 Key Messages
The most effective therapy prescribed by the careful clinician will control HTN only if patients are motivated.
Motivation improves when patients have positive experiences with, and trust in, the clinician.
Empathy builds trust and is a potent motivator.
The responsible physician’s judgment remains paramount.
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Secondary Causes
Pheochromocytoma Coartcation of the aorta Renal disease RAS Hyperaldosteronism Drugs/Medications Thyroid disorder Obstructive sleep apnea
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Symptoms Typically asymptomatic
“Silent killer” Headache – (most common) behind the eyes,
particularly in the AM Dizziness Visual disturbances N/V Confusion Fatigue Dyspnea Symptoms associated with secondary causes
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Signs ????
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Studies Initial Workup
ECG (LVH) Hematocrit BMP (glucose,
creatinine, electrolytes)
Lipids
Secondary workup Thyroid studies Serum
Aldosterone / plasma renin
Echo Renal artery
doppler
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Non-Pharm Management First line for prehypertension and adjunct for mod-severe
Na restriction Weight reduction Moderation of ETOH consumption Smoking cessation Physical Activity/Aerobic exercise Dietary Approaches to Stop Hypertension (DASH)
Rich in fruits, vegetables, lowfat dairy, with reduced sat. and total fat
Address all CVD risk factors
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Pharm Management of HTN Diuretics B-blockers Ace Inhibitors Calcium channel blockers Alpha blockers Angiotensin receptor blockers Direct Aldosterone inhibitors …More
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Ischemic Heart Disease
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Atherosclerosis Lipid deposition, fibrosis, plaque formation
within the intima of arteries Associated with premature CAD, PVD Men affected 4 x more than women but by
age 70 risk is equal. Risks are:
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Ischemic Heart Disease Insufficient oxygen supply to cardiac tissue
Atherosclerotic narrowing of arteries Risks: ??
Clinical features Angina pectoris
Stable angina Prinzmetal’s or Variant
Levine’s sign Radiation
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Ischemic Heart Disease Studies
ECG findings Stress ECG Nuclear scan or Stress echocardiogram MRI or 64 slice CT scan Coronary angiography: GS
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Ischemic Heart Disease: Treatment Preventive???
Reversible Risks Diet Activity
Medical therapy Nitrates
Adverse reaction? Beta Blocker Platelet inhibition ACE Inhibitor Statins
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MI Result of prolonged myocardial ischemia Generally a result of ruptured atherosclerotic
plaque and subsequent thrombus formation Also a result of thromboemboli
1/5th of all die before reaching a hospital Rhythm?
Up to 1/4th of pts have silent MIs Women and DM most likely to have atypical sx
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Clinical Features Severe chest pain Diaphoresis N/V, weakness, syncope, dyspnea, restlessness Dysrhythmias Hypo or hypertensive Lungs: clear to rales and wheezing
Signs of HF? JVD, S4 Pericardial friction rub after 24 hours
Dressler’s syndrome (post MI) Pericarditis, fever, leukocytosis and either pericarial or pleural effusion
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MI Labs/Tests
ECG findings Location of MI
Cardiac enzymes Echocardiogram
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MI Treatment
MONA PTCA or PCI Thrombolytic therapy CABG
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Studies EKG progression
Early peaked T waves ST elevation T wave inversion Q waves
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Studies Cardiac Enzymes
Total CK CKMB
Rapid fall to baseline Troponin
More specific for AMI
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Cardiac EnzymesTest Onset Peak Duration
CK - Total & MB 3-12 hours 18-24 hours 36-48 hours
Troponins 3-12 hours 18-24 hours Up to 10 days
Myoglobin 1-4 hours 6-7 hours 24 hours
LDH 6-12 hours 24-48 hours 6 -8 days
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EKG Localization of MI
RV infarct: ST elevation in V1, V4R
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I Lateral aVR ------------ V1 Septum V4 Anterior
II Inferior aVL Lateral V2 Septum V5 Lateral
III Inferior aVF Inferior V3 Anterior V6 Lateral
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??
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??
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Heart Failure
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Heart Failure Inability of the heart to pump blood
adequately to meet the metabolic demands of the body Abnormalities of filling Abnormalities of pumping Structural heart disease with abnormal blood /
oxygnation
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Epidemiology Prevalence
Symptomatic HF Affects 6 million Americans currently, expected to double over the next 7 years
Many millions more have asymptomatic LV dysfunction or medical conditions predisposing them to HF
Cost Annual direct cost is >10 billion dollars
Frequency It is the most common inpatient diagnosis in the
US for patients over 65 years of age
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Heart Failure Types Low output
Systolic (abnormal pump) Diastolic (abnormal filling)
Right heart failure (cor pulmonale) High output failure (normal heart)
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Flavors of heart failure
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NYHA Classification Class I - symptoms only at activity levels that
would limit normal individuals Class II – only mild symptoms with daily
activities Class III – marked symptoms with daily
activities Class IV - symptoms at rest
GOAL: treat to minimize sx
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Evaluation and Management1. Determine the etiology of HF
2. Detailed history and physical
3. Identify current class
4. Determine therapeutic plan Diagnostics Therapeutics Prognostics
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Symptoms Dyspnea Orthopnea, PND, sleep disturbance Abdominal discomfort, ascites Nausea, early satiety, anorexia Edema Weight gain Chest pain
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Signs Volume and/or Pressure Overload
JVD HJR Ascities S3 Hepatomegaly Pleural effusion Edema Pulmonary rales Resting tachycardia Weight gain
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Diagnostics CBC/diff CMP U/A TSH BNP Iron studies (if suspect
hemochromatosis)
CXR EKG ECHO CATH
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Therapeutics: GOALs Improve survival Improve symptoms Slow progression Avoid adverse events Decrease use of resources (hospitalization)
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Therapeutics: non-pharm
Salt restriction Exercise Smoking cessation Weight loss Treat OSA Fluid restriction*
* In select pts
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Therapeutics ACE Beta-Blocker Digoxin and diuretics Coronary revascularization Valvular repair End of life/Hospice counseling
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Cardiomyopathy
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Cardiomyopathy
General term indicating disease of cardiac muscle resulting in abnormal function
Divided into three types: Dilated cardiomyopathy-ventricular dilation Hypertrophic cardiomyopathy-myocardial
hypertrophy Restrictive cardiomyopathy-impaired
ventricular filling Can have characteristics of more than one
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Incidence and Prevalence Incidence
Dilated cardiomyopathy: 148/100,000/year
Prevalence Dilated cardiomyopathy: 920/100,000 Hypertrophic cardiomyopathy: 50-200/100,000 Restrictive cardiomyopathy is the most rarely
encountered form of heart muscle disease in the western world
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Dilated Cardiomyopathy (DCM) Characterized by dilation and impaired
systolic function of left &/or right ventricle Most common DCM is ischemic
cardiomyopathy Idiopathic (ICM) next most common
Pattern of familial inheritance in 20% of cases.
Role of coxsackie/adenovirus and immune mediated etiology unknown.
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DCM Common causes:
Ischemic Hypertensive Idiopathic Genetic Alcoholism Tachycardia-induced Drug abuse (cocaine,
methamphetamine, and heroin
Chemotherapeutic agents
Pregnancy
Hemochromatosis HIV and antiretroviral
agents used to treat Infectious disease
(coxsackievirus, adenovirus, cytomegalovirus, Rocky Mountain spotted fever, toxoplasmosis, trichinosis, leptospirosis, Lyme, chagas disease)
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DCM- Rare Causes Exposure to toxins,
heavy metals Nutritional deficiency
involving thiamine, selenium, etc.
Endocrine disorders like hypothyroidism, hyperthyroidism, adrenal insuff
Electrolyte abn
Connective tissue disease: SLE, RA, scleroderma
Hematologic disorders- Sickle cell, thalassemia
Muscular dystrophies Sarcoidosis
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DCM Clinical features:
R/L heart failure Arrhythmia Thrombus/Emboli Cardiomegaly Tachycardia JVD 3rd heart sound basiler crackles displaced PMI
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DCM Evaluation
CXR: cardiomegaly EKG: diffuse non specific ST-T wave changes,
LBBB common, tachycardia, conduction abnormalities, arrhythmias
Echo: poor chamber contraction and dilated chambers
If CAD suspected, cardiac catheterization Endomyocardial biopsy for research only.
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DCM Treatment
Beta blcokers Ace Inhibitors Anticoagulation for A.fib/mural thrombus. Diuretics CRT-D (Bi-V AICD) Transplant
Sudden death – Due to V. Tach. or V. Fib
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Hypertrophic Cardiomyopathy (HCM)
Unexplained myocardial hypertrophy (disproportionate to hemodynamic load) with disarray of muscle fibers Principal abnormality is impaired ventricular
compliance Outflow tract obstruction present in only
25% of cases (HOCM, IHSS, ASH) Inherited in 50-75% of cases Most common cardiovascular cause of
death in athletes
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Hypertrophic Cardiomyopathy
Diastolic dysfunction Outflow tract obstruction Myocardial ischemia Arrhythmia
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Symptoms: Asymptomatic Dyspnea Chest pain (angina) Syncope/Pre-syncope (typically with
exertion) Palpitations Sudden Death (arrhythmia)
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Left Ventricular Outflow Tract Obstruction Subvalvular obstruction Different from aortic stenosis (pressure
gradient across valve) Exam to distinguish the systolic murmur of
AS from systolic murmur of HOCM Valsalva- Decreases preload and volume is no longer
holding back the septal wall, obstruction gets worse resulting in a louder murmur (softer with AS)
Squat- increases preload and obstruction gets better resulting in a softer murmur (louder with AS)
Murmur does not radiate to the neck
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HCM
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Evaluation EKG-LVH with ST-T wave changes CXR-normal ECHO is diagnostic XST/Holter
Screen first degree relatives (echo)
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Treatment
B-Blockers Dual chamber pacer Myomectomy Catheter directed ETOH ablation AICD
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Restrictive Cardiomyopathy (RCM)
Restrictive ventricular filling and reduced diastolic volume with normal or near-normal wall thickness “stiff ventricle”
Uncommon in USA Presents with diastolic dysfunction Fewer than 10% of patients live more than
10 years after the initial diagnosis A leading cause of transplant
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Restrictive Cardiomyopathy Amyloidosis (most common in USA) Sarcoidosis Idiopathic Radiation fibrosis Hemochromoatosis Drug inducing fibrosis Endomyocardial fibrosis
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Restrictive Cardiomyopathy Clinical Features
Dyspnea Fatigue Elevated venous pressures
JVD Hepatomegaly Edema Ascites
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Restrictive Cardiomyopathy EKG-
low voltage and ST-T wave abnormalities atrial dilation atrial fibrillation (clot formation common)
Echo Endomyocardial biopsy may be useful. Is it restrictive pericarditis?
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Restrictive Cardiomyopathy Treatment
Management of diastolic dysfunction Treat underlying cause Those with amyloidosis may recur after
transplant
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Amyloidosis Abnormal proteins (amyloid) are produced
by plasma cells in the bone marrow Secondary to cancer (multiple myeloma),
systemic disease, or genetic disorders Deposits in tissues and organs cause
structural and functional damage Hypertrophy and restrictive cardiomyopathy Characteristic low voltage on EKG despite
hypertrophy on echo
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Hemochromatosis Inherited disorder of iron metabolism causing the body
to absorb/store excess iron resulting in “iron overload” Accumulation in:
Liver (cirrhosis and hepatocellular carcinoma) Pancreas (bronze diabetes) Heart (cardiomyopathy) Gonads (atrophy) Skin (bronze or silver-grey) Joints (arthritis)
Restrictive or dilated cardiomyopathy