Cardiology Review

Craig Ernst MHS, PA-C

Lock Haven University

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..."

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

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

Physician Assistant Certification

Cardiology: up to 30-40 % of your

certification exam!

Scope of this review Hypertension Ischemic disease MI CHF Cardiomyopathy

Hypertension

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.

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.

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

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

Hypertension Essential or Primary Hypertension

Hypertension without an identifiable cause Secondary Hypertension

Hypertension secondary to a known underlying cause

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

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

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

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.

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.

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.

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.

Secondary Causes

Pheochromocytoma Coartcation of the aorta Renal disease RAS Hyperaldosteronism Drugs/Medications Thyroid disorder Obstructive sleep apnea

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

Signs ????

Studies Initial Workup

ECG (LVH) Hematocrit BMP (glucose,

creatinine, electrolytes)

Lipids

Secondary workup Thyroid studies Serum

Aldosterone / plasma renin

Echo Renal artery

doppler

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

Pharm Management of HTN Diuretics B-blockers Ace Inhibitors Calcium channel blockers Alpha blockers Angiotensin receptor blockers Direct Aldosterone inhibitors …More

Ischemic Heart Disease

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:

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

Ischemic Heart Disease Studies

ECG findings Stress ECG Nuclear scan or Stress echocardiogram MRI or 64 slice CT scan Coronary angiography: GS

Ischemic Heart Disease: Treatment Preventive???

Reversible Risks Diet Activity

Medical therapy Nitrates

Adverse reaction? Beta Blocker Platelet inhibition ACE Inhibitor Statins

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

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

MI Labs/Tests

ECG findings Location of MI

Cardiac enzymes Echocardiogram

MI Treatment

MONA PTCA or PCI Thrombolytic therapy CABG

Studies EKG progression

Early peaked T waves ST elevation T wave inversion Q waves

Studies Cardiac Enzymes

Total CK CKMB

Rapid fall to baseline Troponin

More specific for AMI

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

EKG Localization of MI

RV infarct: ST elevation in V1, V4R

I Lateral aVR ------------ V1 Septum V4 Anterior

II Inferior aVL Lateral V2 Septum V5 Lateral

III Inferior aVF Inferior V3 Anterior V6 Lateral

??

??

Heart Failure

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

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

Heart Failure Types Low output

Systolic (abnormal pump) Diastolic (abnormal filling)

Right heart failure (cor pulmonale) High output failure (normal heart)

Flavors of heart failure

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

Evaluation and Management1. Determine the etiology of HF

2. Detailed history and physical

3. Identify current class

4. Determine therapeutic plan Diagnostics Therapeutics Prognostics

Symptoms Dyspnea Orthopnea, PND, sleep disturbance Abdominal discomfort, ascites Nausea, early satiety, anorexia Edema Weight gain Chest pain

Signs Volume and/or Pressure Overload

JVD HJR Ascities S3 Hepatomegaly Pleural effusion Edema Pulmonary rales Resting tachycardia Weight gain

Diagnostics CBC/diff CMP U/A TSH BNP Iron studies (if suspect

hemochromatosis)

CXR EKG ECHO CATH

Therapeutics: GOALs Improve survival Improve symptoms Slow progression Avoid adverse events Decrease use of resources (hospitalization)

Therapeutics: non-pharm

Salt restriction Exercise Smoking cessation Weight loss Treat OSA Fluid restriction*

* In select pts

Therapeutics ACE Beta-Blocker Digoxin and diuretics Coronary revascularization Valvular repair End of life/Hospice counseling

Cardiomyopathy

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

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

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.

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)

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

DCM Clinical features:

R/L heart failure Arrhythmia Thrombus/Emboli Cardiomegaly Tachycardia JVD 3rd heart sound basiler crackles displaced PMI

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.

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

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

Hypertrophic Cardiomyopathy

Diastolic dysfunction Outflow tract obstruction Myocardial ischemia Arrhythmia

Symptoms: Asymptomatic Dyspnea Chest pain (angina) Syncope/Pre-syncope (typically with

exertion) Palpitations Sudden Death (arrhythmia)

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

HCM

Evaluation EKG-LVH with ST-T wave changes CXR-normal ECHO is diagnostic XST/Holter

Screen first degree relatives (echo)

Treatment

B-Blockers Dual chamber pacer Myomectomy Catheter directed ETOH ablation AICD

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

Restrictive Cardiomyopathy Amyloidosis (most common in USA) Sarcoidosis Idiopathic Radiation fibrosis Hemochromoatosis Drug inducing fibrosis Endomyocardial fibrosis

Restrictive Cardiomyopathy Clinical Features

Dyspnea Fatigue Elevated venous pressures

JVD Hepatomegaly Edema Ascites

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?

Restrictive Cardiomyopathy Treatment

Management of diastolic dysfunction Treat underlying cause Those with amyloidosis may recur after

transplant

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

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