- Age                                 - Obesity

- Family History

- Abnormal lipids

- Cigarette smoking

- Hypertension

- Diabetes

Tx and Prevention of

Atherosclerosis

Lipid Lowering Therapy

Precursor Lesions

Begin as fatty streaks and progress to small regions of medial wall thickening with scattered macrophages at a young age.  They are not symptomatic.

Advanced Lesions

2 Factors Important For

Cardiac O2 Demands

1.  Rate of coronary perfusion

2.  Myocardial Workload

5 Ways Coronary Perfusion

Impaired

1.  large, stable atherosclerotic plaque

2.  acute platelet aggregation/thrombosis

3.  vasospasm

4.  failure of autoregulation by microcirculation

5.  poor perfusion pressure

Collateral Circulation

Occurs when major vessels are slowly blocked over time.  May help preserve blood flow despite total arterial occlusion.

Angina Pectoris is associated with...

....myocardial ischemia

Anginal Pain Described As...

...burning, crushing, squeezing, choking, elephant on chest, may be mistaken for indegestion or dental pain

Atypical Symptoms of Angina

...back pain, fatigue, weakness

Stable Angina

classic/typical

Characterized by stenotic atherosclerotic coronary vessels that reduce blood flow, onset predictable.

TX for Stable Angina

Rest and Nitroglycerin

Nitroglycerine Therapeutic

Effects

causes coronary ad peripheral vasodilation, reduced preload, and therefore myocardial workload

Variant Angina

aka...

Prinzmetal Variant Angina

Variant Angina

S/S

onset unrelated to physical/emotional exertion, HR, or anything else that would inc. myocardial O2 demand.  DUE TO VASOSPASM!!!

TX of Variant Angina

CCB's

CCB's therapeutic effects

Inhibit vascular smooth muscle contraction.  Used for variant angina.

TX Chest pain, evidence of acute ischemia, and STEMI

Reperfusion strategies

Treatment of unstable angina and

NSTEMI

Antiplatelet's are cornerstone of therapy

What is thought to be the initiatingevent in most MI's?

Development of a thrombus on top of an ulcerated or cracked atherosclerotic plaque.  Platelet plug occurs, clotting cascate, resulting in thrombus.

What happens to myocardial cells within 1-2 minutes of ischemia?

They have impaired ability to contract

What happens within 10 minutes of MI?

ATP levels fall to half of normal

What happens within 30-40 minutes of complete occlusion in MI?

Irreversible cell injury

Nearly all infarcts are located where?

L. Ventricular Walls

When can morphological changes be detected in the heart after MI?

6-12 hours after infarct

What does area of infarct look like at 18-24 hours after MI?

paler than surrounding tissues

turns yellowish and becomes soft with a rim of red vascular connective tissue

What does area of infarction look like 1-2 weeks after MI?

necrotic tissue progressively degraded and cleared away.  Great risk for rupture.

DX Criteria for MI

- S/S: severe crushing, chest pain radiating from arm, shoulder, jaw or back

- Electrocardiographic changes:  ST segment elevation, Q wave

- Elevated CKMB, Troponins I and T

How is ongoing injury and ischemia seen on an ECG?  What efforts should be taken to

reduce injury/ischemia?

ST-segment elevation

Improve perfusion or reduce O2 demand

What does the Q wave represent on ECG?

usually persistent findings, specific for MI, diagnostic for MI.  Q waves may appear abnormally deep or wide.  May have inverted T wave.

What is better NSTEMI or STEMI MI?

Why?

NSTEMI, because infarct size is usually smaller

NSTEMI or STEMI

present with ACS

No ST elevation

ST may be depressed or T wave changes

+ serum markers = NSTEMI

- serum markers = STEMI

What serum markers are used for dx MI?  Which one is most useful?  When are they useful?

Serum Markers:  CK-MB, Troponin I and T

Markers of Choice = Troponin I and T because they remain elevated for a longer time than do CKMB

All serum markers are diagnostically useful only during acute periods of MI

What is the clinical course for MI?

Signs:  cardiac inflammation including fever, leukocytosis, inc. ESR.

Symptoms:  circulatory inadequacy including fatigue, restlessness, anxiety, weakness

Potential Complications Following

MI

cardiac dysrhythmias, heart failure, cardiogenic shock, ventricular rupture, pericarditis, thromboembolism

Sudden Cardiac Death

- unexpected death within 1 hour of onset of symptoms

- Coronary Heart Disease root of vast majority of cases

- Ventricular fibrillation usually the cause

- Ischemia from fibrosis, atrophy, scarring of old MI tissue, electrolyte imbalances,

Chronic Ischemic Cardiomyopathy

Heart failure as a consequence of slow, progressive apoptotic death of myocytes from chronic ischemia.  Usually found in elderly.

Stenosis

Failure of a valve to open completely

Regurgitation

inability of a valve to close completely, thereby allowing blood to flow backward across the valve when no flow should be occuring

Murmurs

abnormal turbulence of blood flow often associated with valvular disorders

Mitral Stenosis

How does the heart remodel to compensate for Mitral Stenosis?

Atrial pressure remains higher than ventricular pressure throughout DIASTOLE.  Increased pressure work of Atrium leads to ATRIAL chamber enlargement and hypertrophy.

If uncorrected, what does Mitral Stenosis lead to?

chronic pulmonary hypertension, R. ventricular hypertrophy, and R. sided HF

What are S/S of mitral stenosis due to?

Due to congestion of blood volume and increase pressure in L. atrium and pulmonary circulation as well as decreased stroke volume b/c L. Ventricle not filling up all the way.

What are S/S of mitral stenosis?

orthopnea, cough, dyspnea on exertion, paroxysmal nocturnal dyspnea, abnormal breath sounds, pooer arterial oxygenation, fatige, poor activity tolerance, weakness, EXERTIONAL DYSPNEA MOST COMMON COMPLAINT

What does mitral valve stenosis sound like?

low pitched, rumbling diastolic murmur at heart apex.  An opening snap may be heard in some patients.

Mitral Valve Prolapse

the mitral valve balloons up into L. atrium during ventricular systole.  usually asymptomatic, associated with other connective tissue disorders

How is mitral valve prolapse heard?

midsystolic click or systolic murmur.  If symptomatic patients may experience palpitations, rhythms abnormalities, dizziness, fatigue, dyspnea, ches pain, depression, anxiety

Aortic Stenosis

Cause?

In the past most commonly due to rheumatic fever.  Now, mainly due to age related calcification.

What compensatory heart mechanisms take place with aortic stenosis?

What kind of heart failure can aortic stenosis produce?

L. sided heart falure

Symptoms of aortic stenosis

Due to diminished CO:  syncope, fatige, low systolic BP, faint pulses, angina, crescendo-decrescendo heart murmur, prominent S4. 

TX of Aortic Stenosis

Surgery only

Aortic Regurgitation what cardiac compensatory mechanisms take place?

L. Ventricly hypertrophies and dilates

S/S or aortic regurgitation?

bounding pulse, head bobbing, high pitched blowing murmur during ventricular diastole

Major complication and TX for aortic regurgitation?

L. sided heart failure due to increased work load.

Well tolerated for years and valve replacement surgery can be delayed.

Rheumatic Heart Disease

due to an immune attack on individual's own tissues, inflammation of heart usually includes all layers.  Skin, joint and brain tissue may undergo inflammation

Infective Endocarditis

- Vegetations

-IV drug abusers particularly susceptible

- risk of embolization or perforation of valve leavlet

- Subacute:  low grade fever, fatigue, weight loss, flu like symptoms

- acute:  heart murmur, fever, chills

Myocarditis

inflammation, leukocyte infltration and necrosis of cardiac muscle cells.  Causes in microbial, immune diseases, physical agents.  CHAGAS DISEASE, T. CRUZI, PENICILLIN

Acute myocarditis characterized by

general dilation of all four heart chambers

flabby ventricular myocardium with lesions

heart muscle inflamed/edematous

white blood cells in heart muscle

endocardial structures normal

S/S of myocarditis

fatigue, dyspnea on exertion, dysrhythmia with associated palpitations

Dilated Cardiomyopathy

cardiac failure associated with dilation of one or both ventricular chambers.  Factors include ETOH toxicity, genetic abnormality, pregnancy, postviral myocarditis

Dilated Cardiomyopathy TX

Characterized by slowly progressing biventricular HF with low EF.  50% mortality rate in 2 years.  Cardiac transplant usually only treatment.

Hypertrophic Cardiomyopathy

Characterized by thickened, hyperkinetic ventricular muscle mass.  Hypertrophy not uniform.  L. ventricle usually more involved than R.  IDIOPATHIC HYPERTROPHIC SUBAORTIC STENOSIS.

Hypertrophic Cardiomyopathy

S/S

Hypertrophic Cardiomyopathy
TX

Beta blockers/CCB's may be used to dampen hypercontractility.  DO NOT USE drugs that INC MYOCARDIAL CONTRACTILITY OR HR as it may worsen symptoms.

Restrictive Cardiomyopathy

Rare.  Characterized by stiff fibrotic ventricle with impaired diastolic filling, abnormal deposition of amyloid protein in tissues.  Results in low stroke volume and HF.  Difficult to manage - no therapy available for most types.

Pericardial Effusion

accumulation of noninflammatory fluid in pericardial sac (serous/serosanguineous/

chylous/blood)

External compression of heart chambers that impairs filling and usually due to accumulation of pericardial fluid. 

S/S: distended neck veins, waxing/waning of BP w/breathing (pulsus paradoxus).

TX:  aspirate fluid

Pericarditis

Acute:  usually idiopathic, NSAIDS used, anginal pain, friction rub, fever, leukocytosis, malaise, tachycardia, ST segment elevation

Chronic:  healing of an acute form of pericarditis - adhesive mediastinopericarditis and constrictive pericarditis.

Shunt

abnormal path of blood flow through heart or great vessels

R. to L. Shunt

cyanotic

L. to R. shunt

acyanotic

Infant Deformations of Heart

Acyanotic

Atrial Septal Defect

Ventricular Septal Defect

Patent Ductus Arteriosus

Coarction of Aorta

Pulmonary Stenosis or Atresia

Infant Deformations of Heart

Cyanotic

Tetralogy of Fallot

Transposition of Great Arteries

Truncus Arteriosus

Tricuspid Atresia