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How does coronary artery disease (CAD; atherosclerosis of the coronary a.) present itself clinically?
- Angina pectoris (chest pain)
- Chronic ischemic heart disease w/ CHF
- Acute myocardial infarction (MI)
- Sudden cardiac death
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What is the underlying mechanism of coronary a. disease?
Myocardial ischemia
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How do atherosclerotic lesions cause acute coronary syndromes?
1) Fissuring of plague w/ clotting
2) Plague ruptures w/ emobolization
3) Results in thromboemboli
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What results from an imbalance between myocardial oxygen demand and myocardial bloody supply?
Ischemic heart disease
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How does coronary occlusion affect myocardial cells?
- @ 10 sec: become hypoxic from inadequate oxygen
- @ 10 mins: lose ability to contract
- @ 20 min: necrosis begins
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What are 4 conditions that increase oxygen demand to the heart?
- High systolic BP
- Increased ventricular volume
- Increased thickness of the myocardium
- Increased HR
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Healthy coronary a. are able to _____ to (increase/decrease) the flow of oxygenated blood to the _____.
Healthy coronary a. are able to dilate to increase the flow of oxygenated blood to the myocardium.
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Narrowing the coronary a. by ___% impairs the flow enough to affect the cell during exertion.
Narrowing the coronary a. by 50% impairs the flow enough to affect the cell during exertion.
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What is angina pectoris?
Chest pain caused by myocardial ischemia
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What causes the actual pain during angina pectoris?
Buildup of lactic acid
Abnormal stretching of the ischemic m.
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What disorders are associate with angina pectoris?
Pallor
Profuse sweating
Dyspnea
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What are the two types of angina?
- Stable
- Unstable
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What causes stable angina? Is it predictable?
Luminal narrowing and hardening of the arterial walls (atherosclerosis)
Predictable
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What causes unstable angina? Is it predictable?
Combination of vasospasm and atherosclerotic lesions
Unpredictable; often occur at rest
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What are some factors that affect the clinical presentation of ischemic disease?
Extent
Location
Type (Fibrolipid plague more likely to rupture)
Speed @ which it develops
Extent of disease in other branches
Other diseases that increase oxygen demand
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What factors can drugs target to help with myocardial ischemia?
BP
HR
Contractility
L. ventricular volume
The goal is to reduce oxygen consumption of the myocardium.
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What is MI?
Myocardial infarction is prolonged ischemia (>20 min) which leads to irreversible hypoxic injury, cellular death, and tissue necrosis.
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Where does necrosis begin with MI?
Necrosis begins in the subendocardial region and extends in the next 3-6 hrs.
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Can ischemic tissue around necrosis be healed?
Ischemic tissue around the area of necrosis may or may not be irreversibly damaged at the outset.
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MI leads to glycolysis (use of glycogen stores for energy) which then causes what?
Accumulation of hydrogen ions and lactic acid, causing acidosis and eventual heart failure
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Oxygen deprivation that occurs with MI also causes what?
Electrolyte imbalance which excites the myocardium leading to dysrhythmias (90% of individuals w/ MI).
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What functional changes occur as a result of MI?
Decreased contractility, SV, and ejection fraction
Increased end-systolic volume
SA node malfunction
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List the 4 main coronary a.
- RCA
- LCA
- LCX
- LAD
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Where does occlusion of the RCA cause infarction?
Poterior infarction
30% of all cases
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Where does occlusion of the LCX cause infarction?
Lateral infarction
20% of all cases
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Where does the occlusion of the LAD cause infarction?
Anterior infarction (widowmaker)
50% of all cases
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Where does occlusion of the l. coronary a. cause infarction?
Anterolateral infarction
Massive MI
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What affects the ability to repair an infarct? Is there inflammation?
The site and size of the lesion
MI causes a sever inflammatory reaction
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What are the problems with collagen repair of infarcts?
Collagen matrix that is initially deposited is weak and may be stressed within 10-14 days post-infarct
After 6 weeks, necrotic area is replaced by scar tissue, which cannot contract and relax (non compliant) like healthy heart tissue
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When do infarcts typically rupture?
May occur anytime within the first 2 weeks (usually between days 4-7)
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What percentage of MI cases lead to rupture? What does rupture often cause?
13% of MI cases lead to rupture
Rupture of an infarct often leads to fatal cardiac tamponade (hemopericardium)
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What are some clinical manifestations of MI?
Sudden chest pain
Indegestion
Fever
Cardiovascular changes
Increased creatine kinase and lactic dehydrogenase
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When are patients at the highest risk for sudden death?
Within the first 24 hours after onset.
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What are some treatments of MI?
Aspirin (inhibits platelets)
Thrombolytic agents
Supplemental oxygen
Pain relief
Bed rest w/ gradual return to activities
Dietary measures
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What is the most common complication associate with MI?
Cardiac arrythmia
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What percentage of MI cases result in sudden coronary death?
25%
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Describe the normal conduction system of the heart
SA Node - atria - AV node - AV bundle - R & L bundle branches - purkinje fibers
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What does it mean that cardiac myocytes are autorhythmic?
They depolarize at regular time intervals without external stimulation
Cardiac m. is an excitable tissue
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What is a sinus rhythm?
A normal cardiac rhythm, originates at SA node
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_____ can be caused by abnormal rate or the abnormal conduction of impulses.
Arrythmias can be caused by abnormal rate or conduction.
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What does the seriousness of an arrythmia depend on?
Its hemodynamic consequences (how much it affects blood flow)
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Valvular damage can be either congenital or ____.
Valvular damage can be either congenital or acquired.
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What can cause acquired valvular dysfunction?
Inflammation
Trauma
Degeneration
Infection
Ischemia
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Abnormal valves are more susceptible to ____.
Abnormal valves are more susceptible to infection,
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What are 3 hemodynamic burdens that occur with abnormal valves?
Stenosis
Regurgitation
Turbulence
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What is valvular stenosis?
Valve orifice is constricted and narrowed, impeding the forward flow of blood
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What do pressure increases in a chamber (like with valvular stenosis) cause?
Myocardial hypertophy - cardiomegaly
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What are the consequences of valvular dysfunction?
Changes in pre/afterload
Enlarged chamber
Decreased contractility and ejection fraction
Increased diastolic pressure
Ventricular failure from overworking
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How does one get rheumatic heart disease?
It is immunologically mediated.
3% of strep (sequella of group A) leads to acute rheumatic fever; 10% of ARF cases lead to rheumatic heart disease
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Rheumatic heart disease happens in ____ episodes.
Rheumatic heart disease happens in recurrent episodes.
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What is rheumatic heart disease?
Acute carditis +
Chronic valvular deformities
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What are some examples of ventricular escape beats?
Atrial standstill
AV block
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Does calcific aortic stenosis occur gradually or acutely?
Gradually, often age-related
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What is MV prolapse?
Cusps of the MV "billow upward" or prolapse into the atrium during systole
Cusps become thickened
Often asymptomatic
Patients may request antibiotics before dental work
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Elongated chordae tedinae are often seen with what?
MV prolapse
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MV prolapse has a high incidence in whom?
Young women
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What is infective (bacterial) endocarditis?
Masses of thrombotic debris and organisms infect the aortic and mitral valves
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Why is infective endocarditis hard to treat?
Because of the avascular nature of valves, antibiotics can't reach
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What are the 2 forms of bacterial endocarditis?
- Acute: organisms with high virulence
- Subacute: organisms of lower virulence
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What is virulence?
The strength, potency, or danger of a pathogen
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What are some conditions that increase the risk of infective endocarditis?
Preexisting conditions
Prosthetic valves
IV drug abuse and indwelling catheters
Hemodynamic trauma
Chronic valve diseases
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Describe the etiology of infective endocarditis
Infection occurs when organisms are implanted on the endocardial surface during episodes of bacteremia
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Describe the steps of the pathogenesis of endocarditis
Bacteria erode endothelium
Site of injury covered with fibrin/platelet clot
Inflammatory cells and bacteria invade the thrombus
Bacteria invade valves and destroy connective tissue
Inflammation heals by fibrosis causing deformity and vegetations
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What are some clinical features of bacterial endocarditis?
Fever
Cardiac murmurs (most characteristic)
Systemic emboli
Renal lesions
Negative blood cultures
May result in CHF and valvular regurgiation/stenosis
Splenomegaly
(was almost always fatal before antibiotics)
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What is myocarditis and what are the different etiologies?
Heart wall inflammation
Viruses (most common)
Parasites
Bacteria
Cardiac allograft rejection
Drug hypersensitivity
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What are the 2 types of pericarditis?
- Primary: uncommon, usually infectious
- Secondary: due to MI, cardiac surgery, radiation
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What are the possible outcomes of pericarditis?
Effusion
Resolution without complication
progress to chronic fibrosis
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What are cardiomyopathies and what is the etiology?
Heart diseases resulting from a primary abnormality in the myocardium
Idiopathic etiology
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What are the 3 major froups of cardiomyopathies?
Dilated
Hypertrophic
Restrictive
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What is dilated cardiomyopathy?
Congestive cardiomyopathy
Progressive dilation of the chambers leading to weak contractions
Associated with alcohol abuse, toxic insult, or viral
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What is hypertrophic cardiomyopathy?
Thickened walls leading to abnormal ventricular diastolic filling
Ineffective ejection because EDV is so small
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What is restrictive cardiomyopathy?
Decrease in ventricular compliance
Inelastic ventricle leading to EDV and SV
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What can all 3 cardiomyopathies lead to?
CHF
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