Alterations in Cardiac Function
Terms in this set (67)
Coronary Heart Disease
also called heart disease and coronary artery disease
characterized by insufficient delivery of oxygenated blood to the myocardium due to atherosclerotic coronary arteries.
Sequelae of CHD
-sudden cardiac death
myocardium becomes damaged, disruption in electrical signals
Etiology of Coronary Heart Disease
atherosclerosis causes narrowing of the arterial lumen that can lead to cardiac ischemia through:
-endothelial cell dyfunction
Known risk factors for CHD
atherosclerosis, microcirculation abnormalities
Mechanisms of coronary atherosclerosis
-lipids are transported via apoproteins
-lipoproteins associated with a greater risk of atherosclerosis. Damage to endothelium and the LDL stick to the endothelium and attracks inflammatory cells, infiltrating artery.
-high density lipoproteins transport cholesterol from peripheral tissue back to the liver, clearing atheromatous plaque. Clean up the area, cardio protective.
-atherosclerotic plaque formation initiated by injury to coronary artery endothelim
-endothelium becomes permeable and recruits leukocytes
-LDL insudation occurs with oxidation by endothelial cells and macrophages
-Oxidized lipids are damaging to endothelial and smooth muscle cells, and stimulate recruitment of macrophages into the vessel.
-Macrophages engulf the lipids; foam cells release inflammatory mediators and growth factors, attracting more leukocytes
-excess lipid and debris accumulate within vessel wall and coalesce into lipid core
-vulnerable plaques may rupture or become eroded, which stimulates clot formation on the plaque
large lipid core
high shear stress = high blood pressure
more collagen and fibrin
less prone to rupture, more collagen
stimulate blood clot formation, further block blood flow and cause heart attack
Increased plaque vulnerability
-active inflmmation within the plaque
-large lipid core with a thin cap
-endotherlial denudation (erosion) with superficial platelet adherence
-fissured or ruptured cap
-severe stenosis predisposing to high shear stress
mainstay of treatment and prevention for atherosclerosis; also, stabilize the plaques, making them less prone to rupture.
Aspirin and coronary atherosclerosis
anti-platelet, minimize platelet aggregation, do not want smooth muscle in the middle of the artery, so this keeps inflammation down
statin drugs on coronary atherosclerosis
lipid lowering drug, and increases HDL.
Has a large lipid core with a thin cap
which plaque is most prone to rupture?
Markers of increased plaque vulnerability
1. active inflammation within the plaque
2. a large lipid core with a thin cap
3. endothelial denudation (erosion) with superficial platelet adherence
4. fissured or ruptured cap
5. severe stenosis predisposing to high shear stress
oxygen supply insufficient to meet metabolic demands of the tissue.
Critical factors in meeting cellular demand:
-rate of coronary perfusion
Medication is aimed at decreasing ischemia so decrease CO so patient has less oxygen demand
Pathophysiology of Ischemia. Altered coronary perfusion
-large, stable atherosclerotic plaque
-acute platelet aggregation and thrombosis
-failure of autoregulation by the microcirculation
-poor perfusion pressure
Chronic occlusion of a coronary vessel
Ischemic pain but the pain is predictable. The patient knows what triggers the attack. Chronic plaques
every organ has the ability to maintain pressure to perfus that specific organ despite arterial pressure
Ischemia: Acute occlusion
plaque disruption and thrombus formation and results in unstable angina or MI .
Thin cap ruptures, and things aggregate and thrombus forms
Myocardial ischemia cause
low perfusion pressure from volume depletion or shock
Coronary syndromes: clinical features and management
-chronic syndromes with slow progression due to chronic obstruction from stable atherosclerotic plaques.
Ex: stable angina pectoris
heart enlarges due to chronic ischemia.
Causes myocardial cells to adapt (hypertrophy)
Heart tries to improve by squeezing harder
Tissue becomes damaged and disorganized
Coronary syndromes: Acute coronary syndrome (ACS)
associated with acute changes in plaque morphology and thrombosis; abrupt and can be life-threatening
Ex: unstable angina
-Chest pain associated with intermittent myocardial ischemia
Sx: burning, crushing, squeesing, choking, referred pain, pressure.
-May result in inefficient cardiac pumping with resultant pulmonary congestion and shortness of breath
-No permanent myocardial damage occurs.
3 Patterns of Angina Pectoris
1. Stable or typical angina
2. Unstable or crescendo angina
3. Prinzmetal or variant angina
Stable or typical angina
-also called classic
-characterized by stenotic atherosclerotic coronary vessels
-onset of anginal pain is generally predictable and elicited by similar stimuli each time
-relieved by rest and nitroglycerin
Unstable or crescendo angina
- May progress to acute ischemia
- If prolonged leads to infarction
Prinzmetal or variant angina
- Unpredictable attacks of anginal pain
- Onset of symptoms is unrelated to physical or emotional exertion, heart rate, or other obviouscauses or increased myocardial oxygen demand.
- Characterized by vasospasms, atherosclerosis-induced hypercontractility, abnormal secretion of vasospastic chemicals by local mast cells, and abnormal calcium flux across vascular smooth muscle
-Responds well to treatment with calcium channel-blocking drugs (decrease contraction of coronary artery by blocking calcium into the cell)
Common in women
Acute Coronary Syndrome
-Chest pain usually more severe and lasts longer than typical angina
-plaque rupture with acute thrombus development
-unstable angina - occlusion is partial (blood is still flowing, no damage to myocardium)
- Myocardial infarction - occlusion is complete
- ECG and biomarkers used for diagnosis
ST segment elevation or STEMI
indicative of myocardial infarction, heart attack.
-Patients with chest pain and evidence of acute ischemia on the ECG.
-Acute reperfusion therpay
-Door to balloon
non ST segment elevation myocardial infarction
-Chest pain, positive cardiac markers but no ST elevation
-Patients presenting with symptoms of prolonged unstable angina and no ST elevation on the ECG
-New T wave inversion or ST depression.
-Go home on Beta blocker
Drugs that the person who just had an MI need to go home on
Beta blocker - decreases myocardial oxygen demand. HR goes down, BP goes down, contractility goes down.
Acute occlusion causes a range of cellular events depending on
-availability and adequeacy of collateral blood flow - good collateral blood flow = good perfusion
-relative workload - if high = more severe injury
-length of time that flow is interrupted
Acute Coronary Syndrome: Time
-after 18 to 24 hours: infarction becomes pale
-5 to 7 days: turns yellowish and soft with a rim of red vascular connective tissue
-1 to 2 weeks: necrotic tissue progressively degraded and cleared away; infarcted myocardiym weakened and susceptible to rupture
-by 6 weeks: necrotic tissue replaced by tough fibrous scar tissue.
Diagnosis of acute coronary syndrome
-Sx - severe crushing, excruciating chest pain that may radiate to the arm, shoulder, jaw or back.
Accompanied by nausea, vomiting, diaphoresis, SOB,
Asymptomatic MI = silent MI
Atypical Sx: fatigue, nausea, back pain, and abdominal discomfort. Women, the elderly and patient with diabetic neuropathies experience atypical Sx.
-ECG changes: St-segment elevation, large Q waves, and inverted T waves.
-Specific serum markers: toponin, lactate dehydrogenase, and creatine kinase. Peak levels around 24 hours.
-Lasts more than 15 minutes and is not relieved by rest or nitroglycerin
Sympathetic activation during acute coronary syndrome
myocardial workload increase
-HR, contractility, BP
Prognosis for ACS or acute MI
difficult to determine because
-how quickly teatment is sought
-extent and location of the infarct
-previous cardiovascular health
-presence of other disease processes
Treatment for ACS
-decreasing myocardial oxygen demand (beta blocker and bed rest)
-Increasing myocardial oxygen supply (thrombolysis, angioplasty, coronary bypass grafting)
-monitoring and managing complications (early detection and mangement of dysrhythmias and conduction disorders; continuous ECG monitoring
MONA for ACS
-pain, vasodilate patient, get rid of feeling of doom
-increase oxygen availability
-chewable to stop platelet aggregation
Chest pain and ST segment elevation
Reperfusion therapy is indicated for the patient with:
Sudden Cardiac Arrest
-Also called sudden cardiac death
-unexpected death from cardiac causes within 1 hour of symptom onset
-use of external defibrillators and CPR has increased survival
-Lethal dysrhythmia (such as ventricular fibrillation) is usually the primary cause
Chronic Ischemic Cardiomyopathy
-heart failure develops insidiously due to progressive ischemic myocardial damage
-typically have history of angina or MI
-appears to be consequence of slow, progressive apoptotic death of myocytes from chronic ischemia (scattered throughout the myocardium)
-more common in older adults
(sympathetic nervous system kicks in and releases catecholamines. the kidney releases renin and angiotensin II which damages cardiac tissue causing apoptosis and left venticular hypertophy)
Endocardial and valvular structure damage
-inflammation and scarring
Cause altered hemodynamics of the heart and increase myocardial workload
Failure of the valve to open completely resulting in extra pressure on the heart.
Blood does not flow normal
Inability of a valve to close completely results in extra volume work for the heart
Volume that does not go anywhere
Common with valvular disorders
-Blood flow from left atrium to left ventricle impaired during VENTRICULAR DIASTOLE
-increased pressure of the left atrium leads to atrial chamber enlargement and hypertrophy
-can lead to chronic pulmonary hypertension, right ventricular hypertrophy, and right-sided heart failure
-Left ventricle is not filling al the way. Fluid backs up into the lungs. Increases CO. chronic hypertension in pulmonary vasculatrue. Can affect the right side of the heart during systole causing hypertophy of the right ventricle as well.
-Characterized by: low-pitched, rumbling diatolic murmur; open snap; atrial dysrhythmias, atrial clots; exertional dyspnea
-Backflow of blood from the left ventricle to the left atrium during ventricular systole.
Valve incompetency, overload in atrium, poor CO, prone to turbulent blood flow and static blood flow, blood clot forms in left ventricle causing ischemic stroke.
-left atrium and ventricle dilate and hypertrophy due to extra volume
-may lead to left-sided heart failure
-High pitched, pansystolic, blowing murmur; giant V waves; chronic weakness and fatigue
Mitral valve prolapse
-displacement (ballooning) of the mirtral valve into the left atrium during ventricular systole
-Women affected more than men
-Midsystolic click or systolic murmur; palpitations; rhythm abnormalities; dizziness; fatigue; dyspnea; chest pain; or depression and anxiety
Increased intrathoracic pressure
-Predominant cause is age-related calcium deposits on the aortic cusps
-results in obstruction of aortic outflow from the left ventricle into the aorta during systole
-left ventricle hypertrophy may result in ischemia and left-sided heart failure.
Hypertrophy because it is over worked. Cells re-arrange causing heart failure.
-crescendo-decrescendo murmur during ventricular systole with prominent S4; syncope; fatigue; angina
S4 = before S1, stiff ventricle
SAD = syncope, angina, dyspnea
-infompetent aortic valve allows blood to leak back from the aorta into the left ventricle during diastole
-causes: abnormal aortic valve or aortic root dilation
-leads to left ventricle hypertrophy and dilation with eventual left-sided heart failure
-High pitched blowing murmur during ventricular diastole; high systolic blood pressure; diastolic blood pressure usually low; palpitations
Disease of the Endocardium: Rheumatic heart disease
-acute inflammatory disease that follows infection with group A Beta-hemolytic streptococci (very similar to our connective tissue antigens, so our body attacks itself)
-damage is due to immune attack on the individual's own tissues
-antibodies against the streptococcal antigens damage connective tissue in joints, heart, skin
-occurs mainly in children
-clinical manifestations: fever, sore throat, joint inflammation, erythema marginatum, involuntary movements (Sydenham chorea abnormal involuntary movements of arms and face); and a distinctive truncal rash
Diseases of the Endocardium: Infective Endocarditis
-Invasion and colonization of endocardial structures by microorgansims with resulting inflammation (vegetations)
-Most common bacteris: Streptococcus and Staphylococcus
-Acute infective endocarditis (poor prognosis, intravenous drug users are susceptible)
-Subacute infective endocarditis (predisposing risk factors typically present)
Myocardial Diseases: Cardiomyopathy
May be genetic or acquired and is non inflammatory
Evolves more insidiously over the years, with few symptoms until the heart slips into failure
-Classified by cause or functional impairment
-primary: dysfunction of unknown cause
-Secondary: known cuase
-Functional classifications: dilated, hypertonic, restrictive
3 Types of cardiomyopathy
Restrictive - comes from protein deposits causing tissues to become non-compliant, fibrotic, does not relax properly.
Hypertonic - small ventricles (tissue is large)
Dilated - ventricles are too big, do not move well.
-Cardiac failure associated with dilation of one or both ventricular chambers
-may be related to: (alcohol toxicity, pregnancy, postviral myocarditis, genetic abnormality (autosomal dominant)
-Slow progression of biventricular heart failure with low ejection fraction (not enough relaxation, contractility, or not enoug space because of hypertrophy)
-thickened, hyperkinetic ventricular muscle mass
-spetum may be affected, leading to idiopathic hypertrophic subaortic stenosis
-Genetic abnormality: autosomal dominant pattern. Pass mutation on to children.
-Clinical course is variable, typically slow progression
-asymptomatic or dyspnea and angina
-RAREST form of cardiomyopathy
-stiff, fibrotic, rigid, noncompliant ventricle with impaired diastolic filling
-most commonly associated with amyloidosis
-decreased cardiac output and left-sided heart failure can result
-exercise intolerance, dyspnea, and weakness
-Presumed known origin
-present functionally as dilated, hypertrophic, or restrictive disorders
Typically sequelae of other disorders such as:
-Metabolic derangement (increase in nitrogenous waste)
-Accumulation of non-inflammatory fluid in the pericardial sac
-composition of usual fluids: Serous, serosanguineous, chylous (milky), blood
- When fluid accumulation in the pericardial sac is large/sudden
-Can lead to external compression of the heart chambers such that filling is impaired
Reduced stoke volume (impaired diastolic filling)
Compensatroy increases in heart rate
Pulsus paradoxus (10 mm or more during filling) Narrowed pulse pressure.
Hypotension (poor CO, distended neck veins from back up, and muffled heart sounds from compression. Called Beck's triad)
-Treatment: pericardiocentesis (removal of fluid from the pericardial sac)
-Acute or chronic inflammation of the pericardium
Healed stage of the acute form that results in chronic pericardial dysfunction
-Most cases idiopathic and presumed viral
-Uncomplicated form resolves spontaneeously
-Complicated forms involve pericardial effusion, or persistent/recurrent inflammation; requires hospitalization
-Typically presents as chest pain; fever, leukocytosis, malaise, and tachycardia; friction rub (leather rubbing together)
Chest pain lying flat, but gets better when they sit up and lead forward
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