Flashcards in Cardiac Pathology 1 - HF, IHD, HTN HD, Deck (55):
What 3 changes occur in an aging heart?
1) myocardium and chambers - LV increased size, increased epicardial fat, myocardial changes*
3) Vascular changes*
What myocardial changes occur with aging?
-Lipofuscin and basophilic degneration
-Fewer myocytes, increased collagen fibers
What valvular changes occur with age?
AV and MV annular calcification
Fibrous thickening of leaflets
What happens to LA with age?
Increases in size due to MV leaflets bucking toward left artrium
What vascular changes occur with age?
Stiffening of the aorta
What is congestive heart failure?
Heart unable to pump blood at a rate to meet peripheral demand (or can only do so with increased filling pressure).
What does CHF result from (2)?
1) Loss of myocardial contractile function (systolic dysfunction)
2) Loss of ability to fill vents during diastole (diastolic dysfunction)
What 2 settings do cardiac myocytes become hypertrophic?
1) Sustained pressure or volume overload
2) Sustained trophic signals (b-adrenergic stim)
What do cardiac myocytes look like in setting of Pressure Overload Hypertrophy? Is this a diastolic or systolic dysfunction?
They become thicker and LV WALL THICKNESS INCREASES CONCENTRICALLY.
Diastolic dysfunction - difficulty filling bc LV too small
What do cardiac myocytes look like in setting of Volume Overload Hypertrophy? Is this a diastolic or systolic dysfunction?
Myocytes elongate and VENTRICULAR DILATION is seen.
Systolic dysfunction - insufficient expelling capacity.
What is a hypertrophic heart vulnerable to?
Ischemia. Because the increase in size is not matched by increased blood supply.
What is the best measure of hypertrophy?
Is left sided heart failure (L-HF) systolic or diastolic failure?
What are 4 things that commonly result in L-HF
1) Myocardial ischemia (atherosclerosis)
2) HTN (LV struggles to pump against increased BP)
3) Left-sided valve disease
4) Primary myocardial disease
What are clinical effects of left sided heart failure due to?
1) Congestion in pulmonary circulation (then edematous).
2) Decreased tissue perfusion.
What is the clinical presentation of L-HF?
Cough, dyspnea, orthopnea, paroxysmal nocturnal dyspnea.
What areas of hypertrophy/dilation do you see if L-HF?
Left ventricular hypertrophy.
LV dysfunction leads to LA DILATION (can lead to afib, stasis, thrombus)
What can be affected systemically as the result of L-HF?
1. Kidney - Decreased Ejection Fraction = decreased GLOM PERFUSION.
2. Brain - decreased cerebral perfusion = HYPOXIC ENCEPHALOPATHY
3. Lungs - PULM EDEMA
What is the most common cause of right sided HF (2)?
2) Isolated R-HF results from any cause of pulmonary HTN (COR PULMONALE; **parenchymal lung dz, primary pulmonary HTN, pulmonary vasoconstriction.
What are signs of PRIMARY R-HF?
Minimal pulm congestion, but marked venous congestion
In Primary R-HF, what does venous congestion result in (5)?
Liver congestion (nutmeg). Splenic congestion=SM. Effusions in peritoneal, pelural, and pericardial spaces. Edema in ANKLES. Renal congestion.
What causes ischemic heart disease (IHD)?
Insufficient coronary artery flow (resulting in insufficient perfusion to meet metabolic demands of the myocardium).
What are consequences of IHD?
MI, angina, chronic IHD with HF, sudden cardiac death
What is the leading cause of death in the US?
IHD! 90%+ are secondary to atherosclerosis (Chronic vascular occlusion and Acute plaque changes like thrombi)
Definition of angina pectoris.
Transient, often recurrent CHEST PAIN induced by myocardial ischemia insufficient to cause MI.
What are the three clinical variants of angina?
1) Stable angina
2) Prinzmetal variant angina
3) Unstable ("crescendo") angina
What does this person have? Stenotic occulsion of the coronary artery, feels like a "squeezing" or burning sensation with exertion. Relieved by vasodilators.
Stable angina - what is it and what does it feel like? How is it relieved?
What does this person have? Episodic coronary artery vasoSPASM. Relieved with vasodilators.
Prinzmetal variant angina - what is it and what does it feel like? How is it relieved?
What does this person have? Caused by rupture of plaque and partial thrombosis. Pain that increases in frequency/duration/severity (eventually at rest). 1/2 have myocardial necrosis.
Unstable ("crescendo") angina - what is it and what does it feel like?
What are 90% of MIs caused by? What are 3 other causes?
1) ATHEROMATOUS PLAQUE + associated risk factors
4) Ischemia secondary to vasculitis, shock, hematologic abnormalities (i.e. sickle cell that causes ischemia in cap beds)
Presentation of what?
*Crushing chest pain radiating to left arm or jaw for more than 30 min.
Classic presentation of an MI
Do all MIs present with the typical symptoms?
No - 25% are "silent MIs" due to: i.e. people with neuropathy or people with denervated transplanted hearts
What is the area of the subendocardium is first at risk after an arterial occlusion? What happens? Time of evolution?
The area farthest away - ischemia and necrosis of subENDOCARDIUM first, then MYOCARDIUM, then EPICARDIUM (1/2 of zone by 2hrs, full zone by 24hrs).
How long is the injury-reversible phase after a MI?
Approx 20-30min for complete recovery.
What 3 coronary vessels are at highest risk of infarct?
1) LAD (40-50%)
2) RCA (30-40%)
3) LCX (15-20%)
Where areas do the LAD , RCA, and LCX supply?
LAD - Apex, LV ant wall, ant 2/3 of septum
RCA - RV free wall, LV post wall, post 1/3 of septum
LCX - LV lateral wall
What does triphenltetrazolium chloride stain and what does it show?
It stains tissue containing lactate dehydrogenase RED. This signifies infarcted tissue.
Evolution of MI (gross and micro)
Generally (1day to months):
Gross - dark to yellow to red to white.
Micro - coagulation necrosis to PMNs to granulation tissue to scar (collagen deposition=blue)
What is the goal of reperfusion?
Limit the infarct size by rescuing the at risk myocardium.
What are four methods of reperfusion?
(1) Thrombolysis. (2,3) Angioplasty and Stent placement. (4) CABG (Coronary Artery Bypass Graft - i.e. vein)
What happens and what do you see (grossly) after reperfusion of an infarcted area?
NECROSIS occurs and CONTRACTION BANDS form.
After temporary occlusion, does tissue immediately have increased viability after reperfusion?
No. It still decreases slightly in viability after and remains its reperfusion injury. The ventricles never fully regain pre-ischemic levels of function.
What are the three useful biomarkers for MI?
Which is the most cardiac myocyte-specific lab findings?
Which peaks earliest?
Which is best for detecting re-infarction days after an MI?
1) Troponins I and T are most specific/sensitive. Peaks about 24 hours after MI.
2) Myoglobin peaks earliest - before symptoms.
3) CK-MB is best for detecting re-infarction because it is normal after 72 hours. rises before troponin, but is not heart specific.
What are 1/2 of all MIs secondary to (and occur within what time frame of onset of this)?
MI within 1 hour of ARRHYTHMIA onset. Arrhythmia reoccur as a result of permanent damage to conducting system from MI.
What are 5 complications of MI?
1) Contractile dysfunction
2) Fibrinous pericarditis
3) Myocardial rupture*
4) Infarct expansion *
5) Ventricular aneurysm *
When does a myocardial rupture (as a complication of an MI) occur after an MI and what are 4 risk factors?
Occurs 2-4 days post-MI.
When inflammation and necrosis weaken the wall - (1) increased age, (2) large transmural anterior MI (LAD), (3) first MI (no scar tissue), and (4) absence of LV hypertrophy.
What is an infarct expansion (as a complication of an MI)?
Muscle necrosis results in weakening, stretching, and thinning of the wall. Mural thrombus often seen.
What are characteristics of a ventricular aneurysm (as a complication of an MI)?
Late complication of large transmural infarct with early EXPANSION.
Composed of thinned wall of scarred myocardium, normally no rupture occurs, associated with mural thrombus.
What precipitates Sudden Cardiac Death and what is SCD?
Coronary artery disease precipitates SCD in 80-90% of cases.
Occurs without symptoms or within 1-24 hours of symptom onset. FATAL ARRHYTHMIA from ischemia-induced myocardial irritability.
What are characteristics of L-sided Hypertensive disease?
Pressure overload results in LV hypertrophy (concentric thickening).
Diastolic dysfunction = LA enlargement = afib
What can L-sided Hypertensive disease lead to?
CHF and risk factor for SCD
What are characteristics of R-sided Hypertensive disease?
Most common cause?
Isolated causes of R-sided HTN disease is the result of pulmonary HTN.
Most common cause is L-sided Heart Disease
What can cause an acute cor pulmonale?
A large pulmonary embolus.
Cor pulmonale definition
RV failure due to increased vascular resistance or pulmonary HTN.