Flashcards in Cardiac Pathology 1 Deck (63):
Myocardial and chamber changes with aging
- Decreased LV size
- Increased epicardial fat
- Lipofuscin buildup in myocytes, basophilic degeneration
- Fewer myocytes, increased collagen (STIFF)
What is lipofuscin? Pathologic?
Normal breakdown product stored in cells
- No known damage to cell
Valvular changes with aging
- Annular calcification (L side valves)
- Fibrous thickening
- Mitral valve buckling toward L atrium --> increased atrial size
- Lambl excrescences
What are lambl excrescences? Pathologic?
Frond-like papillary projections off of cusps
- Pathologic IF abnormally large and embolize
Heart vascular changes with aging
- Coronary atherosclerosis
- Stiffening of aorta
Heart can't pump to meet peripheral demand with normal filling pressure
2 causes (general) of CHF
Systolic dysfunction - loss of contractility of myocytes
Diastolic dysfunction - loss of filling ventricles in diastole
3 causes of cardiac hypertrophy
- Pressure overload (HTN)
- Volume overload
- Sustained beta-adrenergic stimulation
Pathologic finding in pressure overload hypertrophy
Is this a systolic or diastolic dysfunction?
THICKER myocytes, concentric ventricular wall thickening
Diastolic (less filling space)
Pathologic finding in volume overload hypertrophy
Is this a systolic or diastolic dysfunction?
ELONGATED myocytes, ventricular dilation w/ thinner wall
Systolic (less contractility)
Potential danger in cardiac hypertrophy?
Lack of adequate blood supply to myocytes --> ischemia
Describe the pathway by which hypertrophy or dilation occurs
Pressure/volume overload --> increased work --> increased wall stress --> cell stretch --> hypertrophy/dilation
3 RESULTS of cardiac dysfunction (systolic or diastolic)
- Heart failure
- Neurohumoral stimulation
Causes of L-sided heart failure (4)
- Myocardial ischemia (atherosclerosis or hypertrophy)
- L-side valvular disease (aortic or mitral)
- 1º myocardial disease
Clinical effects (seen in clinic) in L-sided failure are DUE TO what?
- Congestion of pulmonary circulation
- Decreased tissue perfusion
Most common clinical symptoms of L-sided failure
Cough, dyspnea, orthopnea, paroxysmal nocturnal dyspnea
Potential morphologic changes in L-sided heart failure
- L atrial dilation (via L ventricular failure)
A patient has L-sided heart failure via chronic systemic HTN. On imaging, the L atrium is dilated. What are the clinical dangers of this finding?
- A. fib --> thrombus --> embolism
- Stasis --> thrombus --> embolism
Lab finding in L-sided heart failure (why?)
- Pre-renal azotemia (decreased renal perfusion)
A patient w/ L-sided heart failure is subject to what neurologic damage?
Hypoxic encephalopathy (decreased brain perfusion)
MOST COMMON cause of R-sided heart failure
L-sided heart failure
Causes of isolated R-sided heart failure
ANY pulmonary hypertension
- Parenchymal lung disease
- 1º Pulmonary HTN
- Pulmonary vasoconstriction
Systemic findings in R-sided heart failure (5)
- Nutmeg liver (partly congested, partly not)
- Splenomegaly (congestion)
- Body space effusions (ascites, pleural, pericardial)
- Peripheral (ANKLE) edema
- Renal congestion
General cause of ischemic heart disease
Decreased blood flow to coronary arteries --> myocardium
Potential RESULTS of ischemic heart disease
- Angina pectoris
- Heart failure
- Sudden cardiac death (fatal arrhythmia)
Most likely cause of ischemic heart disease
What is angina pectoris? Cause?
Transient, RECURRENT chest pain DUE TO myocardial ischemia NOT ENOUGH to cause M.I.
3 types of angina pectoris
- Stable angina (exercise/stress)
- Prinzmetal variant
- Unstable "crescendo" angina
Cause of stable angina
Cause of Prinzmetal angina
Episodic coronary artery spasm
Cause of unstable "crescendo" angina
Complaint by patient?
Plaque rupture --> partial thrombis
Pain of increasing frequency, duration, and severity
Which type of angina pectoris is not generally linked to atherosclerosis?
Common morphologic finding w/ unstable angina
Most COMMON cause of myocardial infarction
Other causes of M.I. besides atherosclerosis
- Vasospasm (cocaine, other)
- Ischemia via vasculitis, shock, other
Classic presentation of M.I.
- Prolonged (> 30 min) chest pain, radiates down L arm
Determinants of M.I. presentation
- Site, degree, rate, duration of arterial occlusion
- Size of perfused area
- Metabolic demands of at-risk area
- Available collateral blood flow
- Arterial spasm or not
Where are the first areas of ischemia/necrosis in an M.I.?
These areas are also the ______
Sub-endocardial myocardium FARTHEST from the artery and NOT able to get oxygen via diffusion from chamber
LAST to heal (if at all)
How long can it take for necrosis to be seen?
How long can it take for the WHOLE wall to be necrotic?
How long can it take for irreversible injury to result?
In ischemic damaged myocardium, levels of ___ drop while levels of ___ rise
Most commonly affected arteries in M.I.
1) LAD (anterior interventricular)
2) R coronary
3) L circumflex
A patient has an M.I. due to LAD occlusion. Where will the areas of myocardial damage be?
Apex, LV anterior wall, anterior 2/3 of septum
A patient has an M.I. due to RCA occlusion. Where will the areas of myocardial damage be?
RV free wall, LV posterior wall, posterior 1/3 of septum
A patient has an M.I. due to LCX occlusion. Where will the area of myocardial damage be?
LV lateral wall
General morphologic progression of M.I. (5 "stages")
Dark mottling (hemorrhage) --> yellow-tan center (necrosis) --> Red-grey (granulation tissue, vessels) --> grey-white (scarring) --> full white (dense collagen)
Nearby myocardial cells that did NOT die during an M.I. will look how?
Hypertrophic and spaced out (to cover dead area)
An M.I. has been reperfused following partial necrosis/death of the myocardium. What pathologic feature will be seen within that area? Why?
CONTRACTION BANDS - living myocytes exposed to calcium from blood (reperfusion) --> contraction
How does myocyte functionality relate to viability (alive) during an M.I.?
They are non-functional within a few minutes, but still completely living for 20 min (at least)
Why do myocytes continue to die slightly after being reperfused (after an M.I.)?
Sudden O2 causes ROS creation by damaged cells
While parts of the myocardium remain alive after a reperfused M.I., what continues to increase?
Fastest lab findings in an M.I.
Intermediate lab finding in an M.I. (timing-wise)
Last and longest lab finding in an M.I. (BEST)
Myoglobin (disappears in hours)
CK-MB (stays for a few days)
Troponin I and T (stays for many days)
Most common cause of death following a treated M.I.
Fatal arrhythmia (50%)
An arrrhythmia following an M.I. is most likely to occur following what type of M.I.? Why?
RCA - conducting system is in posterior of heart
A patient has an M.I. and later shows progressive heart failure. Why?
Contractile dysfunction due to dead myocardium
A patient has an M.I. and later shows chest discomfort and a friction rub. Imaging shows dark red around damaged myocardium. Why?
Fibrinous pericarditis due to attempted healing
A patient has an M.I. and later dies acutely w/ severe chest pain. Why?
Myocardial rupture via weakened, necrotic wall
Risk factors for a myocardial rupture following an M.I. (4)
- Transmural, anterior M.I.
- First M.I. (less protective scar tissue)
- No preceding LV hypertrophy
3 types of myocardial rupture post-M.I.
- External (anterior)
- Septal (L to R shunt)
- Papillary muscle (valvular dysfunction)
Commonly seen formation on imaging following an M.I.
An M.I. is large and transmural, and shows signs of early expansion to surrounding myocardium. Most likely complication?
What makes a "sudden cardiac death"?
Most common cause?
Unexpected death of cardiac cause due to NO symptoms or within 1 day of symptoms starting
Coronary artery disease (sub-clinical level --> occlusion)
Most literal cause of the sudden cardiac death from CAD?
Fatal V fib arrhythmia due to ischemic myocardium