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70 Cards in this Set
- Front
- Back
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what is
1. hypertrophy 2. cardiomegaly 3. dilation |
increased weight/thickness
increased weight/size increased chamber size, will give some increase in force of contraction then drastic decrease in force |
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BV that supply the heart
1. Intramural 2. Coronaries -LAD -RCA -dominant RCA or LCA |
1. within myocardium
2. supplies outside LAD- anterior RCA- R vent dominant- posterior |
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when does systolic fx occur
when does diastolic fx occur |
1. wont let heart pump: ischemia, pressure/volume overload, dilated cardiomyopathy
2. wont let heart fill: LV hypertrophy, myocardial fibrosis, deposition of amyloid, constrictive pericarditis |
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is the following a systolic or diastolic dysfx
1LV hypertrophy 2constrictive pericarditis 3dilated cardiomyopathy 4myocardial fibrosis 5ischemia 6amyloid deposition 7P/V overload |
Systolic: wont let heart pump
Diastolic: wont let heart fill LV hypertrophy- diastolic constrictive pericarditis- diastolic dilated cardiomyopathy- systolic myocardial fibrosis- diastolic ischemia- systolic amyloid deposition- diastolic P/V overload- systolic |
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what are the three mechs that the heart uses to maintain pressure/perfusion when its damaged
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1. Frank starling: increase contractility
2. Hypertrophy (w or w/o dilation) 3. Neurohumoral system activation |
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what are 2 features that characterize CHF
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1. decreased CO (forward failure)
2. Damming of blood (backward failure) **we also see L ventricular remodling |
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what is backwards failure
what is forwards failure |
when blood damms (backs up)
when CO is decreased |
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is CHF a specific Dx
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nope, its a HUGE dx and many many things can cause it
Most commonly caused by: MI HTN DM |
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what are 3 most common causes for CHF
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MI
HTN DM |
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what are some common presentations of CHF
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1. SOB
2. LE edema 3. cough with frothy sputum 4. lack of E 5. Hard to breath at night 6. loss of appetite, swollen abdomen 7. polyuria 8. altered mental status (confusion, memory impairment) |
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what are the 2 patterns of hypertrophy in the heart
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1. Concentric- pressure overload, wall gets thick, seen in HTN,
2. Dilation (eccentric): volume overload, size of chamber increases/stretches to accomadate increased volume **recall the mechs to maintion CO/perfusion were hypertophy, increased contracility and neurohormonal |
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MI, HTN and DM all commonly lead to what
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CHF
**CHF is not a specific dx but can be caused by several things |
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if your heart has hypertrophied in order to maintain CO/perfusion but it still isnt doing the trick what will happen next?
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the heart tries even harder to compensate
1. Dilation- mycardium wont be able to contract and SV/CO decrease 2. Expand blood volume |
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hat are 4 features of a heart in CHF
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1. increased weight
2. wall thins 3. chamber dilation 4. microscopic changes of hypertrophy **cant tell if hypertrophy or dilation happened forst but both things can be ID (cant distinguish damaged compensated heart from a decompensated heart) |
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on a pic what does a concentric heart look like? dilated?
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Concentric: small LV area, huge thick walls (pressure overload like HTN)
Dilation: the whole heart is huge, the chanbers are wide open and the walls arent so thin (volume overload, recall if a heart isnt sending out enough blood it can compensate bu increasing volume) |
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what are the 4 most common causes of Left Heart Failure
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1. Ischemic Heart Disease
2. Hypertension 3. aortic/mitral valve disease 4. non ischemic myocardial disease |
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what side heart failure does this cause
1. ischemia 2. hypertension 3. mitral valve/aortic valve problems 4. non ischemic myocardial disease |
left for all
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what happens to the left atrium in Left sided heart failure
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it dilated, blood is backing up into it
can cause -a fib -stasis in appendage that leads to thrombus (embolus sent to brain) |
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where do thrombi form in the atrium in heart failure caused by HTN
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HTN created L heart failure, L atria dilate and blood is static in appendage and can form clot--> increased risk for embolic stroke
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in Left heart failure (HTN, ischemia, non ischemic cariomyopathy, aortic valve/mitrial valve defect) what are 4 changes seen in the lungs
what are the clinical manifestations of these changes |
1. Increased Pressure in pulm veins: pulm congestion/edema
2. Perivascular/interstitial transudate 3. alveolar septa widen bc of edema 4. alveoar spaces are filled with edematous fluid Dyspnea, orthopena, PND, Cough |
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when do we see Pulm veins have increased pressure, what does this lead to? clinical sx
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in L heart failure blood backs up into the lungs and increases pressure in the pulm vein
**leads to congestion and edema in the lungs (transudates, fluid in alveoi) *clinically: dyspnea, orthopenea, PND, cough |
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what are heart failure cells
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macro with hemosiderin
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are these seen in R or L heart failure
Dyspnea Orthopena PDN Cough |
left- the L heart gets backed up into the lungs and we have congestion/edema in lungs
Dyspnea: breathlessness Orthopenea: dyspnea laying down, releived by sitting up PDN (paroxysmal nocturnal dyspnea): attack of dyspnea at night cough |
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what happens to the kidney in L sided heart failure
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1. poor perfusion- activated renin, ang, aldo system to increase BV
**this makes pulm edema even worse! 2. Ischemic acute tubular necrosis 3. Impaired excretion of waste products |
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what happens to the brain in left sided heart failure
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in advances CHF can lead to cerebral hypoxia
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whats the most common cause of R sided heart failure
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L sided heart failure!
**the L heart backs into the lungs and so the R heart cant pump blood to the lungs **get R vent hypertrophy/dilation |
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Pure R sided heart failure occurs with what? what is it called?
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Pulmonary HTN
cor pulnonale **the R vent has pressure overload bc of the increased pressure in the heart, pulm congestion is minimal but there is lots of engorgement of systemic/portal veins |
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what changes occur in the liver with R sided heart failure
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1. hepatomegaly- increased size/weight
2. NUTMEG LIVER: 3. centrilobular necrosis (stasis of backed up blood that pools around and has no O2) 4. Central Hemmoragic Necrosis 5. Cardiac sclerosis: |
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what happens to the spleen in R sided heart failure
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enlarged
firm sinusoids get thickened CONGESTIVE SPLENOMEGALY **whole portal system backs up |
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what is acites
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trandudates in peritonela cavity
**seen in R sided heart failure |
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what is anasarca
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massive generalized subcutaneous edema
**seen in R sided heart failure, esp in LE |
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what is cor pulmonale
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its pulmonary HTN that leads to pure R sided heart failure
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what is it called when there are transudates in the peritoneal cavity, seen in what sided heart failure
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ascites
seen in R sided heart failure |
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what 2 categories of heart disease account for almost all mortality
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1. ischemic
2. HTN heart disease, pulm HTN heart disease (cor pulmonale, right sided fialure) 3. Valvular disease 4. congenital 5. non ischemic primary myocardial disease |
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what category of heart disease accounts for 80-90% of deaths
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ischemic
**recall the 5 most deadly are: ischemic, HTN, valve, congenical, non ischemic primary mycardial) |
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what is the underlying cause of MI 90% of the time
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artherosclerosis of coronary
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whats another name for IHD
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IDH- general term for a gorup of things resulting from ischemia
*narrowing usually due to artherosclerosis in coronary called CAD CHD |
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whats better, hypoxia or ischemia
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hypoxia, at least we have perfusion to take away waste products
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wht 4 syndromes describe the clinical manifestatinos of IHD
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1. angina
2. MI 3. chronic IHD 4. Sudden cardiac death |
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what 2 thngs have led to a decrease in death due to IHD
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1. Prevention- change lifestyle to decrease risk (decrease artherosclerosis)
2. Dx and theraputic advance |
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angina, MI, chronic ischemic heart disease, sudden cardiac death are all syndromes of what
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ischemic heart disease
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what is acute plaque change?
what disruptions may occur? |
acute plaque change is mycardial ischemia underlying acute coronary syndrome
hemorrhage, rupture/fissuring, erosion/ulceration |
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what are the acute coronary syndromes
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Unstable Angina
Acute MI Sudden cardiac death |
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what can help protect against acute ischemic event
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collaterals
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whats a mural thrombus
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incomplete luminal obstruction
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know these pics
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arteriolo sclerosis
aortic dissection acute plaque change vasculitity aneruysm CHF |
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what is angina
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transient chest pain caused by ischemia
lasts for 15 sec to 15 min so there is NO necrosis |
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what are the 3 patterns of angina
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1. stable: no acute plaque change, just decreased perfusion to coronaries bc of srtherosclerosis, releived with nitro
2. Prinzmetals/Variant: episodic, occurs at rest, due to spasm ST elevation on EKG, releived with No and Ca channel blockers 3. Unstable/Crescendo: gets progressively worse, acute plaque change- preMI angina |
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what are the sx and cause for the 3 patterns of angina
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1. Stable: due to artherosclerotic stenosis and decreased perfusion. releived with Nitro/rest
2. Variant (prinzmetal): due to spasm, occurs at rest. St elevation. releived with nitro and Ca channel blockers 3. Unstable: gets worse, acute plaque change (ulcer,partial thrombus, rupture, fissure of plaque) preceeds MI often |
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what ppl might not know when they are having angina
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DM
old folks |
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what type of angina shows ST elevation
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variant (prinzmetal)
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whats an MI
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death of heart bc of ischemia
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what are the 2 kinds of MI
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1. Transmural: common, necrosis of full thickness of wall in area supplied by one coronary
2. Subendo: necrosis limited to inner 1/3 of vent wall, extends beyond border of a single coronary **can see subendo if we have lots of collaterals supplying the outerwall |
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what kind of MI can we see if we have lots of collaterals
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subendo
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what kind of MI necrosis the enture thickness of the vent wall
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TRANSmural
**necrosis seen in area supplied by one coronary |
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what sex is protected from MI til middle age
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women, estrogen is cardioprotective
**at menopause risk is the same for men/women |
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what things other than artherosclerosis can lead to MI
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(this is only 10% of MI)
1. vasospasm 2. emboli from left mural thrombosis, endocarditis, paradoxic emboli from right 3. unexplained- no artherosclerosis or thrombus |
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what are teh sequence of events that lead to MI (5)
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1. Acute plaque change- hemmorage, fissure/rupture, ulcer/erosion
2. platelets are activated bc they see collagen- they are activated and aggregate, this can lead to emboli or occlusive thrombosis 3/4: thromboplastin, hypercoagulation, can lead to painful vasospasm 5. thrombus becomes completly occlusive |
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90% of MI are what kind (transmural or subendo) and are caused by what
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Transmural
Occlusive thrombus in the coronary overlying an ulcerated/fissured plaque **acute plaque change with thrombus (if there is a partial thrombus they get unstable angina) |
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what 7 things account for location, size and morphology of MI****
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1. the response of myocardium to occlusion (coagulation necrosis after 20-40 min of ischemia)
2. irreversible cell injury 3. locatin, severity, rate of occlusion development 4. Size of vascular bed perfused by infarcted vessel 5. duration of occlusion 6. metabolic/O2 need of myocardium 7. Extent of collaterals (get subendo rather than transmural) |
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how are transmural and subendo infarcts differnet
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1, Transmural: almost always involves L vent. necrosis of the whole thickness of myocardium. limited to area of vessel
2. Subendo: limited to inner 1/3 of myocardium. can extend beyond area of one vessel |
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where is the transmural infarct
LAD L circumflex RCA |
LAD- anterior (leads V1-V4)
L circumflex- lateral (aVL) RCA- posterior/inferior (II III aVF) **recall a transmural is more common, involved the entire thickness of the wall, and is limited to the area supplied by a vessel |
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if you have lots of artherosclerosis building up over time what is a likely MI
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subendo
**there is time for the occlusion to grow slowely and collaterals form |
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what are the gross sequence of events of an MI
2-3 hours |
2-3 hrs can see. stain with TTC, live is red, infarct is white
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what are the microscopic events of an MI****
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1. coagulation necrosis/inflammatin
2. granulation tissue (2-3 weeks) 3. resorption of necrotic mycardium 4. organization of granulation tissue to form a scar (3 months) |
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in the first 30 min of MI what is seen? what about after 30 min
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first 30, nothing seen at gross or light
*after 30 min we get IRREVERSIBLE injury |
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what it TTC
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its a dye that is used to stain hearts to see MI injury 2-3 hrs after infarrct
Dyes healthy tissue red nad infarct is white |
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what are 3 ways to restore blood flow to an infarct
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1. Thrombolysis: streptokinase dissolves thrombus, plaque is still there
2. Balloon angioplasty: removes the thrombus AND some of the plaque 3. Coronary arterial bypass graft (CABG) |
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what will clear a thrombus but do nothing for the plaque
what clears the plaque as well as the thrombus |
streptokinase (thrombolysis)
Balloon Angioplasty |
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what are some bad things associated with reperfusion*
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1. arrhythemis
2. hemmorage with contraction bands 3. irreversible damage due to reperfusion itself 4. microvascular damage 5. prolonged ischemic dysfunction |
