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Patho test 2


inability of the heart to generate an adequate cardiac output to perfuse vital organs Systolic heart failure
pulmonary congestion despite a normal stroke volume and cardiac output Diastolic Heart Failure
occlusion of the Right Coronary artery or Left circumflex artery, manifested by reciprocal changes in V1 and V2 in 12 lead. 20% accompany inferior or lateral MI, 3-11% isolated posterior wall MI
_________ due to the shear stress caused b increased blood velocity close to site of occlusion. Arteriogenesis
This vessel supplies the lateral and inferior portions of the heart and occlusion would manifest as ST elevation in leads I,II,III, aVL, aVF, v5, and v6 Left circumflex artery
this vessel supplies the inferior portion of the heart and posterior septum, occlusion manifests in II,III, aVF Right Coronary Artery
venous tributaries that drain directly into all four chambers of the heart thebesian veins
equation for SVR and normal values SVR= 80[(MAP-CVP)/CO] noramal range 770-1500 dyne/sec/cm-5
pulmonary vascular resistance equation and normal values PVR= 80[(mean PAP- PCWP)/CO] noramal range 20--120 dyne/sec/cm-5
these factors increase SVR VASOCONSTRICTION: excess cathecholamines, hypovolemia, low cardiac output
these factors decrease SVR VASODILATION: septic shock, cirrhosis, aortic regurgitation, anemia
these factors increase PVR vasoconstrictor drugs, hypoxemia, acidemia, hypercapnia
these factors decrease PVR vasodilator drugs, volatile inhaled agents
5 factors affecting Heart Rate bainbridge reflex (r atrial pressure), SNS/PNS, respirations, baroreceptors, intrinisic
4 factors affecting stroke volume preload, afterload, contactility, synchrony
sinus of valsalva specialized outpouching that allow flow into coronary arteries despite position of aortic valve edges
transposition of great arteries aorta originates at the RV and Pulmonary arteries from the LV: results in pulm HTN and unoxygenated blood to body, needs to be fixed w/in a couple days, hopefully have a septal defect, usually have PDA
hypoplastic left heart syndrome LV tin, LA and aorta narrowed, poorly developed, obstructive lesion, usually w/ PDA and PFO
coarctation of the aorta narrowing of aorta, obstructive flow, low CO
4 defects of tetrology of Fallot 1. VSD- high in septum and large 2. overriding aorta- straddles VSD 3. pulmonary stenosis- obstructive 4. RV hypertrophy
tet spell sudden dyspnea, cyanosis, restlessness. probably caused by spasm of RV
why do older tetrology of fallot children squat? increase SVR therefore creating L-->R shunt increasing flow to lungs
VSD- ventrical septal defects most common- 25-33% of all congenital heart disease. L->R shunt, increased pulm circ and workload of LV, long term causes CHF and pulm HTN
ASD- atrial septal defect 4th most common congenital lesion- 5-10%. L->R shunt, increasing pulmonary flow, risk for embolic events, results in pulm htn and RV hypertrophy
PDA- patent ductus arteriosus fails to close, 5-15% congenital heart defects. decreased PVR and increased SVR causes backflow into pulmonary system, increased LV workload, indomethacin given to close, or surgical repair to prevent subacute bacterial endocarditis
causes of heart defects only 10% known cause. infections(rubella, coxsackie, herpesvirus CMV), radiation, metabolic disorders (diabetes), drugs (warfarin, phenytoin, ETOH, thalidamine, lithium, amphetamine), age >40, genetics (trisomy 13 or 18, down syndrome)
transition at birth of Foramen Ovale with 1st breath hypoxic vasoconstriction ends and PVR decreases ending R-->L shunt, tissue flap closes over opening and seals within 30 days
transition at birth of Ductus Arteriosus increase in PaO2 and decrease in prostaglandins path closes in 10-21 days
transition at birth of Ductus Venosus umbilical cord is clamped therefore no more flow, path closes, blood no longer bypasses liver, 7 days
coarctation of aorta, hypoplastic L heart syn., aortic and pulm stenosis obstructive lesions with low CO
tetrology of Fallot & tricuspid atresia lesions that decrease pulm flow R->L shunt, cyanotic lesions
PDA, ASD, VSD lesions that increase pulm flow L->R shunt, acyanotic lesions
cardiac development occurs weeks: 3-7
heart begins contracting week: 4
pericardium outer layer of the heart
pericardial cavity 50 cc of fluid, allows for friction free environment
mycoardium muscular wall of heart, inner 1/3 is subendocardium and outer 1/3 is subepicardium
endocardium innermost layer, lining of heart and valves
collateral arteries connectons between branches of ajacent coronary arteries in response to gradual occlusion
three systems of venous drainage coronary sinus and tributaries, anterior right ventricular veins, and thebesian veins
coronary sinus drains 85% of venous blood from LV, receives blood from small, middle, and cardiac veins, empties into RA
anterior cardiac veins small veins draining directly in to RA
aortic baroreceptors sense increase in pressure send signals through aortic nerve -> vagus nerve -> medulla ->cardio inhibitory center = decreased BP and HR
baroreceptor response to decreased blood pressure sense decrease, signals to cardio accelorator, increase in SNS outflow, decreased PNS outflow = increased HR and and vasoconstriction
carotid barorectors sense increase in pressure glossopharyngeal nerve -> medulla ->cardio inhibitory center = decreased BP and HR: baroreceptor responses are quick but diminish over time- best for short term changes
bainbridge/atrail reflex RA volume increase HR increases to redistribute volume throughout body, involoved in respiratory sinus arrhythmia: HR increased with inspiration do to incrased RA volume when intrathoracis pressure drops
Preload "end diastolic pressure in LV" LVEDP, depends on LVEDV, clinically measurement via PA catheter, or estimated via CVP
myocardial contraction Ca++ realeased from SR, binds to trop. C causing conformational change, Trop. 1 moves out of way, myosin head can bind to actin
actin globular protein chaine of repeating units that form 2 strands of an alpha helix
SNS effect on preload and contractility "shifts curve left" increase CO and SV
Heart failure effect on preload and contractility "shifts curve right" decreases CO and SV
afterload resistance or impedence to ejection of blood from LV; pressure that RV or LV must generate during systole to overcome resistance. force-velocity relationship: less resistance= faster stronger contraction
how does greater afterload effect muscle contraction greater afterload= slower muscle contraction b/c slower velocity of shortening =less work to be done
law of laplace Tension= (IVPxIVR)/wall thickness the thicker the wall the less tension, with increaesd preload incrased wall tension
what is the primary factor of MVO2? myocyte contaction
myocaridal contractility intrinisic ability of cadiac muscle to generate force at given fiber length, inotropic state of heart independent of prelaod. difficult to measure clinically
factors effecting blood flow vessel diameter, vessel length, viscosity of blood
poiseuille's formula R=8nl/πr4 if radius incrased resistance in decreased, if viscosity increases resistance increases, increased length causes increased resistance
isovolumetric periods of cardiac cycle the heard is either contracting or relaxing while ALL VALVES ARE CLOSED
coronary blood flow is affected by: compression of coronary circulation caused by contraction of myocardium, metabolic vasodilation during diastole (NO and adenosine)s
coronary perfusion pressure CPP= AoDP-LVEDP decreased if AoDP decreases or LVEDP increases, HR too fast, or vessels occluded (via spasm)
Myocaridal oxygen demand wall tension (afterload and preload) HR contractility muscle mass
myocaridial oxygen supply arterial oxygen content coronary artery diameter diastolic time (HR) Ao diastolic pressure LVEDP
tunica intima inner layer of all vessels, single layer of endothelial cells, **covered by elestic internal layer in arteries only**
tunica media middle lay of all vessels, smooth muscle, elastin and collogen mediates responses to signals from endothelial cells
tunica adventitia outer covering of vessels, composed of collogen and ANS nerves
arteriosclerosis chronic disease of arteries- abnormal thickening/hardening of inner wall. affects diameter and impairs flow
atherosclerosis accumulation of lipid-laden macrophages in arterial wall forming plaque. caused by smoking, HTN, DM, increased lipids, hyperhomocysteinemia. leads to CAD, PAD, carotid disease
progression of atherosclerosis fatty streak-> fibrous plaque -> complicated lesion
HTN 90-95% are idiopathic, cause unknown aka primary (essential) HTN
causes of secondary HTN (known cause) renovascular disease, renal failure, thyroid disorders, adrenal disorders pheochromocytoma, coarctation or aorta, elevated ICP, PIH, drugs such as MAOI, herbals and apetite supressants
clinical management of HTN lifestyle modification, thiazide diuretics, ACEI, Beta blockers, CA channel blocker or combinations
clinical relevence of HTN startling high # of pts present to OR with undiagnosed or untx HTN= increased risk end organ disease, complicated by shifted autoregulation curve => decreased CPP and coronary perfusion. also variable response to anesthetics and vasoactive drugs
degenerative aneurysm most common type, occur as result of breakdown of connective tissue and muscular layer
dissecting aneurysm occur when tear begins w/in wall or aorta, causing 3 layers to seperate
causes of aneurysm HTN, arterioclerosis, syphilis, marfan syndrome, post MI, trauma
law of laplace and aneurysms Tension= (IVPxIVR)/wall thickness -> the bigger the aneurysm the more likely to rupture: increase radius increases wall tension. repair at 5cm
fusiform aneurysm bulges out on all sides
sacular aneurysm bulges on one side
Thrombi attached to vessel wall, caused by injury inflammation, infection, and low flow/stasis. ie new onset a-fib.
emboli detached from vessel wall, cause damage distal to point of being lodged. thromboembolism air, amniotic fluid, fat foreign material (glass shards), bacteria
Peripheral vascular disease (PVD) intermittent claudication, surgical revascularization, venous disease, varicose veins, venous insufficiency, DVT
Virchow's triad indicates DVT -venous stasis (CHF) -venous endothelial damage (trauma, medications) -hypercoagulable state (malignancy, pregnancy)
Coronary artery disease (CAD) causes changes in structure and function of vessels. vasospasm, impaired relaxation, formation of clots
modifiable risk factors for CAD dyslipidemia, HTN, tobacco abuse, DM, obesisty, sedentary lifestyle, atherogenic diet
non-modifiable risk factors for CAD age, gender (males & post-menopausal women, family hx
TX for CAD goal to restore normal perfusion, reduce O2 demand by decreasing HR, contractility, afterload, or preload. stents, CABG, anti-platelet, anticoag, b-blockers, CCB
myocardial ischemia insufficient blood supply causing myocardium to lose efficient pumping ability and conduction abnormalities w/in seconds
causes of myocardial ischemia arteriosclerotic plaques, coronary spasm, hypotention (decreased AoDP=decreased CPP),arrhythmias, anemia, valvular disease
stable angina chronic narrowing or arteries, occurs with exercise or stress, transient/reversible, neck lower jaw arm pain, sob/restless/nausea/diaphoreisis. ST depression tx w/ b-blockers, CCB
prinzmetal's(varient) angina occurs at night REM sleep, vasospasms, w/ or w/o atherosclerosis, hyperactivity of SNS, Ca, prostaglandins or thromboxane. can cause infarct if long lasting. ST elevations
unstable angina transient formation and dissolution of blood clot w/in coronary artery. chest pain at rest/ supply ischemia. if clot last long can cause infarct
silent ischemia myocardial ischemia w/o symptoms. seen in women, DM, heart transplant r/t denervation
myocardial infarction coronary blood flow interrupted and or insufficient for an extended period of time myocyte death and necrosis occurs
subendocardial infarct only inner layer of myocardium dies, usually non-STEMI, usually lower in heart
transmural infarct full thickness of myocardium dies, manifests as prominent t-waves and STEMI
zone of necrosis area of myocyte death
zone of injury cells surrounding zone of necrosis, can recover if enough collateral circ
zone of ischemia recovers in 2-3 weeks
complications of MI arrhythmias (most common), congestive heart failure/pulm edema (cardiogenic shock-most life threatening), pericarditis, aneurysm formation, thromboembolism, papillary muscle dysfunction/valve regurg
clinical management of MI Think 5 factors of SV 1)HR- b-blockers w/CCB 2)preload: decrease 3)afterload: decrease wall tension, nitrates, diuretics, morphine, phospodiesterase inhibitorss, IABP 4) contractility- decrease/optimize contractility 5)rhythm, dig, anti arrythmics
why give B-blocker with CCB give CCB decrease BP, decreased afterload sensed by baroreceptors, increase HR- increased HR increases O2 demand b-blocker decreases HR
other management of MI O2, ASA, thrombolytics, PCTA
acute pericarditis idiopathic, post-op, infectious, connective tissue disorder, post radiation. server pain worsens with respiration. diffuse ST elevation, friction rub
pericaridal effusion accumulation of fluid in pericardium from CA, radiation, infections , aneurysms, trauma, uremia. tamponade: decrease pulse pressure, fail to fill, emergent needle decompression or pericaridal window
constrictive pericarditis pericardium becomes rigid and scarred, fibrotic due to TB, radiation, uremia. similar to pericaridal effusion but slower to evolve
dilated cardiomyopathy caused by booze or volume overload. large dilated LV no increase in muscle thickness. decreased EF, dyspnea, fatigue, palpitations, dizziness. tx: diuretics dig, anticoag, afterload reducers, corticosteroids, immunosuppress, supportive measures
hypertrophic cardiomyopathy thickened cardiac muscle r/t AS or HTN. pressure overload
asymmetric septal hypertrophy autosomal dominant inherited disorder causes outflow obstruction of LV
hypertensive or valvular hypertrophy secondary to obstruction caused by AS or significant HTN, LV has to compensate for increased workload
valvular dysfunctions cause constriction or narrowing or allows backflow. workload and wall thickness of chamber behind increased
aortic stenosis causes: inflammation r/t rheumatic heart disease, congenital malformation (born as bicuspid valve), degeneration, thickening and calcification. progressive narrowing over time: narrowed pulse pressure, reduced SV, systolic murmur
3 classic s/sx of aortic stenosis 1)angina-increased MVO2, increased LVEDP= decreased CCP 2)dyspnea on exercion 3)syncope
critical aortic stenosis valve orifice less than 0.5 cm2 or pressure gradient is 50 or higher
clinical management of Ao stenosis -HR 60-90- keeps mvo2 low -rhythm maintain sinus- loss atrial kick decreases CO by 40% -pre/afterload- maintain or increase -contractility- maintain NO SPINAL for these pts
mitral stenosis narrowing of open mitral valve orifice difficult flow of blood from LA to LV during diastole. Caused by rheumatic heart disease. LA hypertrophy, afib common complication. can cause pulm HTN. rumbling diastolic murmur
clinical management mitral stenosis -HR keep slow allow for diastolic filling -rhythm keep sinus or slow afib -preload- maintain or slightly decrease -afterload- maintain -contractility- maintain
Ao regurg aortic valve fails to close completely, blood flows back into LV after ejection. causes: rheumatic fever, bacterial endocarditis, HTN, syphilus, connective tissue disorders. widened pulse pressure, diastolic murmur, angina, dilated LV, hypertrophy
clinical management of Ao regurg -HR increase to 80-100 decrease diastolic phase -rhythm- sinus avoid brady -preload- increase to max forward flow -afterload- decrease to favor forward flow -contractility maintain
mitral regurg mitral valve fails to close and blood back flows from LV to LA causing loud systolic murmur. caused by RHD, congenital prolapse, CAD, marfan, cad/MI, CHF sudden MR can cause pulm edema and death, long term pulm HTN & RV failure
clinical management of mitral regurg -HR maintian/increase braday worsens flow -rhythm sinus -preload- maintain or increase to maintain CO -afterload decrease to improve forward flow -contractility- maintain or increase to decrease LV volume
mitral valve prolapse elongated chordae endinae allow mitral vlave susps to balloon backward into LA during systole, inherited or connective tissue disorders (marfan), s/sx: systolic click murmur, palpitations, syncope, fatigue, anxiety, atypical chest pain
clinical management of valve disease medical: dig, diuretics, b-blockers, avoid hypovolemia, abx prophylaxis surgical: repair/replacement -porcine short duration -mechanical require lifelong angicoag and abx
Rheumatic heart disease diffuse inflammatory disease caused by delayed immune response to hemolytic strep. 3% strep throat victims, 10% of rheumatic fever pts get rheumatic heart disease
RHD patho febrile illness: joint pain; scarring on valves, skin, nervous system. bead like vegetation on valves containing platelets and fibrin, deform valves can cause stenosis and regurgitation
infective endocarditis bacteria, viruses, fungi, rickettsiae, parasites attach to valve, colonize and cause dysfunction, conduction changes, thrombus, emboli, stroke, or MI. risks acquired valve disease, prosthetic valve, male, central lines, IV drug abuse, cardiac surgery.
Created by: kaFoster