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119 Cards in this Set
- Front
- Back
cardiac output(CO) formula
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rate of O2 consumption/
(arterial O2 content - venous) |
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mean arterial pressure (MAP) formula
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MAP = CO - TPR
MAP also = 1/3 systolic + 2/3 diastolic |
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stroke volume (SV) formula
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SV = CO/ HR
SV also = EDV-ESV |
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cardiac output variables
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SV CAP
->SV is affected by Contractility, Afterload and Preload |
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contractility/SV increases due to
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increased catecholamines (high activity of Ca pump in SR)
increased [Ca]i decreased [Na]e digitalis admin (increases intracellular Na which leads to increased [Ca]i) |
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contractility/SV decreases due to
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B1 blockers
heart failure acidosis hypoxia/hypercapnea Ca channel blockers |
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force of contraction [starling curve
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is proportional to the initial length of cardiac muscle fiber [PRELOAD]
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ejection fraction (EF) formula
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EF = SV/EDV = (EDV-ESV)/EDV
EF is an index of ventricular contractility EF should be >/= 55% |
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resistance/pressure/flow formula
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change in P = Q x R
Q = flow, R = resistance R= 8 x viscosity x length/ pi radius ^4 *viscostity increased in polycythemia, high protein and hereditary spherocytosis |
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JVP waves
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a: atrial contraction
c: RV contraction(when tricuspid bulges back into RA) v: increased atrial pressure due to atrial filling against closed tricuspid valve |
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cardiac myocyte vs skeletal myocytes
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cardiac muscle:
-> AP has a plateau -> nodal cells SPONTANEOUSLY depolarize [automaticity] -> myocytes are electrically coupled via gap jxns **contraction is due to extracellular Ca |
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AP in atrial/ventricular myocytes and purkinje fibers
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phase O: rapid upstroke (Na)
1: intial repol (inactivation of Na channels) 2: plateau (Ca influx balances slowly increasing K efflux) 3: rapid repol (massive K efflux due to slow K channels and closure of Ca channels) 4: resting potential (K and Ca leak currents + Na/K ATPase and Na/Ca exchanger) |
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AP in pacemaker cells
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phase 0: upstroke due to Ca channels... NO fast Na channels
2: no plateau (pointy) 4: slow diastolic depol (I-f accounts for automaticity of SA/AV nodes) **slope of phase 4 in SA node determines heart rate** |
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wolf parkinson white syndrome
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accessory conduction pathway from atria to ventricle
bypasses the AV node **see a DELTA WAVE before QRS complex can lead to SVTs |
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1st degree AV block
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PR interval prolonged (>200 msec)
is asymptomatic |
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2nd degree AV block
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mobitz type 1:
->progressive lengthening of PR until a beat is dropped. asymptomatic mobitz type 2: ->dropped beats not proceeded by change in PR length. is symptomatic: 2 P waves to 1 QRS |
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3rd degree AV block [complete heart block]
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atria and ventricles beat independantly.
P waves have no relation to QRS. atrial rate > ventricular *Tx = pacemaker rate of ventricular beat: 30-45 stroke volume is increased (high pulse pressure) |
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O2 demand in heart
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high O2 demand drives increased blood flow, NOT increased extraction of O2
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fluid pressure [hydrostatic] starling forces
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Pc = capillary fluid pressure
-> fluid out of capillary Pi = interstitial fluid pressure -> fluid into capillary |
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colloid pressure starling forces
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pi-c: plasma colloid osmotic p
-> moves fluid into capillary pi-i: interstitial colloid p -> moves fluid out of capillary |
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right to left shunts
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=early cyanosis (blue babies)
Teratology of Fallot Transposition of great arteries Truncus arteriosus |
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left to right shunts
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VSD (#1 congenital anomaly)
ASD (loud S1, fixed split S2) PDA (close w/indomethacin) |
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teratology of Fallot
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PROVe
Pulmonary a. stenosis (Px feature) RVH Overriding aorta (overrides VSD) VSD *pts suffer 'cyanotic spells' caused by anteriosuperior displacement of aorta |
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transposition of great vessels
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aorta leavse RV and pulm trunk leaves LV (posterior)
not compatible with life unless shunt is present to mix systemic and pulm circulations (VSD, pDA or pFO) |
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coarctation of aorta
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infants: aortic stenosis proximal to insertion of DA
adults: distal to DA. -> notching of ribs, HTN in upper extremities, weak pulses in lower extremities -> 3:1 male to female ratio **ass'd with Turner Syndrome |
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patent DA
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in fetal pd, shunt R to L (bypasses pulmonary circulation)
birth = lung resistance drops and shut becomes L to R which causes RVH and R heart failure *continuous machine like murmur patency = low O2 tension, PGE |
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congenital cardiac defects
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22q11: truncus arteriosus, teratology of fallot
Ts21: ASD or VSD rubella: septal defects, pDA turner's: coarctation of aorta marfan's: aortic insufficiency mom w/DM: transposition of great vessels |
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monckeburg arteriosclerosis
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calcification of arteries, especially radial or ulnar.
usually benign |
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arteriolosclerosis
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hyaline thickening of small arteries due to essential hypertension
ONION SKINNING in malignant HTN |
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cardiovascular system is derived from which cell layer?
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mesoderm
paired endocardial heart tubes from in cephalic region |
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primitive embryonic heard dilates into five areas (starting at weeks 5-8):
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from cranial to caudal
-truncus arteriosus: proximal aorta and proximal pulm artery -bulbus cordis: smooth parts of right ventricle and LV -primitive ventricle: RV, LV -primitive atrium: RA and LA -sinus venosus (R and L): smooth part of RA, coronary sinus, oblique vein |
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pathophysiology of teratology of Fallot
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aberrant development of aortico-pulmonary septum [which should normally divide aorta and pulmonary trunk]
|
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development of aortic arches
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6 paired aortic arches at 1st
->arch 3: common carotids ->4: aorta and proximal subclavian artery ->6: DA and pulmonary trunk |
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developent of veins
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vitelline veins: ductus venosus carries O2 blood from placenta to fetus
L umbilical vein: ligamentum teres hepatis R umbilical vein: regresses |
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paradoxical emboli
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originate in the venous circulation and pass through pFO or ASD to produce symptoms on arterial side
|
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situs inversus
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all body's organs are transposed
associated with Kartagener's syndrome [immotile cilia] |
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Eisenmerger's syndrome
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change of L to R to R to L shunt secondary to increasing pulmonary HTN
often result of chronic response to VSD |
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acquired arteriovenous fistula
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decreased TPR leads to increased CO (increased HR and SV)
diastolic bp falls b/c blood rapidly exits arterial system but mean bp is relatively normal b/c regulating mechanisms are normal |
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change in pulse pressure with arteriosclerosis
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increases (b/c arteries have hardened... need to push harder [higher systolic bp] to get the blood out)
|
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type of endocarditis in pts with SLE
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Libman-Sacks
->small granular vegetations consisting of fibrin develop on mitral and aortic valves ->leads to aortic stenosis |
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premortum thrombus
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look for Lines of Zahn (composed of platelets)
->b/c has formed over a period of time often due to atrial fibrillation |
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pathology of repeated episodes of stable angina
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gradual loss of myocytes
->small patches of fibrosis and vacuolization ->usually in subendocardial area (poorly perfused) |
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thoracic outlet syndrome with the presence of a cervical rib
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subclavian artery compressed btwn scalenus anterior and the rib
=pain and tingling on affected side |
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effect of severe anemia
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wide pulse pressure
->resting CO is increased due to increased SV and HR also see tachycardia |
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causes of decreased pulse pressure
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aortic valve obstruction
cardiac tamponade heart failure mitral valve obstruction |
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effect of malignant hypertension on arteriole structure
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arteriolar rarefaction
=dissolution and loss of arterioles -due to long term over-perfusion of tissues also, arteriolar wall to lumen ratio INCREASES (thicker wall) |
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syphilitic aneurysm
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massive dilation of aortic root with absence of atherosclerosis
histo = plasma cell lesion in vasa vasorum that supply the aorta [eventually obliterate it and cause aneurysm] |
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cyanosis
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only from R-L shunt
|
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signs of cardiac tamponade
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decreased arterial pressure
small, quiet heart hypotension, tachypnea, tachycardia, increased JVP *pulsus paradoxus |
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signs of pericarditis
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sharp, knife like pain
->usually related to breathing diffuse STEs and upright T waves pericardial rub MAY be present |
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location of femoral vein on CT
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medial to femoral artery
('venous toward the penis') |
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typical bp of someone with aortic regurgitation
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wide pulse pressure (160/80)
systemic pressure drops during diastole b/c blood flows back thru aorta into LV |
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most common cause of sudden cardiac death (SCD)
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ischemic heart disease
*in younger patients, the non-atherosclerotic causes are more common ->hypertrophy, MVP, myocarditis, dilated cardiomyopathy, etc |
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Kawasaki disease
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'mucocutaneous lymph node syndrome'
leading cause of acquired heart disease in kids in the US all sizes of arteries affected *risk of coronary artery aneurysm |
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positive result in starling equation
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=net fluid leaving capillaries
(Pc-Pi) - (pi c - pi i) |
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Dressler's syndrome
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autoimmune phenomenon several weeks post-MI
->fibrinous pericarditis |
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dilated cardiomopathy
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90% of all cardiomyopathies
Alcohol, Beriberi, Coxsackie B, Cocaine, Chagas', Doxorubicin toxicity [chemo], peripartum, hemochromatosis -> SYSTOLIC dysfunction |
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hypertrophic cardiomyopathy
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often asymmetric, involves intraventricular septum
50% familial (AD) sudden death in young athletes loud S4**, strong apical impulse, systolic murmur treat with B-blockers -> DIASTOLIC dysfunction |
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restrictive/obliterative cardiomyopathy
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sarcoidosis, amyloidosis, postradiation, Loffler's
|
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MR
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holosystolic
high pitched, 'blowing' loudest at apex |
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AS
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crescendo-decrescendo systolic, following an ejection click
LV >> aortic pressure in systole radiates to carotids, apex *pulsus parvus et tardus* |
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VSD
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holosystolic
|
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MVP
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late systolic murmur
midsystolic click #1 valvular lesion |
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AR
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high pitched blowing diastolic
associated with wide pulse pressure |
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MS
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delayed rumbling late diastolic
follows opening snap LA >> LV during diastole (takes a lot to open the stenotic MV) **tricuspid stenosis murmur gets louder with INSPIRATION** (b/c more blood to lungs) |
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pDA murmur
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continuous, machine like
throughout systole and diastole loudest at S2 (aortic/pulmonic close) |
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'heart failure cells'
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hemosiderin laded macrophages
|
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cause of orthopnea in CHF
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increased venous return in supine position
exacerbates pulmonary vascular congestion (= SOB) |
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virchow's triad
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stasis
hypercoagulability endothelial damage leads to DVTs |
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features of cardiac tamponade
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compression of heart by fluid leads to low CO
equilibration of pressures in all 4 chambers** hypotension, high JVP, pulsus paradoxus |
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Aschoff bodies
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=granulomas with giant cells
found in rheumatic heart disease also see Anitschkow's cells (activated histiocytes) |
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hydralazine
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increases cGMP: sm musc relaxation
vasodilates arterioles > veins REDUCED AFTERLOAD SEs: tachycardia, fluid retention, lupus like syndrome |
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CCBs
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block L-type Ca channels
->reduced cardiac contractility nifedipine better vascular sm muscle verapamil better heart muscle SEs: cardiac depression, edema, flushing, constipation |
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nitroglycerine, isosoribde dinitrate
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release NO in smooth muscle: increased cGMP
veins >> arteries REDUCED PRELOAD for angina, pulmonary edema |
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digoxin
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inhibits Na/K/ATPase
->increased Na-i leads to increased Ca-i (b/c Na won't come in using Na/Ca antiport) EKG changes ->low QT, scooping of ST, T wave inversion* used for CHF, a-fib (low AV) SEs -> n/v, van gogh vision, arrhymthmias |
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Digoxin drug interaction
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increased [ ] with renal failure
hypokaleima potentiates effects (low K = more K out, Na in) quinidine decreases clearance *treat Dig toxicity with K+ admin (or Mg+) |
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beta blockers with intrinsic sympathomimetic activity
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acebutolol and pindolol
not recommended for pts with angina (can exacerbate) |
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CCBs to avoid in those with CHF
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verapamil
->1st gen CCB that has strong negative inotropic effect dilitiazem ->mild to mod negative inotrope *amlodipine and felodipine are used in CHF pts (can actually increase contractility) |
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treatment of WPW
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don't use an agent that slows AV node conduction (will increase propensity to go to bypass tract)
DO use ibutilide (K channel blocker) ->disrupts reentry circuits and increases refractory period of the bypass tract |
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acute treatment of atrial fibrillation
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dilitiazem (IV)
-inhibits Ca into vascular sm muscle and myocardium -AV node blocker *amiodarine takes 1-3 weeks to work properly |
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most common cardiac anomaly in Ts21
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endocardial cushion defect (??)
or maybe ASD/VSD 20% have congenital cardiac abnormalities |
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mean linear velocity of a RBC is lowest in what vessels?
|
capillaries (have the largest cross-sectional area)
velocity from highest to lowest: aorta > vena cavae > large veins > small arteries > arterioles > small veins > venules > capillaries |
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Churg-Strauss syndrome
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aka allergic granulomatosis and angiitis
variant of PAN--> ass'd with asthma and eosinophilia vascular lesions, granulomas, GI vasculitis |
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polyarteritis nodosa (PAN)
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affects small/med arteries
->esp GI tract and kidneys fibrinoid necrosis of vessels w/ polys, eos, monos often young adult males Tx: steroids, cyclophosphamide |
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severe anemia's affects on vessels
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hypoxia causes dilation of small arterioles and arteries
also: low blood viscosity, decreased PVR, low splanchnic blood flow |
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most common primary cardiac tumor in children
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rhabdomyoma
composed of cells that resemble skeletal muscle **common in kids with tuberous sclerosis |
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mechanism of cocaine-induced hypertension
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blocks re-uptake of NE
|
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arterioles account for ___% of total peripheral resistance
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50% (greatest fall in bp occurs as blood goes thru arterioles)
-highest ratio of wall to cross-sectional area to lumen cross-sectional area |
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leukocytoclastic angiitis
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=microscopic PAN
smaller affected vessels vasculitis w/hemorrhage to skin (palpable purpura) many fragmented neutrophils *penicillin is a common trigger |
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vascular structures that contain the greatest % of total blood volume
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venules and veins (64%)
|
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week of gestation when heart forms
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4th week
(heart forms and starts beating almost immediately) 6th week = heart is fully formed (so difficult to prevent congenital malformations b/c heart forms so early) |
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alpha1 agonists act on...
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smooth muscle cells in media of arterioles
leads to increase in intracellular Ca [smooth muscle contraction] |
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ASD found in Down's syndrome
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ostium primum (most common type in general is the ostium secundum)
can also be associated with tricuspid and mitral valve abnormalities *L-R shunts with late cyanosis (when reversal occurs) |
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mean systemic filling pressure (MSFP)
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pressure that exists when heart has been stopped and blood has been redistribuited equally
as MSFP increases, there is more venous return to heart **venous system is important blood reservoir (normal fxn can be resored w/20% of blood loss) |
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when O2 consumption of the heart increases, this builds up in heart muscle
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adenosine
(ATP degrades to adenosine) adenosine then dilates vessels allowing increased coronary blood flow |
|
graft vascular disease (aka graft arteriosclerosis)
|
develops years after transplant
intimal thickening of coronary arteries w/out atheroma formation or inflammation leads to progressive stenosis chest pain DOES NOT accompany the ischemia--> sudden death **can't be prevented with current immunosuppresive Tx |
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this decreases in old age and causes widened pulse pressure
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arterial compliance (usually due to hardening by arteriosclerosis)
|
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cardiac complications of fragile X syndrome
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mitral valve prolapse and aortic root dilatation
[occur late in adolescence or adulthood] |
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___% of those with ischemic heart disease will present with death
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25%
|
|
Beta-1 selective beta blockers
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A BEAM
atenolol, betaxolol, esmolol, acebutalol, metroprolol non-selective: labetalol (also adds alpha 1), timolol, nadolol |
|
individual cardiac muscles are joined together at
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intercalated disks (that contain gap jxns)
|
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fetal umbilical arteries arise from
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the fetal iliac arteries (supply unoxygenated blood to the placenta)
umbilical vein takes newly oxygenated blood from placenta to fetal liver then to IVC via the ductus venosus |
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fibrinous and serofibrionous pericarditis
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= Dresseler's syndrome (when following an acute MI)
|
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why is atenolol contra-indicated in DM pts?
|
b/c it can block the 'warning signs' of hypoglycemia
|
|
what is a cystic hygroma??
|
lymphatic malformations resembling hemangiomas
-->a feature of Turner syndrome that contributes to the 'webbed neck' (and remember, Turner is associated with coarctation of the aorta) |
|
side effect of metroprolol
|
dyslipidemia
|
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ovary drainage
|
R ovary = ovarian vein to IVC
L ovary = ovarian vein to RENAL VEIN to IVC |
|
best drug for initial treatment of hypertrophic cardiomyopathy
|
beta blocker (metoprolol)
Sx: sustained apical impulse, loud S4, systolic ejection murmur echo = systolic anterior motion of mitral valve, assymetic LVH, early closing of aortic valve |
|
appearance of amyloidosis
|
waxy texture of affected organs
histo = positive Congo red staining |
|
TPR
|
(MAP-RAP) / CO
pressure = flow x resistance (P = Q x R) |
|
removing an organ will ___ the TPR
|
INCREASE
(organs are in parallel.. and adding parallel resistances = lower total) |
|
fully compensated aortic coarctation
|
blood flow normal in upper and lower body
but there is increased arterial pressure in upper body ->lower vascular resistance in lower body (b/c resistance = pressure / flow) |
|
possible finding at autopsy of a SIDS baby
|
RVH
|
|
endocardial fibroelastosis
|
probably related to intrauterine viral infection (mumps)
thickened endocardium w/fibrous and elastic tissue LV is most commonly involved other findings = mural thrombi, flattened trabeculae and stenosed valves *infantile and adolescent forms |
|
artery commonly damaged in knee dislocations
|
popliteal artery
-divides into anterior tibial, posterior tibial and peroneal -emerges from superficial femoral artery |
|
classical findings in ASD
|
prominent RV impulse
systolic ejection murmur heard in pulmonic area fixed split S2 *due to abnormal L-R shunt [creates volume overload on R side] |
|
massive PE affects which part of the heart first?
|
RV
[a saddle PE causes acute cor pulmonale with abrupt RV dilation] *acute cor pulmonale is a surgical emergency |
|
cardiac tamponade causes build up of fluid in which space?
|
between the epicardium [visceral pericardium] and parietal pericardium
(aka the pericardial space) |
|
PO agent similar to lidocaine
|
mexiletine
(class IB anti-arrhythmic for treatment of VT) Na channel blocker and shortens AP duration |