cardio review
Terms
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- cardiac output(CO) formula
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rate of O2 consumption/
(arterial O2 content - venous) - mean arterial pressure (MAP) formula
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MAP = CO - TPR
MAP also = 1/3 systolic + 2/3 diastolic - stroke volume (SV) formula
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SV = CO/ HR
SV also = EDV-ESV - cardiac output variables
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SV CAP
->SV is affected by Contractility, Afterload and Preload - 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) - contractility/SV decreases due to
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B1 blockers
heart failure
acidosis
hypoxia/hypercapnea
Ca channel blockers - force of contraction [starling curve
- is proportional to the initial length of cardiac muscle fiber [PRELOAD]
- 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% - 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 - 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 - 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 - 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) - 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** - 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 - 1st degree AV block
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PR interval prolonged (>200 msec)
is asymptomatic - 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 - 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) - O2 demand in heart
- high O2 demand drives increased blood flow, NOT increased extraction of O2
- fluid pressure [hydrostatic] starling forces
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Pc = capillary fluid pressure
-> fluid out of capillary
Pi = interstitial fluid pressure
-> fluid into capillary - 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 - right to left shunts
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=early cyanosis (blue babies)
Teratology of Fallot
Transposition of great arteries
Truncus arteriosus - left to right shunts
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VSD (#1 congenital anomaly)
ASD (loud S1, fixed split S2)
PDA (close w/indomethacin) - 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 - 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) - 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 - 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 - 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 - monckeburg arteriosclerosis
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calcification of arteries, especially radial or ulnar.
usually benign - arteriolosclerosis
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hyaline thickening of small arteries due to essential hypertension
ONION SKINNING in malignant HTN - cardiovascular system is derived from which cell layer?
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mesoderm
paired endocardial heart tubes from in cephalic region - 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 - pathophysiology of teratology of Fallot
- aberrant development of aortico-pulmonary septum [which should normally divide aorta and pulmonary trunk]
- 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 - 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 - paradoxical emboli
- originate in the venous circulation and pass through pFO or ASD to produce symptoms on arterial side
- situs inversus
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all body's organs are transposed
associated with Kartagener's syndrome [immotile cilia] - 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 - 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 - change in pulse pressure with arteriosclerosis
- increases (b/c arteries have hardened... need to push harder [higher systolic bp] to get the blood out)
- 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 - 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 - 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) - 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 - effect of severe anemia
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wide pulse pressure
->resting CO is increased due to increased SV and HR
also see tachycardia - causes of decreased pulse pressure
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aortic valve obstruction
cardiac tamponade
heart failure
mitral valve obstruction - 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) - 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] - cyanosis
- only from R-L shunt
- signs of cardiac tamponade
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decreased arterial pressure
small, quiet heart
hypotension, tachypnea, tachycardia, increased JVP
*pulsus paradoxus - 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 - location of femoral vein on CT
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medial to femoral artery
('venous toward the penis') - 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 - 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 - Kawasaki disease
-
'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 - positive result in starling equation
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=net fluid leaving capillaries
(Pc-Pi) - (pi c - pi i) - Dressler's syndrome
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autoimmune phenomenon several weeks post-MI
->fibrinous pericarditis - dilated cardiomopathy
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90% of all cardiomyopathies
Alcohol, Beriberi, Coxsackie B, Cocaine, Chagas', Doxorubicin toxicity [chemo], peripartum, hemochromatosis
-> SYSTOLIC dysfunction - 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 - restrictive/obliterative cardiomyopathy
- sarcoidosis, amyloidosis, postradiation, Loffler's
- MR
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holosystolic
high pitched, 'blowing'
loudest at apex - 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* - VSD
- holosystolic
- MVP
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late systolic murmur
midsystolic click
#1 valvular lesion - AR
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high pitched blowing diastolic
associated with wide pulse pressure - 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) - pDA murmur
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continuous, machine like
throughout systole and diastole
loudest at S2 (aortic/pulmonic close) - 'heart failure cells'
- hemosiderin laded macrophages
- cause of orthopnea in CHF
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increased venous return in supine position
exacerbates pulmonary vascular congestion (= SOB) - virchow's triad
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stasis
hypercoagulability
endothelial damage
leads to DVTs - 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 - Aschoff bodies
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=granulomas with giant cells
found in rheumatic heart disease
also see Anitschkow's cells (activated histiocytes) - hydralazine
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increases cGMP: sm musc relaxation
vasodilates arterioles > veins
REDUCED AFTERLOAD
SEs: tachycardia, fluid retention, lupus like syndrome - 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 - nitroglycerine, isosoribde dinitrate
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release NO in smooth muscle: increased cGMP
veins >> arteries
REDUCED PRELOAD
for angina, pulmonary edema - 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 - 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+) - beta blockers with intrinsic sympathomimetic activity
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acebutolol and pindolol
not recommended for pts with angina (can exacerbate) - 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) - 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 - 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 - most common cardiac anomaly in Ts21
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endocardial cushion defect (??)
or maybe ASD/VSD
20% have congenital cardiac abnormalities - mean linear velocity of a RBC is lowest in what vessels?
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capillaries (have the largest cross-sectional area)
velocity from highest to lowest:
aorta > vena cavae > large veins > small arteries > arterioles > small veins > venules > capillaries - 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 - 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 - 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 - 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 - mechanism of cocaine-induced hypertension
- blocks re-uptake of NE
- arterioles account for ___% of total peripheral resistance
-
50% (greatest fall in bp occurs as blood goes thru arterioles)
-highest ratio of wall to cross-sectional area to lumen cross-sectional area - leukocytoclastic angiitis
-
=microscopic PAN
smaller affected vessels
vasculitis w/hemorrhage to skin (palpable purpura)
many fragmented neutrophils
*penicillin is a common trigger - vascular structures that contain the greatest % of total blood volume
- venules and veins (64%)
- 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) - alpha1 agonists act on...
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smooth muscle cells in media of arterioles
leads to increase in intracellular Ca [smooth muscle contraction] - 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) - 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) - 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 - this decreases in old age and causes widened pulse pressure
- arterial compliance (usually due to hardening by arteriosclerosis)
- cardiac complications of fragile X syndrome
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mitral valve prolapse and aortic root dilatation
[occur late in adolescence or adulthood] - ___% of those with ischemic heart disease will present with death
- 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
- intercalated disks (that contain gap jxns)
- 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 - fibrinous and serofibrionous pericarditis
- = Dresseler's syndrome (when following an acute MI)
- why is atenolol contra-indicated in DM pts?
- b/c it can block the 'warning signs' of hypoglycemia
- what is a cystic hygroma??
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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
- 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
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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
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waxy texture of affected organs
histo = positive Congo red staining - TPR
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(MAP-RAP) / CO
pressure = flow x resistance
(P = Q x R) - removing an organ will ___ the TPR
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INCREASE
(organs are in parallel.. and adding parallel resistances = lower total) - fully compensated aortic coarctation
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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?
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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