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262 Cards in this Set

  • Front
  • Back
In the ventricular action potential, what causes the Phase 0 rapid upswing?
opening of voltage gated Na channels
In the phase 2 plateau, Ca++ influx triggers Ca++ release from the SR causing ….
myocyte contraction
What effect does Ach have on HR?
What effect do catecholamines have on HR
Name 4 things that increase contractility:
catecholamines, digitalis, an increase in intracellular Ca++, or a decrease in extracellular Na+
What effect does increased afterload have on myocardial oxygen demand?
how do catecholamines increase contractility?
increase the activity of Ca++ pump in the SR
What effect will and MI have on contractile state of the heart?
what does S1 correspond to?
mitral and tricuspid valve closure
what does S2 correspond to?
aortic and pulmonary valve closure
what does S3 correspond to?
the end of rapid ventricular filling
what is S3 associated with?
dilated CHF
what is S4 and what does it indicate?
an atrial kick associated with a hyptertrophic ventricle (high atrial pressure/stiff ventricle)
what is the a wave?
atrial contraction
what is the c wave?
RV contraction when the tricuspid valve bulges into atrium
what is the v wave?
increase in atrial pressure due to filling against a closed tricuspid valve
what is physiologic S2 splitting
aortic valve closes just before the pulmonic - the difference is increased on inspiration
what is paradoxical splitting
when the split is heard on expiration instead of inspiration … associated with aortic stenosis
what is meant by "HIZ" shrinkage
the H, I, and Z band decrease in length on muscle contraction, the A band (myosin) stays the same length
describe the pathway of smooth muscle contraction
ap - > sm muslce depolarization - > open Ca++ channels -> increase in cytosol Ca++ -> Ca++ bind Calmodulin -> activates MLCK -> relaxation ->MLCP forms a cross bridge and contraction by binding myosin to actin - > MLCK relaxes … cycle continues while Ca is present.
in an EKG, what does the P wave represent?
atrial depolarization
in an EKG, what does the PR segment represent?
conduction delay through the AV (200 msec)
in an EKG, what does the QRS complex represent?
ventricular depolarization(120 msec)
in an EKG, what does the QT interval represent?
mechanical contraction of the ventricle
in and EKG, what does the T wave represent?
ventricular repolarization
do you see atrial repolarization on an EKG?
no, it is masked by the QRS complex
in an EKG, what does the ST segment represent?
isoelectric, ventricles are depolarized
on an EKG, what is a U wave?
caused by hypokalemia
what is Wolff-Parkinson-White syndrome
when an accessory conduction pathway exists from atria to ventricle (bundle of Kent) - bypasses the AV node and ventricles partially depoliarize earlier giving rise to a delta wave. WPW syndrome may lead to recurrent entry and SVTs.
What do you see on and EKG with atrial fibrillation?
chaotic erratic baseline with no disrete P waves in between iregularly spaced QRS complexes
What do you see on an EKG with atrial flutter?
sawtooth, identical back to back P waves
How many kinds of AV block are there?
4: 1st degree, mobitz I, mobitz II, complete
What is 1st degree AV block?
asymptomatic - PR interval longer than 200 msec
What is mobitz II AV block?
driooed beats not proceeded by a progressively lengthening PR interval. Pathological … can progress to complete block
What is mobitz I AV block?
progressive PR lengthening until a beat is dropped … usually asymptomatic
what is a 3rd degree AV block
complete AV block, atria and ventricles beat independently … rx with pacemaker
what is v-fib
completely erradic rhythm with no identifiable waves, fatal without immediate defibrillation
what is the normal right atrial pressure?
what is the normal left atrial pressure
12 (approx with pcwp - swan-ganz)
what is the normal right ventricular blood pressure?
what is the normal pulmonary artery pressure?
what is the normal left ventricular pressure?
what is a normal aortic blood pressure?
of the total body weight, what proportion is blood?
8% … the rest is body fluids and tissues
of the total body blood, what proportion is plasma?
55% plasma … the rest is hematocrit.
what is serum?
plasma without clotting factors
what is the makeup of plasma?
91.5% water, 7% protein, salts, lipids, enzymes, and vitamins
what is the makeup of plasma proteins?
55% albumin, 38% globulin, 7% fibrinogen
what are the three kinds of cells in hematocrit?
erythrocytes, leukocytes, and platelets
what is the typical makeup of WBCs in the blood?
40-70% PMNS, 20-40% lymphocytes, 2-10% monocytes, 1-6% eosinophils, <1% basophils
what is the net filtration pressure
what are 4 common causes edema?
increased capillary pressure, decreased plasma proteins, increased capillary permeability, or increased interstitial colloid pressure
what is a common cause of increased capillary pressure
heart failure
what is a common cause of decreased plasma proteins
nephrotic syndrome or liver failure
what may cause increased capillary permeability?
toxins, infections, burns
what could cause increased colloid presure?
lymphatic blockage
what are the three structures in the carotid sheath?
internal jugular v. (lateral), common carotid a. (medial), vagus n. (posterior)
in most cases, what supplies the SA and AV nodes?
80% of the time, what supplies the inferior portion of the LV via the PD artery?
RCA (right dominant)
when do the coronary arteries fill?
during diastole
what supplies the anterior interventricular septum?
what is the most posterior part of the heart? enlargment can cause what?
left atrium; dysphagia
what artery gives off large obtuse marginal branches that supply the lateral and posterior walls of the LV?
what supplies the anterior 2/3 of IV septum, apical portion of anterior papillary muscle, and the anterior surface of the LV?
where does the RCA travel?
in the right AV groove
what supplies the inferior and posterior wals of the ventricles and the posterior 1/3 of the IV septum?
posterior descending (typically a branch of RCA)
Cardiac output = ?
stroke volume x heart rate
what is the Fick principle?
CO = rate of O2 consumption/ (arterial O2 content - venous O2 content)
how do you calculate mean arterial pressure?
CO x TPR = 1/3SBP + 2/3 DBP
pulse pressure = ?
systolic - diastolic (approx SV)
stroke volume = ?
what variables affect stroke volume?
contractility, afterload, and preload - SV CAP
what effect does increased intracellular calcium have on contractility and SV?
increases contractility and SV
how does decreased extracellular sodium affect contractility and SV?
increases contractility and SV
5 things that decrease contractility and SV?
B1 block, heart failure, acidosis, hypoxea/hypercapnea, Ca++ channel blockers
what effect does digitalis have on contractility and SV?
increases them
preload is equal to what volume?
end diastolic volume
afterload is equal to what presure?
systolic arterial pressure (proportional to peripheral resistance)
what effect do venous dilators (e.g. nitroglycerin) have?
decrease preload
what effect do vasodilators (e.g. hydralazine) have?
decrease afterload
this increases slightly with exercise, increased blood volume (overtransfusion), and excitement (sympathetics)
ejection fraction = ?
SV/EDV = (EDV-ESV)/EDV = index of contractility
ejection fraction is normally greater than or equal to?
resistance is directly proportional to what?
resistance is inversely proportional to what?
radius to the 4th power
delta P = ?
Q x R
resistance = ?
[delta P/Q]/[8xviscosityxlengthxr to the 4th]
what does viscosity mostly depend on? when is it increased?
hematocrit: incrased in polycythemia, hyperproteinemic states (e.g. multiple myeloma), hereditary spherocytosis
when in the cardiac cycle is O2 consumption highest?
isovolumetric contraction
this is the period between mitral valve closing and aortic valve opening
isovolumetric contraction
this is the period between aortic valve opening and closing
systolic ejection
this is the period between aortic valve closing and mitral vale opening
isovolumetric relaxation
when does rapid filling occur?
just after mitral valve opens
when does slow filling occur?
just before mitral valve closes
when is JVD seen?
right heart failure
what is cardiac muscle contraction dependent on?
extracellular calcium, which enters the cells during plateau of action potential and stimulates calcium release from the sarcoplasmic reticulum (calcium-induced calcium release)
what is the plateau in the cardiac muscle action potential due to?
calcium influx
where does the pacemaker action potential occur?
SA and AV nodes
what accounts for the automaticity of the SA and AV nodes?
slow diastolic depolarization - membrane potential spontaneously depolarizes as Na+ conductance increases (funny channel)
what determines heart rate?
slope of phase 4 in the SA node
what are the peripheral chemoreceptors? what do they respond to?
carotid and aortic bodies - they respond to decreased (less than 60 mmHg)/increased PCO2, decreased pH of blood
what do central chemoreceptors respond to?
changes in pH and PCO2 of brain interstitial fluid, which in turn are influenced by arterial CO2
what does the aortic arch respond to? how does it transmit and to where?
responds to increased BP; transmits via vagus to medulla
how and to where does the carotid sinus transmit information?
via glossopharyngeal to the medulla
how do the central chemoreceptors respond to increased intracranial pressure?
hypertension (sympathetic response) and bradycardia (parasympathetic response)
what organ receives the larges share of systemic cardiac output?
what organ receivest eh highest blood flow per gramof tissue?
how does the heart meet increased O2 demand?
incrased coronary blood flow, not by increased extraction of O2
hypoxia in the pulmonary vasculature causes what?
vasoconstriction (unique because in other organs hypoxia causes vasodilation)
what are the local factors in the heart that determine autoregulaton?
O2, adenosine, NO
what are the local factors in the brain that determine autoregulation?
CO2 (pH)
how do the kidneys determine autoregulation?
myogenic and tuboglomerular feedback
what local factors determine autoregulation in skeletal muscle?
lactate, adenosine, K+
what is the most important mechanism for determining autoregulation in the skin?
sympathetic stimulation - temperature control
what is the effect of carotid massage?
incrases pressure on carotid artery - increasing stretch and leading to decreased HR
what is the ultimate consequence of baroreceptors sensing hypotension?
vasoconstriction, incrased HR, contractility, and BP - important in the response to severe hemorrhage
sound of mitral and tricuspid valve closure
sound of aortic and pulmonary valve closure
sound at end of rapid ventricular filling
sound from high atrial pressure/stiff ventricle
what is S3 associated with?
dilated CHF, mitral/tricuspid regurgitation
what is S4 (atrial kick) associated with?
hypertrophic ventricle
what is paradoxical splitting associated with?
aortic stenosis, LBBB
what is fixed splitting associated with?
holosystolic high pitched 'blowing murmur' loudest at apex
mitral regurg (tricuspid regurg)
cresecendo-decrescendo systolic ejection murmur following ejection click
aortic (pulmonic) stenosis
pulsus parvus et tardus
pulses weak compared to heart sounds; seen in aortic stenosis
holosystolic murmur
late systolic murmur with midsystolic click
mitral prolapse
immediate high-pitched blowing diastolic murmur; wide pulse pressure
aortic regurgitation
delayed rubbing late diastolic murmur that follows opening snap
mitral stenosis
how does the murmur in tricuspid stenosis differ from that of mitral stenosis?
tricuspid stenosis differs because it gets louder with inspiration
continuous machine-like murmur
when is the murmur associated with a PDA loudest?
what does the P wave on EKG represent?
atrial depolarization
what does the PR segment on EKG represent? how long is it normally?
conduction delay through AV node - normally <200 msec
what does the QRS complex represent? how long is it normally?
ventricular depolarization (<120 msec)
what does the QT interval represent?
mechanical contraction of the ventricles
what does the T wave represent?
ventricular repolarization
why don't you see atrial repolarization on EKG?
it is masked by the QRS complex
what causes a U wave?
delta wave on EKG is characteristc of what?
Wolff-Parkinson-White syndrome
in this syndrome, there is an accessory conduction pathway from atria to ventricle (bundle of Kent), bypassing the AV node
Wolff-Parkinson-White syndrome
this syndrome may result in reentry current leading to supraventricular tachycardia
Wolff-Parkinson-White syndrome
what is the hallmark of a transmural MI?
pathologic Q wave
increased capillary pressure is seen in what?
heart failure
decreased plasma colloid osmotic pressure is seen in what?
nephrotic syndrome, lver failure
increased capillary permeability is seen in what?
toxins, infections, burns
increased interstitial fluid colloid osmotic pressure is seen in what?
lymphatic blockage
three causes of early cyanosis
tetralogy of fallot, transposition of the great vessels, trucus arteriosis
three causes of late cyanosis
what is the most common congenital cardiac abnormality?
what causes Tetralogy of Fallot?
anterosuperior displacement of the infundibular septum
aortic stenosis proximal to insertion of ductus arteriosus?
preductal - infantile type
aortic stenosis distal to ductus arteriosus?
postductal - adult type
notching of ribs, hypertension in upper extremities, weak pulses in lower extremities?
coarctation of aorta
22q11 syndromes are asscociated with what cardiac defects?
truncus arteriosus, tetralogy of Fallot
what cardiac defects is Down syndrome associated with?
what cardiac defects is congenital rubella associated with?
septal defects, PDA
what cardiac defects are associated with offspring of diabetic mothers?
transposition of great vessels
Marfan's is associated with what congenital cardiac defect?
aortic insufficiency
lipid deposit in cornea
corneal arcus
what characterizes Monckeberg arteriosclerosis?
calcification of arteries, especially radial or unlar; usually benign (involves media - ring-like calcifications; 'pipestem')
arteriosclerosis in essential hypertension?
hyaline thickening of small arteries
arteriosclerosis in malignant hypertension?
hyperplastic 'onion skinning'
fibrous plaques and atheromas form in what part of arteries in atherosclerosis?
risk factors for atherosclerosis?
smoking, hypertension, DM, hperlipidemia, family Hx
progression of atherosclerosis?
fatty streaks - proliferative plaque - complex atheromas
complications of atherosclerosis?
aneurysms, ischemia, infarcts, peripheral vascular resistance, thrombus, emboli
location of atherosclerosis?
abdominal aorta > coronary artery > popliteal artery > carotid artery
angina occurs with coronary artery disease narrowing greater than whta?
retrosternal chest pain with exertion - what type of angina?
angina that occurs at rest secondary to coronary artery spasm?
Prinzmetal's variant
thrombosis but no necrosis/worsening chest pain - what type of angina?
where do red infarcts occur?
in loose tissues with collaterals, such as lungs, intestine, or following reperfusion
where do pale infarcts occur?
solid tissues with single blood supply - brain, heart, kidney, spleen
child with harsh systolic murmur, no diastolic murmur, and increased oxygen saturation in the RV?
cut CN IX and X bilaterally - what is hemodynamic result?
tachycardia with hypertension
EKG with random electrical activity without recognizable QRS complexes
ventricular fibrillation
what can atenolol cause in high doses?
bradycardia and varying degrees of AV block
what causes increased pulse pressure?
stiffening of arteries/ decreased arterial compliance
what maintains a PDA?
PGE analog - alprostadil
what artery is usually compressed in thoracic outlet syndrome?
what is the most common cause of sudden cardiac death in adults?
ischemic heart disease
sudden death in heart transplant patient?
graft vascular disease
cardiac defect associated with Fragile X?
MV prolapse and aortic root dilation
cardiac finding in SIDS?
right ventricular hypertrophy
endocarditis in patient with colon CA?
strep bovis
how does cocaine cause hypertension?
blocks NE reuptake
what substance responsible for calcified valves?
calcium phosphate
high risk for digitoxin therapy with what metabolic problem?
decreased arterial pressure, increased systemic venous pressure, and small, quiet heart
cardiac tamponade
rupture of ventricular wall leading to hemopericardium and cardiac tamponade, rupture of IV septum, rupture of papillary muscle can occur when post-MI?
5-10 days
what is the initial alteration leading to atherosclerosis?
injury to endothelial lining
in compensated aortic coarctation, what is decreased?
vascular resistance in lower body
drugs recommended for patients with diabetes and renal complications (e.g. hyperuricemia)?
ACE inhibitors
bacterial endocarditis in tricuspid valve?
what artery is frequently damaged in knee dislocations?
proper initial treatment for patient with hypertrophic cardiomyopathy?
anti-hypertensive causing gynecomastia?
what increases upon removal of a kidney?
total peripheral resistance
beta blockers with intrinsic sympathomimetic activity not recommended for patients with angina
acebutolol and pindolol
patient with vasculitic symptoms, eosiniophilia, and asthma?
access to vertebral artery via what?
suboccipital triangle
patients who develop digitoxin toxicity gradually during chronic therapy are often taking what type of drugs?
diuretics - hypokalemia and hypomagnesia
increased stroke volume causes what to happen to pulse pressure? in what type of patients is this seen?
wide pulse pressure - anemic patients
endomyocardial fibrosis with myocyte necrosis and a prominent eosinophilic infiltrate?
Loeffler endocarditis - result of direct toxicity to heart by proteins in eosinophil granules designed to kill large parasites
what types of pericarditis may follow acute MI?
fibrinous and serofibrinous pericarditis
what is caseous pericarditis typically due to?
these types of pericarditis can be seen in uremia, chest radiation, rheumatic fever, SLE, and following chest trauma
fibrinous and serofibrinous
this type of pericarditis is seen when pyogenic infections involve the pericardium, e.g. after cardiothoracic surgery
purulent pericarditis
this type of pericarditis is seen in non-infectious inflammations, e.g. rheumatic fever, lupus, scleroderma, tumors, and uremia
serous pericarditis
amyloid deposition in the myocardium results in what type of cardiomyopathy?
restrictive - can be seen in RA and other long-standing inflammatory conditions
what murmur is associated with a bicuspid aortic valve?
immediate diastolic murmur
what structures have the highest ratio of wall cross-sectional area to lumen cross-sectional area?
what type of protein is associated with RA?
AA amyloid protein
another name for hypertrophic cardiomyopathy?
idiopathic hypertrophic subaortic stenosis
administration of epinephrine after what type of drug causes a decrease in BP?
alpha adrenergic antagonist, e.g. phentolamine - blockes epi's vasoconstrictive action on arterioles
flow of blood through PDA?
aorta to left pulmonary artery
ACE inhibitors can cause what type of electrolyte disturbance?
small mass on mitral valve with finger-like projections; non-neoplastic
papillary fibroelastoma
calcium channel blocker associated with accelerated progression of CHF?
drug to slow ventricular response in Wolff-Parkinson White?
hypersensitivity angiitis or microscopic polyarteritis nodosa (can be caused by penicilin)
leukocytoclastic angiitis
in which part of the systemic circulation does the greatest decrease in blood pressure occur?
vasodilator with lupus-like syndrome as side effect?
mechanism of hydralazine?
increases cGMP - smooth muscle relaxation; vasodilates arterioles > veins; reduces afterload
what calcium channel blocker is most selective for peripheral vasculature?
mechanism of calcium channel blockers?
block voltage-dependent L-type calcium channels of cardiac and SM and thereby reduce contractility
which calcium channel blocker is not used to treat arrhythmias?
what is the goal of antianginal therapy?
reduce myocardial O2 consumption by decreasing 1 or more of the determinants of MVO2: EDV, BP, HR, contractility, ejection time
what do nitrates affect in antianginal therapy?
what happens to contractility and HR in nitrate therapy?
increase - reflex response
what do beta blockers affect in antianginal therapy?
how do nitrates affect ejection time and MVO2?
how do beta blockers affect ejection time?
increase it
what do beta blockers do to EDV?
increase it
what do beta blockers do to BP, contractility, and HR?
decrease them
what is digitoxin used for?
CHF (increases contractility) and atrial fibrillation (decreases conduciton at the AV node)
toxicities of digitoxin are increased by what?
renal failure, hpokalemia, and quinidine
blurry yellow vision is side effect of what?
what is the antidote for digitoxin?
slowly normalize K+, lidocaine, cardiac pacer, anti-dig Fab fragments
lupus-like syndrome is associated with what class IA antiarrythmic?
what are the class IA antiarrythmics?
Na+ channel blockers: quinidine, amiodarone, procainamide, disopyramide (queen amy proclaims disco pyramids)
this class IA antiarrhythmic can cause cinchonism (headache, tinnitus, thrombocytopenia), torsades de pointes (due to increased QT interval)
what class of antiarrhythmics are contraindicated post-MI
class IC - proarrhythmic
what beta blocker is very short acting?
what is the antiarrhythmic action of beta blockers?
decrease cAMP and calcium currents; suppress abnormal pacemaker by decreasing slope of phase 4 - AV node particularly sensitive - increased PR interval
toxicity of amiodarone?
pulmonary fibrosis, hepatotoxicity, hypo/hyperthroidism;corneal deposits, skin deposits resulting in photodermatitis, neuro effects, constipation, bradycardia, heart block, CHF
K+ channel blockers that can cause torsades de pointes
soltalol, ibutilide
K+ channel blocker that can cause new arrhythmias and hypotension?
wha type of cells do Ca2+ channel blockers primarily affect?
AV nodal cells
what type of antiarrhythmics are used for prevention of nodal arrhythmias?
class IV - Ca2+ channel blockers
what class IV antiarrhythmic can cause torsades de pointes?
what is the drug of choice for diagnosing/abolishing AV nodal arrhythmias?
what depresses ectopic pacemakers, especially in digitoxin toxicity?
Mg+ is effective for treating what?
torsades de pointes and digitoxin toxicity
drug for hypertension in patient with PKD?
ACE inhibitor
anti-hypertesive for pregnant woman?
in patients with wolff parkinson white and atrial fibrillation, what can digitoxin do?
enhance transmission through accessory pathways that can predispose to v tac