Flashcards in Cardiology_1 Deck (351):
Truncus arteriosus gives rise to what?
ascending aorta and pulmonary trunk
bulbus cordis gives rise to what?
smooth parts (outflow tract) of left and right ventricles
primitive ventricle gives rise to what?
trabeculated left and right ventricles
primitive atria give rise to what?
trabeculated left and right atria
left horn of sinus venosus gives rise to what?
right horn of SV gives rise to what?
smooth part of right atrium
right common cardinal vein and right anterior cardinal vein give rise to what?
what happens in the normal development of the truncus arteriosus?
neural crest migration → truncal and bulbar ridges that spiral and fuse to form the aorticopulmonary (AP) septum→ ascending aorta and pulmonary trunk
what are the truncus arteriosus pathologies?
1. TGA • 2. ToF • 3. TA
what is the defect in transposition of the great vessels?
failure to spiral
what is the TA defect in tetralogy of Fallot?
skewed AP septum development
what is the defect in persistent TA?
partial AP septum development
3 steps in embryologic formation of interventricular septum?
1. muscular ventricular septum forms- opening= interventricular foramen • 2. AP septum rotates and fuses with muscular ventricular septum to form membranous interventricular septum, closing interventricular foramen • 3. Growth of endocardial cushions separates atria from ventricles and contributes to both atrial separation and membranous portion of the interventricular septum
improper neural crest migration into the TA can result in what?
transposition of the great arteries or a persistent TA
in interventricular septum development, membranous septal defect causes what?
an initial left to right shunt, which later reverses to a right to left shunt due to onset of pulmonary hypertension (Eissenmenger's syndrome)
8 steps in interatrial septum development?
1. foramen primum narrows as septum primum grows toward endocardial cushions • 2. perforations in septum primum form foramen secundum (foramen primum disappears • 3. foramen scundum maintains right to left shunt as septum secundum begins to grow • 4. septum secundum contains a permanent opening (foramen ovale) • 5. foramen secundum enlarges and upper part of septum primum degenerates • 6. remaining portion of septum primum forms the valve of the foramen ovale • 7. septum secundum and septum primum fuse to form the atrial septum • 8. foramen ovale usually closes soon after birth because of ↑ LA pressure
what happens in pathology of interatrial septal development?
patent foramen ovale, caused by failure of the septum primum and septum secundum to fuse after birth
when is there fetal erythropoiesis in the yolk sac?
when is there fetal erythropoiesis in the liver?
when is there fetal erythropoiesis in the spleen?
when is there fetal erythropoiesis in the bone marrow?
mnemonic for fetal erythropoiesis?
young liver synthesizes blood
structure of HbF?
structure of HbA?
O2 content of fetal blood in the umbilical vein?
PO2~30 • 80% saturated with O2
O2 sat of umbilican arteries?
sites of 3 important shunts of fetal circulation?
1. ductus venosus • 2. foramen ovale • 3. ductus arteriosus
action of shunt at ductus venosus in fetal circulation?
blood entering the fetus through the umbilical vein is coducted via the ductus venosus into the IVC to bypass the hepatic circulation
action of the shunt at the foramen ovale in fetal circulation?
most oxygenated blood reaching the heart via the IVC is diverted through the foramen ovale and pumped out the aorta to the head and body
action of the shunt at the ductus arteriosus in fetal circulation?
deoxygenated blood entering the RA from the SVC enters the RV, is expelled into the pulmonary artery, then passes through the ductus arteriosus into the descending aorta
what happens to fetal circulation at birth when the infant takes a breath?
↓ resistance in pulmonary vasculature causes ↑ LA pressure vs RA pressure→ • foramen ovale closes (now called fossa ovalis) → • ↑ in O2 leads to ↓ in prostaglandins, causing closure of ductus arteriosus
what helps close PDA?
what keeps PDA open?
post natal derivative of the umbilical vein?
ligamentum teres hepatis, contained in falciform ligament
postnatal derivatives of umbilical arteries?
medial umbilical ligaments
postnatal derivatives of ductus arteriosus?
postnatal derivative of ductus venosus?
postnatal derivative of foramen ovale?
postnatal derivative of allantois?
urachus-median umbilical ligament
what is the urachus part of?
the allantoic duct between the bladder and the umbilicus
what finding is a remnant of the urachus?
urachal cyst, or sinus
postnatal derivative of the notochord?
nucleus pulplosus of intervertebral disc
LCX supplies what?
lateral and posterior walls of left ventricle
LAD supplies what?
anterior 2/3 of interventricular septum, anterior papillary muscle, and anterior surface of left ventricle
PD supplies what?
posterior 1/3 of interventricular septum and posterior walls of ventricles
acute marignal artery supplies what?
SA and AV nodes are usually supplied by what?
frequency and features of right dominant coronary circulation?
85% • PD arises from RCA
frequency and features of left-dominant coronary circulation?
8% • PD arises from LCX
frequency and features of codominant circulation?
7% • PD arises from both LCX and RCA
coronary artery occlusion most commonly occurs where?
when do coronary arteries fill?
most posterior part of the heart is what?
enlargement of LA can cause what?
dysphagia (due to compression of the esophagus) or hoarseness (due to compression of the left recurrent laryngeal nerve)
transesophageal echocardiography is useful for diagnosing what?
LA enlargement • aortic dissection • thoracic aortic aneurysm
equations for cardiac output?
CO= SV x HR • • Fick's: • CO= (rate of O2 consumption)/((arterial O2 content)- (venous O2 content))
equation for MAP?
MAP= CO x TPR • • MAP= 2/3 diastolic pressure + 1/3 systolic
systolic pressure - diastolic pressure
pulse pressure is proportional to what?
equations for stroke volume?
SV = CO/HR = EDV - ESV
during the early stages of exercise CO is maintained by what?
↑ HR and ↑ SV
during the late stages of exercise, CO is maintained by what?
↑ HR only (SV plateaus)
what happens during exercise if HR is too high?
diastolic filling is incomplete and CO ↓
cardiac variables that affect stroke volume?
SV CAP • Stroke Volume affected by Contractility, Afterload, and Preload
↑ SV when what?
↑ preload, ↓ afterload, ↑ contractility
contractility (and SV) ↑ with what?
1. catecholamines • 2. ↑ intracellular Ca++ • 3. ↓ extracellular Na+ • 4. Digitalis
how do catecholamines ↑ contractility?
↑ activity of Ca++ pump in sarcoplasmic reticulum
how does a ↓ in extracellular Na+ ↑ contractility?
↓ activity of Na+/Ca++ exchanger
how does digitalis ↑ contractility?
blocks Na+/K+ pump → ↑ intracellular Na+ →↓ Na+/Ca++ exchanger activity → ↑ intracellular Ca++
contractility and SV ↓ with what?
1. β blockade • 2. heart failure (systolic dysfunction) • 3. acidosis • 4. hypoxia/hypercapnia (↓PO2/↑PCO2) • 5. Non-dihydropyridine Ca++ channel blockers
effect of anxiety, exercise, and pregnancy on SV?
myocardial O2 demand is ↑ by what?
↑ afterload (proportional to arterial pressure) • ↑ contractility • ↑ heart rate • ↑ heart size (↑wall tension)
preload = ?
MAP (proportional to peripheral resistance)
agents that ↓ preload?
agents that ↓ afterload?
preload ↑ with what?
1. exercise (slightly) • 2. ↑ blood volume (overtransfusion) • 3. excitement (↑ sympathetic activity)
on Starling curve, force of contraction is proportional to what?
end-diastolic length of cardiac muscle fiber (preload)
on Starling curve, what are the factors that increase contractility?
sympathetic stimulation • catecholamines • digoxin
on starling curve, which factors ↓ contractility?
loss of myocardium (MI) • β blockers • Ca++ channel blockers
equation for EF?
EF= SV/EDV = (EDV-ESV)/EDV
EF is an index of what?
EF ↓ in what?
systolic heart failure
Q x R
equation for resistance?
resistance = (driving pressure ΔP)/(Flow Q)= (8ηl)/πr^4
equation for total resistance of vessels in series?
1/Toral Resistance of vessels in parallel?
= 1/R1 + 1/R2 + 1/R3...
viscosity ↑ in what?
1. polycythemia • 2. hyperproteinemic states (multiple myeloma) • 3. hereditary spherocytosis
viscosity ↓ in what?
pressure gradient drives blood flow where?
from high pressure to low pressure
resistance is proportional to what?
viscosity and vessel length
viscosity is inversely proportional to what?
the radius to the 4th power
what accounts for most of total peripheral resistance?
what vessels regulate capillary flow?
where is the operating point of the heart on the cardiac and vascular function curve?
intersection where cardiac output and venous return are equal
what causes the operating point of the heart on the cardiac and vascular function curve to shift straight down?
↑ TPR, hemorrhage before compensation can occur
what causes the operating point of the heart on the cardiac an vascular function curve to shift straight up?
↓ TPR, exercise, AV shunt
what causes the operating point of the heart to shift downward and rightward along the venous return curve on the cardiac and vascular function curve?
heart failure • narcotic overdose
what causes an upward shift in the CO curve?
what causes a downward shift in the CO curve?
what causes a rightward shift in the venous return curve?
↑ blood volume
what causes a leftward shift in the venous return curve?
↓ blood volume
what is the X intercept of the venous return curve?
mean systemic filling pressure
what are the 5 phases of the left ventricle in the cardiac cycle?
1. isovolumetric contraction • 2. systolic ejection • 3. isovolumetric relaxation • 4. rapid filling • 5. reduced filling
what is isovolumetric contraction?
period between mitral valve closure and aortic valve opening
what is the period of highest O2 consumption during the cardiac cycle?
what is systolic ejection?
period between aortic valve opening and closing
what is isovolumetric relaxation?
period between aortic valve closing and mitral valve opening
what is rapid filling?
period just after mitral valve opening
what is reduced filling?
period just before mitral valve closure
what causes a rightward EDV expansion without an upward pressure expansion in the LV cardiac cycle P/V curve?
↑preload → ↑SV
what causes a leftward ESV expansion with an upward pressure expansion on a LV cardiac cycle P/V curve?
↑ contractility • ↑ SV • ↑ EF • ↓ ESV
what causes a leftward ESV contraction with an upward pressure expansion on a LV cardiac cycle P/V curve?
↑ afterload • ↑ aortic pressure • ↓ SV • ↑ ESV
what causes S1 sound?
mitral and tricuspid valve closure
S1 is loudest where?
at mitral area
what causes S2 sound?
aortic and pulmonary valve closure
where is S2 loudest?
at left sternal border
when is S3 heard?
in early diastole during rapid ventricular filling phase
S3 is associated with what?
↑ filling pressures (MR, CHF)
S3 is more common in which types of ventricles?
dilated ventricles, but normal in children and pregnant women
when do you hear S4?
atrial kick in late diastole
what causes S4?
high atrial pressure • LA must push against stiff LV wall
S4 associated with what?
what does JVP a wave correspond to?
what does the JVP c wave correspond to?
RV contraction (closed tricuspid valve bulging into atrium)
what does the JVP x descent correspond to?
atrial relaxation and downward displacement of closed tricuspid valve during ventricular contraction
what does the JVP v wave correspond to?
↑ right atrial pressure due to filling against closed tricuspid valve
what does the JVP y descent correspond to?
blood flow from RA to RV
what happens in normal splitting?
inspiration → • drop in intrathoracic pressure → • ↑ venous return to the RV → • ↑ RV stroke volume → • ↑ RV ejection time → • delayed closure of the pulmonic valve
what else contributes to the delayed closure of the pulmonic valve in normal splitting?
↓ pulmonary impedance ( ↑ capacity of the pulmonary circulation)
what does normal splitting sound like?
A2 and P2 are close during expiration, • A2 and P2 are only slightly more separated during inspiration
wide splitting is seen in which conditions?
those that delay RV emptying (pulmonic stenosis, RBB block)
what happens in wide splitting?
delay in RV emptying causes delayed pulmonic sound (regardless of breath)
what does wide splitting sound like?
an exaggeration of normal splitting • Ex: A2 and P2 are split as wide as normal inspiration • Ins: A2 and P2 are split much wider than normal
fixed splitting is seen in what?
what happens in fixed splitting?
ASD → left to right shunt → ↑ RA and RV volumes → ↑ flow through pulmonic valve such that, regardless of breath, pulmonic closure is greatly delayed
paradoxical splitting is seen in what?
conditions that delay LV emptying (aortic stenosis, LBB block)
what happens in paradoxical splitting?
normal order of valve closure is reversed so that P2 sound occurs before A2.
what does paradoxical splitting sound like?
on inspiration, P2 closes later and moves closer to A2, thereby 'paradoxically' eliminating the split
what can cause a systolic murmur in the aortic area?
aortic stenosis • flow murmur • aortic valve sclerosis
where is the aortic auscultation area?
2nd intercostal space RSB
what causes a systolic ejection murmur in the pulmonic area?
pulmonic stenosis • flow murmur (ASD, PDA)
where is the pulmonic area for ausculation?
2nd interspace LSB
what causes a pansystolic murmur at the tricuspid area?
tricuspid regurgitation • ventricular septal defect
what causes diastolic murmur at the tricuspid area?
tricuspid stenosis • ASD
where is the tricuspid area for auscultation?
5th interspace LSB
what causes a systolic murmur in the mitral area?
what causes a diastolic murmur in the mitral area?
where is the mitral area for auscultation?
5th interspace mid clavicular line
what causes diastolic murmur at the left sternal border?
aortic regurgitation • pulmonic regurgitation
what causes systolic murmur at left sternal border?
what are the auscultation findings in ASD?
pulmonary flow murmur • diastolic rumble (tricuspid) • blood flow across the ASD doesn't cause a murmur because there is no pressure gradient • murmur → louder diastolic murmur of pulmonic regurgitation from dilation of pulmonary artery
the continuous, machine-like murmur of PDA is best appreciated where?
left infraclavicular region
what is the effect of inspiration on ausculation?
↑ intensity of right heart sounds
what is the effect of expiration on auscultation?
↑ intensity of left heart sounds
what is the effect of hand grip maneuver on auscultation (↑ systemic vascular resistance)?
↑ intensity of MR, AR, VSD, MVP murmurs • ↓ intensity of AS, hypertrophic cardiomyopathy murmurs
what is the effect of the vasalva maneuver (↓ venous return) on auscultation?
↓ intensity of most murmurs • ↑ intensity of MVP, hypertrophic cardiomyopathy murmurs
what is the effect of rapid squatting (↑ venous return, ↑ preload, ↑afterload with prolonged squatting)?
↓ intensity of MVP, hypertrophic cardiomyopathy murmurs
conditions associated with systolic heart sounds include what?
aortic/pulmonic stenosis • mitral/tricuspid regurgitation • VSD
conditons associated with diastolic heart sounds include what?
aortic/pulmonic regurgitation • mitral/tricuspid stenosis
what does mitral/tricuspid regurgitation sound like?
holosystolic, high-pitched "blowing murmur"
mitral regurgitation is loudest where?
at apex and radiates to toward axilla
mitral regurgitation sound is enhanced by what?
maneuvers that ↑ TPR (squatting, hand grip) or LA return (expiration)
MR is often due to what?
ischemic heart disease, mitral valve prolapse, LV dilation
where is tricuspid regurgitation loudest?
loudest at tricuspid area and radiates to right sternal border
tricuspid regurgitation sound enhanced by what?
maneuvers that ↑ RA return (inspiration)
TR can be caused by what?
rheumatic fever and infective endocarditis can cause which heart sounds?
MR or TR
what does Aortic stenosis sound like?
crescendo-decrescendo systolic ejection murmur following ejection click • radiates to carotids/heart base
what causes ejection click in aortic stenosis?
EC due to abrupt halting of valve leaflets
pressure gradient in aortic stenosis?
LV>> aortic pressure during systole
pulse findings in aortic stenosis?
pulsus parvus et tardus' • pulses are weak with a delayed peak
aortic stenosis can lead to what?
Syncope, Angina, Dyspnea on exertion (SAD)
aortic stenosis is due to what?
age related calcific aortic stenosis or bicuspid aortic valve
what does VSD sound like?
holosystolic, harsh sounding murmur
where is VSD loudest?
VSD sound can be accentuated how?
hand grip maneuver due to increased afterload
what does MVP sound like?
late systolic crescendo murmur with midsystolic click
what causes MC?
sudden tensing of the chordae tendineae
what is the most frequent valvular lesion?
MVP is best heard where?
when is MVP loudest?
severity of MVP?
MVP can predispose to what?
MVP can be caused by what?
myxomatous degeneration • rheumatic fever • chordae rupture
MVP enhanced by what?
maneuvers that ↓ Venous return (standing or vasalva)
what does aortic regurgitation sound like?
immediate high pitched "blowing" diastolic decrescendo murmur
pulses in AR?
wide pulse pressure when chronic; can present with bounding pulses and head bobbing
AR is often due to what?
aortic root dilation, bicuspid aortic valve, endocarditis, rheumatic fever
what ↑ murmur in AR?
effect of vasodilators on AR?
↓ intensity of murmur
what does MS sound like?
follows opening snap • delayed rumbling late diastolic murmur
what causes OS in MS?
abrupt halt in leaflet motion in diastole, after rapid opening due to fusion at leaflet tips
pressure gradient in MS?
LA>>LV during diastole
MS often occurs secondary to what?
chronic MS can result in what?
MS sound is enhanced by what?
maneuvers that ↑ LA return (expiration)
what does PDA sound like?
continuous machine like murmur
when is PDA loudest?
PDA is often due to what?
congenital rubella or prematurity
where is PDA best heard?
left infraclavicular area
ventricular action potential also occurs where?
in bundle of His and Purkinje fibers
what happens in Phase 0 of ventricular action potential?
rapid upstroke- voltage gated Na+ channels open
what happens in Phase 1 of ventricular action potential?
initial repolarization- inactivation of voltage gated Na+ channels. Voltage gated K+ channels begin to open
what happens in Phase 2 of ventricular action potential?
plateau-Ca++ influx through voltage gated Ca++ channels balances K+ efflux • Ca++ influx triggers Ca++ release from sarcoplasmic reticulum and myocyte contraction
what happens in phase 3 of ventricular action potential?
rapid repolarization= massive K+ efflux due to opening of voltage-gated slow K+ channels and closure of voltage gated Ca++ channels
what happens in phase 4 of the ventricular action potential?
resting potential- high K+ permeability through K+ channels
difference between cardiac muscle AP and skeletal muscle?
1. cardiac muscle AP has a plateau, which is due to Ca++ influx and K+ efflux, myocyte contraction occurs due to Ca++ induced Ca++ release from the sarcoplasmic reticulum • 2. cardiac nodal cells spontaneously depolarize during diastole resulting in automaticity due to If channels • 3. Cardiac myocytes are electrically coupled to eachother by gap junctions
what do If chanels do?
funny current channels responsible for a slow, mixed Na+/K+ inward current
what is the direction of the leak currents in cardiac ventricular myocytes?
K+ out • Na+, Ca++ in
pacemaker action potential occurs where?
in the SA and AV nodes
what happens in phase 0 of the pacemaker action potential?
upstroke- opening of VG Ca++ channels • fast VG Na channels are permanently inactivated because of the less negative resting voltage of these cells
permanent fast VG Na channel inactivation in the pacemaker cells results in what?
slow conduction velocity that is used by the AV node to prolong transmission from the atria to the ventricles
what happens in Phase 2 or pacemaker potential?
plateau is absent
what happens in phase 3 of the pacemaker potential?
inactivation of the Ca++ channels and ↑ activation of K+ channels→ ↑ K+ efflux
what happens in phase 4 of the pacemaker potential?
slow diastolic depolarization- membrane potential spontaneously depolarizes as Na+ conductance ↑ (If different from Ina in phase 0 of ventricular action potential)
phase 4 of the pacemaker potential accounts for what?
automaticity of SA and AV nodes
slope of phase 4 in the SA node determines what?
effect of ACh/adenosine on SA node?
↓ the rate of diastolic depolarization and ↓ HR
effect of catecholamines on SA node?
↑ depolarization and ↑ heart rate
effect of sympathetic stimulation on SA/AV node?
↑ the chance that If channels are open and thus ↑ HR
P wave corresponds to what?
atrial repolarization in ECG?
masked by QRS complex
PR interval corresponds to what?
conduction delay through AV node
normal PR interval?
QRS complex correspondes to what?
normal duration of QRS complex?
QT interval corresponds to what?
mechanical contraction of the ventricles
T wave corresponds to what?
T wave inversion may indicate what?
ST segment corresponds to what?
isoelectric, ventricles depolarized
U wave is caused by what?
hypokalemia • bradycardia
relative speed of conduction in the heart?
purkinje > atria > ventricles > AV nodes
relative speed of conduction in the pacemaker cells?
SA node> AV> Bundle of his/purkinje/ventricles
what is the conduction pathway in the heart?
SA node → atria → AV node → common bundle→ bundle branches→ purkinje fibers→ ventricles
dominant pacemaker in heart?
SA node pacemaker inherent dominance with slow phase of the upstroke
what is the delay in the AV node?
100ms delay- atrioventricular delay; allows time for ventricular filling
what happens in torsades de pointes?
ventricular tachycardia, characterized by shifting sinusoidal waveforms on ECG, can progress to ventricular fibrillation
what predisposes to torsades de pointes?
anything that prolongs the QT interval
treatment for torsades de pointes?
congenital long QT syndromes are most often due to what?
defects in cardiac sodium or potassium channels
what condition has long QT syndrome that presents with severe sensorineural deafness?
Jervell and Lange-Nielsen syndrome
how does atrial fibrillation look?
chaotic and erratic baseline (irregularly irregular) with no discrete P waves in between irregularly spaced QRS complexes
atrial fibrillation can result in what?
atrial stasis and lead to stroke
tx for atrial fibrillation?
rate control • anticoagulation • possible cardioversion
what does atrial flutter look like?
a rapid succession of identical, back-to-back atrial depolarization waves • 'saw tooth' appearance
pharmacologic conversion to sinus rhythm in atrial flutter?
Class IA, IC, or III antiarrhythmics
rate control in atrial flutter?
β-blocker or calcium channel blocker
what does ventricular fibrillation look like?
a completely erratic rhythm with no identifiable waves
severity of ventricular fibrillation?
fatal arrhythmia without immediate CPR and defibrillation
features of 1st degree AV block?
prolonged PR interval >200ms • asymptomatic
features of 2nd degree AV block Mobitz type I (Wenckebach)?
progressive lenghtening of the PR interval until a beat is dropped • usually asymptomatic
features of Mobitz type II?
dropped beats that are not preceded by a change in the length of the PR interval
severity of Mobitz type II?
these abrupt, nonconducted p waves result in a pathologic condition
mobitz type II is often found as what?
2:1 block, where there are >=2 p waves to 1 QRS
mobitz type II often treated with what?
mobitz type II may progress to what?
3rd degree block
what happens in 3rd degree (complete) heart block?
the atria and ventricles beat independently of each other • both p waves and QRS complexes are present, though P waves bear no relation to the QRS complexes
which rate is faster in 3rd degree heart block?
atrial rate is faster than ventricular rate
3rd degree heart block is usually treated with what?
which disease can result in 3rd degree heart block?
ANP is released from where?
ANP is released in response to what?
↑ blood volume and pressure
ANP causes what?
generalized vascular relaxation and ↓ Na+ reabsorption at the medullary collecting tubule
effect of ANP on renal blood flow?
constricts efferent renal arterioles and dilates afferent arterioles (cGMP mediated), promoting diuresis and contributing to the escape from aldosterone mechanism
aortic arch baroreceptors transmit info where?
via vagus nerve to solitary nucleus of medulla (responds only to ↑ BP)
carotid sinus baroreceptor transmits info where?
via glossopharyngeal nerve to solitary nucleus of medulla (responds to ↑ and ↓ in BP)
what happens at baroreceptors in response to hypotension?
↓ arterial pressure → • ↓ stretch → • ↓ afferent baroreceptor firing→ • ↑ efferent sympathetic firing and ↓ efferent parasympathetic stimulation → • vasoconstriction, ↑ HR, ↑ contractility, ↑ BP
baroreceptors are important in the response to what?
effect of carotid massage on baroreceptors?
↑ pressure on carotid artery → ↑ stretch → ↑ afferent baroreceptor firing → ↓ HR
baroreceptors contribute to which reaction?
what happens in Cushing reaction?
triad of hypertension, bradycardia, and respiratory depression
mechanism of Cushing reaction?
↑ ICP constricts arterioles→ cerebral ischemia and reflex sympathetic increase in perfusion pressure (hypertension)→ ↑ stretch → reflex baroreceptor induced-bradycardia
what happens in stimulation of peripheral chemoreceptors?
carotid and aortic bodies are stimulated by ↓ PO2 (<60mmHg), ↑ PCO2, and ↓ pH of blood
what happens in stimulation of central chemoreceptors?
are stimulated by changes in pH and PCO2 of brain interstitial fluid, which in turn are influenced by arterial CO2
central chemoreceptors do not directly respond to what?
what is the organ with the largest blood flow?
Lung (100% of CO)
what is the organ with the largest share of systemic cardiac output?
which organ has the highest blood flow per gram of tissue?
which organ has the largest arteriovenous O2 difference?
why does heart have the largest arteriovenous O2 difference?
becuase O2 extraction is 80%
how is O2 demand met in heart?
↑ O2 demand is met by ↑ coronary blood flow, not by ↑ extraction of O2
what is the normal pressure in the RA?
what is the normal pressure in the RV?
what is the normal pressure in the PA?
what is the normal pressure in the LA?
what is the normal pressure in the LV?
what is the normal pressure in the aorta?
PCWP is a good approximation of what?
left atrial pressure
when is PCWP> LV diastolic pressure?
how is PCWP measured?
Swan Ganz catheter
what is autoregulation?
how blood flow to an organ remains constant over a wide range of perfusion pressures
what are the factors determining autoregulation in the heart?
Local metabolites (vasodilatory)-CO2, adenosine, NO
what are the factors determining autoregulation in the brain?
Local metabolites (vasodilatory)-CO2 (pH)
what are the factors determining autoregulation in the kidneys?
myogenic and tubuloglomerular feedback
what are the factors determining autoregulation in the lungs?
hypoxia causes vasoconstriction
what are the factors determining autoregulation in skeletal muscle?
local metabolites- lactate, adenosine, K+
what are the factors determining autoregulation in the skin?
sympathetic stimulation most important mechanism-temperature control
what determines fluid movement through capillary membranes?
what are the 4 starling forces?
Pc • Pi • πc • πi
what is Pc?
capillary pressure- pushes fluid out of capillary
what is Pi?
interstitial fluid capillary- pushes fluid into capillary
what is πc?
plasma colloid osmotic pressure- pulls fluid into capillary
what is πi?
interstitial fluid colloid osmotic pressure-pulls fluid out of capillary
equation for net filtration pressure?
Pnet= [(Pc - Pi) - (πc - πi)]
what is Kf?
filtration constant (capillary permeability)
what is Jv?
net fluid flow= Kf x Pnet
what is edema?
excess fluid outflow into interstitium
edema is commonly caused by what?
↑ capillary pressure (heart failure) • ↓ plasma proteins (nephrotic syndrome, liver failure) • ↑ capillary permeability (toxins, infections, burns) • ↑ interstitial colloid osmotic pressure (lymphatic blockage)
what is the most common cause of early cyanosis?
Tetralogy of Fallot
which congenital heart diseases make up the right to left shunts (early cyanosis)-blue babies?
5T's • Tetralogy of Fallot • Transposition of the great vessels • persistent Truncus arteriosus • Tricuspid atresia • Total anomalous pulmonary venous return
features of Persistent Truncus Arteriosus?
failure of truncus arteriosus to divide into pulmonary trunk and aorta
most patients with persistent truncus arteriosus have what?
tricuspid atresia is characterized by what?
absence of tricuspid valve and hypoplastic RV
tricuspid atresia requires what for viability?
both ASD and VSD
what happens in TAPVR?
pulmonary veins drain into right heart circulation (SVC, coronary sinus, etc)
TAPVR is associated with what?
ASD and sometimes PDA to allow for right to left shunting to maintain CO
which congenital heart abnormalities make up the left to right shunts (late cyanosis)-blue kids?
VSD • ASD • PDA
what is the most common congenital cardiac anomaly?
findings in ASD?
loud S1, wide, fixed split S2
what do you use to close PDA?
what is the frequency of the congenital left to right shunts?
VSD > ASD > PDA
what happens in Eisenmenger's syndrome?
uncorrected VSD, ASD, or PDA causes compensatory pulmonary vascular hypertrophy, which results in progressive pulmonary hypertension
what happens in Eisenmenger's syndrome as pulmonary resistance increases?
the shunt reverses from left to right to right to left, which causes late cyanosis, clubbing, and polycythemia
tetralogy of fallot is caused by what?
anterosuperior displacement of the infundibular septum
what is the mnemonic for the components of ToF?
PROVe • 1. Pulmonary infundibular stenosis • 2. RVH • 3. Overriding aorta (overrides the VSD) • 4. VSD
what is the most important determinant for prognosis in ToF?
pulmonary infundibular stenosis
in ToF early cyanosis (tet spells) caused by what?
a right to left shunt across the VSD
difference between isolated VSD and VSD in ToF?
isolated VSDs usually flow left to right (acyanotic) • in tetralogy, pulmonary stenosis forces right to left (cyanotic) flow and causes RVH
how does RVH in ToF look?
boot shaped heart on CXR
patients with ToF learn what compensatory mechanism?
squat to relieve cyanotic symptoms
why do patients with ToF squat?
reduces blood flow to the legs, ↑ PVR, and thus ↓ the cyanotic right to left shunt across the VSD
what is the preferred treatment for ToF?
early, primary surgical correction
what happens in transposition of great vessels?
aorta leaves RV (anterior) and pulmonary trunk leaves LV (posterior)→ separation of systemic and pulmonary circulations
transposition of the great vessels not compatible with life unless what?
a shunt is present to allow adequate mixing of blood (VSD, PDA, or patent foramen ovale)
transposition of great vessels is due to what?
failure of aorticopulmonary septum to spiral
prognosis of transposition of great vessels?
without surgical correction, most infants die within the first few months of life
coarctation of the aorta can result in what?
what is infantile type of coarctation of the aorta?
aortic stenosis proximal to insertion of ductus arteriosus (preductal)
preductal coarctation of the aorta is associated with what?
what needs to be checked in infantile coarctation of the aorta?
check femoral pulses on physical exam
what is adult type coarctation of the aorta?
stenosis is distal to ligamentum arteriosum (postductal)
postductal coarctation of the aorta is associated with what?
notching of the ribs (due to collateral circulation), hypertension in upper extremities, weak pulses in lower extremities
postductal coarctation of the aorta is most commonly associated with what?
bicuspid aortic valve
what is going on in patent ductus arteriosus in the fetal period?
shunt is right to left (normal)
what happens to patent ductus arteriosus in the neonatal period?
lung resistance ↓ and shunt becomes left to right with subsequent RVH and/or LVH and failure (abnormal)
patent ductus arteriosus is associated with what finding?
continuous machine like murmur
in PDA, patency is maintained with what?
PGE synthesis and low O2 tension
uncorrected PDA can eventually result in what?
late cyanosis in the lower extremities (differential cyanosis)