Card Set Information
Why is the ventricular AP very long?
inward calcium current: L-type Ca2+ channels --> longer plateau phase
What is the trigger for excitation-contraction coupling in cardiac myocytes?
depolarization --> Na+ influx, triggers voltage-sensitive L-channels
calcium entering from T-tubule via L-channels (i.e. dihydropyridine)
triggers calcium elease from SR via ryanodine receptors
How does calcium promote muscle contraction?
calcium stimulates troponin C
troponin C moves --> disinhibition of thick and thin filaments from each other
How does an intracellular calcium burst relate to muscle contraction timing?
intracellular calcium burst precedes muscle contraction/force generation
What does a non-linear length-tension relationship of myocytes reflect?
steeply increasing stiffness with stretching
What is the dominant component of the diastolic passive elastic property of cardiac muscle?
What cardiac properties is connectin/titin responsible for?
diastolic passive elastic property
diastolic stiffening with diastolic heart failure
Why does the force of contraction increase with increased muscle length?
because of increased sensitivity to calcium
What increases the force of a (cardiac) muscle contraction?
increased muscle length
increased sensitivity to calcium
increased intracellular calcium
increased overlap between thick/thin filaments
increased passive force
increased heart rate
What component of cardiac muscle is responsible for length dependent calcium sensitivity?
Increase in what parameter results in cardiac dilatation?
Why is heart failure associated with cardiomegaly?
heart failure --> decrease in contractility --> heart muscle lengthens to compensate and maintain force of contraction --> cardiomegaly
i.e. during heart failure the heart takes advantage of the length-tension relationshiop
What is responsible for the cardiac muscle length-tension relationship?
increased sensitivity to calcium
What determines length of cardiac muscle fibers?
End Diastolic Volume
What it used as a measure of left heart afterload?
What affects stroke volume?
True/False: Stroke volume is a function of afterload.
What does heart rate effect?
Can a decreased heart rate ever increase the force of cardiac contraction?
yes, during rest potentiation a decreased beat frequency may result in increased force of contraction
What would you suspect if a patient has normal cardiac contractility but decreased cardiac performance?
leaky valves (i.e. regurgitation)
low blood volume
What increases (cardiac) muscle contractility?
increased SNS discharge
increased intracellular calcium
What effects do epi and norepi have on cardiac myocytes?
increased rate of relaxation
increased force of contraction
increased peak force
increased rate of force develpment
What effect does contractility have on stroke volume?
increasing contractility increases the amount of shortening --> increased stroke volume
When does the ejection fraction change?
systolic heart failure
increasing afterload --> decreasing ejection fraction
increasing contractility --> increasing efection fraction
changing preload --> no effect on efection fraction
What are some clinical features of left ventricular systolic failure?
stroke volume stabilized by increased preload (i.e. increased muscle fiber length)
How can afterload reduction benefit a patient with severe systolic heart failure?
decrease afterload --> decrease BP --> increase SV --> increase Ef
Is cardiac myocyte relaxation a passive process?
no: calcium actively pumped back into SR
What does an ECG record?
summation of millions of AP's over space/time
What does the P wave signify in a cardiac cycle?
slight atrial pressure increase
In the cardiac cycle, what is signified by a R wave?
increased ventricular pressure
In the cardiac cycle, what is signified by a S wave?
increased aortic pressure (isovolumetric contraction)
In the cardiac cycle, what is signified by a T wave?
peak aortic/ventricular pressure
In the cardiac cycle, what is signified after the T wave?
decreased ventricular pressure (steep)
decreased aortic pressure (gradual)
What is happening during isovolumic ventricular contraction?
ventricular pressure is still less than aortic pressure, aortic valve closed
pressure rises but volume remains constant
correlates to S wave on ECG
What is happening during isovolumic relaxation?
ventricular pressure lower than aortic pressure and higher than atrial pressure, all valves closed
volume remains same as ventricular relaxation continues
When does the ventricle fill with blood at the fastest rate?
rapid ventricular filling phase
i.e. phase F
: ventricular pressure decreases --> atrial P > ventricular P --> mitral valve opens
i.e. immediately after mitral valve opens
i.e. early diastole
What are the normal heart sounds? What produces them?
normal heart sounds are produced by closing of heart valves
S1 = AV valves closing
S2 = PV and Aortic (i.e. semilunar) valves closing
What produces the atrial "a" wave?
What produces the atrial "c" wave?
What is the "v" venous wave from?
venous filling (relative to atria)
Which closes first, aortic or pulmonic valves?
aortic valves (esp. during inspiration)
What could cause wide splitting of S2 (i.e. A2/P2) during inhalation and exhalation?
Right bundle branch block
What can cause fixed splitting of the S2 heart sounds during inspiration and exspiration?
atrial septal defect
What could cause paradoxical splitting (i.e. reversal of P2/A2 sounds, splitting during exhalation and not inhalation)?
left bundle branch block
advanced aortic stenosis
What are the common causes of valvular heart disease and what are common risk factors?
: aortic and pulmonic stenosis, tricuspid and mitral stenosis (rare), bicuspid aortic valve
: aortic stenosis and insufficiency, mitral insufficiency, mitral valve myxomatous disease
: mitral sentosis/insufficiency, aortic stenosis/insufficiency
: usually tricuspid, mitral, and aortic insufficiency
atherosclerosis risk factors
What heart valves do rheumatic diseases generally affect?
usually both at same time
What is the most common etiology of aortic stenosis today vs 30 years ago?
: degenerative valvular disease
30 years ago
: bicuspid aortic valve (i.e. congenital)
What is the least common etiology of aortic stenosis vs 30 years ago?
: post-infectious (Group A Strep)
30 years ago
: degenerative valvular disease
How can you measure added pressure load on heart in stenotic patients?
measure pressure gradient across aortic valve (i.e. between LV and Aorta)
What would you expect on clinical exam with a patient with aortic stenosis?
diminished and delayed upstroke = pulsus parvus et tardus
difference between systolic blood pressures of LV and aorta (i.e. increased LV afterload)
harsh diamond-shaped systolic murmur
: RUSB radiating to carotids
: increased stiffness
What are the clinical consequences of aortic stenosis?
unable to increase SV with decrease in SVR, i.e. resistance does not drop normally
LV wall stress:
increased O2 demand
ECG and echo findings
impaired diastolic function
dyspnea on exertion
What are the 3 main components of the Bernoulli equation and which is most important with stenotic valves?
1. convective acceleration
2. flow acceleration
3. viscous friction
stenotic valves: convective acceleration component predominates
What is useful about the Bernoulli equation and CV?
can calculate effects of increased flow rates through valves/vessels
What are some pathological causes of a change in cardiac output?
What are some normal causes of a change in cardiac output?
What are some common treatments for aortic stenosis?
aortic stenosis = mechanical problem, treatment = mechanical solution
mechanical valve replacement
anticoagulation therapy (prevent thrombus)
treatment usually only for symptomatic patients
What are the clinical consequences of mitral stenosis?
need for long diastolic period
sensitivity to high heart rates
pulmonary venous congestion:
shortness of breath
dyspnea on exertion
harsh diastolic murmur (apex)
In a patient with aortic stenosis, what is the average survival rate for a person with angina, syncope, CHF, and/or atrial fibrillation?
: 5 yrs
: 3 yrs
: 2 yrs
: 6 mo
What are some common treatments for mitral stenosis?
many non-surgical options, unlike with aortic stenosis
maintenance of sinus rhythm
What are some common etiologies of mitral insufficiency?
mitral annular dilation
ruptured mitral chordae tendinae
leaflet/chord abnormality (congenital, rheumatic, infectious)
(mitral valve prolapse: CT disorders, Marfan's, myxomatous degenerative disease)
What are some common clinical findings for mitral regurgitation?
increased PVP --> pulmonary congestion, dyspnea
right-heart failure uncommon
holosystolic murmur at apex
: LA enlargement, AF
: LA and LV enlargement
rate of progression is highly variable
How is mitral regurgitation treated?
trace/mild mitral regurgitation = common normal variant
main treatment = diuretics
i.e. main treatment = reduce afterload
45% 5 yr survival
surgical repair of valve
What are common etiologies of mitral valve prolapse?
genetic CT disorders
: Marfan's, Ehlers-Danlos
What are common etiologies for aortic insufficiency?
: bicuspid aortic valve
: from asc. aorta dilation
How does left ventricular pressure relate to coronary artery flow?
increased LV pressure --> decreased cornary artery blood flow
What are common clinical findings of aortic insufficiency?
dyspnea (most common)
angina/palpitations (less common)
wide pulse pressure (Corrigan's pulse)
head bob (de Musset)
capillary pulsations (Quincke's sign)
diastolic flow reversal (Duroziez's sign)
diastolic, decresendo murmur
**left ventricular dilation/dysfunction
How do the effects of vasodilators differ from aortic and mitral insufficiencies?
: reduce afterload
: vasodilators relieve symptoms
: vasodilators slow progression of disease
What is the prognosis for someone with severe aortic insufficiency?
severe AR but normal LV and asymptomatic
: good 10 year prognosis
: 4 year survival
: 2 year survival
diuretics can reduce symtpoms
What are the pathological heart sounds? What causes them? Can they ever be "normal"?
S3 = early ventricular filling, always pathological
S4 = atrial filling, can be normal
How are heart murmurs described?
: systolic, diastolic, continuous
: systolic grade +3 = pathological , diastolic grade +1 = pathological
: high frequency = high gradient
: near source
: direction of flow
What are some common correlates to cardiac output?
CO is dependent on SV and HR
decreases with age
decreases with supination (i.e. sitting/standing up)
What can cause an error in calculating Fick cardiac ouput?
anything that can change the oxygen content of blood/air of vlume of air
perforated ear drums
change in resting lung volume
small air bubbles in syringes
What is the effective cardiac output and how is it measured?
effective cardiac output = amount of blood actually being pumped throughout the body
measured by Fick equation (i.e. O2 consumption)
How is cardiac output determined?
1. effective cardiac output
: effective transport (Fick equation), dilution method (temp. indicator)
2. stroke volume
: volumetric techniques (imaging), flow techniques (Doppler)
What are the common causes of acute rheumatic fever?
autoimmune complication of Strep pyogenes Group A beta-hemolytic pharyngitis
bacterial glycoproteins similar to cardiac antigens (valve glycoproteins, sarcolemmal/smooth muscle)
possibly direct toxic effect by bacteria endotoxins
What are common clinical features of acute rheumatic fever?
: all layers of the heart
: effusions, fibrin deposition
: lymphocyte/macrophage infiltration
: fibrinoid necrosis, myocyte loss, lymphocyte/marophage infiltration
: ulceration, collagen damage
What are some common causes of chronic rheumatic heart diseae?
develops 10-30 years after initial episode of rheumatic fever
chronic inflammation and scarring of cardiac valves and chordae tendinae
mitral valve > mitral + aortic > aortic > tricuspid > pulmonic
What is the most common cause of mitral stenosis?
chronic rheumatic heart disease
What is the most common cause of mitral regurgitation?
(asymptomatic) mitral valve prolapse
What are some common clinical features of chronic rheumatic heart disease?
inflammation/scarring of (mitral/aortic) valves and chordae tendinae
fusion of valvular commissures
fusion/shortening of chordae tendinae
: fusion of valves
: rigid leaflets, short chordae
right- and left- sided heart failure
What are some common findings with mitral valve prolapse?
genetic CT disorders
: Marfan's, Ehler's-Danlos
myxomatous tissue degeneration --> gelatinous appearance
fragmentation of collagen fibers
redundant valvular leaflets
myxomatous tissue in CT
What is clinically significant about calcification of the mitral valve annulus?
common in elderly, usually asymptomatic
can interfere with valve closure
can cause regurgitation
can affect valvular leaflets and interventricular septum
What are the 3 main ways a myocardial infarction can cause mitral regurgitation?
1. dilation of mitral valve annulus
2. papillary muscle rupture
3. papillary muscle dysfunction/scarring
What are the main pathological findings of fibrocalcific aortic stenosis?
nodular fibrosis of leaflets
inflammatory cell accumulation
What are common complications of fibrocalcific aortic stenosis?
myocardial ischemia --> MI
What are the common features of Marfan's syndrome?
genetic CT disorder
: autosomal dominant
: fibrillin, microfibrils
musculoskeletal abnormalities (e.g. arachnodactly)
CV structural complications
mitral valve prolapse
mitral regurgitation (kids)
aortic regurgitation (adults)
**cystic medial degeneration
What is tricuspid stenosis usually from?
What usually causes tricuspid regurgitation?
dilation of tricuspid annulus
: pressure/volume overload
(i.e. rarely a primary valvular disease)
What usually causes pulmonary valve stenosis?
congenital abnormailty: Tetralogy of Fallot, isolated pulmonary stenosis
What usually causes pulmonary valve regurgitation?
dilation of the valve annulus
severe pulmonary hypertension
What is the most common cause of infectious endocarditis? rarest?
: bacterial endocarditis
: fungal endocarditis
What are predisposing factors to developing infectious endocarditis?
abnormal valves (e.g. bicuspid aortic valve, congenitally stenotic valves, rheumatic valves, MVP, fibrocalcific valves)
IV drug use (S. aureus most common)
Iatrogenic bacteremia (e.g. dental procedures, urinary catheterization)
What are common clinical features of infectious endocraditis? complications?
inflammed myocardial tissue
immune complex glomerulonephritis
What is non-bacterial thrombotic endocardosis?
a.k.a. Marantic (Wasting) Endocarditis
vegetations can be colonized --> infectious endocarditis
associated with wasting syndromes, end stage cancers
What causes carcinoid heart disease?
overproduction of serotonin, bradykinin, histamine, prostaglandins
stimulate fibroblastic cells in endocardium, chordae, valve leaflets
i.e. overproduction hormones resulting in overproduction of ECM in myocardium
What are the common clinical features of carcinoid heart disease?
fibrosing valvular disease
fusion of chordae
fibrous plaques on leaflets
lesions are predominantly right-sided
How do carcinoid heart disease, drug-induced valvular disease, and chronic rheumatic heart disease present differently clinically?
carcinoid heart disease
: predominance of right-sided lesions
drug-induced valvular disease
: predominance of left-sided lesions
What causes drug-induced valvular disease?
: methylsergide, ergotamines
What physical factors determine the rate of fluid flow (i.e. resistance) through a tube?
viscosity of the fluid
radius of the tube
length of the tube
How does the Poiseuille equation relate to CV?
shows the relationship between flow and resistance
flow occurs only when there is a pressure difference
small changes in radius result in large changes in resistance
What does the ascending limb of the arterial pulse wave represent?
rapid ventricular ejection
What does the incisura/dicrotic notch of the arterial pulse wave represent?
aortic valve closure
end of systole
What does the apex the arterial pulse wave represent? the nadir?
apex = systolic pressure
nadir = diastolic pressure
What is the pulse pressure?
pulse pressure = systolic - diastolic pressure = apex - nadir of arterial pulse wave
How is mean arterial pressure determined?
MAP = average pressure over time
MAP = baseline of arterial pulse wave
sphygmomanometer on brachial artery
MAP = diastolic pressure + 1/3 pulse pressure
How does the heart make peripheral blood flow less pulsatile?
arterial tree is distensible (Windkessel effect)
elastic recoil of arteries preparing for diastole
artery recoil ejects part of stroke volume that remains after systole
Why does pulse pressure increase with age?
inreasing age relates to decreasing arterial compliance
i.e. increasing age relates to increasing hardening of arteries
What are the Korotkoff sounds when using a sphygmomonometer?
1st sound = cuff pressure falls below systolic pressure, intermittent systolic squirts
1st sound increases in amplitude until muffled during diastole
2nd sound = disspearance of 1st sound, diastolic pressure
What is mean transmural pressure?
meaured with a sphygmomanometer
equal to blood pressure when the subject is lying down
affected by hydrostatic effect if not meaured at heart level
Does the arterial pulse wave amplitude increase or decrease as it travels down the arterial tree?
increases with arterial tree progression
increase in systolic pressure, decrease in diastolic pressure
**mean pressure declines
Why is the total resistance of the capillary bed less than the arteriolar bed even though they are narrower?
capillary bed = several parallel resistor systems
What are the 3 harmonic changes in the arterial pulse wave as it progresses through the arterial tree?
: increase systole, decrease diastole
: high frequency waves faster than low frequency
: decreased compliance relates to increased amplitude
True/False: It is normal for the ankle systolic pressure to be less than or equal to the systolic pressure measured in the upper arm.
It is normal the ankle systolic pressure to be 20mmHg higher than the systolic pressure of the upper arm.
True/False: Intracellular free Ca2+ can occur both with and without changes inthe membrane potential.
How is the effect of caclium on muscle contraction different for smooth muscle and skeletal/cardiac muscle?
: calcium --> troponin C disinhibits actin --> faster ATP consumption
: calcium --> calmodulin --> activates/phosphorylates myosin --> slower ATP consumption
Through which range of arterial pressure is autoregulation active?
Which cranial nerve innervates the carotid sinus?
CN IX: glossopharyngeal
What happens when the carotid sinus baroreceptors are stretched?
decrease in heart rate
arterial pressure reflexively decreases
How is the SA node innervated?
: CN X
: bulbospinal pathway
What areas of the heart are supplied by the left coronary artery?
anterior portion of interventricular septum
anterior wall of RV
What areas of the heart are supplied by the right coronary artery?
posterior portion of the interventricular septum (dominant right coronary artery)
What are Thebesian veins?
veins that drain directly into the ventricular and atrial chambers wihtout passing through an epicardial vein
shunts with unknown functions
How is coronary blood flow regulated?
strong metabolic control
: flow higher for greater level of metabolism
: maximal dilation: small drop in pressure decreases flow greatly
large during diastole, small during systole
: myocardium squeezes on own blood flow during systole
small flow during systole
: increased aortic pressure
subendocardium perfused first, then subepicardium
: tissue pressure gradient, waterfall third pressure
Nitric Oxide --> increases cGMP --> vasodilation
What can threaten subendocardial perfusion?
decreases in diastolic pressure difference across aortic valve (e.g. hypotension)
shortened diastole (e.g. tachycardia)
prevention of autoregulatory vasodilation
decrease in coronary blood flow (e.g. atherosclerosis)
Why is cardiac oxygen consumption almost the same as overall myocardial metabolism?
barely any anaerobic respiration, even in resting cardiac muscle
Where does the most blood oxygen extraction occur in the body?
coronary artery flow: 70% of oxygen extracted by myocardium
What is clinically useful about the "double product"?
double product = Heart Rate x Systolic BP
i.e. = heart rate x tension development
indicates myocardial oxygen consumption
What are the ranges of critical coronary artery stenosis?
: 90% diameter narrowing
during increased blood flow/exercise
: 40% diameter narrowing
What are the 3 main causes of subendocardial ishemia during exertion?
1. exponential pressure drop across a stenosis as a function of flow
2. exhaustion of vasodilation reserve
3. tachycardia during exercise
What causes the majority of CHD events (e.g. heart attack, unstable angina, sudden cardiac death)?
epicardial coronary atherosclerosis
What are risk factors for developing atherosclerosis?
age: look at 40yo, esp 50+yo
elevated total cholesterol (more than 240mg/dL)
elevated triglycerides (>150mg/dL)
elevated LDL:HDL ratio (risk when ration >5)
elevated apo B
low HDL (less than 40mg/dl for men, less than 50mg/dl for women)
low apo A1
elevated ratio total cholesterol
: HDL (risk when ratio greater than 5-6)
elevated ratio of apo B
: apo A1
elevated lipoprotein and lipoprotein-associated phospholipase A2
hypertension: SBP above 115mmHg
diabetes: types I and II
elevated waist to hip ratio (> 1.6)
elevated C reactive protein
increased oxidant stress
increased physical stress
altered shear stress
What are some correlates of low endothelial shear stress?
low blood flow
increased oxidative sterss on endothelium
attenuation of nitric oxide inflammation
LDL cholesterol uptake
smooth muscle cell migration
When does coronary remodeling take place?
lumen diameter is maintained until the plaque area increases to 40% of total cross-sectional area
when plaque area is greater than 40% of lumen, compensatory expansion is overcome and lumen narrows
What predisposes a coronary artery to developing an aneurysm?
lesions with excessive expansive remodeling
lesions with thin fibrous cap
What can cause a cornary thrombus?
plaque disruption, rupture of fibrous cap
endothelial erosion, no fibrous cap disruption
intra-plaque hemorrhage, no fibrous cap disruption
What makes a coronary plaque more likely to rupture?
thin fibrous cap overlying a large necrotic lipid core
presence of inflammatory cells in fibrous cap
: foam cells, T-cells --> proteases (MMP); interferon-gamma
extensive expansive remodeling
minimal/mild lumen narrowing
neovessels within plaque
previous asymptomatic coronary embolism episodes
(sudden) physical exertion
True/False: The presence of matrix metalloproteinases (MMP) indicates that a coronary plaque is less likely to rupture.
The presence of matrix metalloproteinases (MMP) indicates that a coronary plaque is MORE likely to rupture.
What is characterized by metabolic syndrome?
combination of 3 or more of following:
According to the Framingham Interheart Study, what are the 9 reasons that 90% of people get myocardial infarctions?
elevated apoB/apoA1 ratio (esp. decreased A1)
lower consumption of fruits and vegetables
lower consumption of alcohol
What commonly causes stable angina?
fixed coronary obstruction
: limits maximal coronary blood flow
maximal coronary blood flow reduced when coronary lesion exceeds 60-70% diameter stenosis
marked increase in O2 demand with normal coronary flow: aortic stenosis, hypertrophic cardiomyopathy, dynamic outflow tract obstruction
Why do patients with aortic stenosis present with stable angina?
elevated ventricular wall stress
low diastolic blood pressure
What are clinical features of classic angina?
: clenched fist over chest
substernal chest pressure/tightness
can radiate to arms, neck, jaw
associated with dyspnea, nausea, diaphoresis
What exercise test outcomes are associated with high MI risk?
poor exercise capacity (<5 METs)
poor heart rate repsonse from rest to exercise (chronotropic incompetence)
fall in blood pressure during exercise, especially below baseline
poor heart rate recovery in the first minute of recovery (<12bpm)
exercise-induced ventricular tachycardia
high density of PVCs, ventricular couplets, or non-sustained ventricular tachycardia during recovery
What are the variables of the Duke Score of heart disease risk?
horizontal/downsloing ST depression
How is atherosclerosis diagnosed?
stress test/exercise capacity
: CT, MRI, angiography, intracoronary ultrasound
Why does coronary angiography miss early-stage atherosclerosis?
cornary artery lumen narrowing only happens at later stages of atherosclerosis
In the absence of high risk findins, what should be the medical treatment of someone with angina/ischemia?
: reduce risk of ACS
: lower preload, vasodilator
: lower HR, lower BP, lower O2 demand
: lower HR, lower BP, lower O2 demand
: e.g. ranolazine
lipid-lowering therapy (e.g. statins)
: reduce risk of ACS, lower mortality
What are some common complications of MI?
decreased coronary perfusion
papillary muscle infarction/ischemia
ventricular septal defect
What are the 3 basic components of cardiogenic shock?
1. decreased coronary perfusion
2. ventricular dysfunction
: increased ischemia
What are risk factors for developing NSTEMI?
(possible) ECG changes
: ST depression, T wave inversion, tansient ST elevation
: hemodynamic instability
presentation with heart failure (e.g. pulmonary congestion)
recurrent angina despite initial medical therapy
elevated cardiac enzymes
What are the vairiable sin teh GRACE Risk Score?
systolic blood pressure
cardiac arrest at admission
elevated cardiac enzymes
ST segment deviation
What are the 3 basic embyrological principles that determine cardiac development?
1. function of endocardial cushion
2. division of turncus arteriosus
3. role of flow
What is the function of the foramen ovale and ostium secundum in fetal circulation?
permits right-to-left flow
prevents left-to-right flow
Where are the most common ventricular septal defects?
membranous septum (last to develop)
Where are the most common atrial septal defects?
ostium secumdum: last to develop
What structures develop from the endocardial cushion?
: anterior leaflet continuity with aorta
offset of AV valves
What are some common endocardial cushion defects?
primum atrial septal defect
inlet type of ventricular defect
cleft anterior mitral leaflet
cleft septal tricuspid leaflet
: atrioventricular septal defect
What describes an AVSD?
atrioventricular septal defect
1. cleft anterior mitral leaflet
2. cleft septal tricuspid leaflet
3. loss of offset between valves
also: primum atrial septal defect, inlet ventricular septal defect
What types of complications can arise from dysfunctional truncus arteriosus develpment?
septation, no twist:
twist, incomplete septation:
displacement of septum:
(anterior) Tetralogy of Fallot
(anterior) double outlet LV
(posterior) double outlet RV
What is related to tricuspic atresia in cardiac develpment?
hypoplastic RV, Pulmonic valve, PA
What is related to mitral atresia in cardiac develpment?
hypoplastic LV, Aortic valve, ascending aorta
How does fetal ciculation maintain flow with tricuspic atresia, mitral atresia, and/or other blood flow defects?
other "side" of heart still functional
: right-to-left shunt in pulmonary artery to asc. aorta
What causes hypoplastic left heart syndrome?
severe mitral stenosis
mitral atresia --> hypoplastic LV, Aortic valve, Asc. Aorta
What causes a "peach-pit" right ventricle?
: right ventricle is exposed to a pressure load while there is little flow
simultaneous RV hypoplasia and hypertrophy
pulmonary stenosis --> pulmonary atresia:
hypoplastic pulmonary vein
hypoplastic pulmonary artery
hypoplastic right ventricle
hypertrophic right ventricle
How does fetal circulation accomodate high vascular resistance in lungs and prevent right ventricular pressure overload?
: alternate outlet for RV blood flow
: prevents backup in RA
What is are the immediate post-partum changes to fetal circulation?
1. pulmonary vascular resistance decreases
2. lung blood flow increases
3. sytemic blood flow decreases
4. ductus arteriosus shunt reverses to become L-to-R shunt
5. increased pulmonary flow --> increased left atrial pressure --> closure of foramen ovale
6. ductus arteriosus closes (~days)
7. ductus venosus obliterates (~weeks)
8. ductus arteriosus obliterates (~1year)
9. foramen ovale obliterates (~decades)
What is clinically significant about a patent foramen ovale?
prevalence depends on age distribution
increased risk for paradoxical embolization
increased risk for migraines (?)
What is the most common clinical sign of a congenital heart defect?
heart murmur (not specific)
abnormal heart sounds (e.g. splitting of A2/P2)
pulmonary edema, dyspnea
True/False: Most congenital heart defects involve isolated lesions.
What are the 3 "levels" of congenital heart defects?
open ductus arteriosus
What is the most common ASD?
(ostium) secundum ASD
What are common signs of ASD?
True/False: Most patients with an ASD are symptomatic.
Most patients with an ASD are asymptomatic.
What is Eisenmenger's syndrome?
abnormally high blood flow through lungs --> permanent damage of pulmunary arterioles --> permanent elevation of pulmonary vascular resistance --> reversal of shunt to R-to-L
direct repair of defect not possible
permanent lung damage
Which congenital heart defects are likely to develop Eisenmenger's syndrome?
increaesd pulmonary circuit blood flow
patent ductus arteriosus
What can keep a ductus arteriosus open?
What promotes ductus arteriosus closure?
What is coarctation of the aorta?
significant narrowing of aorta
What is the most common location for a coarctation of the aorta?
: area in descending aorta near where the ductus arteriosus is
: hypoplasia of aortic arch
What are long-term complications of coarctation?
What can lead to an increase in systolic loads (pressure) and cause hypertrophy?
peripheral pulmonic stenosis
Which shunts are cyanotic?
Right to left: mix deoxygenated blood with oxygenated blood
What is the direction of shunt resulting from an isolated, restrictive defect?
Left to Right: follows normal pressure gradient
What can cause right-to-left shunts or reversal of left-to-right shunts?
decreased systemic arterial pressure
preductal coarctation (with hypoplasia of aorta)
any condition which raises the RV EDP
any condition where QP<QS
What are common consequences of shunts?
chamber enlargement: ASD --> RA/RV dilation; VSD --> LA/LV dilation
pulmonary hypertension --> Eisenmenger's syndrome
endocarditis (not ASD)
decreased exercise tolerance (decreased cardiac function, normal O2 sat)
decreased exercise tolerance (decreased oxygen saturation)
What are the ductus dependent lesions?
systemic flow obstruction:
pulmonary flow obstruction:
tetralogy of Fallot
no other connections:
Which murmurs are usually pathological?
What are some normal murmurs?
When should you administer PGE2 to an infant? What are counter-indications?
clinical signs of ductus dependent congenital heart defect
failure to thrive
tetralogy of Fallot
What are the 3 main causes of edema?
increased capillary hydrostatic pressure
: increased venous pressure in heart failure
reduced capillary osmotic pressure
: nephrotic syndrome, liver disease
increased tissue oncotic pressure
: filariasis, tissue injury (changes permeability)
How does arteriole pressure change affect capillary pressure?
increasing arteriole pressure --> decreases capillary pressure
decreasing arteriole pressure --> increases capillary pressure
What part of the heart is most posterior?
Why choose a lateral view of heart with CXR than A-to-P view?
inspect right ventricle
(better) left atrium inspection
right ventricle obscured
What are common radiographic findings in heart failure?
enlarged lung vessels, equalization, rarely cephalization
: Kerley B lines, "fluffy" or hazy alveolar filling
What are common sites and causes of calcification as seen with CXR?
: viral, TB, other chronic pericarditis
: remote infarction, rheumatic disease
: sclerosis, degeneration, rheumatic disease
What is the sequence of the myocardial ischemia cascade?
: perfusion abnormailities
diastolic and regional systolic dysfunction
: wall motion abnormalities
: electrical transit abnormalities
: angina, MI, death
Which vessel layers are disturbed in a pseudoaneurysm? true aneurysm?
: always t. intima and t. media layers involved, sometimes t. adventitia intact
: all layers involved
Where do Berry aneurysms typically develop?
near Circle of Willis
What is the most common cause of pseudoaneurysms?
catheter puncture sites
: femoral artery
break-down of suture lines of bypass grafts swen to femoral arteries
What is the most common cause of peripheral arterial aneurysms?
artherosclerosis (not from occlusion; from direct arterial wall degeneration)
(genetic CT disorders)
What are common causes of mycotic aneurysms?
: following dental work
True/False: Aneurysms are typically lined with thrombi due to blood stasis.
True/False: Arteriograms of a patient with an aneurysm may appear normal.
Arteriograms only demonstrate flowing blood, not stasis
What is the classic triad of aneurysm symptoms indicating surgery?
palpable, pulsatile abdominal mass
(impending rupture: sudden back/abdominal tenderness)
What is the most common cause of aortic dissection?
Where are the most common sites of aortic dissection? common treatments?
most commonly begins beyond the arch vessels
spirals down into iliac vessels
vasodilators (e.g. nitroprusside)
: surgical replacement of aorta
What are symptoms of aortic dissection?
acute onset of tearing back pain
symptoms associated with occlusion of branch vessels
involvement of other arteries
: stroke, renal failure, mesenteric ischemia
ascending aorta dissection: acute aortic insufficiency, occlusion of coronary arteries, causing acute myocardial ischemia, dissection into pericardium, pericardial tamponade
What is acute ischemia and what causes it?
acute ischemia = sudden decrease in blood flow +/- sudden increase in myocardial O2 demand
: atherosclerotic plaque
What are some potential complications of acute ischemia?
: vasculogenesis, angiogenesis
loss of limb
What are the 6 P's of acute ischemia?
What are the typical treatments for acute ischemia?
surgical thrombectomy, embelectomy, bypass
: catheter-directed, tissue-plasminogen-activation factor
revascularization (systemic and local complications
: compartment syndrome, hyperkalemia, etc.)
What causes compartment syndrome? what are its symptoms?
leaking of capillaries caused by reperfusion injury within muscular fascial compartments
pain on passive stretch
loss of sensation
How is acute hyperkalemia treated?
glucose/insulin IV (some bicarbonate)
What is Buerger's disease? What causes it and what are its symptoms?
Brueger's disease = thromoangitis obliterans = inflammatory process of small/medium blood vessels related to smoking addiction
causes: occlusion of distal tibial/digital arteries
symptoms: ulcers of tips of fingers and toes, loss of digits
How is acute myoglobinemia treated?
fluid, osmotic diuretics (e.g. mannitol)
True/False: In a patient with intermittent claudication, their chance of losing a limb at 10 years is greater than losing their life.
In a patient with intermittent claudication their chance of losing a limb at 10 years is 22% and chance of losing life is 61%.
What are varicose veins and which veins are commonly affected?
varicose veins = enlarged superficial veins, veins elongate and widen, benign
common site: branches of saphenous veins (greater and lesser)
What is Virchow's triad of deep vein thrombosis? How are these related to risk factors?
damage to endothelium (e.g. inflammation, smoking)
stasis (e.g. sedentary lifestyle, immobilization, aneurysm)
hypercoagulable state (e.g. genetic disorders, pregnancy, cancer, etc.)
What are (7) major risk factors for DVT?
prior history of DVT
major surgical procedure
genetic procoagulant abnormalities
What does a (-) d-dimer test rule out?
What are the signs/symptoms of a pulmonary embolism?
(+) d-dimer levels
What is post-thrombotic syndrome?
post-thrombotic syndrome = long-term result of chronic ambulatory venous hypertension due to valve damage and loss of calf-pump mechanism
mechanism: increased capillary pressure results in exudation of protein into interstitial space, calf narrows at ankle, RBC infiltrate tissue --> hyperpigmentation
How are venous ulcers different from arterial ulcers?
arterial ulcers = dry, pale, painful, toes-distal foot
venous ulcers = moist, pink, ankle-mid calf
What is carotid disease associated with embolization of plaque and not actual arterial occlusion?
intracerebral circulation has rich collateralization: Circle of Willis
Where does carotid heart disease typically occur and why?
: bifurcation in neck
: low, oscillating shear
What are the common symptoms of carotid disease?
focal, hemispheric neurologic deficits
ipsilateral amaurosis fugax (monocular blindness)
When should you intervene on carotid artery disease?
when >70% stenosis of carotid artery