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?
calcium-induced-calcium release 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 prevents overstretching
What is the dominant component of the diastolic passive elastic property of cardiac muscle?
connectin/titin
What cardiac properties is connectin/titin responsible for?
diastolic passive elastic property cardiac hypertrophy stress-sensing 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 contractility increased preload increased muscle length increased sensitivity to calcium increased intracellular calcium increased overlap between thick/thin filaments increased passive force increased shortening-velocity increased SNS increased heart rate
decreased afterload
What component of cardiac muscle is responsible for length dependent calcium sensitivity?
troponin C
Increase in what parameter results in cardiac dilatation?
increasing volume
Why is heart failure associated with cardiomegaly?
heart failure --> decrease in contractility --> heart muscle lengthens to compensate and maintain force of contraction --> cardiomegaly
What is responsible for the cardiac muscle length-tension relationship?
increased sensitivity to calcium
What determines length of cardiac muscle fibers?
preload End Diastolic Volume
What it used as a measure of left heart afterload?
diastolic BP
What affects stroke volume?
preload afterload contractility
True/False: Stroke volume is a function of afterload.True False
True
What does heart rate effect?
calcium kinetics contractile strength
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 epi/norepi increased intracellular calcium
What effects do epi and norepi have on cardiac myocytes?
increased contractility 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) increased EDV increased EDP decreased Ef unchanged afterload cardiomegaly
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?
isovolumic relaxation 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 opensi.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?
atrial contraction
What produces the atrial "c" wave?
ventricular contraction
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 pulmonic stenosis
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 Left-sided CHF
What are the common causes of valvular heart disease and what are common risk factors?
causes: congenital : aortic and pulmonic stenosis, tricuspid and mitral stenosis (rare), bicuspid aortic valvedegenerative : aortic stenosis and insufficiency, mitral insufficiency, mitral valve myxomatous diseaserheumatic : mitral sentosis/insufficiency, aortic stenosis/insufficiencyinfectious : usually tricuspid, mitral, and aortic insufficiencyrisk factors: age atherosclerosis risk factors family history hypertension
What heart valves do rheumatic diseases generally affect?
mitral valve aortic valve usually both at same time
What is the most common etiology of aortic stenosis today vs 30 years ago?
today : degenerative valvular disease30 years ago : bicuspid aortic valve (i.e. congenital)
What is the least common etiology of aortic stenosis vs 30 years ago?
today : 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 carotidsS4 : increased stiffnessstrong PMI pulmonary congestion
What are the clinical consequences of aortic stenosis?
outflow obstruction: unable to increase SV with decrease in SVR, i.e. resistance does not drop normally syncope LV wall stress: increased O2 demand chest pain LV thickness: ECG and echo findings impaired diastolic function LA size: atrial fibrillation PV pressure: pulmonary congestion/edema 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 valve grafts balloon valvuloplasty
anticoagulation therapy (prevent thrombus)
treatment usually only for symptomatic patients
What are the clinical consequences of mitral stenosis?
valve gradient: need for long diastolic period sensitivity to high heart rates dyspnea onexertion LA enlargement: atrial fibrillation stasis thrombus formation emboli pulmonary venous congestion: shortness of breath dyspnea on exertion physical exam: harsh diastolic murmur (apex) opening "snap"
In a patient with aortic stenosis, what is the average survival rate for a person with angina, syncope, CHF, and/or atrial fibrillation?
angina : 5 yrssyncope : 3 yrsCHF : 2 yrsAtrial fibrillation : 6 mo
What are some common treatments for mitral stenosis?
many non-surgical options, unlike with aortic stenosis maintenance of sinus rhythm : medicationballoon valvulplasty
What are some common etiologies of mitral insufficiency?
myxomatous degeneration mitral annular dilation ruptured mitral chordae tendinae ventricular dilation ischemic disease 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 ECG : LA enlargement, AFCXR : LA and LV enlargementrate 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 severe : 45% 5 yr survival surgical repair of valve
What are common etiologies of mitral valve prolapse?
genetic CT disorders : Marfan's, Ehlers-Danlosmyxomatous degeneration normal variant
What are common etiologies for aortic insufficiency?
rheumatic congenital : bicuspid aortic valvedegenerative infectious annular dilation : 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 CXR : cardiomegaly
**left ventricular dilation/dysfunction
How do the effects of vasodilators differ from aortic and mitral insufficiencies?
vasodilators : reduce afterloadmitral insufficiency : vasodilators relieve symptomsaortic insufficiency : 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 prognosisangina : 4 year survivalCHF : 2 year survivalvasodilators can diuretics can reduce symtpoms surgical options
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?
timing : systolic, diastolic, continuousintensity : systolic grade +3 = pathological , diastolic grade +1 = pathologicalpitch/character : high frequency = high gradientshape : de/crescendolocation : near sourceradiation : direction of flowmaneuvers
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 improper technique 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?
causes : 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?
pancarditis : all layers of the heartpericarditis : effusions, fibrin depositionmyocarditis : lymphocyte/macrophage infiltrationAschoff bodies : fibrinoid necrosis, myocyte loss, lymphocyte/marophage infiltrationendocarditis : ulceration, collagen damage
What are some common causes of chronic rheumatic heart diseae?
causes: 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 valvular stenosis : fusion of valvesvalvular regurgitation : rigid leaflets, short chordaecomplications: atrial fibrillation thrombosis pulmonary hypertension right- and left- sided heart failure
What are some common findings with mitral valve prolapse?
genetic CT disorders : Marfan's, Ehler's-Danlosmyxomatous 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 marked calcification inflammatory cell accumulation serum-derived lipids
What are common complications of fibrocalcific aortic stenosis?
aortic stenosis aortic regurgitation LV hypertrophy myocardial ischemia --> MI arrhythmias sudden death
What are the common features of Marfan's syndrome?
genetic CT disorder : autosomal dominantgenes : fibrillin, microfibrilsmusculoskeletal abnormalities (e.g. arachnodactly) CV structural complications mitral valve prolapse mitral regurgitation (kids) aortic regurgitation (adults) aneurysms **cystic medial degeneration
What is tricuspid stenosis usually from?
rheumatic disease mitral disease
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?
most common : bacterial endocarditisrarest : 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) prosthetic 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?
vegetations inflammed myocardial tissue complications: valve perforation CHF septic embolization immune complex glomerulonephritis
What is non-bacterial thrombotic endocardosis?
a.k.a. Marantic (Wasting) Endocarditis sterile vegetations vegetations can be colonized --> infectious endocarditis unknown mechanism associated with wasting syndromes, end stage cancers
What causes carcinoid heart disease?
neuroendocrine tumors 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 lesionsdrug-induced valvular disease : predominance of left-sided lesions
What causes drug-induced valvular disease?
serotonergic drugs : methylsergide, ergotaminesappetitie suppressants : fenfluramine
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?
reflections : increase systole, decrease diastoleharmonic dispersion : high frequency waves faster than low frequencyelastic tapering : 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.True False
False 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.True False
True electromechanical coupling pharmacomechanical coupling
How is the effect of caclium on muscle contraction different for smooth muscle and skeletal/cardiac muscle?
skeletal/cardiac muscle : calcium --> troponin C disinhibits actin --> faster ATP consumptionsmooth muscle : calcium --> calmodulin --> activates/phosphorylates myosin --> slower ATP consumption
Through which range of arterial pressure is autoregulation active?
60-140mmHg
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?
PNS : CN XSNS : bulbospinal pathway
What areas of the heart are supplied by the left coronary artery?
anterior portion of interventricular septum anterior wall of RV LA LV
What areas of the heart are supplied by the right coronary artery?
posterior portion of the interventricular septum (dominant right coronary artery) RA posterior RV
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?
autoregulation (60-140mmHg) strong metabolic control : flow higher for greater level of metabolismbelow 60mmHg : maximal dilation: small drop in pressure decreases flow greatlylarge during diastole, small during systole : myocardium squeezes on own blood flow during systolesmall flow during systole : increased aortic pressuresubendocardium perfused first, then subepicardium : tissue pressure gradient, waterfall third pressureNitric 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?
at rest : 90% diameter narrowingduring 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
gender: male
lipid disorders: elevated total cholesterol (more than 240mg/dL) elevated triglycerides (>150mg/dL) elevated LDL 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 A1elevated lipoprotein and lipoprotein-associated phospholipase A2
hypertension: SBP above 115mmHg
smoking
diabetes: types I and II
obesity : elevated BMI elevated waist to hip ratio (> 1.6) sedentary lifestyle endothelial injury/activation : 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 LDL permeability 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
What predisposes a coronary artery to developing an aneurysm?
atherosclerosis lesions with excessive expansive remodeling lesions with thin fibrous cap intense inflammation
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-gammaextensive expansive remodeling minimal/mild lumen narrowing neovessels within plaque pro-thrombotic state previous asymptomatic coronary embolism episodes emotional stress (sudden) physical exertion
True/False: The presence of matrix metalloproteinases (MMP) indicates that a coronary plaque is less likely to rupture.True False
False 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: central obesity low HDL elevated triglycerides hypertension glucose intolerance diabetes
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) smoking hypertension diabetes central obesity psychosocial stress sedentary lifestyle lower consumption of fruits and vegetables lower consumption of alcohol
What commonly causes stable angina?
fixed coronary obstruction : limits maximal coronary blood flowmaximal 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
increased afterload
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?
Levine's sign : clenched fist over chestsubsternal 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?
exercise capacity horizontal/downsloing ST depression angina
How is atherosclerosis diagnosed?
clinical history stress test/exercise capacity calcium deposition noninvasive imaging : 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?
aspirin : reduce risk of ACSnitrates : lower preload, vasodilatorbeta-blockers : lower HR, lower BP, lower O2 demandcalcium-channel blockers : lower HR, lower BP, lower O2 demandsodium-channel blockers : e.g. ranolazinelipid-lowering therapy (e.g. statins) : reduce risk of ACS, lower mortality
What are some common complications of MI?
embolism ischemia decreased coronary perfusion cardiogenic shock arrhythmias pericarditis papillary muscle infarction/ischemia mitral regurgitation ventricular septal defect ventricular rupture cardiac tamponade CHF
What are the 3 basic components of cardiogenic shock?
1. decreased coronary perfusion 2. ventricular dysfunction : increased ischemia3. hypotension
What are risk factors for developing NSTEMI?
(possible) ECG changes : ST depression, T wave inversion, tansient ST elevationhypotension : hemodynamic instabilitypresentation 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?
age systolic blood pressure heart rate serum creatinine Killip class : symptomscardiac 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?
atrial septum ventricular septum mital valve : anterior leaflet continuity with aortatricuspid valve 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 AVSD : atrioventricular septal defect
What describes an AVSD?
atrioventricular septal defect
requirements: 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?
twist, incomplete septation: aorto-pulmonary window 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 ductus arteriosus : 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?
pulmonary stenosis/atresia : right ventricle is exposed to a pressure load while there is little flowsimultaneous 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?
ductus arteriosus : alternate outlet for RV blood flowforamen ovale : prevents backup in RA
What is are the immediate post-partum changes to fetal circulation?
first breath: 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?
normal variant 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)
cyanosis abnormal heart sounds (e.g. splitting of A2/P2) cyanosis pulmonary edema, dyspnea rales
True/False: Most congenital heart defects involve isolated lesions.True False
True
What are the 3 "levels" of congenital heart defects?
ASD VSD open ductus arteriosus
What is the most common ASD?
(ostium) secundum ASD
What are common signs of ASD?
RV dilation RA dilation murmur
True/False: Most patients with an ASD are symptomatic.True False
False 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 ASD VSD patent ductus arteriosus
What can keep a ductus arteriosus open?
PGE2
What promotes ductus arteriosus closure?
prostaglandin inhibitors e.g. indomethacin
What is coarctation of the aorta?
significant narrowing of aorta
What is the most common location for a coarctation of the aorta?
juxtaductal coarcatation : area in descending aorta near where the ductus arteriosus ispreductal coarctation : hypoplasia of aortic arch
What are long-term complications of coarctation?
re-coarctation late hypertension aneurysm cardiac defects
What can lead to an increase in systolic loads (pressure) and cause hypertrophy?
RV: pulmonary stenosis peripheral pulmonic stenosis pulmonary hypertension LV: aortic stenosis coarctation systemic hypertension
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?
Eisenmenger's syndrome tricuspid stenosis pulmonary stenosis pulmonary hypertension decreased systemic arterial pressure preductal coarctation (with hypoplasia of aorta) Valsalva effect 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
L-to-R: pulmonary hypertension --> Eisenmenger's syndrome endocarditis (not ASD) heart failure decreased exercise tolerance (decreased cardiac function, normal O2 sat) R-to-L: systemic emboli polycythemia hyperviscosity decreased exercise tolerance (decreased oxygen saturation) hypoxemic spells
What are the ductus dependent lesions?
systemic flow obstruction: mitral atresia coarctation aortic stenosis pulmonary flow obstruction: tricuspid atresia tetralogy of Fallot pulmonary stenosis
Which murmurs are usually pathological?
diastolic murmurs continuous murmurs >grade3 harsh murmurs radiating murmurs
What are some normal murmurs?
functional/flow murmurs
stills pulmonic venous hum subclavian bruit
When should you administer PGE2 to an infant? What are counter-indications?
clinical signs of ductus dependent congenital heart defect
sx: failure to thrive cyanosis shock acidosis murmur differential pulses dx: TGA pulm. stenosis aortic stenosis mitral atresia tricuspid atresia coarctation tetralogy of Fallot counterindications: difficult birth respiratory distress prematurity
What are the 3 main causes of edema?
increased capillary hydrostatic pressure : increased venous pressure in heart failurereduced capillary osmotic pressure : nephrotic syndrome, liver diseaseincreased 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?
left atrium
Why choose a lateral view of heart with CXR than A-to-P view?
lateral view: inspect right ventricle (better) left atrium inspection A-to-P view: right ventricle obscured
What are common radiographic findings in heart failure?
cardiomegaly enlarged lung vessels, equalization, rarely cephalization edema : Kerley B lines, "fluffy" or hazy alveolar fillingpleural effusions
What are common sites and causes of calcification as seen with CXR?
pericardium : viral, TB, other chronic pericarditiscoronary artery : atherosclerosismyocardium : remote infarction, rheumatic diseasevalve : sclerosis, degeneration, rheumatic disease
What is the sequence of the myocardial ischemia cascade?
ischemia : perfusion abnormailitiesdiastolic and regional systolic dysfunction : wall motion abnormalitiesECG changes : electrical transit abnormalitieschest pain : angina, MI, death
Which vessel layers are disturbed in a pseudoaneurysm? true aneurysm?
pseudoaneurysm : always t. intima and t. media layers involved, sometimes t. adventitia intacttrue aneurysm : all layers involved
Where do Berry aneurysms typically develop?
cerebral vessels near Circle of Willis
What is the most common cause of pseudoaneurysms?
catheter puncture sites : femoral arterybreak-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?
bacteremia : following dental workcholecystits (Salmonella) syphilis
True/False: Aneurysms are typically lined with thrombi due to blood stasis.True False
True
True/False: Arteriograms of a patient with an aneurysm may appear normal.True False
True Arteriograms only demonstrate flowing blood, not stasis
What is the classic triad of aneurysm symptoms indicating surgery?
abdominal pain hypotension palpable, pulsatile abdominal mass
(impending rupture: sudden back/abdominal tenderness)
What is the most common cause of aortic dissection?
hypertension
Where are the most common sites of aortic dissection? common treatments?
sites: most commonly begins beyond the arch vessels spirals down into iliac vessels tx: reduce HTN vasodilators (e.g. nitroprusside) beta antagonists severe : 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
causes: embolism thrombotic occlusion : atherosclerotic plaqueaorta dissection traumatic disruption vasospasm : drugs
What are some potential complications of acute ischemia?
CHF renal failure collateral circulation : vasculogenesis, angiogenesisloss of limb
What are the 6 P's of acute ischemia?
Pain Pallor Poikilothermia (cold) Pulselessness Parasthesia (numbness) Paralysis (weakness)
What are the typical treatments for acute ischemia?
anticoagulation therapy : heparinsurgical thrombectomy, embelectomy, bypass thrombo-lytic agents : catheter-directed, tissue-plasminogen-activation factorrevascularization (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
symptoms: tense compartment pain on passive stretch loss of sensation motor weakness
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
How is acute myoglobinemia treated?
fluid, osmotic diuretics (e.g. mannitol) bicarbonate
True/False: In a patient with intermittent claudication, their chance of losing a limb at 10 years is greater than losing their life.True False
False 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
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?
age prior history of DVT major surgical procedure malignancy genetic procoagulant abnormalities estrogen drugs acute paraplegia
What does a (-) d-dimer test rule out?
pulmonary embolism
What are the signs/symptoms of a pulmonary embolism?
decreased osygenation hyperventilation hypotension intravascular thrombosis (+) 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
How are venous ulcers different from arterial ulcers?
arterial ulcers = dry, pale, painful, toes-distal foot
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?
common site : bifurcation in neckwhy : low, oscillating shear
What are the common symptoms of carotid disease?
focal, hemispheric neurologic deficits contralateral numbness contralateral weakness aphasia ipsilateral amaurosis fugax (monocular blindness)
When should you intervene on carotid artery disease?
when >70% stenosis of carotid artery
