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Why is the ventricular AP very long?
inward calcium current: L-type Ca2+ channels --> longer plateau phase
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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
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How does calcium promote muscle contraction?
- calcium stimulates troponin C
- troponin C moves --> disinhibition of thick and thin filaments from each other
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How does an intracellular calcium burst relate to muscle contraction timing?
intracellular calcium burst precedes muscle contraction/force generation
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What does a non-linear length-tension relationship of myocytes reflect?
- steeply increasing stiffness with stretching
- prevents overstretching
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What is the dominant component of the diastolic passive elastic property of cardiac muscle?
connectin/titin
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What cardiac properties is connectin/titin responsible for?
- diastolic passive elastic property
- cardiac hypertrophy
- stress-sensing
- diastolic stiffening with diastolic heart failure
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Why does the force of contraction increase with increased muscle length?
because of increased sensitivity to calcium
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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
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What component of cardiac muscle is responsible for length dependent calcium sensitivity?
troponin C
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Increase in what parameter results in cardiac dilatation?
increasing volume
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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
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What is responsible for the cardiac muscle length-tension relationship?
increased sensitivity to calcium
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What determines length of cardiac muscle fibers?
- preload
- End Diastolic Volume
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What it used as a measure of left heart afterload?
diastolic BP
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What affects stroke volume?
- preload
- afterload
- contractility
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True/False: Stroke volume is a function of afterload.
True
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What does heart rate effect?
- calcium kinetics
- contractile strength
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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
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What would you suspect if a patient has normal cardiac contractility but decreased cardiac performance?
- leaky valves (i.e. regurgitation)
- low blood volume
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What increases (cardiac) muscle contractility?
- increased SNS discharge
- increased epi/norepi
- increased intracellular calcium
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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
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What effect does contractility have on stroke volume?
increasing contractility increases the amount of shortening --> increased stroke volume
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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
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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
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How can afterload reduction benefit a patient with severe systolic heart failure?
decrease afterload --> decrease BP --> increase SV --> increase Ef
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Is cardiac myocyte relaxation a passive process?
no: calcium actively pumped back into SR
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What does an ECG record?
summation of millions of AP's over space/time
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What does the P wave signify in a cardiac cycle?
slight atrial pressure increase
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In the cardiac cycle, what is signified by a R wave?
increased ventricular pressure
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In the cardiac cycle, what is signified by a S wave?
increased aortic pressure (isovolumetric contraction)
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In the cardiac cycle, what is signified by a T wave?
peak aortic/ventricular pressure
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In the cardiac cycle, what is signified after the T wave?
- isovolumic relaxation
- decreased ventricular pressure (steep)
- decreased aortic pressure (gradual)
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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
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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
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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
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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
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What produces the atrial "a" wave?
atrial contraction
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What produces the atrial "c" wave?
ventricular contraction
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What is the "v" venous wave from?
venous filling (relative to atria)
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Which closes first, aortic or pulmonic valves?
aortic valves (esp. during inspiration)
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What could cause wide splitting of S2 (i.e. A2/P2) during inhalation and exhalation?
- Right bundle branch block
- pulmonic stenosis
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What can cause fixed splitting of the S2 heart sounds during inspiration and exspiration?
atrial septal defect
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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
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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 valve
- degenerative: aortic stenosis and insufficiency, mitral insufficiency, mitral valve myxomatous disease
- rheumatic: mitral sentosis/insufficiency, aortic stenosis/insufficiency
- infectious: usually tricuspid, mitral, and aortic insufficiency
- risk factors:
- age
- atherosclerosis risk factors
- family history
- hypertension
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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 disease
- 30 years ago: bicuspid aortic valve (i.e. congenital)
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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
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How can you measure added pressure load on heart in stenotic patients?
measure pressure gradient across aortic valve (i.e. between LV and Aorta)
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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
- S4: increased stiffness
- strong PMI
- pulmonary congestion
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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
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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
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What is useful about the Bernoulli equation and CV?
can calculate effects of increased flow rates through valves/vessels
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What are some pathological causes of a change in cardiac output?
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What are some normal causes of a change in cardiac output?
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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
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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"
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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 yrs
- syncope: 3 yrs
- CHF: 2 yrs
- Atrial fibrillation: 6 mo
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What are some common treatments for mitral stenosis?
- many non-surgical options, unlike with aortic stenosis
- maintenance of sinus rhythm: medication
- balloon valvulplasty
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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)
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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, AF
- CXR: LA and LV enlargement
- rate of progression is highly variable
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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
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What are common etiologies of mitral valve prolapse?
- genetic CT disorders: Marfan's, Ehlers-Danlos
- myxomatous degeneration
- normal variant
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What are common etiologies for aortic insufficiency?
- rheumatic
- congenital: bicuspid aortic valve
- degenerative
- infectious
- annular dilation: from asc. aorta dilation
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How does left ventricular pressure relate to coronary artery flow?
increased LV pressure --> decreased cornary artery blood flow
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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
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How do the effects of vasodilators differ from aortic and mitral insufficiencies?
- vasodilators: reduce afterload
- mitral insufficiency: vasodilators relieve symptoms
- aortic insufficiency: vasodilators slow progression of disease
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What is the prognosis for someone with severe aortic insufficiency?
- severe AR but normal LV and asymptomatic: good 10 year prognosis
- angina: 4 year survival
- CHF: 2 year survival
- vasodilators 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, continuous
- intensity: systolic grade +3 = pathological , diastolic grade +1 = pathological
- pitch/character: high frequency = high gradient
- shape: de/crescendo
- location: near source
- radiation: direction of flow
- maneuvers
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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)
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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
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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)
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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)
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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
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What are common clinical features of acute rheumatic fever?
- pancarditis: all layers of the heart
- pericarditis: effusions, fibrin deposition
- myocarditis: lymphocyte/macrophage infiltration
- Aschoff bodies: fibrinoid necrosis, myocyte loss, lymphocyte/marophage infiltration
- endocarditis: ulceration, collagen damage
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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
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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
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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 valves
- valvular regurgitation: rigid leaflets, short chordae
- complications:
- atrial fibrillation
- thrombosis
- pulmonary hypertension
- right- and left- sided heart failure
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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
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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
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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
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What are the main pathological findings of fibrocalcific aortic stenosis?
- nodular fibrosis of leaflets
- marked calcification
- inflammatory cell accumulation
- serum-derived lipids
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What are common complications of fibrocalcific aortic stenosis?
- aortic stenosis
- aortic regurgitation
- LV hypertrophy
- myocardial ischemia --> MI
- arrhythmias
- sudden death
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What are the common features of Marfan's syndrome?
- genetic CT disorder: autosomal dominant
- genes: fibrillin, microfibrils
- musculoskeletal abnormalities (e.g. arachnodactly)
- CV structural complications
- mitral valve prolapse
- mitral regurgitation (kids)
- aortic regurgitation (adults)
- aneurysms
- **cystic medial degeneration
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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
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What is the most common cause of infectious endocarditis? rarest?
- most common: bacterial endocarditis
- rarest: fungal endocarditis
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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)
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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
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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
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What causes drug-induced valvular disease?
- serotonergic drugs: methylsergide, ergotamines
- appetitie suppressants: fenfluramine
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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
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What does the apex the arterial pulse wave represent? the nadir?
- apex = systolic pressure
- nadir = diastolic pressure
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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
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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
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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 diastole
- harmonic dispersion: high frequency waves faster than low frequency
- elastic 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.
- 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
- 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 consumption
- smooth 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 X
- SNS: bulbospinal pathway
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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 metabolism
- below 60mmHg: 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?
- at rest: 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
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 A1
- elevated 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
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?
- 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-gamma
- extensive 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.
- 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 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
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 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?
- 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 ACS
- nitrates: lower preload, vasodilator
- beta-blockers: lower HR, lower BP, lower O2 demand
- calcium-channel blockers: lower HR, lower BP, lower O2 demand
- sodium-channel blockers: e.g. ranolazine
- lipid-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 ischemia
- 3. hypotension
-
What are risk factors for developing NSTEMI?
- (possible) ECG changes: ST depression, T wave inversion, tansient ST elevation
- hypotension: 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?
- age
- systolic blood pressure
- heart rate
- serum creatinine
- Killip class: symptoms
- 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)
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Where are the most common atrial septal defects?
ostium secumdum: last to develop
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What structures develop from the endocardial cushion?
- atrial septum
- ventricular septum
- mital valve: anterior leaflet continuity with aorta
- tricuspid valve
- offset of AV valves
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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
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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
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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
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What is related to tricuspic atresia in cardiac develpment?
hypoplastic RV, Pulmonic valve, PA
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What is related to mitral atresia in cardiac develpment?
hypoplastic LV, Aortic valve, ascending aorta
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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
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What causes hypoplastic left heart syndrome?
- severe mitral stenosis
- mitral atresia --> hypoplastic LV, Aortic valve, Asc. Aorta
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What causes a "peach-pit" right ventricle?
- pulmonary stenosis/atresia: 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
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How does fetal circulation accomodate high vascular resistance in lungs and prevent right ventricular pressure overload?
- ductus arteriosus: alternate outlet for RV blood flow
- foramen ovale: prevents backup in RA
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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)
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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 (?)
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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
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True/False: Most congenital heart defects involve isolated lesions.
True
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What are the 3 "levels" of congenital heart defects?
- ASD
- VSD
- open ductus arteriosus
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What is the most common ASD?
(ostium) secundum ASD
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What are common signs of ASD?
- RV dilation
- RA dilation
- murmur
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True/False: Most patients with an ASD are symptomatic.
- 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
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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 is
- preductal coarctation: hypoplasia of aortic arch
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What are long-term complications of coarctation?
- re-coarctation
- late hypertension
- aneurysm
- cardiac defects
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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
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Which shunts are cyanotic?
Right to left: mix deoxygenated blood with oxygenated blood
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What is the direction of shunt resulting from an isolated, restrictive defect?
Left to Right: follows normal pressure gradient
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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
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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
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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
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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?
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 filling
- pleural effusions
-
What are common sites and causes of calcification as seen with CXR?
- pericardium: viral, TB, other chronic pericarditis
- coronary artery: atherosclerosis
- myocardium: remote infarction, rheumatic disease
- valve: sclerosis, degeneration, rheumatic disease
-
What is the sequence of the myocardial ischemia cascade?
- ischemia: perfusion abnormailities
- diastolic and regional systolic dysfunction: wall motion abnormalities
- ECG changes: electrical transit abnormalities
- chest 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 intact
- true 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 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?
- bacteremia: following dental work
- cholecystits (Salmonella)
- syphilis
-
True/False: Aneurysms are typically lined with thrombi due to blood stasis.
True
-
True/False: Arteriograms of a patient with an aneurysm may appear normal.
- 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)
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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
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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 plaque
- aorta dissection
- traumatic disruption
- vasospasm: drugs
-
What are some potential complications of acute ischemia?
- CHF
- renal failure
- collateral circulation: vasculogenesis, angiogenesis
- loss of limb
-
What are the 6 P's of acute ischemia?
- Pain
- Pallor
- Poikilothermia (cold)
- Pulselessness
- Parasthesia (numbness)
- Paralysis (weakness)
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What are the typical treatments for acute ischemia?
- anticoagulation therapy: heparin
- surgical thrombectomy, embelectomy, bypass
- thrombo-lytic agents: catheter-directed, tissue-plasminogen-activation factor
- revascularization (systemic and local complications: compartment syndrome, hyperkalemia, etc.)
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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
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)
- bicarbonate
-
True/False: In a patient with intermittent claudication, their chance of losing a limb at 10 years is greater than losing their life.
- 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
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.)
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What are (7) major risk factors for DVT?
- age
- prior history of DVT
- major surgical procedure
- malignancy
- genetic procoagulant abnormalities
- estrogen drugs
- acute paraplegia
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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
mechanism: increased capillary pressure results in exudation of protein into interstitial space, calf narrows at ankle, RBC infiltrate tissue --> hyperpigmentation
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How are venous ulcers different from arterial ulcers?
arterial ulcers = dry, pale, painful, toes-distal foot
venous ulcers = moist, pink, ankle-mid calf
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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 neck
- why: 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
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