CV Final

inward calcium current: L-type Ca2+ channels --> longer plateau phase

• 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

• calcium stimulates troponin C
• troponin C moves --> disinhibition of thick and thin filaments from each other

intracellular calcium burst precedes muscle contraction/force generation

• steeply increasing stiffness with stretching
• prevents overstretching

connectin/titin

• diastolic passive elastic property
• cardiac hypertrophy
• stress-sensing
• diastolic stiffening with diastolic heart failure

because of increased sensitivity to calcium

• 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

troponin C

increasing volume

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

increased sensitivity to calcium

• preload
• End Diastolic Volume

diastolic BP

• preload
• afterload
• contractility

True

• calcium kinetics
• contractile strength

yes, during rest potentiation a decreased beat frequency may result in increased force of contraction

• leaky valves (i.e. regurgitation)
• low blood volume

• increased SNS discharge
• increased epi/norepi
• increased intracellular calcium

• increased contractility
• increased rate of relaxation
• increased force of contraction
• increased peak force
• increased rate of force develpment

increasing contractility increases the amount of shortening --> increased stroke volume

• systolic heart failure
• increasing afterload --> decreasing ejection fraction
• increasing contractility --> increasing efection fraction
• changing preload --> no effect on efection fraction

• stroke volume stabilized by increased preload (i.e. increased muscle fiber length)
• increased EDV
• increased EDP
• decreased Ef
• unchanged afterload
• cardiomegaly

decrease afterload --> decrease BP --> increase SV --> increase Ef

no: calcium actively pumped back into SR

summation of millions of AP's over space/time

slight atrial pressure increase

increased ventricular pressure

increased aortic pressure (isovolumetric contraction)

peak aortic/ventricular pressure

• isovolumic relaxation
• decreased ventricular pressure (steep)
• decreased aortic pressure (gradual)

• ventricular pressure is still less than aortic pressure, aortic valve closed
• pressure rises but volume remains constant
• correlates to S wave on ECG

• ventricular pressure lower than aortic pressure and higher than atrial pressure, all valves closed
• volume remains same as ventricular relaxation continues

• 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

• normal heart sounds are produced by closing of heart valves
• S1 = AV valves closing
• S2 = PV and Aortic (i.e. semilunar) valves closing

atrial contraction

ventricular contraction

venous filling (relative to atria)

aortic valves (esp. during inspiration)

• Right bundle branch block
• pulmonic stenosis

atrial septal defect

• left bundle branch block
• advanced aortic stenosis
• Left-sided CHF

• 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

• mitral valve
• aortic valve
• usually both at same time

• today: degenerative valvular disease
• 30 years ago: bicuspid aortic valve (i.e. congenital)

• today: post-infectious (Group A Strep)
• 30 years ago: degenerative valvular disease

measure pressure gradient across aortic valve (i.e. between LV and Aorta)

• 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

• 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

• 1. convective acceleration
• 2. flow acceleration
• 3. viscous friction

stenotic valves: convective acceleration component predominates

can calculate effects of increased flow rates through valves/vessels

• stenosis
• shock
• fever
• anemia

• pregnancy
• exercise

• aortic stenosis = mechanical problem, treatment = mechanical solution
• mechanical valve replacement
• valve grafts
• balloon valvuloplasty

anticoagulation therapy (prevent thrombus)

treatment usually only for symptomatic patients

• 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"

• angina: 5 yrs
• syncope: 3 yrs
• CHF: 2 yrs
• Atrial fibrillation: 6 mo

• many non-surgical options, unlike with aortic stenosis
• maintenance of sinus rhythm: medication
• balloon valvulplasty

• 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)

• 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

• 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

• genetic CT disorders: Marfan's, Ehlers-Danlos
• myxomatous degeneration
• normal variant

• rheumatic
• congenital: bicuspid aortic valve
• degenerative
• infectious
• annular dilation: from asc. aorta dilation

increased LV pressure --> decreased cornary artery blood flow

• 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

• vasodilators: reduce afterload
• mitral insufficiency: vasodilators relieve symptoms
• aortic insufficiency: vasodilators slow progression of disease

• 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

• S3 = early ventricular filling, always pathological
• S4 = atrial filling, can be normal

• 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

• CO is dependent on SV and HR
• decreases with age
• decreases with supination (i.e. sitting/standing up)

• 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

• effective cardiac output = amount of blood actually being pumped throughout the body
• measured by Fick equation (i.e. O2 consumption)

• 1. effective cardiac output: effective transport (Fick equation), dilution method (temp. indicator)
• 2. stroke volume: volumetric techniques (imaging), flow techniques (Doppler)

• 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

• 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

• 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

chronic rheumatic heart disease

(asymptomatic) mitral valve prolapse

• 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

• genetic CT disorders: Marfan's, Ehler's-Danlos
• myxomatous tissue degeneration --> gelatinous appearance
• fragmentation of collagen fibers
• redundant valvular leaflets
• myxomatous tissue in CT

• common in elderly, usually asymptomatic
• can interfere with valve closure
• can cause regurgitation
• can affect valvular leaflets and interventricular septum

• 1. dilation of mitral valve annulus
• 2. papillary muscle rupture
• 3. papillary muscle dysfunction/scarring

• nodular fibrosis of leaflets
• marked calcification
• inflammatory cell accumulation
• serum-derived lipids

• aortic stenosis
• aortic regurgitation
• LV hypertrophy
• myocardial ischemia --> MI
• arrhythmias
• sudden death

• 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

• rheumatic disease
• mitral disease

• dilation of tricuspid annulus: pressure/volume overload
• (i.e. rarely a primary valvular disease)

congenital abnormailty: Tetralogy of Fallot, isolated pulmonary stenosis

• dilation of the valve annulus
• severe pulmonary hypertension

• most common: bacterial endocarditis
• rarest: fungal 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)

• vegetations
• inflammed myocardial tissue

• complications:
• valve perforation
• CHF
• septic embolization
• immune complex glomerulonephritis

• a.k.a. Marantic (Wasting) Endocarditis
• sterile vegetations
• vegetations can be colonized --> infectious endocarditis
• unknown mechanism
• associated with wasting syndromes, end stage cancers

• 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

• fibrosing valvular disease
• fusion of chordae
• fibrous plaques on leaflets
• lesions are predominantly right-sided

• carcinoid heart disease: predominance of right-sided lesions
• drug-induced valvular disease: predominance of left-sided lesions

• serotonergic drugs: methylsergide, ergotamines
• appetitie suppressants: fenfluramine

• viscosity of the fluid
• radius of the tube
• length of the tube

• 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

rapid ventricular ejection

• aortic valve closure
• end of systole

• apex = systolic pressure
• nadir = diastolic pressure

pulse pressure = systolic - diastolic pressure = apex - nadir of arterial pulse wave

• MAP = average pressure over time
• MAP = baseline of arterial pulse wave
• sphygmomanometer on brachial artery
• MAP = diastolic pressure + 1/3 pulse pressure

• arterial tree is distensible (Windkessel effect)
• elastic recoil of arteries preparing for diastole
• artery recoil ejects part of stroke volume that remains after systole

• inreasing age relates to decreasing arterial compliance
• i.e. increasing age relates to increasing hardening of arteries

• 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

• meaured with a sphygmomanometer
• equal to blood pressure when the subject is lying down
• affected by hydrostatic effect if not meaured at heart level

• increases with arterial tree progression
• increase in systolic pressure, decrease in diastolic pressure
• **mean pressure declines

capillary bed = several parallel resistor systems

• reflections: increase systole, decrease diastole
• harmonic dispersion: high frequency waves faster than low frequency
• elastic tapering: decreased compliance relates to increased amplitude

• False
• It is normal the ankle systolic pressure to be 20mmHg higher than the systolic pressure of the upper arm.

• True
• electromechanical coupling
• pharmacomechanical coupling

• skeletal/cardiac muscle: calcium --> troponin C disinhibits actin --> faster ATP consumption
• smooth muscle: calcium --> calmodulin --> activates/phosphorylates myosin --> slower ATP consumption

60-140mmHg

CN IX: glossopharyngeal

• decrease in heart rate
• arterial pressure reflexively decreases

• PNS: CN X
• SNS: bulbospinal pathway

• anterior portion of interventricular septum
• anterior wall of RV
• LA
• LV

• posterior portion of the interventricular septum (dominant right coronary artery)
• RA
• posterior RV

• veins that drain directly into the ventricular and atrial chambers wihtout passing through an epicardial vein
• shunts with unknown functions

• 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

• 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)

barely any anaerobic respiration, even in resting cardiac muscle

coronary artery flow: 70% of oxygen extracted by myocardium

• double product = Heart Rate x Systolic BP
• i.e. = heart rate x tension development

indicates myocardial oxygen consumption

• at rest: 90% diameter narrowing
• during increased blood flow/exercise: 40% diameter narrowing

• 1. exponential pressure drop across a stenosis as a function of flow
• 2. exhaustion of vasodilation reserve
• 3. tachycardia during exercise

epicardial coronary 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

• low blood flow
• increased oxidative sterss on endothelium
• attenuation of nitric oxide inflammation
• LDL cholesterol uptake
• LDL permeability
• smooth muscle cell migration

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

• atherosclerosis
• lesions with excessive expansive remodeling
• lesions with thin fibrous cap
• intense inflammation

• plaque disruption, rupture of fibrous cap
• endothelial erosion, no fibrous cap disruption
• intra-plaque hemorrhage, no fibrous cap disruption

• 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

• False
• The presence of matrix metalloproteinases (MMP) indicates that a coronary plaque is MORE likely to rupture.

• combination of 3 or more of following:
• central obesity
• low HDL
• elevated triglycerides
• hypertension
• glucose intolerance
• diabetes

• 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

• 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

• elevated ventricular wall stress
• low diastolic blood pressure

• Levine's sign: clenched fist over chest
• substernal chest pressure/tightness
• can radiate to arms, neck, jaw
• associated with dyspnea, nausea, diaphoresis

• 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

• exercise capacity
• horizontal/downsloing ST depression
• angina

• clinical history
• stress test/exercise capacity
• calcium deposition
• noninvasive imaging: CT, MRI, angiography, intracoronary ultrasound

cornary artery lumen narrowing only happens at later stages of atherosclerosis

• 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

• embolism
• ischemia
• decreased coronary perfusion
• cardiogenic shock
• arrhythmias
• pericarditis
• papillary muscle infarction/ischemia
• mitral regurgitation
• ventricular septal defect
• ventricular rupture
• cardiac tamponade
• CHF

• 1. decreased coronary perfusion
• 2. ventricular dysfunction: increased ischemia
• 3. hypotension

• (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

• age
• systolic blood pressure
• heart rate
• serum creatinine
• Killip class: symptoms
• cardiac arrest at admission
• elevated cardiac enzymes
• ST segment deviation

• 1. function of endocardial cushion
• 2. division of turncus arteriosus
• 3. role of flow

• permits right-to-left flow
• prevents left-to-right flow

membranous septum (last to develop)

ostium secumdum: last to develop

• atrial septum
• ventricular septum
• mital valve: anterior leaflet continuity with aorta
• tricuspid valve
• offset of AV valves

• primum atrial septal defect
• inlet type of ventricular defect
• cleft anterior mitral leaflet
• cleft septal tricuspid leaflet
• AVSD: atrioventricular septal defect

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

• septation, no twist:
• TGA

• twist, incomplete septation:
• aorto-pulmonary window

• displacement of septum:
• (anterior) Tetralogy of Fallot
• (anterior) double outlet LV
• (posterior) double outlet RV

hypoplastic RV, Pulmonic valve, PA

hypoplastic LV, Aortic valve, ascending aorta

• other "side" of heart still functional
• ductus arteriosus: right-to-left shunt in pulmonary artery to asc. aorta

• severe mitral stenosis
• mitral atresia --> hypoplastic LV, Aortic valve, Asc. Aorta

• 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

• ductus arteriosus: alternate outlet for RV blood flow
• foramen ovale: prevents backup in RA

• 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)

• normal variant
• prevalence depends on age distribution
• increased risk for paradoxical embolization
• increased risk for migraines (?)

heart murmur (not specific)

• cyanosis
• abnormal heart sounds (e.g. splitting of A2/P2)
• cyanosis
• pulmonary edema, dyspnea
• rales

True

• ASD
• VSD
• open ductus arteriosus

(ostium) secundum ASD

• RV dilation
• RA dilation
• murmur

• False
• Most patients with an ASD are asymptomatic.

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

• increaesd pulmonary circuit blood flow
• ASD
• VSD
• patent ductus arteriosus

PGE2

• prostaglandin inhibitors
• e.g. indomethacin

significant narrowing of aorta

• juxtaductal coarcatation: area in descending aorta near where the ductus arteriosus is
• preductal coarctation: hypoplasia of aortic arch

• re-coarctation
• late hypertension
• aneurysm
• cardiac defects

• RV:
• pulmonary stenosis
• peripheral pulmonic stenosis
• pulmonary hypertension

• LV:
• aortic stenosis
• coarctation
• systemic hypertension

Right to left: mix deoxygenated blood with oxygenated blood

Left to Right: follows normal pressure gradient

• 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

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

• systemic flow obstruction:
• mitral atresia
• coarctation
• aortic stenosis

• pulmonary flow obstruction:
• tricuspid atresia
• tetralogy of Fallot
• pulmonary stenosis

• no other connections:
• TGA

• diastolic murmurs
• continuous murmurs
• >grade3
• harsh murmurs
• radiating murmurs

functional/flow murmurs

• stills
• pulmonic
• venous hum
• subclavian bruit

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

• 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)

• increasing arteriole pressure --> decreases capillary pressure
• decreasing arteriole pressure --> increases capillary pressure

left atrium

• lateral view:
• inspect right ventricle
• (better) left atrium inspection

• A-to-P view:
• right ventricle obscured

• cardiomegaly
• enlarged lung vessels, equalization, rarely cephalization
• edema: Kerley B lines, "fluffy" or hazy alveolar filling
• pleural effusions

• pericardium: viral, TB, other chronic pericarditis
• coronary artery: atherosclerosis
• myocardium: remote infarction, rheumatic disease
• valve: sclerosis, degeneration, rheumatic disease

• ischemia: perfusion abnormailities
• diastolic and regional systolic dysfunction: wall motion abnormalities
• ECG changes: electrical transit abnormalities
• chest pain: angina, MI, death

• pseudoaneurysm: always t. intima and t. media layers involved, sometimes t. adventitia intact
• true aneurysm: all layers involved

• cerebral vessels
• near Circle of Willis

• catheter puncture sites: femoral artery
• break-down of suture lines of bypass grafts swen to femoral arteries

• artherosclerosis (not from occlusion; from direct arterial wall degeneration)
• (genetic CT disorders)

• bacteremia: following dental work
• cholecystits (Salmonella)
• syphilis

True

• True
• Arteriograms only demonstrate flowing blood, not stasis

• abdominal pain
• hypotension
• palpable, pulsatile abdominal mass

(impending rupture: sudden back/abdominal tenderness)

hypertension

• 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

• 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

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

• CHF
• renal failure
• collateral circulation: vasculogenesis, angiogenesis
• loss of limb

• Pain
• Pallor
• Poikilothermia (cold)
• Pulselessness
• Parasthesia (numbness)
• Paralysis (weakness)

• 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.)

leaking of capillaries caused by reperfusion injury within muscular fascial compartments

• symptoms:
• tense compartment
• pain on passive stretch
• loss of sensation
• motor weakness

glucose/insulin IV (some bicarbonate)

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

• fluid, osmotic diuretics (e.g. mannitol)
• bicarbonate

• 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%.

varicose veins = enlarged superficial veins, veins elongate and widen, benign

common site: branches of saphenous veins (greater and lesser)

• damage to endothelium (e.g. inflammation, smoking)
• stasis (e.g. sedentary lifestyle, immobilization, aneurysm)
• hypercoagulable state (e.g. genetic disorders, pregnancy, cancer, etc.)

• age
• prior history of DVT
• major surgical procedure
• malignancy
• genetic procoagulant abnormalities
• estrogen drugs
• acute paraplegia

pulmonary embolism

• decreased osygenation
• hyperventilation
• hypotension
• intravascular thrombosis
• (+) d-dimer levels

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

arterial ulcers = dry, pale, painful, toes-distal foot

venous ulcers = moist, pink, ankle-mid calf

intracerebral circulation has rich collateralization: Circle of Willis

• common site: bifurcation in neck
• why: low, oscillating shear

• focal, hemispheric neurologic deficits
• contralateral numbness
• contralateral weakness
• aphasia
• ipsilateral amaurosis fugax (monocular blindness)

when >70% stenosis of carotid artery