cardiac Flashcards
non modifiable risk fx heart disease
age, male, family history
modifiable risk fx heart disease
smoking, htn, diet, hyperlipidemia, physical inactivity, obesity DM, pvd, l ventricular wall motion dysfunction
majority mis caused by
atherosclerosis
patho MI
emoli–>ischemia–>acidosis–>inflammatory/cellular response–>preservation measures (collateral circ)–?zones of necrosis—>signs of MI
ami caused by
ruptured plaque emboli lodging in a coronary vessel
cessation of perfusion causes
aerobic production (38 ATP) to anaerobic (2ATP)
ischemia occurs when
ATP deman is greater than atp production
myocardial acidosis
first 6 hours of onset mi symptoms:
- H+accumulate
- ca++ displace from SR
- K= shift outside cell and NA+ inside, altered cell membrane action potential causing edema and arrhythmias
- myocardial acidosis
anerobic waste leads to
lactic acide, increased intracellular ph and inhibition of anaerobic atp production
continued hpoxia leads to
cell death and necrosis
necrotic myocardial cells release
cytokines that mediate acute inflamm process
what accumulates at infarct site- proteolytic enzymes that spills proteins into smaller peptides
this exacerbates injury
myocardial o2 reserve is gone within
8 seconds
immediaely after total occlusion how many normal heartbeats can be completed
sufficient o2 and atp in tissue to sustain 27
ecg changes in
30 seconds
pain with mi
60 seconds after ischemia
myocardial cells are irreversibly injured after
30-40 minutes of ischemia
zone of necrosis
center, contains dead tissue
zone of injury
inner ring- tissue cannot contract but not necrotic
zone of ischemia
inner and outer ring, superimposed upon the zone of injury, separates the other two zones from undamaged tissue
effects of MI
decrease ventricular stroke volume—> decreased CO
- increased LV filling pressure
- decreased cardiac output—> decreased compliance left ventricle= resultant stiff muyocardiam increases BP
- decreased CO and arterial pressure–> baroreceptor mediated
- pain stimulates vasoconstriction and HTN
- SNS increases o2 demand, enlarging the infarcted region and preciptating arrhythmias and impairing cardiac function
s/s AMI
substernal chest pain
progressing hypoxia
dizziness, nausea
itachycardia, increased resp and dyspnea
class i nyh assoc
no limit physical activity
class II (mild)
slight limitation activity, physical activity leads to fatigue, dyspnea, palpitation
class III (moderate)
marked limitation physical activity, ok at rest but less then ordinary physical activity causes fatigue, palp, dysp
class IV (severe)
unable to carry out any physical tast
what lead is most sensitive for detecting ischemia
V5
lead II can detect
ischemia of RCA distribution and most useful for monitroing p waves
V5 and lead II
highest sensitivity to detect ischemia
MI drugs of choice
fentanyl vs. inhaled
inhaled agents cause
vasodilation, decreased preload, decreased CO
o2 demand determined by
wall tension, hr and contractility
o2 delivery
determined by o2 content, coronary blood flow
increased wall tension factors
increased preload, increased afterload will increase o2 demand
increased contractility in response to sympathetic stim or inotropes will
increase o2 demand
increased heart rate
increases contractility but decreases ventricular diameter, decreases wall tension, decreases o2 demand
tee can detect with mi
new segmental wall motion abnormalities
goal periop
maintain supply and demand
what should be avoided with mi
ketamine
muscle relax with mi
vec, roc (pan increases hr)
malignant hypertension
systolic greater than 200 or dbp>120
stage 1 htn
140-159 or 90-99 confirm in 2 months
stage 2 hypertension
> 160 or >100
htn during anesthesia may be due to
depth of anesthesia, hypoxia, hypercarbia
systolic dyfunction
reduced ability for heart to eject, lvef <40%
factors affecting CO
preload, contractility, afterload,(stroke volume), heart rate
compensatory mech co
neurohormonal, frank starling, inflammatory cytokines, ventric remodeling
neurohormonal activation sns- adaptive
- catecholamine induced augmentation ventricular contractility and hr
- systemic and pulmonary vasoconstriction leads to enhanced venous tone, leads to increased preload, maintains blood pressure
maladaptive neurohumoral activation
elevation catechoamine, leads to direct myocyte toxicity leads to apoptosis and myocardial removeling
RAAS
angiotensin II leads to vaocostriction leads to increased preload
aldosterone leads to increase NA resorption, leads to increased preload
maladaptive RAAs
angiotensin II lacts directly on myocytes to promote pathologic removeling leading to decreased contractility
release of atrial and brain natriuretic peptides released following
atrial and ventricular vent, decreased perivpheral vascular resistance and promote sodium excretion
one of fist signs heart failure
increased BNP
frank starling curve
increased sarcomere length, increased CO to a point
ventricular remodeling-
hemodynamic stresses on the heart lead to this, changes compensatory initially to increase ventricular volume, greater stroke volume, higher CO, then ventricle continues to enlarge and myocardium hypertrophies, leading to impaired ontractility
s/s systolic dysfunction
dyspnea, orthopnea, paroxysmal nocturnal dyspnea, dry/nonprod cough, fatigue and weakness, nocturia, decreased exercise toleratnce
systolic dysfunction clinical signs
caxechia, ansious, expir wheeze and rhonchi, cough, tachypnea, laterally displaced PMI, S3, cool and pale extremitie
Stage A
risk factors present, no heart failure
stage b
structural heart disease, no smptoms heart failure
stage c
structural disease with prior or current symptoms of heart failure and lv dyfunction (high risk of decompensation)
stage d
refractory end stage heart disease (highest risk anesthesia)
intraop with systolic dysfunction
avoid nitrous, etomidate for induction, opiods, positiove pressure and peep
hemodynamic goals systolic dyfunction
maintain co, o2 delivery, tissue perfusion, maintain contractility, avoid increases in afterloa
maintain contractiity and co with
epinephrine, dobutamine, milrinone, iabp, vad
diastolic dysfunction
functional abnormality of diastolic relaxation (lusitropy), filling or distensibility of the left ventricle, regardless of ejection fraction. abnormal cardiac relaxation stiffness and filling
diastolic heart failure
diastolic dysfuction with s/s of heart failure, having anormal EF
dyastolic dysfunction vs. systolic dysfunction
diastolic (can’t relax and fill), systolic (too relaxed, cant contract)
systolic dysfunction
decreased EF, progressive chamber dilation eccentric remodeling EF <50
diastolic dysfunction
normal EF, normal LVEDV, abnormal diastolic function, concentric remodeling/hypertrophy
grading system diastolic dysfunction
I-relaxation abnormality
II psudonormal
III- restrictive (reversible)
IV- irreversible
dyastolic heart failure
ef>50
etiology diastolic ysfunction
abn stiffness left vent
abn relaxation left vent
abn filling left vent
isovolumetric relaxation
period between aortic valve closre and mitral valve opening, no change in volume, lv pressure declines
increase in LV diastolic pressure causing and increase in pulm venous pressure can cause
heart failure
hypertrophic remodeling
caused by hypertension
concentric hypertrophy
lv muscle mass thicker, diminishing volume while maintaing a normal ef of blood
anesthesia contraindications
severe aortic or mitral valve stenosis
uncontrolled heart failure
mi less than 1 month
prevent intraop diastolic heart failure
keep HR within narrow range (allow filling)
tachycardia bad
bp withina narrow range
careful with volume
careful with volatile agents and induction as they may decrease inotropy
complication of stenosed valves
obstructed blood flow forward, pressure overload
stenosed valve can lead to
compensation via increas in chamber wall thickness (concentric hypertrophy)
stenosis implications
slow and steady heart rate
maintain preload
maintain SVR
regurgitation problem
back flow of blood, volume overload
regurgitation leads to
compensation via chamber dilation (eccentric hypertropy)
implications of regurgitation
after load reduction for fast, full, forward flow
MR TRAPS
systole
MS. PARTS
diastole
tricuspid stenosis leads to
right sided heart failure- hepatomegaly, ascies, peripheral edema, fatigue, dyspnea
tricuspid regurgitation- r
right atrial volume overload
tricuspid regur leads to
a fib, rv systolic dysfunction, rv hypertrophy, r sided heart failure, dyspnea
serous pericarditis
non infectious
fibrinous
dry with a fine granulare roughening (friction rub)
serofibrinous
more intense inflammatory process with cloudy pericardial fluid d/t leukoscytes/red blood cells fibrin
purulent/suppurative
invasion of the pericardial space with microbes
hemmorhagic
blood with a fibrous/serious mix
caseous
most often with tb, direct spread from TB foci
most common pericarditis
serofibrinus
friction rub assoc with
fibrinous pericarditis
caseous necrosis is
a form of cell death when tissue maintains a cheese like appearance
acute pericarditis clinical presentation
sharp peuritic pain ant chest, increasing pain with recumbent position (may be leaning forward), low grade fever, malaise, tachycardia, ecg, duration hours to days, elevated wbc, troponin may be elevated
pericardial friction rubs are
present throughtout the cardiac cycle
normal pericardium
intrathroacic pressure decreases during inspiration, leading to an increas in venous return to the right heart and increase in right ventricular chamber size. b/c normal pericardium accomodates the increased venous return, return does not impair left vent filling
pericardium
anchors, reduces friction, acts as a barrier, limits acute dilation of ventricles, promotes diastolic coupling
acute pericarditis
acute inflammation of the pericardial layers
constrictive pericarditis
chronic inflammation can lead to fibrosis and calcification and eventually impaired diastolic filling
st elevation with pericarditis
widespread, concave, t waves inverted when st segments have normalized
result of scarring with constrictive pericarditis
adhesion of pericardium to epicardium
constrictive pericarditis is
typically chronic, can be acute, transient, occult constriction
constrictive pericarditis leads to
diminished elasticity of pericardium, prevents the normal inspitory decrease in intrathoracic pressure, rapid early diastolic filling, ultimately reduced SV
s/s constrictive
fluid overload- peripheral edema, ascites, jvd, fatique, pericardial knock
pericarditis diagnosis
TEE- pericardial thickening, atrial enlargement, abn septal movement, echo with doppler, ct/mri, coronary angiography
cardiac tamponade
cardiac filling is impeded by external foce, ventricular interdependence, decrease in stroke volume and CO
in chronic tamponade symptoms may not occur until
effusion>2L
s/s tamponade
cp, tachypnea, dyspnea, increased JVP, muted heart sounds, hypotension, tachycardia, pulsus paradoxus, cyanosis, decreased UO, pericardial rubb
constrictive pericarditis treatment
nsaids, steroids, chemotherapy, ace plus diuretics, pericardiectomy only definitive tx option
cardiac tamponade
pericardiocentesis
acute pericarditis in the absence of assoc pericardial effusion or scarring does
not alter cardiac function
surgery and acute pericarditis
focus on underlying disease, case cancelled if possible,
pericardiotomy
large bore IV, CPB available, arterial monitoring, ketamine/etomidate/nitrous/benzos, vaa with caution avoid ppv if possible
goal with hemodynamics in pericardiotomy
preserve contractility, hr, preload and afterload
cardiac tamponade and anesthesia
optimize clinical status, cvc/art line, local infiltration anesthesia only, no positive pressure vent, inotrope if needed
after pericardiocentesis
preserve hr, co, preload, afterload, myocardial contractility
primary cardiac tumors are
rare
clinical manifestation of cardiac tumors
location
obstruction of circulation thru heart valves leads to
heart ailure sysmptoms
interference with heart falves
regurgitation
direvt infasion of myocardium
impaired heart
invasion of adjacent lung
pulm symptoms
left atrial tumors
mimic symptoms of obstructing AV flow or causing mitral regurgitation
direct invasion of myocardium leads to
impaired contractility, arrhythmias,heart block, or pericardial effusion with or without tamponade
s/s heart tumor
fever, malaise, arthralgias, raynauds, rash, clubbing
lab findings heart tumor
increased igm, increased ESR
tumor embolism
tumor fragments. systmic- mi, cva, pe- pah, cor pulmonale
majority of benign cardiac tumors are
myxomas
where are most tumors
left atrium
myxomas
produce vascular endothelial growth factor. 35% are friable or billous.
myxoma patho
obstruct pulm or systemic venous drainage, impair av flow
s/s myxoma
fever, weight loss, raynauds, myalgia, etc
tx myxoma
surgical resection
carney omplex- inherited autosomal dominant disorder hcar by multiple tumors including atrial, extracardiac myxomas
true
2nd most common cardiac tumor
papillary fibroelastomas 80% in heart valves- usually left side heart
fibroelastoma most common presentation
stroke or tia, angina, sudden death hf, pe
cardiac lipoma
benign fatty cells, mainly in adults, half in subendocardial regions
cardiac lipoma
not a true tumor, exxagerated growth of normal fat in septum
rhabdomyomas
exclusively in children less than 1 year old
location rhabdomyoma
ventricular walls or av valves
s/s rhabdomyomas
rhythm disturbances, heart block, v tach
second most common pediatric tumor
cardiac fibromas- ventricular muscle 5x more in left then right
teratomas
benign tumors located in the pericardium, mainly in peds
purkinje cell tumors/hamartomas
benign tumors, small, flat sheets cells, usually young children
purkinje cell tumors located
left ventrical endocardial and epicardial surfaces
s/s purkinje cell tumors
incessant V tach
can you se epurkinje cell tumor on echo
no
mesothelioma
most arise in pleura, can arise from pericardium
mesothelioma
malignant
location mesothelioma
av node, may produce heart block
s/s mesothelioma
cardiac tamponade, constriction
sarcomas
primary malignant tumors- proliferate rapidly and invade myocardium, obstruct blood flow to heart
la tumors
pulm congestion, s4, loud s1, diastolic murmur
ra tumors
r sided congestion, diastolic mumur, tricuspid regurg
rv tumors
r sided chf, s3
lv tumors
positional changes of murmur and bp, buaortic hypertrophic cardiomyopathy
outflow obstruction causes
hypotension d/t posture
hypotension during induction avoid
epinephrine
left atrium myxoma may mimic
mitral stenosis with pulmonary hyptertension
what needs to be avoided in cardiac tumor surgery
tachycardia, max. vent filling- slow HR, high afterload to maintain perfusion setting, adequate preload
3 layers aorta
tunica intima, tunica media, tunica dventitia
localized abnormal dilation of a blood vessel or the wall of the heart.
aneurysm
most common cause aneurysm
aaa, htn, older age
patho aortic aneurysm
degeneration and wekening of the normal elastic medial layer from constant stress, arterial wall thinning secondary to plaque that originates in the intima, dilation from effect of blood stream across obstructive vascular plaque, causes turbulance and weakens wall
laplace and aneurysm
aneurys will get progressively larger regardless of cause. as radius expands, wall tension increases
true aneurysm
bounded by arterial wall components
false aneurysm
breach in vascular wall
fusiform aneurysm
make up majority, uniform dilation involves entire vessel
saccular
less common- localized, balloon shaped outpoutching that involves only portion of vessel wall
crawford1
originates distal to subclavian artery
crawford 2
involves entire aorta distal left subclavian
crawford3
involves distal half of descending thoracic aorta and entire abd aorta
crawford4
involves infradiaphragmatic aorta
dissection
an expanding hematoma within aortic wll, caused by either an intimal tear or degeneration of media
4 major inherited disorders that are known to effect major arteries
marfans, ehlers-danlos, biscupid aortic valve, nonsyndromic familial aortic dissection
marfans
most prevelent connective tissue disorders- mutations in fibrillin-1 gene
ehlers danlos
group connective tissue disorders, syndrom type IV only type with increased risk death- mutations type III procollagen gene
bicuspid aortic valve
most common congenital anomaly resulting in aortic dilation/dissection
nonsyndromic familial aortic dissection
no criteria marfans,
dissection usually
in right lateral wall of ascending aorta or close to ligamentum arteriosum
patho dissection
tear in intima, inflow of blood along aortic media, separates intima and media, creates false lumen
debakey type 1- dissection
intimal tear originates in prox ascenting aorta- involves variable lenghts of arch, descending and abd aorta
debakey type 2-dissection
contained to ascending aorta
type 3
confined to desending thoracic aorta
type iiib
extends into abd aorta and iliacs
dissection and anesthesia
minimize increases blood pressure
perfusion pressures distal to the clamp in aortic surgery are
directly dependent on proximal aortic pressures (above the clamp) not CO or intravascular volume
goal in aortic surgery is to
maintain distal aortic pressures (permissive hypertension), decrease afterload, normalize preload, coronary blood flow and contractility
hemodynamic responses to aortic unclamping
decreased SVR and bp, CO no change, LVEDP decreases, Myocardial blood flow increases, hypotension (hypoia mediate, central and vasoactive
clamping aorta hemodynamics
increased filing pressures- cvp, lvedp, pcwp, increased SVR and BP, decreased CO, increased pulm vascular resistance, systemic hypertension causes increased afterload,
risks with aortic surgery
spinal cord ischemia, mi and heart failure, hypothermia, coagulopathy, renal insufficiency, pulm complications
if la is used during aorta it may
produce sensory and motor anesthesia which delays the recognition of anterior and spinal artery syndrome
primary cardiomyopathy
genetic, mixed, acquired
genetic cardiomyopathy
hypertrophi, arrhythmogenic, left ventricular noncompaction
mixed cardiomyopathy
dilated cardiomyopathy, primary restrictive nonhypertrophic cardio
acquired cardiomyopathy
myocarditis, peripartum, stress
secondary cardiomyopathies
toxic, inflammatory, infiltrative, storage, endomyocardial, endocrine, neuromuscular, autoimmune
hypertrophic cardiomyopathy
genetic- autosomal dominant. lv hypertrophy (most common anterolateral)
s/s hypertrophic cario
fatigue, dyspnea, chest pain, palpitations, syncopeecho lv wall thick>15mm, ecg, mri, myocardial biopsy
diagnosis HCM
diagnosis, ef>80, lv wall>15
manifestations HCM
myocardial hypertrophy, lv outflow tract, diastolic dysfunction, myocardial ischemia, dysrhythmias
most common arrhythmias with HCM
a fib
tx HCM
beta blockers, CCB, diuretic, amiodarone, ICd
anesthesia and hypertropic cardiomyopathy
avoid increase LVOT obstruction
what increases LVOT
increase in myocardial contractility, decrease in preload, decrease in afterload
what decreases preload
vasodilators, hypovolemia, tachycardia
what decreases afterload
hypotension, vasodilators
what increases myocardial contractility
beta adrenergic stim, digitalis
hypertrophic cardiomyopathy avoid
atropin/glyco b/c increase HR
goal anesthesia hypertorophic cardiomyopathy
avoid tachycardia, maintain preload, maintain afterload, maintain contractiity, maintain NSR do not inactivate DDD pacemaker if placed for gradient reduction
what do you use for hypotension with HCM
phenylephrine, not ephedrine, dopamine, dobutamine
most common cardiomyopathy
dilated
s/s dilated cardiomyopathy
heart failure (initial), chest pain on exertion, dyspnea
dilated cardiomyopathy diagnosis
echo: ef<40%, ecg- lbbb, s segment abn, r heart cath- increased wedge pressure, increased SVR, decreased CO
tx dilates cardiomyopathy
gen supportive measures- adequate weight loss, na and diet, fluid restriction
anesthetic management dilated cardiomyopathy
ppv and peep may be beneficial, fluid management, monitoring
stress induced cardiobyopathy mimics
signs of mi
cardiac transplant patient reminders
aseptic technique, these pateints are denervated- no sympathetic innervation, no parasymp innervation, no sensory
consequences denervation
loss of vagal tone, carotid massage and valsalva have no effect, nod irect symp restponse to DL or TE, blunt hr response to pain, no immed response to hypovolemia
pvd
slow, progressive circulatory disorder may involve arteries, veins, lymphatics
PAD
atherosclerosis major
progression of atherosclerosis
endothelial injury accumulation of LDL monocyte adhesion to endothelium transformation of monocytes into macrophages and foam cells platelet adhesion smooth muscle cell recruitment, prolif lipid acumulation extra and intra cell
progression atherosclerosis
damaged endothelium, fatty streak and lipid core, fibrous plaque, complicated lesion, trhombus, plaque is complicated by red thrombus depositoin
most commonly effected vessles pad
pelvis, le
assessment findings
diminished/absent pulses, dry/shiny/hairless skin, pallor on elevation, dusky pale mottled skin, cool or cold limb, deep small, round ulcers
s/s pad
intermittent claudication (main), pain, burning, tightening, cramping, fatigue, lower extrem- triggered by activity and relieved by rest
diagnosis pad
doppler, abi, angiography ratio is less than 0.9 with claudication
abi normal
1.0-1.2
severe pad 0-0.4
true
rutherford scale
o- asymptomatic
1-mild claudication
2-moderate
3-severe claudication
4-rest pain
5- ischemic ulceration not exceeding ulcer of digits foot
6- severe ischemic ulcers or frank gangrene
when pad present
6-7x higher risk MI, CVA
intraop
avoid/limit pure alpha agonists aggressive hr and bp control
virchows triad in thrombosis
endothelial injury,, hypercoagulability, abnormal blood flow
endothelial injury
loss of endothelium>exposure of subendothelium>adhesion platelets>release tissue factor>local depletion of prostacylin>plasminogen activators
abnormal blood flow
promotes endothelial activation and enhances procoagulant activity, disrupts laminar flow and brings plt in contact with endothelium
turbulence
primary causative factor in arterial and cardiac circulation, causes endothelial injury and pockets of stasis
primary causative factor in venous circulation for thromboembolism
stasis
risk thromboembolism
age,metabolic syndrome, trauma, surgery, immobiliation, cancer, pregnancy
arterial thromboembolism form in
areas of turbulence and endothelial injury
myocardial infarction is main cause of
intracardiac thrombi by causing dyskinetic wall motion and damage to endocardium
venous thromboembolism
occur at sites of stasis, primarily lodge in pulm capillary beds
arterial thromboemoblism most arise from
mural thrombi- 2/3 left vent infarct, 1/4 left atrial dilation and fibrillation
most common severe manifestations of atherothrombosis
mi and stroke
most common source of cerebral artery thromboemb
cardiac mural thrombi or a fib and valve disease
where is most often affected in cerebral artery thromboemb
middle cerebral artery
mi most common source
ruptured atherosclerotic plaques
venous thromboembolism triggered by
procoag activity on intat endothelium from inflammation and/or stasis
what is most significant clinical manifestation of venous thromboembolism
pulm embolism
2 main pathophysiologic consequences pe
respiratory compromise from non-perfused, ventilated alveoli, circulatory compromise from increased resistance in pulm blood flow
clinical manifestation pe
dyspnea, chest pain, fever, tachypena, cough, blood tinged sputum, coarse breath sounds, new s4
regional and decreased incidence dvt
sympathectomy- increased lower extrem. blood flow, decreased plt activity, faster ambulation post op,
acyanotic heart defects
vsd, asd, coarc of aorta
cyanotic defects
tetrology, total anomolous pulm vascular connection
left to right shunt
not initially assoc with cyanosis, increased pulm blood flow can lead to pulm htn and rv hypertrophy. potential for rv hf
what does l to r shunt lead to
eventually pvr increases above svr which will reverse shunt right to left (unoxygenated blood will enter the ystemic circ)
ostium secundum
located near intrarterial septum most
ostium primum
large opening in the interatrial septum, adjacent to av valve
sinus venosus
located near entracnce SVC
ASD s/s
dyspnea, supravent dyshryth, r heart failure, paradoxical embolism, recurrent pulm infections, systolic ejection murmur
asd large shunt
2 cm left to right
small asd
0.5cm- no hemodynamic compromise
if pulm blood flow is 1.5x systemic blood flow
asd should be closed to prevent rv dysfunction adn irreversible pulm htn
ASD anesthetic managment
what not to do
avoid increased SVR, avoid decreased PVR b/c leads to increased L-R shunting
avoid high fio2- decreases pvr and increases pulm blood flow
no air bubbles
what to do with asd and anesthesia
decrease left to right shunt- decrease SVR (VA) increase PVR (ppv)
antibiotic prophylaxis
valve with artifical material, hx of endocarditis, heart transplant, certain congenital defects- cyanotic not repaired, or congentital repaired with artificial material or a device for the fist 6 monts after procedure
3 types VSD
membranous, supracristal, muscular
VSD s/s
small- may not have s/s
large- svr exceeds pvr left to right shunting
diagnosis vsd
systolic holistic murmur, enlarged l atria/vent on ecg/ xray with atrial/vent enlargement, echo, heart cath
VSD surgery what not to do
avoid increase in svr, avoid decrease pvr b/c leads to increased shunting, avoid hypovolemia, avoid increased myocardial contractility
coarctation of aorta
preductal- proximal to ductus arteriosus or ligamentum arteriosum, ductal occurs at the insertion of ductious arteriosus, postductal- distal to ductus arteriosus
s/s coarctation of aorta
htn with absent femoral pulse, headache, dizziness, palpitations, harsh systolic ejection murmur
tet anesthesia managment
avoid decreased SVR, avoid increased PVR avoid increased myocardial contractility…. why? increased right to left shunt, increased arterial hypoxemia
