Cardiac Flashcards
Emptying problems include
SHF, dilated cardiomyopathy, aortic stenosis, pulmonic stenosis
Considerations for SHF & DCM include:
- ) optimize inotropy (balance w/ causing increased MVO2)
- ) decrease afterload (as long as it doesn’t cause drop in BP)
- Maintain NSR to allow for atrial kick
- Don’t fluid overload
Systolic heart failure (pathophys)
an emptying problem that is triggered by volume overload causing eccentric remodeling
known as heart failure with reduced ejection fraction
Systolic heart failure characteristics include
decreased LVEF, Increased LV chamber size, volume overload, LV hypertrophy on ECG, S3 gallop, compliant, eccentric remodeling
Heart failure is
reduce forward flow
Causes for the heart to fail include:
volume overload, pressure overload (two most common), myocardial contractile impairment d/t ischemia or infarct), restrictive filling (pericarditis, tamponade), idiopathic remodeling of sarcomeric or extracellular matrix proteins, myocardial inflammation
Chronic vs. acute heart failure
chronic: stable where BP is maintained b/c of physiological compensations
Acute: sudden decrease in CO resulting in hypotension; medical emergency and can turn into flash pulmonary edema
Acute heart failure can occur due to
worsening chronic HF, new onset HF (i.e. valve or septal wall rupture, MI, or severe HTN crisis)
NYHA Class 1
no symptoms and no limitation in ordinary physical exercise
NYHA Class 2
mild symptoms (mild SOB and/or angina) and slight limitation during ordinary activity
NYHA Class 3
Marked limitation in activity d/t symptoms even during less than ordinary activity; comfortable only at rest
NYHA Class 4
Severe limitations; experiences symptoms even while at rest; mostly bedbound patients
Describe differences between left versus right sided heart failure
Left side: pulmonary congestion, dyspnea, increased LVEDP, pulmonary edema, dyspnea
Right side: increased RVEDP, systemic congestion, hepatomegaly
Most common causes of left heart failure include
HTN, CAD, MI, valvular disease
Most common causes of right heart failure include
Left-sided heart failure
may also be caused by pulmonary arterial hypertension or MI of right ventricle
Describe low output vs. high-output heart failure
Both are d/t heart being unable to pump enough blood to meet oxygen demand of tissues
low-output: filling or emptying problem; CO can be normal but only b/c of compensation
High-output: not a filling or emptying problem; problem is metabolic demand and/or SVR; cardiac output can be normal or above normal but CO is insufficient to meet global metabolic demands
Causes of low-output HF
CAD, chronic HTN, cardiomyopathy, valvular disease, pericardial disease
Causes of High-output HF
Anemia, septicemia, hyperthyroidism
Common causes of HF include:
pressure overload, volume overload, MI, idiopathy cardiomyopathy, hypertrophy/cardiac remodeling
Increased catecholamines cause cardiotoxicity and promote
cardiac remodeling
ANP & BNP promote
diuresis, natriuresis, inhibition of RAAS and SNS, vasodilation, and INHIBIT REMODELING
Concentric remodeling is
caused by increased pressure and results in sarcomeres being laid down in parallel; smaller chamber radius and thicker/less compliant chamber wall
Results in a filling problem
associated with DHF
Eccentric remodeling is
caused by volume overload resulting in sarcomeres being laid down in series; larger chamber radius and more compliant chamber wall
results in an emptying problem
associated with SHF
diastolic heart failure is
a filling problem (occurs L>R)
triggered by pressure overload
stiff/non-compliant ventricles impair filling
heart failure with preserved EF
Diastolic heart failure characteristics include
normal LVEF, decreased chamber size, pressure overload, LV hypertrophy on EKG, S4 gallop, decreased compliance, concentric ventricular remodeling
In patients who develop acute heart failure during surgery, the immediate goal is to
increase CO and decrease LVEDP
Heart failure responses include
increased SNS, increased RAAS, increased humoral and biochemical, increased remodeling
The key difference between SHF & DCM is
etiology!
DCM risk factors include
African American Men (Dark Dads- DDD)
Cardiomyopathy is a
chronic disease of the heart
heart muscle is structurally and functionally abnormal in the absence of CAD, HTN, valvular disease, & congenital heart disease
associated with mechanical and/or electrical abnormality
Etiology of cardiomyopathies (in general):
are genetic, genetic/non-genetic (mixed), or acquired
not caused by other CV diseases
Are not congenital diseases
Can include metabolic, inflammatory or toxic
Etiology of HCM
Genetic
Etiology of DCM & RCM
mixed genetic/non-genetic
Causes of DCM include
caused by genetic & non-genetic factors
non-genetic factors include: alcoholism, cocaine, infection, thyroid disease, pheochromocytoma, chemotherapy or radiation
Dilated cardiomyopathy pathophysiology
increased cardiomyocyte apoptosis, increased sarcomeric proteins in eccentric pattern resulting in eccentric remodeling of the chamber–> emptying problem
Sarcomeric protein changes that reduce contractile filament senstivity to Ca2+ and decrease force generation
Remodeling can lead to conduction abnormalities
s/s consistent with SHF
Signs/symptoms of DCM include
mimic angina pectoris, chamber is hypokinetic and dilated so increased thrombus risk, valve regurgitation possible d/t dilated ventricles, dysrhythmias
Diagnosis of DCM is via
Echo or chest XR that shows LV dilation
The anesthetic goals for DCM & SHF:
Prevent acute drop in CO and increase in LVEDP
Restrictive cardiomyopathy is
rare but lethal
has changes to sarcomeric proteins that impair relaxation and infiltrations/deposits stiffen ventricle
no concentric or eccentric remodeling
a filling problem
RCM etiology
caused by genetic and non-genetic factors
non-genetic causes: infection, chemo or radiation, diseases of infiltration like amyloidosis, sarcoidosis
The pathophysiology of RCM includes:
1) ventricular stiffness
2) impaired relaxation d/t altered Ca2+ cycling
3) system diseases that cause ventricular infiltration w/ substances that stiffen the ventricle
Results in high LVEDP, reduced filling, reduced SV, and reduced CO
can progress to DHF
Signs and symptoms of RCM include
same as those for DHF- congestion in pulmonary or systemic systems, decreased CO to tissues–> syncope, decreased myocardial contractility
conduction abnormalities d/t deposition of infiltrative substances
Diagnosis of RCM
Echo- diastolic dysfunction, atria enlarged not ventricles
The quintessential for DHF & restrictive cardiomyopathy:
SV limited: maintain HR in NSR, do not decrease afterload
Need their preload (titrate carefully so as not to fluid overload)
Have inotropy- maintain
Ischemia- avoid hypotension b/c CorrPP is at risk since can’t increase SV to compensate
Etiology of HCM:
caused in whole or part by genetic abnormality
Pathophysiology of HCM:
excessive growth of left ventricular muscle for no apparent reason
usually concentric remodeling which can result in obstruction of LVOT and mitral regurgitation
LVOT is primary cause of HCM clinical manifestations
Describe LVOT:
left ventricle hypertrophy w/ unfavorable mitral valve anatomy results in obstruction of the LVOT
decreased forward blood flow d/t:
narrowed tract & leaflet of the mitral valve obstructs LVOT
The most common cardiomyopathy is
HCM: 1 in 500
S/S of HCM include:
vary widely but similar to SHF (d/t outflow obstruction) and DHF (d/t prolonged relaxation and decreased ventricular compliance)
angina, fatigue, syncope, tachydysrhythmias, HF
Positioning is important in this cardiomyopathy:
HCM- supine reduces LVOTO
Diagnosis of HCM:
Echo & ECG: looking for LV hypertrophy
Cardiac cath to measure increased LVEDP
Anesthetic considerations for HCM:
Avoid acute HF by minimizing decreased LVOTO
- Avoid increased contractility- makes LVOTO worse
- Avoid decreased afterload- makes LVOTO worse d/t venturi affect
- Avoid tachycardia- does not allow for filling time
- Maintain adequate preload b/c they need filling
With regional anesthesia there is a risk for
decreased SVR and venodilation which causes decreases afterload
Describe DHF from triggering event to response:
Pressure load–> concentric remodeling–> collagen stiffness–> reduced compliance–> decreased filling–> DHF–> diastolic dysfunction
Describe restrictive cardiomyopathy from triggering event to response:
Genetic/acquired–> sarcomeric proteins–> impaired relaxation–> decreased filling–> diastolic dysfunction
Describe HCM from triggering event to response:
Genetic–> LVH–> obstruct LVOT–> emptying–> SHF–> systolic dysfunction
Genetic–> collagen, sarcomeric proteins–> decreased compliance and decreased relaxation–> decreased filling–> DHF & RCM–> diastolic dysfunction
Describe DCM from triggering event to response:
genetic/acquired–> eccentric–> increased chamber size–> decreased Ca2+ sensitivity–> decreased force–> decreased emptying–> systolic dysfunction
Describe systolic HF from triggering event to response:
Volume load–> eccentric–> increased chamber size–> increased L to W ratio–> decreased force–> decreased emptying–> SHF–> systolic dysfunction
What is acute pericarditis?
inflammation of the pericardium
How much fluid can the pericardial space contain?
15 to 50 mL
How many layers surround the heart?
3 layers:
outermost: fibrous pericardium
middle: parietal pericardium
inner: visceral pericardium
Where is the pericardial cavity or pericardial space located?
between the parietal and visceral pericardial layers
Common causes of acute pericarditis:
viral infection or MI
Result: benign unless pericardial effusion occurs
S/s of acute pericarditis
no change in cardiac function unless there is an associated pericardial effusion
Diagnosis of acute pericarditis:
more often in men commonly between 20-50 years
chest pain
ECG changes d/t inflammation of superficial myocardium
friction rub
Tx of acute pericarditis:
Salicylates, NSAIDs, and corticosteroids to treat inflammation
Corticosteroids are second line b/c withdrawal is associated with increased incidence of pericarditis relapse
Describe pericardial effusion
collection of fluid in the pericardial space that may occur with or without pericardial inflammation
Describe cardiac tamponade
Collection of fluid in the pericardial sac sufficient to cause increased pericardial pressure that results in reduced cardiac filling
Describe the pathophysiology of cardiac tamponade:
pressure reduces ventricular dilation, diastolic filling and increases RAP
depends on how rapidly the fluid collection occurs- slow chronic stretch dissipates the pressure
Result: FILLING PROBLEM
Filling and emptying problems include:
HCM w/ LVOTO
Filling problems include:
cardiac tamponade, constrictive pericarditis, restrictive cardiomyopathy, DHF, mitral valve stenosis, tricuspid valve stenosis
What is the difference between transudative & exudative?
transudative: a filtrate of the blood; it accumulates in tissues outside the blood
Exudative: any fluid that filters from the circulatory system into lesions or areas of inflammation
Common causes of pleural effusion/cardiac tamponade include:
fluid in pericardial space d/t disease (cancer, TB, etc.), trauma (implantation of pacemaker or CVC), exposure to radiation
Describe the difference between acute and chronic pericardial effusion.
chronic- the effusion develops overtime so the pericardium has time to stretch & no increase in intrapericardial pressure
acute- occurs rapidly and the pericardium is unable to stretch and thus increase intrapericardial pressure and symptoms occur
Beck’s triad includes:
hypotension, increased JV pressure, distant heart sounds (pericardial fluid muffles)- s/s of cardiac tamponade
S/S of cardiac tamponade include
Increased RAP, BP normal if compensated or hypotensive, CVP elevated, compression of adjacent intrathoracic structures leading to anorexia, cough, hoarseness, dyspnea, chest pain, & hiccup
Beck’s triad: hypotension, increased JV pressure, distant heart sounds
ultimately decrease in CO
PULSUS PARODOXUS is classic
What is pulsus paradoxus?
decrease in systolic BP > 10 mmHg during inspiration (more common if the tamponade is acute rather than chronic)
Inhibition of RV into pericardial space on inspiration and thus it moves toward the LV and impairs filling –> decreased LVEDV–> decreased SV–> decreased SBP
Diagnosis of cardiac tamponade:
echo
Anesthetic implications of cardiac tamponade:
Goal: relieve pressure before surgery
During: maintain CO & BP
Optimize volume, give catecholamines, avoid decreased HR, decreased SVR, decreased VR
An issue when tamponade is relieved is
significant hypertension
Quintessential of cardiac tamponade:
avoid decreased HR because SV limited avoid decreased afterload b/c SV limited Maximize preload to engage F/S & avoid anything that impacts VR (PEEP, coughing) high risk of ischemia d/t high LVEDP maintain contractility
What is constrictive pericarditis?
constriction of the heart due to changes in the pericardial sac
What is the difference between chronic constrictive pericarditis & subacute constrictive pericarditis?
Chronic: fibrous scarring and adhesions that create a rigid shell
Subacute: fibroelastic, more common & less serious
The pathophysiology of constrictive pericarditis:
pericardium scarring and adhesions–> decreased compliance of sac–> decreased diastolic filling
Thickening of pericardial space—> constricts heart–> increased intrapericardial pressure
FILLING problem
Causes of constrictive pericarditis:
usually idiopathic
can be caused by: radiation, TB, aberrant wound repair of myocardium d/t trauma or surgery
The s/s of constrictive pericarditis:
similar to right-sided HF: increased RVP leads to back up of blood, atrial dysrhythmia d/t compression and remodeling of SA node, reduced cardiac filling leads to decreased VR, decreased F/S, decreased SV, and decreased CO
Kussmaul’s sign
What is Kussmaul’s sign?
Increase in JV distension during inspiration
RV unable to expand normally during inspiration so increased VR d/t abdominal compression on inspiration goes to JV
How is constrictive pericarditis diagnosed?
increased CVP w/ other signs of heart disease
pericardial thickening on ECHO
ECG may or may not display minor abnormalities
Anesthetic implications of constrictive pericarditis?
Avoid decrease in VR as this reduces cardiac filling
Avoid increased HR as this reduces cardiac filling
avoid decreased SVR since heart cannot compensate (SV LIMITED)
Optimize preload
Common themes with filling disorders:
Stroke volume limited so maintain HR and do not decrease afterload; careful titration of preload b/c need volume to fill but do not overload
What factors increase MVO2?
Preload, HR, inotropy, afterload
CO is work and works is proportional to MVO2
What factor increases MVO2 the least?
preload
The afterload equation:
Afterload= (LVP x chamber radius )/Wall thickness
What factors cause an increase in LVEDP?
increased volume–> increases LVEDV and thus LVEDP
Increased elastance of ventricle or poor relaxation
What type of hypertrophy reduces afterload?
concentric hypertrophy
When we say heart rate is a double whammy we are referring to the idea that
heart rate affects both supply and demand- increased heart rate increases the MVO2 demand and decreases the supply (less time in diastole= less coronary perfusion time)
Coronary perfusion pressure is equal to
CorrPP=aortic DP-LVEDP
Coronary perfusion pressure is
diastolic dependent
depends on time in diastole (HR)
Diastolic BP (hypotension)
LV pressures during diastole (diastolic dysfunction)
Any kind of internal or external pressures squeezes the arteries which means
resistance goes up and supply goes down
Factors that affect coronary vascular resistance include:
Cardiac work output, cardiac extravascular compressive forces, neurohumoral and endothelial factors
Supply is affected by
coronary blood flow and O2 carrying capacity
Neurohumoral regulation of coronary VSMC tone:
vasodilation: adenosine, hypoxia, nitric oxide, PSNS stimulation, SNS stimulation (B2)
Vasoconstriction: SNS stimulation (a1), Ang II, endothelin (also PSNS acts on endothelin receptors)
Coronary blood flow is directly proportional to
CorrPP/coronary resistance
Blood flow to the coronaries occurs mainly during
diastole
Myocardial ischemia occurs when
O2 supply cannot keep pace with O2 demand
Ischemic heart disease is
insufficient coronary blood flow to meet the metabolic demands of the cardiomyocytes
The two major components of cardiac ischemia are
metabolism in cardiomyocytes (demand) & delivery of O2 and nutrients to cardiomyocytes (supply)
Most ischemic heart disease results from
coronary artery disease which can be atherosclerotic or non-atherosclerotic
Atherosclerosis is
abnormal deposition of a plaque in the artery wall–> arterial narrowing–> increased resistance–> decreased blood flow
Non-atherosclerotic decreased coronary blood flow can result from
coronary artery dissection, coronary artery spasm, coronary artery embolism and congenital abnormalities of the heart
CAD is a problem at
the level of the coronary arteries
The two most common reasons for myocardial ischemia:
coronary artery narrowing (atherosclerosis) & occlusion (thrombus)
Coronary microvascular disease affects
women more than men and it affects the tiny arteries in the heart muscle (can occur with or without CAD)
Risks associated with ischemic heart disease include:
increased risk for periop CV events including MI, HF, and death
recent UA or MI further increase the risk
What is stable angina?
chest pain or discomfort due to CAD
Stable means frequency and severity of symptoms consistent for >2 months
usually occur on exertion so demand is what is changing
S/S of stable angina include
chest pain, pressure, or heaviness; may or may not radiate to neck, arms, shoulder or jaw
epigastric discomfort
pain characterized by crescendo-decrescendo
lasts several minutes
Diagnosis of stable angina:
induced by physical exertion, emotional tension, or cold
ECG changes coincide with chest pain- ST segment depression or T wave inversion
Acute coronary syndrome includes:
unstable angina, NSTEMI, and STEMI
SA is NOT an ACS
occurs when atherosclerotic coronary plaque becomes unstable, leading to a series of events that eventually results in partial or total thrombotic occlusion of a coronary artery
STEMI definition
MI caused by complete blockage of coronary artery
Pathophysiology of STEMI
ischemia–> injury–> death
S/S of STEMI include:
same as for NSTEMI/UA
chest pain (back, neck, jaw, abdomen, shoulders, or arms)
pain could be absent in elderly
anxious, pale, diaphoretic, sinus tach, hypotension, dyspnea, N/V, dizziness, sudden weakness, fatigue
STEMI is characterized by
ST elevation on more than one EKG
Cardiac biomarkers
imaging may show abnormal ventricular wall motion
STEMI is treated with
TPA because it can get at fibrin to break it down
may need PCI or CABG
NSTEMI definition:
MI caused by a partially blocked coronary artery
NSTEMI is characterized by
ECG showing absence of elevated ST segment (transient ST elevation, T wave inversion, ST depression), elevated cardiac biomarkers
S/S of NSTEMI:
same as those for STEMI/UA
chest pain (back, neck, jaw, abdomen, shoulders, or arms)
pain could be absent in elderly
anxious, pale, diaphoretic, sinus tach, hypotension, dyspnea, N/V, dizziness, fatigue
Definition of unstable angina:
chest pain or discomfort due to coronary artery disease that occurs randomly and unpredictably without any of the obvious triggers (physical exertion, emotional stress, or cold)
Causes of unstable angina include:
decreased myocardial oxygen supply (vasospasm, worse narrowing, inflammation) or increased myocardial oxygen demand
Descriptive pathology of unstable angina:
angina at rest, angina of new onset, increase in the severity or frequency of previously stable angina, no elevation of cardiac biomarkers
Unstable angina treatment
still needs to be treated like a medical emergency
Reduce myocardial O2 consumption
Rest, increased FIO2, analgesia, BB, Ca2+ inhibitor, NO, anticoagulant
Diagnosis of unstable angina:
no elevation of ST segment (other EKG changes)
no elevation of cardiac biomarkers
Management of patients with IHD:
take a thorough cardiac history of patients with suspected
avoid triggering SNS elevation during intubation or laryngoscopy (increased SNS increases demand)
monitor for ischemia- continuous ECG w/ ST analysis, cardiac biomarkers, TEE monitoring
The goals for patients with IHD are
avoid ischemia, monitor ischemia, treat ischemia
Perioperative MI has a ____ risk of death
20% which occurs 24-48 hours post surgery
Risk of periop MI is increased if:
history of IHD, high-risk vascular surgery, emergency surgery
Diagnosis of periop MI is difficult because
hemodynamic instability is common post-op, post-op analgesia may mask MI pain, measure cardiac troponin to understand duration of ischemia
For patients getting a PCI and stents:
if PCI was recent then patient will be on anti-platelet therapy
monitor patient closely for MI or infarct
Volume overload problems include:
AVR & MVR
High ischemia risks patients include:
HCM-LVOTO, Cardiac tamponade, AS, AVR
Patients with baseline elevated afterload include
AS, SHF
Patients with elevated inotropy include:
Constrictive pericarditis, cardiac tamponade, Tricuspid valve stenosis, aortic stenosis, pulmonic stenosis
Any of the diastolic/filling problems can advance
to DHF
Any of the emptying problems can advance to
SHF
Regional anesthesia will decrease
SVR
Hypotension is defined as
systolic blood pressure < 90 mmHg
Neuraxial anesthesia can lead to
hypotension and bradycardia d/t anesthesia of spinal sympathetic nerve fibers
Patients with preexisting hypertension are at higher risk for
intraoperative hypotension
& increased risk of mortality and/or MI
The duration of hypotension
increases risk
Hypotensive effects may occur at
normal BP in patients with uncontrolled hypertension (autoregulatory adaptation to higher pressures)
Hypotension can result from:
arterial vasodilation, myocardial depression, venodilation, bradycardia, volume: hemorrhage or third space (starling forces)
Causes of intra-operative hypotension includes:
hypovolemia, induction of general anesthesia, sympathectomy due to neuraxial block, inhibition of RAAS, periop MI or acute HF causing hypotension
For severe or refractory hypotension (treatment):
infusion of a short-acting vasopressor/inotropic agent, aggressive treatment
Acute post-operative hypotension is defined by
systolic BP <90 mmHg, mean BP <65 mmHg, or relative decrease in BP 20% below baseline
Post-op hypotension may occur due to:
chronic or recent administration of hypertensive agents, inadequate intraoperative fluid replacement, blood loss, residual anesthetic effects, allergic drug reactions, adrenal insufficiency, myocardial ischemia or acute congestive heart failure
Hypertension is defined by
BP >130/80 mmHg or higher
1/3rd of non-cardiac patients will be hypertensive & 2/3rds of cardiac patients will be hypertensive
Patients with chronic HTN are at significant risk for
IHD, HF, CVA, arterial aneurysm, and ESRD
Even short durations of MAP <65 was associated with
increased overall mortality, AKI, myocardial injury and stroke
Anesthetic implications for hypertensive patients:
prevent end-organ damage, reduce periop risk of adverse events (vessel injury)
Isolated systolic hypertension is primarily a result of
stiffening of the arteries
suspect in patients >65 years
Widening pulse pressure is better than
SBP alone as diagnostic for intraoperative hemodynamic instability and adverse postoperative outcomes
Distinguish hypertensive urgency from emergency:
presence of end organ damage: emergency
Hypertensive crisis is defined as
BP >180/120 mmHg
The cause of hypertensive emergency is
pheochromocytoma
S/S of hypertensive urgency:
HA, epistaxis, anxiety
Chronic HTN patients are more likely to experience a hypertensive
urgency than emergency
S/S of hypertensive emergency:
acute CV emergency (ACS, acute decomp. HF, pulm edema, dissecting aortic aneurysm), acute RF, postop complications exacerbated by the elevated BP (hemorrhage, increased ICP), neurologic s/s
Treatment of hypertensive emergency includes:
using short-acting vasodilators such as nitroprusside (need to bring SVR down)
Pheochromocytoma is
adrenal gland chromaffin cell tumor that has NE release greater than Epi release
S/S of pheochromocytoma:
tachycardia, diaphoresis, HA, paroxysmal HTN, HTN, hyperglycemia
For patients diagnosed with pheochromocytoma
pre-treat to inhibit alpha 1 adrenergic
2 in 1 million patients have undiagnosed pheochromocytoma
Define stenosis:
abnormal narrowing of a passage or orifice
valve stenosis thickens and stiffens the valve and increases resistance to blood flow through the orifice
Mitral valve stenosis is
a narrowing of the mitral valve resulting in a LV filling problem
Pathology of mitral valve stenosis:
increased resistance to blood flow through the mitral valve–> reduced LV filling–> decreased SV–> decreased CO
back up of blood in the LA results in increased LAP
when LAP >25 mmHg then blood is backed up into pulmonary circulation
S/S of mitral valve stenosis begin when
orifice narrowing is >50%
heart murmur, pulm arterial HTN, 1/3rd of patients have afib
Diagnosis of mitral valve stenosis:
Echo, increased transvalvular pressure gradient, LA hypertrophy
Treatment of mitral valve stenosis:
goal is to decrease LAP
diuretics, control a-fib (thrombus risk), surgery to repair leaflet
Anesthetic implications of mitral valve stenosis:
Goal: avoid pulm edema or decreased CO
avoid increased HR- causes reduced LV filling time and ultimately decreased CO
Careful fluid balance to avoid hypotension but prevent fluid overload
Avoid increased pulmonary vascular resistance–> may lead to RHF
Causes of aortic valve stenosis:
calcification of aortic valve leaflet occurs with increasing age
infective endocarditis
rheumatic fever
risk factors: HTN, hypercholesterolemia
Aortic valve stenosis is:
a narrowing of the aortic valve resulting in an obstruction to the flow of blood from the left ventricle to the aorta
results in an LV emptying problem
In advanced stages of aortic valve stenosis,
concentric remodeling may occur resulting in a LV filling problem
Pathology of aortic valve stenosis
Myocardial oxygen demand problem: increased LVSP, increased LVEDP, increased afterload
Myocardial oxygen supply problem: increased afterload: emptying is not complete and increased LVEDV and LVEDP leads to compression of coronary arteries
S/S of aortic valve stenosis:
systolic murmur, exercise intolerance, syncope, LV hypertrophy, can lead to LH failure
Diagnosis of aortic valve stenosis:
ECG LV hypertrophy, Echo/doppler shows decreased aortic valve area, increased transvalvular pressure gradient increases
Treatment of aortic valve stenosis:
surgical valve replacement
Anesthetic implications of aortic valve stenosis:
goal is to maintain CO and decrease risk of myocardial ischemia/infarct
AVOID HYPOTENSION AND KEEP HR NORMAL
avoid hypotension b/c decreased coronary perfusion
keep NS b/c need atrial kick to improve SV via F/S
Tricuspid valve stenosis is
a narrowing of the tricuspid valve opening resulting in an obstruction to the flow of blood from the RA to the RV
results in a RV filling problem
Tricuspid valve stenosis the the result of
rheumatic fever
S/S of tricuspid valve stenosis include:
systemic venous congestion with JVD, ascites, and peripheral edema; decreased CO, abdominal discomfort d/t hepatomegaly, Kussmaul’s sign, NO pulmonary congestion unless have mitral valve stenosis
Diagnosis of tricuspid valve stenosis:
echo
differential diagnosis: r/o other causes of systemic venous HTN
Treatment of tricuspid valve stenosis includes:
diuretics to avoid congestion
Anesthetic implications of tricuspid valve stenosis:
balance fluids so that decreased CO is avoided but that systemic congestion is not exacerbated
Normal HR for infants:
113-145 bpm
Normal HR for child:
75-113 bpm
Normal HR for adult:
60-90 bpm
MHR declines with
age- normal MHR for older adult ~73 bpm
Cardiac dysrhythmia is a
cardiac rhythm that displays abnormal rate, interval length or conduction path
Tachydysrhythmias can result in
HTN increased CO & IHD (decreased supply/ increased demand)
Sinus tachycardia is defined as
HR: 100-160
tolerable unless history of cardiac disease
Supraventricular tachycardia is defined as
HR 160-180 initiated at or sustained by tissue at or above the AV node
more common Young>old, women>men
Ventricular tachycardia is defined as
HR>170 + 3 or more PVCs
common after MI, cardiac infection
Atrial fibrillation is defined as
no ECG P wave
multiple areas of the atrium continuously depolarize, quivering atrial wall
Big risk with atrial fibrillation is
blood clots
Atrial flutter differs from atrial fibrillation because
atrial to ventricular beat rate is 1:2
Ventricular fibrillation is defined by
no pulse or BP
most common cause of sudden cardiac death
common in IHD, risk declines with statins, ACEi, beta-blockers
Sinus bradycardia is defined by
HR <60 (athletes, sleeping)
Premature ventricular contractions
arise from single or multiple foci below the AV node
s/s: palpitations, syncope, near syncope
management: keep defib handy, rule out acid-base or electrolyte triggers
Heart blocks can be precipitated by:
MI, myocarditis, lyme disease, rheumatic fever, infiltrative disease, mononucleosis, overdose of beta blockers or Ca2+ channel blockers
1st degree AV block is defined by
PR interval >200msec (slow conduction through AV node)
inconsequential except increased risk for a-fib
2nd degree heart block is defined by
impaired conduction in “conduction fibers” (MI, fibrosis, calcification, infiltration, inflammation)
P wave and no corresponding QRS
may require atropine or pacing
3rd degree heart block is defined by
“complete heart block” atrial electrical system disconnected from ventricular
MI, aged, or diseased heart
treatment: pace, beta-agonists
Bundle branch blocks are defined as
conduction error in conducting fibers
RBBB- ASD, IHD, valve disease, DCM
LBBB- IHD, valve disease, HTN, cardiomyopathy
The goal of cardioversion is to
re-coordinate the electrical pathways
Defibrillation creates
a fire risk in the OR b/c it arcs electricity
electrical discharge to correct dysrhythmias when cardioversion is not possible (no R wave or no pulse)
Aneurysm is
dilation of all three layers of the artery wall (intima, media, and adventitia)
rupture is a medical emergency
Dissection is
when blood enters the medial wall layer d/t intimal layer tear
Risk factors for aortic aneurysm:
HTN, family history, smoking, atherosclerosis, male, older age, Marfan’s syndrome (dissecting aneurysm, atherosclerosis
Factors that precipitate dissection:
deceleration injuries, crack cocaine, pregnancy, aortic cannulation/clamping, aortic valve replacement
S/S of thoracic aortic aneurysm:
usually asymptomatic, stridor, hoarseness, dysphagia, superior vena cava edema, aortic valve incompetence–> aortic regurgitation–> HF
S/S of aneurysm dissection:
severe sharp pain in chest, neck, shoulder blades, progress to high SVR, shock, absence of peripheral pulses, myocardial ischemia, ischemic stroke
When the thoracic aortic is cross-clamped–>
there is an increased blood flow to the brain and reduced blood flow to the spinal cord
release of the clamp can result in hypotension (severe)
Surgical considerations for aortic aneurysm:
increased risk for: high blood loss, hypoperfusion of end organs
Peripheral arterial disease is defined by
atherosclortic plaque deposition in peripheral artery, narrowed artery, reduced blood flow (chronic); embolism (acute); or vasculitis (inflammation)- rare
Risk factors for peripheral arterial disease include
smoking, age, family history, DM, HTN, obesity, dyslipidemia
Diagnosis of PAD includes:
ankle to brachial index <0.9
SBP is reduced at ankle in PAD
S/S of PAD include:
intermittent claudication (muscle pain/cramps), leg coolness, pallor, atrophy, hair loss, leg symptoms worse when supine, absent or decreased peripheral arterial pulse
Anesthetic considerations for PAD
similar to that for surgical repair of AAA b/c aortic clamping occurs
issues revolve around hypotension with unclamping
PVD formation is promoted by
Virchow’s triad: venous stasis (immobility), hypercoagulability, and injury to vascular endothelium
Congenital heart disease is
a defective heart structure
gene-environmental interactions account for 90% of cardiac congenital abnormalities
single or multi-gene abnormalities account for 10%
Atrial septal defect results in
RH and pulm circulatory volume overload
septal wall between right and left atria is defective
allows blood flow through the septum
decreased systemic blood flow because LA kick is reduced
Atrial septal defect accounts for
1/3rd of all cardiac congenital defects
more likely in females
With septal defects the goal is to avoid
increased shunt volume or right to left shunt (can lead to hypoxemia)
Decreased SVR will increase right to left shunt and increased PVR will increase right to left shunt
Ventricular septal defect is
the most common cardiac congenital defect
pulm circulation and left heart volume overload (volume overload in pulm circulation transmitted to left heart)
Pulmonic valve stenosis is
a narrowing of the pulmonic valve resulting in an obstruction to the flow of blood from the right ventricle to the pulmonary artery
Prevalence of pulmonic valve stenosis:
accounts for 10% of all congenital heart disease; acquired is rare, PVS usually discovered in childhood
Cause of pulmonic valve stenosis:
congenital»> rheumatic heart disease, infective endocarditis, carcinoid heart disease, iatrogenic causes (radiation or chemo)
Pulmonic valve stenosis results in
a RV emptying problem, increased MVO2
With pulmonic valve stenosis, right ventricle
outflow tract can also be obstructed
In pulmonic valve stenosis, RV pressures become elevated d/t increased
pulmonic valve resistance and RVOT obstruction–> RV hypertrophy–> RV diastolic dysfunction occurs
S/S of pulmonic valve stenosis include
Mild disease: asymptomatic, good long term survival
Severe disease: present during childhood–> RV failure and cyanosis
adult: exertional dyspnea, fatigue RV hypertrophy, RV failure
Diagnosis of pulmonic valve stenosis:
echo
a systolic ejection murmur
Treatment of aortic valve stenosis:
valve surgery
balloon pulmonary valvuloplasty
Anesthetic implications of pulmonic valve stenosis:
goal is to maintain CO & avoid RV decompensation
volume needs to be sufficient but don’t overload
inotropes may be necessary
Aortic valve regurgitation is defined by:
during diastole a portion of the SV moves backwards from aorta into the LV
results: decreased CO, LV volume overload, Increased LVEDV & LVEDP, and decreased coronary perfusion
Aortic valve regurgitation is a
volume overload and ischemia problem
Chronic aortic regurgitation is due to
rheumatic fever, idiopathic, Marphan’s syndrome, Rheumatoid arthritis
Acute aortic regurgitation is due to
infective endocarditis, aortic dissection
Rapid deterioration in LV function results in (aortic valve regurgitation)
LHF; coronary ischemia
S/S of aortic valve regurgitation
patients may be asymptomatic for decades; initial symptoms are exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea
Descriptive pathology of aortic valve regurgitation:
regurgitant flow increased LVEDV, LV remodeling–> eventually LHF
With aortic valve regurgitation, volume regurgitated is
directly proportional to duration of diastole, directly proportional to the pressure across the valve, directly proportional to size of aortic valve orifice
Diagnosis of aortic valve regurgitation
diastolic murmur, decrease DBP d/t backflow, enlarged LV on ECHo
acute s/s include CV collapse
Treatment of aortic valve regurgitation:
surgically replace valve
Anesthetic management of aortic valve regurgitation:
Maintain LV forward flow & CO
Summary: desire slight increase in HR and slight decrease in SVR, adequate volume
Heart rate- Increase >80 bpm; decreased duration in diastole and increased CO
Preload: need preload for F/S and SV/CO
Afterload: decreased afterload favors forward flow; avoid increased SVR
Mitral valve regurgitation is
during systole a portion of the SV moves backwards from LV into the LA
Mitral valve regurgitation is a
Volume overload problem
Causes of chronic mitral regurgitation include
rheumatic fever, incompetent valve
Causes acute mitral regurgiation include
myocardial ischemia/infarct, infective endocarditis, chest trauma
Descriptive pathology of mitral valve regurgitation:
decreased forward flow, regurgitation into LA, increased LAP, pulmonary congestion
Diagnosis of mitral valve regurgiation:
murmur, echo, ECG atrial or ventricular hypertophy
Treatment of mitral valve regurgitation
surgery
Anesthetic management of mitral valve regurgitation:
avoid increased CO
HR- normal or slight increase
preload: need preload for F/S and SV but overload increases pulmonary congestion
use inotropes to improve forward flow and decrease LV volume
Summary: inotropes increase SV, vasodilators decrease SVR, titrate volume
