Cardiac Flashcards
Heart Failure Classification
New York Heart Association Functional Classification of Breathlessness (for heart failure patients)
NYHA Class I
No symptoms and no limitation in ordinary physical activity i.e. SOB when walking, climbing stairs, etc.
NYHA Class II
Mild symptoms (SOB and/or angina) and slight limitation during ordinary activity
NYHA Class III
Marked limitation in activity d/t symptoms even during less-than-ordinary activity i.e. walking short distances (20-100m)
Comfortable at rest
NYHA Class IV
Severe limitations
Experiences symptoms even while at rest
Mostly bedbound patients
Heart Failure Causes
Volume overload
Pressure overload
Myocardial contractile impairment d/t ischemia or infarct
Restrictive filling (constrictive pericarditis, cardiac tamponade, restrictive myocarditis)
Idiopathic remodeling - cardiomyopathy
Myocardial inflammation
Left-Sided HF Causes
↑LVEDP Hypertension CAD Valvular disease MI
Right-Sided HF Causes
↑RVEDP
Most common cause L-sided HF
Pulmonary arterial hypertension
R ventricle MI
Low Output HF Causes
Result from FILLING or EMPTYING problem CAD Chronic HTN Cardiomyopathy Valvular disease Pericardial disease
High Output HF Causes
↑ metabolic demand
Anemia
Septicemia
Hyperthyroidism
Volume Overload
SHF ↓LVEF ↑LV chamber size S3 gallop Compliant ECCENTRIC remodeling
Pressure Overload
DHF Normal LVEF ↓LV chamber size S4 gallop ↓ compliance CONCENTRIC remodeling
Eccentric
New sarcomeres in series
Hypertrophy
↑radius (chamber size)
EMPTYING problem
Concentric
New sarcomeres in parallel Hypertrophy ↓chamber radius Cardiomyocyte thickening FILLING problem
Heart Failure Physiological Compensations
↑SNS
Arterial VSMC vasoconstriction ↑SVR ↑afterload
↑venomotor tone ↑VR
Frank-Starling mechanism engagement
SA node ↑HR
Myocardium ↑inotropy ↓catecholamine sensitivity
Adrenal gland ↑circulating catecholamines
RAAS activation d/t ↓renal blood flow
Cardiac remodeling
Neural Compensations
Atrial & arterial baroreceptors trigger catecholamine release & ↑vasopressin
Catecholamines → cardiotoxicity (apoptosis & necrosis) promotes cardiac remodeling
Vasopressin ↑SVR ↑Na+/H2O retention
Local Compensations
↓renal blood flow → RAAS activation promotes remodeling
Ischemic cardiomyocytes release inflammatory mediations (cytokines) that trigger cardiac remodeling
Ischemic endothelial cells release endothelin
Stretched atrial & ventricular cells release ANP/BNP (cardioprotective)
ANP promoted diuresis, natriuresis, inhibits RAAS & SNS, anti-inflammatory, inhibits remodeling
Systolic Heart Failure
Emptying problem occurs in the L ventricle > R ventricle
Triggered by volume overload → eccentric remodeling
Diastolic Heart Failure
Filling problem occurs in the L ventricle > R ventricle
Triggered by pressure overload → concentric remodeling
Acute Heart Failure
Anesthetic Implications
Immediate goal ↑CO ↓LVEDP
End organ perfusion
Tools include inotropes, vasodilators, diuretics, Ca2+ sensitizers, BNP, NO inhibitors, & mechanical devices
Chronic Heart Failure
Anesthetic Implications
Goal to prevent acute heart failure episode
Hemodynamic stability
Full preop workup
Check medications, complete cardiac history, hepatic/renal/electrolyte panels, recent EKG or Echo
FILLING
DHF Restrictive cardiomyopathy Hypertrophic cardiomyopathy Constrictive pericarditis Cardiac tamponade Hypotension Mitral valve stenosis (L ventricle) Tricuspid valve stenosis (R ventricle)
EMPTYING
SHF Dilated cardiomyopathy Hypertrophic cardiomyopathy w/ LVOTO Myocardial infarction Aortic valve stenosis (L ventricle) Pulmonary valve stenosis (R ventricle)
Volume Overload
Aortic regurgitation (L ventricle) Mitral regurgitation (L atrium)
SHF or DCM Considerations
EMPTYING problem
Heart rate - maintain NSR (atrial kick) ↓HR ↑filling time ↓CO
Preload - maximize Frank-Starling & prevent fluid volume overload or pulmonary congestion
Afterload - ↓SVR ↑CO (ΔP) w/o hypotension (maintain BP) ↓BP ↓CorrPP
Contractility/inotropy - admin inotropes to help improve forward flow
Ischemia - monitor to prevent
DHF or RCM
Considerations
FILLING problem
Heart rate - maintain NSR ↑HR ↓filling time SV limited
Preload - maximize Frank-Starling & prevent fluid volume overload
Afterload - maintain ↓SVR → SNS activation ↑HR
Contractility/inotropy - maintain (not an emptying problem) ↑contractility ↑MVO2
Ischemia - avoid ↑LVEDP
HCM w/ LVOTO
Considerations
FILLING & EMPTYING problem
Heart rate - avoid ↑HR ↓filling time
Preload - maintain w/o fluid volume overload
Afterload - do NOT ↓afterload (worsens LVOTO d/t Venturi effect)
Contractility/inotropy - ↑contractility worsens LVOTO
Ischemia - HIGH risk
Aortic Valve Stenosis
Considerations
L ventricle EMPTYING problem
Heart rate - maintain NSR (atrial kick) SV limited ↑HR ↑demand ↓supply ↓HR → L ventricle overdistension
Preload - maintain w/o fluid volume overload
Afterload - do NOT ↓afterload (unable to compensate to maintain BP)
Contractility/inotropy - maintain or ↑contractility ↑CO
Ischemia - HIGH risk
Pulmonic Valve Stenosis Considerations
R ventricle EMPTYING problem
Heart rate - maintain NSR ↓HR → volume overload
Preload - maintain w/o fluid volume overload
Afterload - minimal impact ↑SVR to maintain CO
Contractility/inotropy - maintain or ↑contractility
Ischemia - monitor ↑MVO2
Prevent ↑PVR → worsens R ventricle congestion & cardiac demand
Aortic & Mitral Valve Regurgitation Considerations
VOLUME overload
Heart rate - AVOID bradycardia >80bpm ↓filling time
Preload - maintain w/o fluid volume overload
Afterload - avoid ↑SVR ↓SVR as tolerated (ΔP) but maintain adequate perfusion
Contractility/inotropy - maintain & admin inotropes as needed to promote forward flow
Ischemia - ↑LVEDP ↓CorrPP
