Case 4: Alessandra W. - CHF

Atrial Contraction

Signal propagation through atria cause depolarization and contraction

SA node → AV node

During P wave

Ventricular Contraction

Signal propagation through ventricles cause depolarization and contraction

AV node → His-Purkinje system

End of QRS to start of T wave

Ejection Fraction (EF)

Percentage of blood pumped out of left ventricle per heartbeat

Normal: 55-70%

Low: <40% → Heart failure

Left Heart Pressure

Higher

• Pump to systemic circulation

Wiggers diagram

Right Heart Pressure

Lower

• Pump to pulmonary circulation

Swan-Ganz (pulmonary artery) catheter

Pressure Variables

Depend on compliance and volume

High Pressure: Low compliance, high volume

Low Pressure: High compliance, low volume

Left Atrium Pressure

a Wave: Atrial contraction

• Increase pressure

• During P wave

c Wave: Mitral valve moving into atrium

• Increase pressure

• During QRS

v Wave: Venous atrial filling

• Increase pressure

• After T wave

Left Ventricle Pressure

Systolic Pressure: Ventricular contraction

• Increase pressure

  • All valves closed (isovolumic contraction)

• Ejection

  • Aortic valve opens

• Decrease pressure

  • All valves closed (isovolumic relaxation)

Diastolic Pressure: Ventricular relaxation

• Mitral valve opens

• Passive blood flow into ventricle

• Small pressure increase: Atrial contraction (atrial kick)

Aorta Pressure

Systolic Pressure: Aortic valve opens for ventricular emptying

• Increase pressure

Diastolic Pressure: Aortic valve closes

• Decrease pressure

  • Slow from elastic artery stretch

• Small pressure increase: Aortic valve closes and bulges into aorta

  • Dicrotic notch

  • After T wave and during diastole

Right Atrium Pressure

a Wave: Atrial contraction

• Increase pressure

• During P wave and late diastole

c Wave: Tricuspid valve moving into atrium

• Increase pressure

• During QRS and systole

x Descent: Atrial relaxation + tricuspid valve moves out of atrium

• Decrease pressure

• After QRS and during systole

v Wave: Venous atrial filling

• Increase pressure

• During T wave and late systole

y Descent: Tricuspid valve opens for atrial emptying

• Decrease pressure

• After T wave and early diastole

Right Ventricle Pressure

Systolic Pressure: Ventricular contraction

• Increase pressure

• Higher than right atrium

• During QRS and systole

Diastolic Pressure: Pulmonic valve opens for ventricular emptying

• Decrease pressure

• Same as right atrium

• During T wave and late systole

• Small pressure increase: Ventricular relaxation

  • Before P wave

Pulmonary Artery Pressure

Systolic Pressure: Pulmonary artery filling

• Increase pressure until same as right ventricle

• During T wave

Diastolic Pressure: Pulmonary artery emptying

• Decrease pressure

• Higher than right ventricle (diastolic step-up)

• Small pressure increase: Pulmonary valve closes

  • Dicrotic notch

  • After T wave and during diastole

Ventricular Performance

Determined by stroke volume (SV) and cardiac output (CO)

• CO = HR x SV

• SV = EDV - ESV

Determinants of Ventricular Performance

1. Preload

2. Afterload

3. Contractility (inotropic state)

4. HR

Frank-Starling Mechanism

LV adjust SV to match EDV

1: Preload

Volume of blood in ventricle at end of diastole (EDV)

• Myocardial stretch at end of diastole

Greater distension during diastole = Greater volume ejected during systole

• Frank-Starling relationship

Preload: PV Loop Changes

Increase Preload:

• Increase EDV

• Increase SV = Constant ESV

Decrease Preload:

• From stiff ventricles (low compliance)

• Decrease EDV

• Decrease SV = Constant ESV

2: Afterload

Force ventricles need to overcome to empty (aortic pressure)

• Myocardial tension during systole

Determined by wall stress (Laplace relationship)

• Increased wall thickness = Decreased wall stress

Afterload: PV Loop Changes

Increase Afterload:

• Increase ejection/systolic pressure = Increase ESV

• Decrease SV = Constant EDV

Decrease Afterload:

• Decrease ejection/systolic pressure = Decrease ESV

• Increase SV = Constant EDV

3: Contractility

Inotropic state

• Change in myocardial force

Independent from prelaod and afterload

Frank-Starling Relationship:

• Increased contractility = Curve shift up = Increase SV

• Decreased contractility = Curve shift down = Decrease SV

Contractility: PV Loop Changes

Increase Contractility:

• Steep end-systolic pressure-volume relationship (ESPVR)

  • Up and left

• Increase SV = Decrease ESV

Decrease Contractility:

• Shallow ESPVR

  • Down and right

• Decrease SV = Increase ESV

4: HR

Heartbeats/contractions per minute

High HR:

• Decrease diastolic filling time

• Increase diastolic filling pressure

• Decrease SV

Low HR: 

• Increase diastolic filling time

• Decrease diastolic filling pressure

• Increase SV

Pulmonary Edema

Fluid accumulation in lung interstitium and alveolar spaces

• Medical emergency = Require immediate treatment

Clinical Presentation: Bibasilar lung crackles (auscultation) and dyspnea

Pulmonary Edema From CHF

Frank-Starling mechanism

Increased EDV (preload) in LV = Ventricle cannot increase SV

Increase pulmonary vein pressure = Increase capillary hydrostatic pressure = Fluid leak out of capillaries

Peripheral Edema

Fluid accumulation in interstitium of extremities

Peripheral Edema From CHF

Frank-Starling Mechanism

• Same as left heart (pulmonary edema)

Neurohormal Activation

• Baroreceptors sense effective arterial blood volume (to perfuse tissues)

• Increase vascular resistance and Na+/water retention

  • Adrenergic NS

  • RAAS

  • Increase ADH production

• Maintain BP (perfusion) → BP = CO x TPR

  • CO decreased in HF = Increase TPR

Impaired Lymphatic Drainage

• Increased interstitial fluid > Lymphatic system drainage capacity = Fluid accumulates

Congestive Heart Failure (CHF): Description

Structural/Functional impairment of ventricular filling or ejection fraction

• Reduced heart function

CHF Types

HF with reduced EF (HFrEF): “Systolic”

• Low SV

• Low LV EF

HF with preserved EF (HFpEF): “Diastolic”

• Low SV

• Normal/low EDV

• Preserved LV EF

• Increased LV filling pressure

Not often used since both present with systolic and diastolic dysfunction

CHF: Epidemiology

Risk factors:

• Older age

• Hypertension

• Obesity and metabolic syndrome

• Impaired renal function

CHF: Etiology

Usually ischemia

• Coronary artery disease (low O2 to myocardial tissue)

Valvular diseases

• Aortic stenosis

• Aortic and mitral regurg

Stages:

• A: At risk, asymptomatic

• B: Pre-HF, asymptomatic

• C: Symptomatic HF

• D: Advanced HF

CHF: Presentation

Profile A: Warm and dry

• No reduced CO and vasoconstriction

• No increased LV filling pressure (congestion)

Profile B: Warm and wet

• No reduced CO and vasoconstriction

• Increased LV filling pressure

Profile L: Cold and dry

• Reduced CO and vasoconstriction

• No increased LV filling pressure

Profile C: Cold and wet

• Reduced CO and vasoconstriction

• Increased LV filling pressure

CHF Pathogenesis: HFrEF

Decreased contractility = Ventricular dysfunction in systole = Decreased blood pumped (LVEF)

Decrease CO

CHF Pathogenesis: HFpEF

Decreased ventricular compliance = Ventricular dysfunction in diastole = Decrease ventricular filling (preload) + Increased diastolic pressure

Decrease CO

CHF Pathogenesis: Left-Sided HF

Increased Afterload:

• Increased aortic pressure (arterial hypertension)

• Outflow obstruction (aortic stenosis)

Increased Preload:

• LV volume overload (aortic regurg)

CHF Pathogenesis: Right-Sided HF

Increased Afterload:

• Increased pulmonary artery pressure (pulmonary hypertension)

Increased Preload:

• RV volume overload (tricuspid regurg, L to R shunt)

CHF: Investigations

Clinical features

Imaging

Blood test

CHF: Imaging

ECG

CXR

Echo (TTE)

CHF Imaging: ECG

HFpEF: Normal

ST-segment and T-wave changes

• Elevation

• Depression

P wave changes

• Biphasic

Long QTc interval

CHF Imaging: CXR

Changes in cardiac silhouette

• Cardiomegaly

• Pericardial effusion

Pulmonary congestion

Valve calcification

CHF Imaging: Echo

LV systolic/diastolic dysfunction

• Reduced filling and contraction

Thick or dilated atria and ventricles

CHF Investigation: Blood Test

Brain natriuretic peptide (BNP)

• Vasodilator and diuretic hormone produced by cardiomyocytes during stretch and ventricular wall stress

• Elevated

  • >35 (chronic)

  • >100 (acute)

CHF: Clinical Presentation

Nocturia (urinating at night)

Fatigue

Tachycardia and arrythmia

S3/S4 sounds

CHF: Treatment/Management

Lifestyle changes

• Increase exercise

• Weight loss

• Healthy eating (low Na+)

• Smoking and alcohol cessation

Treat underlying conditions

Pharmacological: Decrease BP

Devices:

• Automated implantable cardioverter defibrillator

• Cardio resynchronization therapy

CHF Management: Pharmacological

Beta-1 blocker

Diuretics

Sodium-glucose cotransporter 2 (SGLT2) inhibitor

Renin-angiotenin-aldosterone system (RAAS) inhibitor

Mineralocorticoid receptor antagonist

CHF Management: Beta-1 Blocker

First-line

Ex: Metoprolol, Propranolol

MOA:

1. Inhibit beta-1 receptors in heart = Decreaes HR and contractility = Decrease work for heart during pumping

2. Decrease BP and energy needs = Reverse pathological remodelling

CHF Management: Diuretics

Ex: Spironolactone, furosemide

MOA: Increase Na+, ion, water excretion = Decrease edema

CHF Management: Sodium-Glucose Cotransporter 2 (SGLT2) Inhibitor

First-line

Ex: Empagliflozin

MOA: Decrease glucose (+ water) reabsorption = Decrease edema

HF Management: Renin-Angiotensin-Aldosterone System (RAAS) Inhibitor

Ex: Ramipril, Losartan

MOA:

1. Prevent angiotensin-2 binding to receptors to decrease Na+ and water retention

2. Decrease vasoconstriction and preload

CHF Management: Mineralocorticoid Receptor Antagonist (MRA)

Ex: Spironolactone

MOA:

1. Inhibit aldosterone effects to decrease Na+ reabsorption and H+/K+ excretion

2. Decrease water retention

3. Decrease pathological remodelling

HCF Treatment: Automated Implantable Cardioverter Defibrillators (AICDs)

Detect tachyarrhythmias = Deliver electrical impulse to reset sinus rhythm

CHF Treatment: Cadiac Resynchronization Therapy (CRTs)

Generate pulse to synchronize right and left ventricle contraction