Heart Failure

“The inability of the heart to supply adequate blood flow and therefore oxygen delivery to peripheral tissues and organs”

Warwick Cardiology Society

http://www.cvphysiology.com/Heart%20Failure/HF002.htm

& Starling’s Law

Learning Objectives 1• Understand how the pumping activity of the heart is

affected by changes in venous return and total peripheral resistance

Quick review on Starling’s Law• Relation of venous return (and hence preload) to stroke volume (due to

force generation)– Stretch Sarcomere lengthening ↑ force generated ↑ SV– Length-tension and force-velocity relationships

• Note other non-Starling relationship (Trop C-calcium sensitivity due to increased sarcomere length)

• Not just one Starling curve – curve depends on ionotropy/afterload state– High afterload/decreased ionotropy Curve shifted down and R-wards– Low afterload/increased ionotropy Shifts curve up and leftwards

Learning Objectives 2

• Explain the pathophysiology of heart failure• Describe the clinical characteristics of the principal types

of heart failure, and the circumstances which lead to its development

• Identify targets for drug action for the manipulation of cardiac output

• Describe the principles involved in the general management of heart failure, and the categories of drugs used in its therapy.

• Principle types of heart failure & Circumstances for development

• Pathophysiology• Clinical characteristics• Principles of management• Categories of drugs and their targets

HF types

Type CircumstanceAcute Hours/days

Low output state/decompensated CHF

MI, Ventricular septal rupture, IE ( Acute MR/AR), Sepsis, severe arrhythmias, valve dysfunction

Chronic Months/years

Associated w/ cardiac adaptive response to precipitating cause (e.g. CAD, congenital defects, valvular disease, arrhythmias etc)

Adaptive responses: e.g. hypertrophy, dilatation

Type Circumstance

SystolicDiastolic

LeftRight

Biventricular

ForwardBackward

High OutputLow Output

Impaired ejection fraction (contractility)Impaired ventricular filling (stiffness)

Involves left side of the heartInvolves left side of the heart often due to LHF. If isolated, then due to cor pulmonale

Both sides

Unable to maintain adequate COUnable to accommodate venous return

HF due to demand for increased COHF associated with poor CO

Pathophysiology

• Causes:– Intrinsic – e.g. dilated and hypertrophic

cardiomyopathies– Extrinsic – uncontrolled HTN, ↑SV, hormonal

(e.g. Hyperthyroidism), Pregnancy, Drugs (alcohol, cocaine)

‘HEART FAILED’

• H – Hypertension• E – Endocarditis/environment (e.g. heat wave)• A – Anaemia• R – Rheumatic Heart Disease and other valvular disease• T - Thyrotoxicosis• F – Failure to take medications• A – Arrhythmia• I – Infection/Ischaemia/Infarction• L – Lung problems (PE, pneumonia, COPD)• E – Endocrine (Phaeochromocytoma, hyperaldosteronism)• D – Dietary indiscretions

Pathophysiology cont…• Cardiac dysfunction changes to:

– Vascular function• Systolic and Diastolic

– Neurohumoral status• Vasoconstriction via:

– Sympathetics– R-A system– ADH– ANP

• Increases preload and afterload aggravate HF

– Blood volume• ↓ renal perfusion• Sympathetic adrenergic• RAAS• ADH• Relate to Venous pressure & oedema

Purpose:

Maintain cardiac output +

Arterial Blood Pressure

Some of these compensatory changes can worsen cardiac function

Clinical Characteristics

Left Failure Right Failure

Low CO (Forward) FatigueSyncopeSystemic hypotensionCool extremitiesSlow capillary refillPeripheral cyanosisPulsus alternansMitral regurgitationS3 – 3rd heart sound; Ken-tucky

RHF can mimic most of the Sx of forward left heart failure if decreased RV output leads to LV underfilling

Venous Congestion (Backward)

DyspnoeaOrthopnoeaPNDCoughCrackles

Peripheral oedemaElevated JVP with AJR/HJR and Kussmaul’s signHepatomegalyPulsatile Liver

• Others:• Ascites• Pleural effusion (excess fluid between 2 pleural layers)• Cardiac dilatation (increased ventricular end-diastolic

volume) or hypertrophy (increased end-systolic ventricular pressure)

• AF

Management Principles

• Aim:– Improve QOL via symptomatic relief– Prevent hospital admission and reduce length

of stay of any admissions

• How:– Non-pharmacological– Pharmacological

Non-pharmacological

• Lifestyle advice:– Smoking cessation– Low salt diet– Safe alcohol use– Weight loss for BMI >30– Exercise regimes– Secondary prevention for CAD– Once only pneumococcal vaccination and

annual Influenza vaccination

Categories of drugs & targets

• Beta Blockers (-lols)• ACEi or ARBs (-prils, -sartans)• Digoxin• Aldosterone antagonists/K+ sparing

diuretics (Spironolactone, Eplerenone)• Loop diuretics (Furosemide/Bumetanide)• Stop/avoid aggravating drugs (nSAIDs,

Calcium antagonists, steroids, glitazones)

• Carvedilol, Bisoprolol, Metoprolol targets the SNS via B1 receptor and dampens activity

• Lisinopril, Ramipril target ACE and downregulates activity• Candesartan, Losartan, Valsartan target AT Receptor and

downregulates activity• Digoxin targets Na+/K+ pump in cardiomyocytes to indirectly

increase intracellular calcium• Aldosterone antagonists target MR to decrease aldosterone

binding• Loop diuretics target the loop of Henle to cause increased

diuresis

RAAS

Investigations• CXR (HERB-B)

• Heart enlargement• Pleural Effusion• Re-distribution (alveolar

oedema)• Kerley B-Lines• Bronchiolar-alveolar cuffing

• ECG– Likely abnormal

• Bloods– Anaemia, thyrotoxicosis etc,

BNP (re: V distension – hence 1st line test)

• ECHO– Underlying anatomical

problems (cardiomyopathy, valves, pericardial effusion)

• MRIoedematous

Bilateral effusions

References

• http://www.cvphysiology.com/Heart%20Failure/HF002.htm

• Last year’s lecture by Dr Banerjee• Wikipedia (I know…naughty)• USMLE 2012• Toronto Notes 2012

Remember, a common cause of RHF is LHF!

Questions?