Armaan Khalid

Heart Failure 101

HF is a syndrome that manifests as the inability of the heart to fill with or eject blood

HF can result from any structural/functional cardiac disorder that impairs the ability of the heart to function normally

Coronary Artery Disease (CAD) is the most commonest cause of HF

Anything that ↑ myocardial work may aggravate/initiate HF

What is Heart Failure?

Ischaemic Heart Disease (35-40%)Cardiomyopathy (dilated) (30-34%)Hypertension (15-20%)

Common Causes of HF

EXTREMELY COMPLEX!Compensatory physiological changes that

eventually get overwhelmed & become pathological

Factors involved are:Venous return (preload)Outflow resistance (afterload)Myocardial contractility (inotropic state)Salt & water retention

Pathophysiology

Stroke work is increased as ventricular end diastolic volume is raised (e.g. ↓ ejection fraction)↑ Preload will ↑ cardiac contractilityCompensatory mechanism

Frank-Starling’s Law of the Heart

SV is the volume of blood pumped from one ventricle of the heart with each heart beatUsually assumed to be the Left

SV = EDV – ESVEjection Fraction = SV / EDVDeterminants

PreloadSV is controlled by preload due to Frank-Starling’s Law

Afterload↑ Afterload will ↓ SV

Contractility↑ Ca2+

Stroke Volume

In HF, ejection fraction ↓Can be compensated by ↑ heart rate (sinus

tachycardia)In severe myocardial dysfunction, cardiac output can

only be maintained by ↑ venous pressure (Preload) &/ ↑ tachycardiaLow functional reservePerfusion only maintained to vital organs (huge

impact)Causes dyspnoea,

hepatomegaly, ascites, oedemaDue to ↑ venous pressure

Venous Return (Preload)

Afterload is defined as the myocardial wall tension developed during systolic ejection

It is formed by:Pulmonary & systemic resistancePhysical characteristics of the vessel wallsVolume of blood that is ejected

↑ in afterload ↓ cardiac output↑ end-diastolic volume↑ dilatation of the ventricle↑ AFTERLOAD

Vicious cycle

Outflow Resistance (Afterload)

Sympathetic nervous system is activated in early HF as a compensatory mechanism Inotropic support & maintains cardiac output

Chronic sympathetic activation leads to ↑ neurohormonal activation & myocyte apoptosis

Also causes ↑ cytosolic Ca2+ entryAugments myocardial contractility Impairs myocardial relaxation (lusitropy)

Myocardial Contractility

↓ CO leads to diminished renal perfusionActivation of RAAS↑ Aldosterone production to retain salt &

waterExacerbates increased venous pressure

Salt & Water Retention

Primary response to chronic ↑ wall stress is myocyte hypertrophy, apoptosis & regeneration

Myocardial remodelling is pathological (eccentric)Worsens the situation↑ stress on remaining myocytes

Myocardial Remodelling

Left Heart FailureClinical features

Fatigue, dyspnoeaCardiomegalyOn auscultation,

gallop rhythmCrackles in lung

basesPulmonary oedema

Clinical featuresFatigue, dyspnoea,

anorexia, nauseaJugular venous

distensionHepatomegalyPitting oedemaAscitesPleural transudates

Findings

Right Heart Failure

FBE/LFT/U&E/TFT/Cardiac troponinsCXR (to be discussed)ECG

Signs of ischaemia, MI, ventricular hypertrophy, LBBB

Echo (TTE/TOE)? Stress

BNPHighly indicative of CHF & poor prognosis factor

? Cardiac Biopsy? Cath Lab

Workup

Diagnosing Heart Failure

EducateObesity controlDietary modification

Low salt, minimise EToH +/- fluid restrictionSmokingSexual activityExercise

Light exercise is encouragedVaccination

General Lifestyle Advice

Heart Failure Treatment Guidelines

Overall Management Plan

Presents typically as 1 of 2 radiographic patterns:Pulmonary interstitial oedemaPulmonary alveolar oedema

Which radiographic pattern appears depends on the pulmonary (venous) capillary wedge pressure (PCWP)

Radiological Findings in CHF

4 key radiographic signs:Thickening of the interlobular septa

Kerley B linesNamed after Irish neurologist & radiologist, Peter

James KerleyPeribronchial cuffingFluid in the fissuresPleural effusions

Pulmonary Interstitial Oedema

Spot diagnosis!

Thickening of the interlobular septaNot visible on normal CXROnly visible when it accumulates excessive

fluid, PCWP about 15 mm HgVisible on frontal CXR, @ lung bases, @/ near

costophrenic anglesVery short (1-2cm), very thin (1mm) &

horizontal in orientationChronic Kerley B Lines

After repeated episodes of pulmonary interstitial oedema, fibrosis occurs

Kerley B Lines

A, B, C!

Yes, there are A & C lines unfortunatelyKerley A Lines

Appears when connective tissue around the bronchoarterial sheaths in the lungs distends with fluid

Extends from the hila (up to 6 cm) & don’t extend to the lung peripheries

Kerley C LinesIf you know what they are, you are wasting

time in this lecture? Overlap b/w A & B Lines? Myth

Kerley A Lines

Doughnuts!

Bronchi may only be visible when seen on-end in the region of the pulmonary hilaAnywhere else, it is pathological

Fluid collects in the interstitial tissue surrounding the wall of the bronchiBronchial wall becomes ‘thicker’ & appears as

doughnuts when seen on-endSame mechanics as air bronchograms

Peribronchial Cuffing

Normal & Pathological

The fissures may normally be visible however, are almost never thicker than a line drawn with a sharp pencil

Fluid may collect b/w the 2 layers of the visceral pleura or subpleural spaceAccumulated fluid distends the fissure(s)

Thicker, irregular & more visible

Fluids in the Fissures

Spot the Difference

Pleural effusions caused by CHF are usually bilateralWhen it is unilateral, almost always right-sided

Therefore when you see a left-sided pleural effusion, considerMets, TB, thromboembolic disease, etc

Laminar Pleural EffusionThin, band-like density along lat chest wall,

esp. near costophrenic angles (still sharp)Almost always due to left atrial pressure ↑↑↑

CHFLymphangitic spread of malignancy

Pleural Effusions

Which one is it?

Fluid spills out of the interstitium & into the airspaces when PCWP is sufficiently ↑↑↑ (25 mm Hg)

Almost known as Pulmonary OedemaRadiographic finding

Fluffy, indistinct patchy airspace densitiesOuter 1/3 usually sparedLower zones > Upper zonesButterfly/Bat-wing appearancePleural effusions usually present when the

oedema is cardiogenic in nature

Pulmonary Alveolar Oedema

Cardiogenic VS Non-cardiogenic Pulmonary Oedema

Imaging Findings Cardiogenic Non-cardiogenic

Pleural Effusions Common Infrequent

Kerley B Lines Common Infrequent

Heart Size Usually enlarged May be normal

PCWP Elevated Normal

Different forms of Pulmonary Oedema

Mr XY, 80 y/o pensionerHOPC sudden & extreme SOBWheezing & diaphoreticCoughing with pink frothy sputumCold peripheriesGallop rhythm

DifferentialsInvestigationsManagement

Emergency!!!

a) Asthmab) COPDc) Pneumoniad) Pulmonary oedemae) All of the above

Differentials???

CXRECGU&E, Cardiac Troponins, ABGBNPEcho

Investigation!!!

Could this be Pneumonia?

Sit upright & OxygenIV access & ECG monitoringMorphine (5-10mg) +/- metoclopramide (10mg)

Beware of morphine systolic BP < 90 mm HgIV diuretics (furosemide 40-80 mg slowly)GTN (spray 2 puffs/ 2 x 0.3 mg SL)

Don’t give if systolic BP < 90 mm HgConsider nitrate infusion if systolic BP > 100 mm Hg

Isosorbide dinitrate 2-10mg/h IVEvaluate situation

If worsening, consider more diuretics & venesectionGet HELP!!!

Management