Armaan Khalid

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

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

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

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

SV is the volume of blood pumped from one ventricle of the heart with each heart beat Usually assumed to be the Left SV = EDV – ESV Ejection Fraction = SV / EDV Determinants Preload SV is controlled by preload due to Frank-Starling’s Law Afterload ↑ Afterload will ↓ SV Contractility ↑ Ca 2+

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) &/ ↑ tachycardia Low functional reserve Perfusion only maintained to vital organs (huge impact) Causes dyspnoea, hepatomegaly, ascites, oedema Due to ↑ venous pressure

Afterload is defined as the myocardial wall tension developed during systolic ejection It is formed by: Pulmonary & systemic resistance Physical characteristics of the vessel walls Volume of blood that is ejected ↑ in afterload ↓ cardiac output ↑ end-diastolic volume ↑ dilatation of the ventricle ↑ AFTERLOAD Vicious cycle

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 Ca 2+ entry Augments myocardial contractility Impairs myocardial relaxation (lusitropy)

↓ CO leads to diminished renal perfusion Activation of RAAS ↑ Aldosterone production to retain salt & water Exacerbates increased venous pressure

Primary response to chronic ↑ wall stress is myocyte hypertrophy, apoptosis & regeneration Myocardial remodelling is pathological (eccentric) Worsens the situation ↑ stress on remaining myocytes

Left Heart Failure Clinical features Fatigue, dyspnoea Cardiomegaly On auscultation, gallop rhythm Crackles in lung bases Pulmonary oedema Clinical features Fatigue, dyspnoea, anorexia, nausea Jugular venous distension Hepatomegaly Pitting oedema Ascites Pleural transudates Right Heart Failure

FBE/LFT/U&E/TFT/Cardiac troponins CXR (to be discussed) ECG Signs of ischaemia, MI, ventricular hypertrophy, LBBB Echo (TTE/TOE) ? Stress BNP Highly indicative of CHF & poor prognosis factor ? Cardiac Biopsy ? Cath Lab

Educate Obesity control Dietary modification Low salt, minimise EToH +/- fluid restriction Smoking Sexual activity Exercise Light exercise is encouraged Vaccination

Presents typically as 1 of 2 radiographic patterns: Pulmonary interstitial oedema Pulmonary alveolar oedema Which radiographic pattern appears depends on the pulmonary (venous) capillary wedge pressure (PCWP)

4 key radiographic signs: Thickening of the interlobular septa Kerley B lines Named after Irish neurologist & radiologist, Peter James Kerley Peribronchial cuffing Fluid in the fissures Pleural effusions

Thickening of the interlobular septa Not visible on normal CXR Only visible when it accumulates excessive fluid, PCWP about 15 mm Hg Visible on frontal lung near costophrenic angles Very short (1-2cm), very thin (1mm) & horizontal in orientation Chronic Kerley B Lines After repeated episodes of pulmonary interstitial oedema, fibrosis occurs

Yes, there are A & C lines unfortunately Kerley 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 Lines If you know what they are, you are wasting time in this lecture ? Overlap b/w A & B Lines ? Myth

Bronchi may only be visible when seen on-end in the region of the pulmonary hila Anywhere else, it is pathological Fluid collects in the interstitial tissue surrounding the wall of the bronchi Bronchial wall becomes ‘thicker’ & appears as doughnuts when seen on-end Same mechanics as air bronchograms

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 space Accumulated fluid distends the fissure(s) Thicker, irregular & more visible

Pleural effusions caused by CHF are usually bilateral When it is unilateral, almost always right-sided Therefore when you see a left-sided pleural effusion, consider Mets, TB, thromboembolic disease, etc Laminar Pleural Effusion Thin, band-like density along lat chest wall, esp. near costophrenic angles (still sharp) Almost always due to left atrial pressure ↑↑↑ CHF Lymphangitic spread of malignancy

Fluid spills out of the interstitium & into the airspaces when PCWP is sufficiently ↑↑↑ (25 mm Hg) Almost known as Pulmonary Oedema Radiographic finding Fluffy, indistinct patchy airspace densities Outer 1/3 usually spared Lower zones > Upper zones Butterfly/Bat-wing appearance Pleural effusions usually present when the oedema is cardiogenic in nature

Cardiogenic VS Non-cardiogenic Pulmonary Oedema Imaging FindingsCardiogenicNon-cardiogenic Pleural EffusionsCommonInfrequent Kerley B LinesCommonInfrequent Heart SizeUsually enlargedMay be normal PCWPElevatedNormal

Mr XY, 80 y/o pensioner HOPC sudden & extreme SOB Wheezing & diaphoretic Coughing with pink frothy sputum Cold peripheries Gallop rhythm Differentials Investigations Management

a) Asthma b) COPD c) Pneumonia d) Pulmonary oedema e) All of the above

CXR ECG U&E, Cardiac Troponins, ABG BNP Echo

Sit upright & Oxygen IV access & ECG monitoring Morphine (5-10mg) +/- metoclopramide (10mg) Beware of morphine systolic BP < 90 mm Hg IV diuretics (furosemide mg slowly) GTN (spray 2 puffs/ 2 x 0.3 mg SL) Don’t give if systolic BP < 90 mm Hg Consider nitrate infusion if systolic BP > 100 mm Hg Isosorbide dinitrate 2-10mg/h IV Evaluate situation If worsening, consider more diuretics & venesection Get HELP!!!