1. Dilated Cardiomyopathy (most common, ~90% cases)

Characterised by dilation of chamber walls with only minor hypertrophy. The heart becomes weakened and enlarged - Systolic Dysfunction. Cause is usually idiopathic. Other causes incl: Viral myocarditis, Alcohol toxicity, Chemotherapeutic drugs, Cocaine, Heroin, Specific Gene mutations (eg Duchenne Muscular Dystrophe), Hyperthyroidism etc

2. Hypertrophic Cardiomyopathy (most common cause of sudden cardiac death in young athletes) is characterised by significant thickening in chamber walls and a decrease in chamber size, which results in low stroke volume (diastolic dysfunction). Causes: Genetic predisposition, hypertensive heart disease and ageing.

3. Restrictive cardiomyopathy (least common of them all!) Chamber walls DO NOT enlarge or dilate. They become FIBROTIC and STIFF. Stiff ventricles fail to fill adequately during diastole. (Diastolic dysfunction) Causes; Endocarditis, Amyloidosis, Sarcoidosis, Haemachromatosis, Radiation Fibrosis, Endocardial Fibrocardosis

Peripheral Oedema, Raised JVP, Ascites, Anasarca: the failing heart - poor perfusion to kidneys, sympathetic activation- sets off the R.A.A.S. This causes Na⁺ and H₂O retention & Vasoconstriction. ↑ Intravascular volume - ↑ Venous pooling & Venous back pressure = Peripheral Oedema (may gravitate to ankles, tibia etc), Raised JVP

Dyspnoea: Poor Left Ventricle filling, therefore poor perfusion to lungs causing shortness of breath. DIFFERENT from LV Heart Failure caused Dyspnoea.

Tender Epigastric Region, Hepatomegaly: Activation of R.A.A.S - vasoconstriction & Water retention - increased venous pooling - increased back venous pressure - buildup of fluid in liver - liver becomes congested with fluid, toxins, nutrients etc.

Fatigue, Weakness, Cold peripheries: vasoconstriction and poor LV filling - poor perfusion to skeletal muscle and extremeties - cold hands and feet. Also lactic acidosis - fatigue and weakness.

Ischaemic Heart Disease

Valvular Disease (eg, Aortic Valve Stenosis, Mitral Insufficiency)

Hypertensive Heart Diseaase

Cardiomyopathy

LFT - liver congestion can lead to impaired hepatic function, and therefore ↑ Bilirubin/Hepatic enzymes

BNP - ↑ Brain Natriuretic Peptide in serum, because the body responds to the Na⁺ and water retention by trying to lose the Na⁺, ie, Natriuresis.

Arterial Blood Gases - Shows poor perfusion, hypoxia and metabolic acidosis. Pt's who are hypoxic may need artifical ventilation.

Electrolytes&Renal Function - shows Hypokalaemia, Hypernatraemia

ECG - Shows ichaemic/hypertensive changes, maybe axis deviation in Cardiomyopathy

Chest X-Ray - Cardiomegaly? Dilated Ventricle? Pulmonary Oedema?

Echocardiogram - LV,RV dimensions, valvular defects? regurgitation? pressures in each chamber? back pressures in major blood vessels? intracardiac thrombus? Ischaemic heart tissue?

ACE Inhibitors - Ramipril - dilatation of blood vessels, ↓ Blood Pressure

Angiotensin 2 Receptor Antagonist - Irbesartan - ↓ secretion of aldosterone, vasodilation, ↓ Blood Pressure

βeta Blockers - Metoprolol - blocks effect of catecholamines on β-1 adrenergic receptors, ↓ cardiac sympathetic stimulation.

Diuretics:
1. Loop - Furosemide - blocks the Na⁺K⁺2Cl^- Symporter, inhibiting Na⁺, Cl^- absorption. Ultimately causing diuresis.

2. Thiazide - Hydrochlorothiazide - blocks the thiazide sensitive Na⁺Cl^- symporter, inhibiting reabsorption of Na⁺, Cl^- and ultimately water, causing diuresis.

3. K-Sparing - Spironolactone - weak diuretic, used in conjunction with other diuretics to avoid Hypokalaemia.

Cardiac Glycosides - Digoxin - inhibits sarcolemmal Na^+/K⁺ Pumps to ↑intracellular [Ca²⁺] = Positive Ionotropic effect

Nitrates -  Isosorbide Dinitrate - Directly dilates blood vessels

Pulmonary Oedema - increased pressure buildup in pulmonary circuit, forces fluid out into lung tissues, causing pulmonary oedema, frothy pink sputum, cough.

Cold Peripheries and renal impairment due to poor LV output.

Fatigue and weakness - due to poor LV Cardiac output, 

Bilateral Basal Crepitations -  Alveoli that have collapsed form the Oedema 'pop' open during expiration, making crackly sounds in both lungs.

LV 3rd Heart Sound - heard at Apex (due to mitral regurgitation usually)

Paroxysmal Nocturnal Dyspnoea - this is due to return of venous interstitial fluid to lungs and nocturnal depression of respiratory function.

1. Activation of the Sympathetic Nervous System.
Adrenalin and Noradrenalin activate the β-1 Adrenergic receptors, and keep doing so even when the max limit of cardiac contractility is reached -> leading to tachycardia, fatigue and weakness, and only a slight ↑ in Cardiac output.

2. ↑ Myocardial Stretch.

In an attempt to boost cardiac output, and under high pressure, the myocardium becomes stretched and thin. The leads to ↓ contractility, and a large ↑ in pulmonary capillary back pressure -> Oedema

3. Elevated Catecholamine activity

Peripheral vasocontriction. Blood is directed to most important vital organs, away from peripheries and skeletal muscle. This results in underperfusion, cold extremities, lactic acidosis.

4. Activation of R.A.A.S in response to poor renal perfusion.

Aldosterone causes Na⁺, H₂O retention, ↑ Intravascular volume, ↑ Cardiac Load, this exacerbates cardiac failure, and causes Raised JVP, Oedema

In Congestive Heart Failure, and in Left Ventricle Failure, the left ventricle, is not pumping adequately to push blood through all the tissues of the body, and so blood and interstitial fluid is retained in the pulmonary circuit. The fluid begins to leak out and congest the pulmonary tissue - alveoli, and they fill up with fluid and can no longer function as a respiratory surface. There is less of functioning respiratory surface available, and less oxygen available to the patient - causing exertional dyspnoea, tachycardia and dyspnoea. When the patient lies supine, the total blood volume is augmented because of the reabsorption of oedema from other parts of the body. This exacerbates the already existing pulmonary congestion, and can leave the patient breathless and wheezing halfway through the night when recumbent.

1. Congestive Heart Failure - the heart fails to pump blood adequately, and fluid slowly collects in the periphery or in lung tissue (pitting, peripheral oedema, tibial/ankle oedema, pulmonary oedema)

2. Hypoalbuminaemia - Albumin acts like a sponge to keep fluid in blood vessels. Low albumin can cause non-pitting oedema (Ascites in Liver failure/Chronic Hepatitis)

3. Obstruction of flow - blocking lymph ducts/blood vessels can cause fluid build up in surrounding tissues. (Radical Mastectomy, Deep Venous Thrombosis)

4. Nephrotic Syndrome - Glomeruli innappropriately allow albumin to be lost via urine, causing non-pitting oedema, and sometimes ascite.