Heart Failure Flashcards
Congestion
A relative excess of blood in the vessels of a tissue/organ
Congestive heart failure pathophysiology
Heart is unable to pump sufficient blood from the ventricles
↓ cardiac output
activates renin-angiotensin-aldosterone system
↑ Na+ and H2O retention
↑ amount of fluid in body = fluid overload in veins
Causes of vascular congestion
DVT,
Hepatic cirrhosis,
Congestive cardiac failure,
Exudate
Due to increased vascular permeability
(part of the inflammatory process),
Higher protein/albumin and cell content
Transudate
Due to altered haemodynamic forces acting across the capillary wall. (e.g. cardiac failure)
Low protein/albumin and cell content
Starling forces in capillaries
HYDROSTATIC PRESSURE: forces fluid out of the capillary (higher at the arterial side - filtration)
ONCOTIC PRESSURE: forces fluid into the capillaries (higher at the venous side - reabsorption)
Factors affecting net flux and filtration of fluid in the capillaries
Hydrostatic pressure
Oncotic pressure
Permeability and area of endothelium
*Disturbance of normal components = oedema
oedema
accumulation of abnormal amounts of fluid in the extravascular compartment (tissues and body cavities)
Disturbances in starling forces leading to oedema
LVF = ↑ left atrial pressure = ↑ pulmonary vascular pressure = ↑ hydrostatic pressure = ↑ filtration = pulmonary oedema
RVF = blood retained in systemic veins = ↑ hydrostatic pressure in systemic capillaries = ↑ filtration = peripheral oedema
Lymphatic obstruction = ↓ lymph drainage = ↑ vascular fluid volume = ↑ hydrostatic pressure = lymphoedema
Abnormal renal function = NaCl and H2O retention = ↑ vascular fluid volume = ↑ hydrostatic pressure = oedema
Hypoalbuminaemia = ↓ oncotic pressure = ↑ filtration = peripheral oedema
Permeability oedema
Damage to endothelial lining = fluid (+ proteins etc.) leak out = oedema
e.g. acute inflammation, burns
Aetiology of heart failure
Any structural heart disease:
*LV systolic dysfunction* Valvular heart disease Pericardial constriction/effusion LV diastolic dysfunction Cardiac arrhythmias Myocardial ischaemia/infarction Restrictive cardiomyopathy RV failure
Causes of left ventricular systolic dysfunction
Myocardial ischaemia/infarction
Severe aortic valve disease
Severe mitral regurgitation
Dilated cardiomyopathy (DCM)
Inherited Toxins Infective Systemic disease Muscular dystrophies Hypertension
Epidemiology of heart failure
Affects 1-2% UK population increasing in prevalence due to: -aging population -hypertension -CHD -diabetes -obesity
Prognosis for heart failure
Worsens with increasing NYHA class (I - IV)
average = 30-40% mortality at 1 year
Symptoms of heart failure
Dyspnoea
Fatigue
Oedema
Reduced exercise capacity
Signs of heart failure
Oedema Tachycardia Raised JVP Chest crepitations or effusions 3rd heart sound Displaced or abnormal apex beat
Investigations for heart failure
to show evidence of cardiac dysfunction
Bloods: BNP elevated in HF
ECG: LVSD unlikely if ECG normal
Echo: Shows dysfunction, effusion/tamponade, hypertrophy, shunts, congenital defects etc.
Cardiac MRI: Possible causes e.g. inflammation/ infarction/ fibrosis. LVEF
CXR: Cardiomegaly, hypertrophy, effusion etc.
Radionucleotide imaging: To assess ventricular function if echo not available
- Left ventriculogram: LVEF
- MUGA: Accurately obtains LVEF
Screening tests for heart failure
12 lead ECG (90-95% sensitive)
BNP (Brain natriuretic peptide) - elevated in HF
Treatment for heart failure
due to LVSD
Symptomatic treatment:
Diuretics (Furosemide)
Inhibition of RAAS:
ACE Inhibitors
ARBs
Aldosterone antagonist (spironolactone)
Enhance natriuretic peptide system: Neprysilin inhibitor (or ARNI)
Enhance cardiac function/ reduce workload:
Positive inotropes (Digoxin)
Nitrovasodilators
β-blockers
Ivabradine
Anticoagulant:
Warfarin (dilated ventricle gives rise to thrombus formation)
Strengths of loop diuretics therapy in the treatment of congestive heart failure
Loop diuretics = the main stay of treatment
Loop diuretics can be used with thiazide-like diuretics in diuretic resistant patients
Loop diuretics ADRs
Dehydration Hypotension Hypokalaemia Hyponatraemia Gout
Strengths of ACE inhibitors in the treatment of heart failure
Improve symptoms AND survival
Also prevent onset of heart failure
More effective than ARBs
ACEIs drug-drug interactions
NSAIDS: acute renal failure
Potassium supplements: hyperkalaemia
Potassium sparing diuretics: hyperkalaemia
Strengths of beta blockers in the treatment of heart failure
Improves survival
Weaknesses of beta blockers in the treatment of heart failure
POTENTIALLY HAZARDOUS (may precipitate severe deterioration): Only for stable, dry patients Must start at a low dose
Must be used in combination with ACEI/ARB and diuretic
Neprysilin inhibitor
inhibits nepryilin which breaks down ANP and PNP
Decreases blood pressure
Often combined with an ARB making “angiotensin receptor neprysilin inhibitor” (ARNI)
Furosemide drug-drug interactions
Lithium: renal toxicity NSAIDs: renal toxicity Vancomycin: renal toxicity Aminoglycosides: aural + renal toxicity Antihypertensives: profound hypotension
Body’s response to heart failure + therapeutic intervention
↓ CO is perceived as a loss in circulatory volume
= sympathetic activation (vasoconstriction, myocyte hypertrophy etc) + RAAS
[↑ in circulatory volume dilates heart = further ↓ CO]
Drug therapy:
- inhibits RAAS
- inhibits sympathetic response (↓ cardiac workload)
- diuretics (↓ salt + water retention from RAAS)
- ehance natriuretic peptide system (↓ BP)
