Heart Failure

Question 1

Congestion

Answer 1

A relative excess of blood in the vessels of a tissue/organ

Question 2

Congestive heart failure pathophysiology

Answer 2

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

Question 3

Causes of vascular congestion

Answer 3

DVT,
Hepatic cirrhosis,
Congestive cardiac failure,

Question 4

Exudate

Answer 4

Due to increased vascular permeability
(part of the inflammatory process),
Higher protein/albumin and cell content

Question 5

Transudate

Answer 5

Due to altered haemodynamic forces acting across the capillary wall. (e.g. cardiac failure)
Low protein/albumin and cell content

Question 6

Starling forces in capillaries

Answer 6

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)

Question 7

Factors affecting net flux and filtration of fluid in the capillaries

Answer 7

Hydrostatic pressure
Oncotic pressure
Permeability and area of endothelium

*Disturbance of normal components = oedema

Question 8

oedema

Answer 8

accumulation of abnormal amounts of fluid in the extravascular compartment (tissues and body cavities)

Question 9

Disturbances in starling forces leading to oedema

Answer 9

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

Question 10

Permeability oedema

Answer 10

Damage to endothelial lining = fluid (+ proteins etc.) leak out = oedema

e.g. acute inflammation, burns

Question 11

Aetiology of heart failure

Answer 11

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

Question 12

Causes of left ventricular systolic dysfunction

Answer 12

Myocardial ischaemia/infarction
Severe aortic valve disease
Severe mitral regurgitation
Dilated cardiomyopathy (DCM)

Inherited
Toxins
Infective
Systemic disease
Muscular dystrophies
Hypertension

Question 13

Epidemiology of heart failure

Answer 13

Affects 1-2% UK population
increasing in prevalence due to:
-aging population
-hypertension
-CHD
-diabetes
-obesity

Question 14

Prognosis for heart failure

Answer 14

Worsens with increasing NYHA class (I - IV)

average = 30-40% mortality at 1 year

Question 15

Symptoms of heart failure

Answer 15

Dyspnoea
Fatigue
Oedema
Reduced exercise capacity

Question 16

Signs of heart failure

Answer 16

Oedema
Tachycardia
Raised JVP
Chest crepitations or effusions
3rd heart sound
Displaced or abnormal apex beat

Question 17

Investigations for heart failure

to show evidence of cardiac dysfunction

Answer 17

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

Question 18

Screening tests for heart failure

Answer 18

12 lead ECG (90-95% sensitive)

BNP (Brain natriuretic peptide) - elevated in HF

Question 19

Treatment for heart failure

due to LVSD

Answer 19

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)

Question 20

Strengths of loop diuretics therapy in the treatment of congestive heart failure

Answer 20

Loop diuretics = the main stay of treatment

Loop diuretics can be used with thiazide-like diuretics in diuretic resistant patients

Question 21

Loop diuretics ADRs

Answer 21

Dehydration
Hypotension
Hypokalaemia
Hyponatraemia
Gout

Question 22

Strengths of ACE inhibitors in the treatment of heart failure

Answer 22

Improve symptoms AND survival
Also prevent onset of heart failure
More effective than ARBs

Question 23

ACEIs drug-drug interactions

Answer 23

NSAIDS: acute renal failure
Potassium supplements: hyperkalaemia
Potassium sparing diuretics: hyperkalaemia

Question 24

Strengths of beta blockers in the treatment of heart failure

Answer 24

Improves survival

Question 25

Weaknesses of beta blockers in the treatment of heart failure

Answer 25

``` 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

Question 26

Neprysilin inhibitor

Answer 26

inhibits nepryilin which breaks down ANP and PNP Decreases blood pressure Often combined with an ARB making "angiotensin receptor neprysilin inhibitor" (ARNI)

Question 27

Furosemide drug-drug interactions

Answer 27

``` Lithium: renal toxicity NSAIDs: renal toxicity Vancomycin: renal toxicity Aminoglycosides: aural + renal toxicity Antihypertensives: profound hypotension ```

Question 28

Body's response to heart failure + therapeutic intervention

Answer 28

↓ 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: 1. inhibits RAAS 2. inhibits sympathetic response (↓ cardiac workload) 3. diuretics (↓ salt + water retention from RAAS) 4. ehance natriuretic peptide system (↓ BP)