Heart Failure

Question 1

4 clinical peices of evidence that someone may have a heart structural/functional abnormality

Answer 1

ECG, murmur, raised natriuretic peptide, cardiomegaly

Question 2

How is HF classified? (3)

Answer 2

1. Acute vs Chronic
2. L side vs R side (or congestive = both)
3. Reduced vs Preserved ejection fraction (or both)

Question 3

What’s the difference between a reduced and preserved ejection fraction? Name examples of each

Answer 3

Reduced: problem with systole (impaired contractility/increased afterload)

Preserved: problem with diastole (EF stays higher)
L ventricular hypertrophy, tamponade, restrictive cardiomyopathy, etc

Question 4

3 scenarios that could cause the body to demand a higher output from the heart

Answer 4

Pregnancy, anemia, hyperthyroidism

Question 5

What are the 2 main causes of L sided Heart failure?

Answer 5

Coronary heart disease, hypertension

Question 6

What is the main cause of R sided Heart failure?

Answer 6

L sided HF

Question 7

What is the latin term for what occurs in the R side of the heart during R sided heart failure

Answer 7

Cor pulmonale

Question 8

What are 3 pathologies that could increase the preload and 2 things that could increase an afterload?

Answer 8

Hypervolemia, valve regurg, HF

HTN, vasoconstriction

Question 9

Symptoms of LEFT Ventricular failure

Answer 9

Pulmonary congestion: orthopnea, paroxysmal nocturnal dyspnoea, pink/frothy nocturnal cough, breathless on exertion

Lower O2: muscle wasting, fatigue

Question 10

Signs of RIGHT ventricular failure

Answer 10

pitting edema/Swollen ankles, raised JVP, ascites, hepatomegaly (back up in hepatic veins)

+fatigue, nausea, anorexia

Question 11

How is staging classified for heart failure? List the stages and their brief characteristics

Answer 11

Staged depending on how functional the heart still is

Class 1: no symptomatic limitation of physical activity

Class 2: Mild physical limitation, (i.e symptoms when doing ordinary physical activity)

Class 3: Marked physical limitation, (i.e symptoms when doing ordinary daily activity)

Class 4: symptoms at rest + severe discomfort/inability to do physical activity without symptoms

Question 12

3 compensatory mechanisms the body tries to bring the CO back to normal

Answer 12

Ventricular remodelling, starling law, neurohormonal alterations

Question 13

Describe the starling law mechanism in HF

Answer 13

Increase L ventricle force -> brings SV and CO up

*HF decreases CO and SV so blood accumulates in ventricle

Question 14

When are neurohormonal alterations activated and what are their 2 overall goals?

Answer 14

Low CO activates..
1. Increase TPR as this brings up BP and CO

2. Increase preload by retaining salt and water

Question 15

What does the RAAS system lead to as a neurohormonal alteration?

Answer 15

Fluid retention/increase preload

Angiotensin II:

1. increases thirst
2. Vasoconstriction
3. Produces aldosterone: retains Na+, excretes K+ and H+

Question 16

How can neurohormonal alterations become an issue chronically? (4 things)

Answer 16

Too much
Vasoconstriction: wall stress, hypotension

HR: increases heart’s metabolic/O2 needs

TPR: high afterload that reduces SV and CO further

Volume: further pulmonary and peripheral congestion

Question 17

What does ADH/Vasopressin do as a neurohormonal alteration?

Answer 17

Released via hypovolaemia, increases fluid retention (aquaporins)

Question 18

What 2 things activate the start of RAAS?

Answer 18

Sympathetic NS and reduced renal blood flow

-> Renin secreted from JGA cells in kidney

Question 19

Describe the two natriuretic peptides, what is their relationship with RAAS?

Answer 19

ANP: atrial myocytes in response to high blood volume/atrial pressure -> vasodilation and decreased Na absorption

B type natriuretic peptide (BNP): ventricular myocytes in response to high pressure

-> BALANCE RAAS: vasodilation, increase Na+ and water excretion, decrease renin and angiotensin II action

Question 20

What are the 3 main components to Ventricular Remodelling and what is the eventual outcome?

Answer 20

Hypertrophy, fibrosis, apoptosis

Eventually overstretch of myocyte -> thin/weak -> blood backs up into L atria and pulmonary vessels

Question 21

Why is BNP not always reliable?

Answer 21

Highly sensitive but low specificity

*many things affect it; may be decreased with certain meds, obesity, etc

Question 22

What is the main goal in medical management of heart failure? List 3 things

Answer 22

Symptomatic improvement, delay progression

Reduce fluid: Loop diuretics, ACE inhibitors
Reduce sympathetic response: beta-blockers
Veno/vasodilation: nitrates

Question 23

What are 3 main surgical interventions that can be done to manage heart failure?

Answer 23

Implantable defibrillator, pacemaker, surgery (transplant, valve, revascularisation, etc)

Question 24

What defines acute heart failure? List 5 symptoms and 7 signs

Answer 24

Sudden onset of symptoms

Severe SOB, sweating, nausea, anxious, dry or productive (wet and chesty) cough

Hypotension, edema, crackles, S3, raised JVP, tachycardia, orthopnea