Heart Failure Flashcards

1
Q

Pathophysiology of HF? Discuss compensatory mechanism for HF.

A

(1. ) Inability of cardiac output to meet the physiological demands of the body.
(2. ) This can be systolic or diastolic failure. In both cases it causes pulmonary congestion
(3. ) Compensatory mechanisms (a-c) are activated in attempt to restore heart functioning, CO and tissue perfusion.

(a. ) Sympathetic Adrenergic Systems
- Inc HR + contractility

(b.) Myocyte size inc (LVH)

(c. ) Renal and peripheral alterations
- reduced GFR –> RAAS activation –> fluid retention –> Inc Preload and BP
- Peripheral vasoconstriction –> Inc resistance and thus BP

(4.) Chronic activation of compensatory mechanism can worsen HF and leads to cardiac damage. Thus CO declines, reduced tissue perfusion, hypoxic organs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Systolic failure

A
  1. Inability of ventricles to contract normally so not enough blood is pumped out during systole
  2. Dec CO and dec EF (<40%)
  3. Causes: IHD, MI, Cardiomyopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Diastolic failure

A
  1. Inability of ventricles to relax and fill normally causing inc filling pressure
  2. Not enough blood fills into the ventricles during diastole - reduced preload.
  3. EF will look normal (>50%) despite SV being low. This is because EDV is low. Referred to as HF with preserved EF, HFPEF
  4. Causes: heart cannot relax and ventricle walls become stiffer. This can be due to:
    - Less elasticity as we get older.
    - Muscles get larger and thicker in high BP
    - CAD
    - Obesity
    - Diabetes
    - ventricular hypertrophy
    - constrictive pericarditis
    - tamponade
    - reconstructive cardiomyopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Left-Sided SYSTOLIC HF pathophysiology?

A

(1. ) Systolic HF = heart can’t contract as forcefully and thus cannot pump efficiently.
(2. ) Dec BP -> dec renal blood flow -> activates RAAS -> inc blood volume -> inc preload which increases contractility via Frank Starling mechanism.
(3. ) H/E long term fluid retention in vessels causes leakage and build up in tissues.
(4. ) Eventually, LV function declines and will cause blood to back up into pulmonary circulation -> pulmonary congestion
(5. ) Fluid filled capillaries in lungs can rupture, leaking blood into the alveoli.
(6. ) Alveolar macrophages engulf leaking RBC, which causes them to become brownish colour from iron build-up, these are called “hemosiderin-laden macrophages”, also known as “heart failure cells”.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Clinical features of left-sided HF

A

Signs of LV pump dysfunction

(1. ) Dyspnea - trouble breathing
(2. ) Orthopnea: difficulty breathing when lying down flat
(3. ) Fatigue
(4. ) Exercise intolerance

Signs of volume overload

(1. ) Pulmonary Crackles - heard on auscultation while patient breathes.
(2. ) Peripheral oedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Aetiology of left-sided systolic HF

(what causes LV to become weaker?) [3].

A
  1. IHD (most common cause) E.g. CAD, atherosclerosis
  2. Longstanding HTN
  3. Dilated cardiomyopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Left-Sided DIASTOLIC HF pathophysiology?

A

(1. ) This is a filling dysfunction but LV function is preserved
(2. ) LV can no longer relax and becomes stiff.
(3. ) LV is stiff - dec compliance and impaired relaxation this causes increased resistance to filling (reduced EDV). So little blood leaves the ventricles (reduced SV). EF is preserved.
(4. ) There is an inc EDP and this can impact pulmonary circulation and lead to pulmonary congestion, dyspnea, and other symptoms of heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Aetiology of left-sided diastolic HF (what makes it stiffer?) [4].

A

(1. ) Chronic HTN (most common cause)
- LVH: reduces cardiac compliance and reduces EDV

(2. ) Aortic stenosis
- AS reduces blood flow through aortic valves so there is an increase afterload and so heart has to work with more force and causes LVH.

(3. ) Hypertrophic cardiomyopathy
- Heart becomes abnormally thick

(4. ) Restrictive cardiomyopathies
- heart gets stiffer and less compliant
- LV can’t easily stretch and fill with as much blood.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Why might you get arrhythmias in HF? and how would it be managed?

A

(1. ) In HF, myoctes stretch and thin out, or thicken and become ischaemic. This can lead to arrhythmias.
(2. ) Ventricles don’t contract in sync anymore making them less able to pump out blood.

(3. ) Mx = cardiac resynchronization therapy pacemakers
- stimulate ventricles to contract at same time and improve blood pumped out.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Aetiology of Right-sided HF (3)

A

(1. ) Left-sides heart failure
- When LV fails, increased fluid pressure is, in effect, transferred back through the lungs, ultimately damaging the right side

(2. ) Atrial or ventricular septal defect
- left-to-right cardiac shunt allows blood to flow from left to right side down pressure gradient, which inc fluid volume on right side and can lead RVH

(3. ) Chronic lung disease, Cor Pulmonale
- Lung diseases make it harder to exchange oxygen - hypoxia
- In response to hypoxia, pulmonary arterioles constrict, which raises pulmonary BP
- High BP in pulmonary circulations makes it harder for RV to pump against and can lead to RVH and HF.
- Chronic lung disease leading to RVH and failure is known as cor pulmonale.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Clinical Features of Right-sided HF (5)

A

(1. ) Jugular venous distention
(2. ) Hepatosplenomegaly
(3. ) Cardiac Cirrhosis and liver failure
(4. ) Ascites
(5. ) Pitting Oedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How may you get Biventricular HF?

A
  • Both ventricles are affected.
  • RSHF is often caused by LSHF
  • Inc pulmonary arterial BP makes it harder for the right side to pump blood into pulmonary circulation.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Aetiology of LSHF & RSHF

A

Causes of left-sided HF
- CAD, HTN, valve disease, myocardial disease

Causes of right-sided HF
- LSHF, valve disease, lung disease

Other causes:

  • Dilated CM, hypertrophic CM
  • Renal failure
  • Haemochromatosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Signs and Symptoms of LSHF & RSHF

A

Left Sided HF Symptoms:

  • Dyspnoea
  • Orthopnoea
  • Paroxysmal nocturnal dyspnoea
  • Pink sputum caused by pulmonary oedema.
  • Exercise intolerance

Right Sided HF Symptoms

  • Jugular venous distention
  • Hepatomegaly
  • Ascites
  • GI upset: N+V
  • Pitting Oedema in lower extremities
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe severity of HF using New York Classification

A

(1. ) Class 1 = Heart disease present but no undue dyspnoea from ordinary activity
(2. ) Class 2 = Comfortable at rest, dyspnoea during ordinary activities
(3. ) Class 3 = Less than ordinary activity causes dyspnoea, which is limiting
(4. ) Class 4 = Dyspnoea present at rest, all activity causes discomfort

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Investigations of HF (4)

A

(1. ) Blood tests
- NT-proBNP = High in myocardial stress
- U&Es = electrolyte abnormalities due to fluid overload
- Troponin = if considering recent MI
- Lipids/HbA1c = ischaemic risk profile

(2. ) 12-lead ECG
- Look for ischaemia, MI, ventricular hypertrophy
- A normal ECG makes HF very unlikely

(3.) TTE (1st line imaging) = confirm the presence or absence of LV dysfunction.

(4. ) CXR, ABCDE:
- Alveolar oedema
- Kerley B lines: small, horizontal, peripheral straight lines. Represents interstitial oedema
- Cardiomegaly
- Dilated upper lobe vessels
- Pleural Effusion, blunted costophrenic angles

17
Q

Treatment and Management of chronic HF

A

(1. ) Lifestyle: Fluid + salt restriction, exercise, smoking cessation, reduce alcohol
- Management of co-morbidities
- Vaccination: for influenza and pneumococcal disease.

(2.) Remove any exacerbating factors e.g. NSAIDs (fluid retention), CCB (-ve inotrope)

(3. ) BANDAID2
- Beta-blocker (small + titrate)
- ACEi/ARB
- Nitrate, hydralazine, vasodilators
- Diuretics (loop)
- Aldosterone antagonist
- Ivabradine
- Digoxin = slows HR inc filling
- Devices (CRT, ICD, VAD)

(4. ) Surgery
- Revascularisation - CABG, PCI
- Aortic valve replace/repair
- Heart Transplant (rare and strict criteria)

18
Q

When would you suspect acute HF? And how would it be managed?

A

(1.) Suspect = breathlessness, peripheral oedema, reduced exercise tolerance, fatigue

Mx

(1. ) Stabilise
- Identify and treat underlying cause
- Oxygen, IV diuretics, nitrates

(2. ) Once Stable, if EF >40%:
- loop diuretic
- ACEi or B-blockers
- Aldosterone antagonist