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- Y6 Cardiovascular > Cardiac failure (acute and chronic) > Flashcards

Cardiac failure (acute and chronic) Flashcards

1
Q

What are the different types of heart failure?

A

HFrEF = heart failure with reduced ejection fraction

HFpEF - heart failure preserved ejection fraction

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2
Q

Define HF.

What is the CO equation?

A

The failure of the heart to maintain the cardiac output (CO) needed to meet the body’s requirements

CO= HR x SV

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3
Q

How common is HF?

A

Incidence increases rapidly with advanced age:

  • -1-2% of those <70 yrs
  • -10-20% of those > 70 years
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4
Q

Define chronic HF.

A

A long-term condition in which the heart fails to maintain an adequate circulation for the needs of the body.

  • Develops and progresses slowly
  • Can have periods of acute decompensation
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5
Q

Define acute HF.

A

Rapid onset or worsening of symptoms & signs of HF, requiring urgent treatment and evaluation.

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6
Q

What is the pathophysiology of HF?

A

SNS –> increased HR and SV –> increased CO

Long term activation of SNS can have a -ve effect =increased wall stress, dilation, ventricular remodelling –> disease progression and further SNS activation

Left ventricular remodelling = change in ventricular size, shape, function which could be due to MI, HTN, cardiomyopathy, valvular disease.

Hallmarks include hypertrophy, loss of myocytes and interstitial fibrosis –> left ventricle dilates, assuming more globular shape –> mitral regurgitation

MR –> increasing volume overload and progresison of HF

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7
Q

What is the difference between high and low output cardiac failure and which is more common?

A

Low output HF - CO is reduced and fails to increase normally with exertion - MORE COMMON

High output HF - CO is normal but you have increased need (e.g. hyperthyroidism, pregnancy). HF occurs when heart fails to meet those increased needs (heart is overworked)

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8
Q

What is congestive heart failure?

A

When RHF and LHF occur together.

CCF is a term used for patients who are breathless with oedema due to abnormal salt and water retention (signs of LVF and RVF)

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9
Q

What is the aetiology of left heart failure? (reduced CO state)

A

1)Valvular:

  • Aortic stenosis,
  • Aortic Regurgitation
  • Mitral Regurgitation

2) Heart Muscle:

  • Ischaemic Heart Disease
  • Cardiomyopathy
  • Myocarditis
  • Arrhythmias (AF)
  • Congenital
  • Pericardial

3) Systemic:

  • Hypertension,
  • Amyloidosis
  • Drugs (e.g. cocaine, alcohol, BBs*, chemotherapeutics - eg doxorubicin
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10
Q

How does aortic stenosis contribute to LHF?

A

Aortic stenosis → causes excessive afterload as ventricle has to push harder to eject blood.

(NB: afterload = the pressure the heart must work against to eject blood during systole)

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11
Q

How does aortic regurgitation cause LHF?

A

Aortic regurgitation: There is increased pressure in the LV due to the regurgitant blood form the aorta to the LV (the LV in addition to having to pump the normal volume of blood, has to pump the regurgitant blood as well).

These changes lead to cardiac remodeling (dilatation, hypertrophy) leading to heart failure.

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12
Q

How does mitral regurgitation cause LHF?

A

Mitral regurgitation: If significant (moderate to severe) MR is present, the LV must work harder to keep up with the body’s demands for oxygenated blood.

Over time, the heart muscle and circulatory system undergo a series of changes to maintain this increased demand – due to mechanical overload the LV overtime can become, hypertrophied, fibrotic, dilated and scarred, ending up with an impaired myocardial function.

This can lead to LHF (mitral regurgitation increases preload)

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13
Q

How does hypertension cause LHF?

A

Hypertension: increases afterload. LV has to push harder in order to push blood against high systemic pressures. This over time puts strain in the LV leading to LHF.

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14
Q

How does amyloidosis cause LHF?

A

Amyloidosis: In amyloidosis, an abnormal protein called amyloid builds-up in tissues and organs. If amyloid gets deposited in the heart, the heart becomes increasingly stiff and eventually the pumping function deteriorates.

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15
Q

Why can beta blockers exacerbate HF?

A

BBs can exacerbate the HF, bc they have negative chronotropic and inotropic effects –> symptomatic hypotension and acute decompensated HF

But selective beta1‐blockers or non‐selective combined alpha‐ and beta‐blockers are now a part of the standard treatment of heart failure since a number of trials showed beneficial effects

metoprolol, bisoprolol, or carvedilol

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16
Q

What is the aetiology of RHF? (reduced CO state)

A

1) LHF
2) Lungs:

  • Pulmonary HTN (can lead to cor pulmonale)
  • PE
  • Chronic Lung Disease (interstitial lung disease, pulmonary fibrosis, cystic fibrosis)

3) Heart valves:

  • TR
  • Pulmonary valve Disease
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17
Q

How does pulmonary hypertension cause RHF?

A

Heart cannot pump to the stiffened pulmonary arterial vessels. So RV needs to work harder, becomes enlarged and weakened.

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18
Q

How does chronic lung disease cause RHF?

A

Chronic lung disease can result in chronic hypoxia: The pulmonary vasculature results to chronic hypoxia by vasoconstriction.

This increases vascular resistance and and results in increased pulmonary arterial pressure. The right heart reacts to this by remodelling (hypertrophy and dilatation). Over time it can lead to RHF.

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19
Q

What is the aetiology of high output HF?

A

Caused by conditions that require a ↑ CO and put strain on the heart.

2 things that medical students need to deal with a high output state: NAP MEALS

  • Nutritional (B1: thiamine)
  • Anaemia
  • Pregnancy
  • Malignancy (multiple myeloma)
  • Endocrine (hyperthyroidism)
  • AV malformations
  • Liver cirrhosis
  • Sepsis

High output HF initially presents with RHF then LHF

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20
Q

What are the signs and symptoms of LHF vs RHF?

A

LHF: respiratory symptoms due to fluid accumulation in the lungs

RHF: symptoms due to fluid accumulation in the periphery

  • So since the LV pumps the blood coming from the lungs to the rest of the body, if the LV fails fluid will accumulate into the lungs causing symptoms*
  • Accordingly, if the RV that pumps blood coming from the peripheries fails, fluid will accumulate in the periphery.*
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21
Q

What are the symptoms of LHF? What are the signs?

A

Symptoms:

  • Exertional dyspnea
  • Orthopnoea (SOB when lying flat)
  • Paroxysmal nocturnal dyspnea – PND (attacks of SOB at night)
  • Fatigue
  • Nocturnal Cough (+/- pink frothy sputum)
  • Wheeze

Signs:

Heart:

  • ↑HR, ↑RR
  • Irregularly Irregular heart beat (AF often co-exists)
  • Pulsus alternans- alternating strong and weak pulses
  • Displaced apex beat
  • S3 Gallop rhythm
  • S4 in severe HF
  • Murmur (AS, MR, AR)

Lungs:

  • Fine end-inspiratory crackles at lung bases (pulmonary oedema)
  • Wheeze (cardiac asthma)
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22
Q

What is the reason for S4 heart sounds?

A

Poor compliance of the ventricle – compliance against a stiff ventricle

23
Q

What are the signs and symptoms of RHF?

A

Symptoms:

  • Swelling (ankles, facial engorgement, ascites)
  • Weight gain (due to oedema)
  • Fatigue
  • Reduced exercise tolerance
  • Anorexia
  • Nausea
  • Nocturia - as fluid returns as patient lies down

Signs:

  • Face: face swelling
  • Neck: ↑JVP
  • Heart/Chest: TR murmur, ↑HR, ↑RR
  • Abdomen: Ascites, hepatomegaly
  • Other: pitting oedema in ankles & sacrum
24
Q

Name 3 differentials for a raised JVP.

A

1) RHF
2) Tricuspid regurgitation
3) Constrictive pericarditis

25
Q

What are the investigations for HF?

A

Bedside: ECG

Bloods: FBC*, U&Es, LFTs, TFTs, BNP (sensitive but non-specific) - check for abdo congestion and hypo/hyperthyroidism

Imaging: CXR, TTE

If BNP is raised –> thransthoracic echocardiogram (if not then HF is unlikely). BNP is used to exclude HF.

Anaemia and high lymphocyte counts are strong RF and prognostic factors of poor survival.

26
Q

What causes BNP release?

A

Cardiac hormone secreted by cardiomyocytes in response to stretching caused by increased ventricular volume.

Its physiologic effects include reduction in renal sodium reabsorption, which in turn lead to reduction in circulating blood volume.

Non-cardiac - PE, COPD

27
Q

What does TTE show in HF?

A

HFpEF= inability of the ventricle to relax and fill normally (EF > 50%). Basically you font get pump blood bc the heart doesn’t relax, so even if the proportion of blood you are sending is fine, the total amount of blood going out isn’t fine.

28
Q

What are the features of HF on X ray?

A
  1. Alveolar oedema
  2. B-lines (kerley)
  3. Cardiomegaly
  4. Dilated upper lobe vessels
  5. Effusion (pleural, transudative)

ABCDE

29
Q

What is the clinical diagnostic criteria used for heart failure?

A

Framingham Criteria: 2+ major, OR 1 major and 2 minor

Major:

  • Paroxysmal nocturnal dyspnoea
  • Bibasal Crepitations
  • S3 gallop
  • Cardiomegaly
  • Increased central venous Pressure
  • Weight loss
  • Neck vein distension
  • Acute pulm oedema
  • Hepatojugular reflux

Minor

  • bilateral ankle oedema
  • dyspnoea on ordinary exertion
  • tachycardia
  • decrease in vital capacity by 1/3
  • nocturnal cough
  • hepatomegaly
  • pleural effusion
30
Q

How do you manage HF conservatively?

A

Smoking cessation, weight management (exercise), diet (reduce salt intake )

31
Q

How do you manage HF medically?

A
  • ACEi (enalapril):
    • ALL pts with LV dysfunction
    • improves survival and slows progression.
  • BBs (carvedilol, bisoprolol):
    • reduce O2 demand
    • for ALL patients with CHF once established on ACEi – improve survival & synergistic effects with ACEi.
  • Diuretics (furosemide, chlorothiazide, spironolactone):
    • use if fluid retention,
    • monitor electrolytes (spironolactone can cause hyperkalaemia)
  • Digoxin:
    • +inotrope (increases heart contractility),
    • helps improve symptoms but does NOT increase overall survival.

Other: hydralazine nitrate, cardiac resynchronization, implantable cardiac defibrillator TREAT THE CAUSE

32
Q

If ACE inhibitors are not tolerated which drugs would you give?

A

ARBs (eg losartan)

33
Q

Which of the medical treatments does not improve prognosis in HF?

A

Furosemide (diuretics)

34
Q
A
35
Q

What is the aetiology of acute HF?

A

1) Decompensation of previous chronic HF
2) Acute Coronary Syndrome

* Factors that can lead to acute decompensation include: MI, Arrhythmias, Infection, Hypo/hyperthyroidism, Uncontrolled HTN

36
Q

How does acute HF present? (history and examination)

A

Signs and Symptoms due to fluid congestion in various organs. Presentation similar to chronic, but ACUTE onset and the patient is really UNWELL (struggling to breath)

Symptoms:

  • Dyspnoea
  • Cough
  • Wheeze
  • Pink frothy sputum
  • Swelling of the legs
  • Symptoms of the underlying condition

Examination:

  • ↑HR, ↑RR
  • Pulsus alternans
  • Cyanosis
  • Peripheral shutdown
  • S3 gallop rhythm
  • Fine end inspiratory crackles
37
Q

How do you manage acute HF?

A

ABCDE - medical emergency

  1. Sit patient up
  2. High-glow Oxygen via non rebreathe mask (Target SpO2 = 94-98%)
  3. Furosemide 40-80mg IV over 10mins
  4. GTN infusion/oral - evidence of pulmonary oedema AND SBP > 90mmHg)
  5. IV or IM morphine 2-5mg over 2mins (+ antiemetic)
  6. Consider CPAP (if sats are dropping)
  7. Treat cardiogenic shock if BP < 90mmHg with positive inotropes (e.g. dobutamine)
38
Q

How does CPAP work in HF?

A

CPAP: improves ventilation by recruiting more alveoli, driving fluid out of alveolar spaces and into vasculature. CPAP provides continuous positive airway pressure throughout the breathing cycle - same pressure when breathing in and out

39
Q

What are the complications of HF? What is the prognosis?

A

Complications:

  • Pleural effusion
  • Renal failure (long standing HF can lead to hypoperfusion)
  • Acute exacerbations
  • Death

Prognosis:

  • 50% of severe HF pts die within 2 years
  • In AHF, in hospital mortality: 2-20%
40
Q

A 67-year-old woman presents to her GP complaining of increasing shortness of breath, which becomes worse when trying to sleep. She has a history of hypertension and hyperlipidaemia. On examination, her blood pressure is 148/83 mmHg and heart rate is 126 beats per minute. There is an audible S3 gallop and the jugular venous pressure is elevated 3 cm above normal.

Which investigation would be best to confirm the diagnosis?

  • A.ECG
  • B.Brain natriuretic peptide (BNP)
  • C.Endothelin levels
  • D.Echocardiogram
  • E.CXR
A

D

A.ECG - Not diagnostic

B.Brain natriuretic peptide (BNP) - Used to exclude HF but not diagnostic as it is sensitive and not specific

C.Endothelin levels - It is raised in HF, and is associated with poor prognosis but it is not diagnostic

D.Echocardiogram

E.CXR - Not diagnostic

41
Q

A 62 year old man, 3 months after an MI presents with increasing shortness of breath. He is currently on aspirin, atenolol and simvastatin. An echocardiogram shows an ejection fraction of 30% in the left ventricle. What additional medication should he be given?

  • A.Carvedilol
  • B.Furosemide
  • C.Digoxin
  • D.Enalapril
  • E.Morphine
A

D

  • A.Carvedilol - This is a BB – She is already on a BB
  • B.Furosemide - This is a loop diuretic – important in the management of acute HF. Also given in chronic HF is signs of fluid retention
  • C.Digoxin - Can be given in chronic HF but not first line
  • D.Enalapril
  • E.Morphine - Opiates can be given in acute HF but not used routinely anymore
42
Q

What signs of acute pulmonary oedema can be seen here?

A
  • Cardiomegaly
  • Prominent upper lobe veins
  • Diffuse interstitial shadowing
  • Classic perihilar “bat wings” shadowing
43
Q

Why shouls you avoid CCBs in the acute setting?

A

They have a negative ionotropic effect

44
Q

What is cardiogenic shock?

A

AKA circulatory collapse

i.e. poor peripheral perfusion, oliguria, hypotension

45
Q

Which high output states can cause heart failure?

A
  • Anaemia
  • Thyrotoxicosis
  • Pregnancy
  • AV shunts
  • Beri-beri
  • Paget’s disease
  • Nephritis
  • Septicaemia
46
Q

What are the lifestyle management options for HF?

A

Limit/avoid alcohol

Stop smoking

Encourage exercise

Check drugs prescribed and taken - treat hypertension, lipids, arrhythmias

Reduce salt intake

Flu immunisation

47
Q

Why is furosemide given over 10mins in acute HF?

A

Prevents ototoxicity

48
Q

What is the first management step?

Patient post primary-angioplasty/PCI is breathless and has BP of 80/50. His CXR is shown below.

A

CPAP - this pushes fluid back into the vasculature so that any diuretics to be given afterwards will not cause further hypotension.

49
Q

What BNP levels make HF unlikely?

A

Serum BNP<100 pg/ml (29 pmol/litre)

OR NT-proBNP <400 pg/ml (47 pmol/litre)

50
Q

Describe the NYHA classification of heart failure.

A

Class 1: No limitation of physical activities

Class 2: Slight limitation of physical activity in which ordinary physical activity leads to fatigue, palpitation, dyspnea, or anginal pain; the person is comfortable at rest

Class 3: Marked limitation of physical activity in which less-than-ordinary activity results in fatigue, palpitation, dyspnea, or anginal pain; the person is comfortable at rest

Class 4: Inability to carry on any physical activity without discomfort but also symptoms of heart failure or the anginal syndrome even at rest, with increased discomfort if any physical activity is undertaken

51
Q

What are the signs/symptoms of heart failure from early to late signs?

A

Tachycardia initially → pulmonary oedema late

52
Q

What is cardiogenic shock?

A

Failure to perfuse even the heart and brain

Treated with dobutamine (analogue of dopamine only having the middle function of the ones below) - still has high mortality

53
Q

What are the causes of apex displacement?

A

- Y6 Cardiovascular (47 decks)

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