Cardiac failure Flashcards

1
Q

What is heart failure?

A

Inability of CO to meet the body’s demands without increasing DBP.

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2
Q

What is the aetiology of heart failure?

A
  • LOW OUTPUT (decreased CO):
  • Left heart failure: IHD, hypertension, cardiomyopathy, aortic valve disease, mitral regurgitation
  • Right heart failure: secondary to LHF, IHD, pulmonary hypertension, cardiomyopathy, pulmonary valve disease, tricuspid regurgitation, PE, chronic lung disease, constrictive pericarditis
  • Bi ventricular failure: arrythmia, cardiomyopathy, myocarditis, drug toxicity
  • HIGH OUTPUT (increased demand):
  • Anaemia, beriberi, septicaemia, pregnancy, Paget’s disease, hyperthyroidism, arteriovenous malformation
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3
Q

What are the different types of heart failure? (x2)

A

Acute (rapid onset or worsening of symptoms/signs of heart failure), chronic

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4
Q

How is heart failure classified based on ejection fraction? Interpretation?

A
  • HF with reduced ejection fraction (HFrEF): LVEF less than 40%
  • HF with mid-range ejection fraction (HFmrEF): LVEF between 40% and 49%
  • HF with preserved ejection fraction (HFpEF): LVEF over 50%
  • If there is reduced ejection fraction, the heart failure is because of DIASTOLIC dysfunction i.e., there is decreased compliance leading to restrictive filling defect. If ejection fraction is preserved, there is SYSTOLIC dysfunction.
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5
Q

What is ejection fraction and its normal value?

A

Usually at least 60%. It is a measure of SV/EDV (not ESV).

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6
Q

What is the pathophysiology of heart failure?

A
  • INITIALLY or ACUTELY: there is compensatory activation of SNS which leads to tachycardia, increased contractility, and increased myocardial O2 consumption. There is also RAAS activation with retention of water and salt
  • There is also neurohormonal vasoconstriction leading to hypertension, increased myocardial wall stress, and decreased renal perfusion
  • Sustained SNS activation leads to ventricular remodelling which also potentiates SNS activation
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7
Q

What are the risk factors of heart failure?

A

CVS disease, old age, diabetes, FH, smoking, hypertension, chemotherapy.

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8
Q

What is the epidemiology of heart failure: Age?

A

10% of over 65-year-olds.

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9
Q

What are the signs and symptoms of left heart failure?

A
  • ACUTE: tachycardia, S3 (rapid ventricular filling in diastole), cyanosis, peripheral shutdown, pulsus alternans, pulmonary congestion
  • PULMONARY CONGESTION: tachypnoea, orthopnoea, paroxysmal nocturnal dyspnoea, wheeze (cardiac asthma), pink frothy sputum, fine crackles throughout lung
  • CARDIOMYOPATHY: displaced apex beat (but also common sign of ACUTE heart failure)
  • Pansystolic murmur (functional mitral regurgitation from increasing volume overload on the left ventricle)
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10
Q

What are the signs and symptoms of right heart failure?

A
  • SYSTEMIC CONGESTION: raised JVP, hepatomegaly, ascites, ankle/sacral pitting, oedema
  • Signs of functional tricuspid regurgitation
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11
Q

What is pulsus alternans?

A

Highly specific for LHF and describes arterial pulse waveform showing alternating strong and weak pulses.

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12
Q

What happens to BP in heart failure?

A

Preserved or raised.

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13
Q

What happens to ejection fraction in heart failure?

A

Reduced or preserved.

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14
Q

! What are the investigations for heart failure? (x5)

A
  • First investigations, echo and ECG, then always order CXR and bloods. Best test for chronic is echocardiogram – other investigations are good only for first presentation
  • ECG: may have ischaemic changes, arrythmia
  • ECHOCARDIOGRAM: assess ventricular contraction and LV-ejection fraction. This determines treatment
  • BLOODS: NT-proBNP, BNP (raised in acute heart failure, but also ACS, myocarditis, PE), high troponin. FBC, TFTs, HbA1c for aetiology, U&Es for baseline, LFTs and CRP for complications
  • CXR
  • ABG: if patient in cardiogenic shock
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15
Q

What are the signs of heart failure in a CXR? (x5)

A
  • A - alveolar oedema (bat wing opacities – pattern of bilateral pulmonary oedema)
  • B - Kerley B lines
  • C - cardiomegaly
  • D - dilated upper lobe vessels (congestion falls to bases, resulting in engorgement of pulmonary vessels at the apex)
  • E - pleural effusion
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16
Q

What are Kerley B lines?

A

Thin lines 1-2 cm in length in the periphery of the lung(s). They are perpendicular to the pleural surface and extend out. They represent thickened subpleural interlobular septa and are usually seen at the lung bases.

17
Q

What additional investigations are there for chronic heart failure? (x2)

A
  • Exercise stress testing
  • Swan-Ganz catheter: allows measurements of RA, RV, pulmonary artery, pulmonary wedge and LV end-diastolic pressures
18
Q

How is acute LVF managed? (x3)

A
  • CARDIOGENIC SHOCK: inotrope (increases contractility e.g., dopamine, dobutamine, digoxin) and/or vasopressor (raise BP e.g., dobutamine, dopamine)
  • PULMONARY OEDEMA: sit up patient, administer oxygen and consider CPAP. Can also be treated with diamorphine (venodilator and later diuretic effect), GTN infusion (decreases preload), IV furosemide (venodilator and later diuretic effect)
  • TREAT CAUSE
19
Q

How is chronic LVF managed medically? (x7)

A
  • TREAT CAUSE
  • ACEi (enalapril, perindopril): inhibit intracardiac RAAS which contributes to remodelling
  • B-blockers (bisoprolol, carvedilol): block the effects of chronically activated SNS and therefore slow heart failure progression
  • LOOP DIURETICS (furosemide): correct fluid overload
  • ALDOSTERONE ANTAGONISTS (spironolactone): correct fluid overload
  • ARBs: may be added to ACEi
  • HYDRALAZINE and a NITRATE: may be added to ACEi
  • DIGOXIN: positive inotrope to reduce hospitalisation
20
Q

How is chronic LVF managed surgically?

A

Cardiac resynchronisation therapy: biventricular pacing with moderate to severe HF despite medical management. Patients are also candidates for implantable cardiac defibrillator.

21
Q

What are the complications of heart failure?

A

Respiratory failure, cardiogenic shock, death.

22
Q

Why are patients with heart failure given beta-blockers? (x2)

A

Beta blockers decrease HR, so more time is spent between each heartbeat in DIASTOLE. Only in diastole are the coronary arteries perfused, so beta blockers increase coronary artery blood flow. IN ADDITION, beta blockers increase the duration of systole. When you have aortic stenosis, less blood can pass through the aortic valve, so increased length of systole (which also causes decreased HR) gives more time for blood to be pumped through the aortic valve.