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Year 3 > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

What is cardiac output?

A

Volume of blood pumped per minute, calculated as stroke volume x heart rate, typically around 5l/min.

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2
Q

What is stroke volume a proportion of?

A

End diastolic volume.

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3
Q

What is ejection fraction?

A

Ejection fraction is the volume of blood ejected out of the ventricles calculated by stroke volume/ end diastolic failure. Normal is 55%-70%

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4
Q

Which value for ejection fraction indicates mild left ventricular systolic failure?

A

45-55%

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5
Q

Which value for ejection fraction indicates severe left ventricular systolic failure?

A

Severe LVSD below 35%

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6
Q

What is heart failure?

A

A clinical syndrome where the heart’s pumping capacity reduces, failing to meet the body’s myocardial demand.

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7
Q

What are the common causes of systolic heart failure?

A

Ischaemic heart disease
Chronic hypertension
Dilated cardiomyoapthy
Myocarditis

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8
Q

What are the common causes of diastolic heart failure?

A

Left ventricular hypertrophy
Cardiac tamponade
Fibrosis
Amyloidosis
Sarcoidosis
Haemochromatsois
Valvular disease
Duchenne muscular dystorphy

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9
Q

What is left ventricular systolic dysfunction?

A

Commonly results in systolic heart failure

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10
Q

What are common causes of heart failure?

A
  • Ischaemic heart disease
  • Increased demand due to hypertension
  • Valvular heart disease
  • Metabolic conditions
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11
Q

How is metabolic conditions can lead to heart failure?

A

High demand Oxygen states such as anaemia, thyrotoxicoss or arteriovenous fistulas and Paget’s disease.

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12
Q

Which ventricle is typically affected in heart failure?

A

Left ventricle.

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13
Q

What compensatory mechanisms occur with reduced ejection fraction?

A
  • Increased sympathetic outflow
  • Increased preload
  • Increased venous return
  • Increased peripheral resistance
    Decreased renal blood flow activates the RAAS system causes increased vasoconstriction salt and water retention, resulting in further increase in preload. These occur to maintain arterial blood pressure and tissue perfusion.
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14
Q

How do compensatory mechanisms cause heart?

A

Increased preload overstretches the cardiomycytes, resulting in eccentric hypertrophy that further increases oxygen demand, resulting in dilatation and risk of valvular regurgitation with myocardial ischaemia. Congestion eventually occurs in pulmonary oedema due to high ventricular pressure backflow, resulting in peripheral and alveolar oedema.

Excessive RAAS activation causes left ventricular remodelling with myocardial thinning and fibrosis.

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15
Q

What are common co-morbidities in patients with heart failure?

A

Hypertension and Coronary artery disease - number 1 cause
Diabetes mellitus
Renal impairment - linked to poorer prognsois
COPD- linked to poorer mortality and morbidiity
Anaemia
Gout- worsened with the use of loop diuretics due to dehydration

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16
Q

What factors can worsen heart failure?

A
  • Renal dysfunction
  • Non-compliance to lifestyle changes
  • Infection
  • Embolus
  • Atrial fibrillation
  • Bradycardia
  • Myocardial ischaemia
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17
Q

What does the Frank-Starling mechanism state?

A

Increased end diastolic volume stretches the myocardium, increasing sarcomere length and stroke volume.

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18
Q

What causes an increase in preload?

A

Preload increases with greater blood volume, venous return
Pregnancy, exercise and Excesssive fluid or sodium intake
Arteriovenous fistula
High sympathetic tone.

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19
Q

What are the causes of reduced ejection fraction heart failure?

A

Reduced ejection fraction heart failure is associated with reduced contractility/systolic heart failure due to:
*Coronary artery disease
*Volume overload
* Arrythmias that result in un-coordinated contraction
*Valvular heart disease

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20
Q

What can cause volume overload?

A

Volume overload from valvular disease such as regurgitation or stenosis or dilated cardiomyopathy which weakens the myocardium.

It is commonly idiopathic but can occur due to alcohol toxicity, viral myocarditis or chemotherapeutic drugs like doxorubicin and trastuzumab.

It increases the risk of valvular regurgitation and mural thrombus for emboli event.

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21
Q

What is systolic heart failure associated with?

A

Reduced contractility due to conditions like coronary artery disease or volume overload.

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22
Q

What is systolic heart failure assoicated with?

A

Systolic heart failure is associated with left-sided heart failure and progression to congestive heart failure with pulmonary hypertension. Risk factors include obesity, hypertension, diabetes and renal disease

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23
Q

What are the findings with pulmonary hypertension?

A

Pulmonary hypertension produces a parasternal heave due to right ventricular hypertrophy, loud P2 with splitting due to issues with pulmoanry valve closure, raised JVP, prominent branch vascular markings, cardiomegaly on chest x-ray, opacity at hilum known as bats wing oedema and pleural effusion.

Superior vena cava rises in pressure, causing raised veins
Inferior vena cava rises in pressure to cause pulsatile hepatomegaly due to high stroke volume
Portal vein hypertension, pedal oedema from ankle up and Budd-CHir syndrome

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24
Q

What is the order of CXR findings for

A
  1. Bronchovasuclar markings at apices
    Pulmonary oedema
    Pleural effusions at bases
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25
Q

What is Budd-Chiari syndrome?

A

Budd-Chiari syndrome is a rare condition where hepatic veins are occluded, presenting with a triad of:
->Abdominal pain in right upper quadrant
-> Ascites
-> Hepatomegaly

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26
Q

What are the complications with left sided heart failure?

A

Coarctation of aorta
Aortic stenosis
MI
Mitral regurgitation
Pulmonary fibrosis and hypertension
Tricuspid regurgitation
Budd-CHiari syndrome

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27
Q

What is the first line treatment for stabilised patients with reduced ejection fraction heart failure?

A

ACE inhibitor and Beta blockers are first line treatment once condition has stabilised following haemodynamic stabilisation with intravenous diuretics therapy. ACE inhibitors therapy should start at low dose and titrate upwards
-> sodium, potassium, blood pressure and renal function should be measured before beginning ACE inhibitor and after change in dose
-> once target dose in ACE is reached, monitor treatment monthly for 3 months then at least every 6 months

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28
Q

Which drug is used as an addition for resisting symptomatic REF heart failure?

A

Mineral corticoid receptor antagonists should be in addition to ACE/ARB and beta blockers if there are resisting symptoms which includes spironolactone amiloride and traimterene

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29
Q

What should be used for severe REF heart failure that is worsening?

A

Digoxin is reccomended for worsening severe heart with reduced ejection fraction. It acts by inhibtiing the Na+/K+ ATPase channel which reduces chronotropy and increases inotropy at REST and best for sedentary patients.

It can cause arrythmias and should be avoided with constrictive pericarditis, arrythmias such as bradycardia, heart block, Wolff-Parkinson white and hypertrophic cardiomyopathy.

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30
Q

Which drug should be avoided in systolic heart failure?

A

Calcium channel blockers should be avoided because they depress cardiac function

31
Q

What is preserved ejection fraction associated with?

A

Reduced filling of chambers, known as diastolic heart failure.

32
Q

What are the common causes of preserved ejection fraction heart failure?

A

*Chronic hypertension which results in Ventricular concentric hypertrophy which reduces chamber size for filling
*Aortic stenosis
*Restrictive cardiomyopathy due to fibrosis from scar tissue- associated with amyloidosis or endomyocardial fibrosis.
*Pericardial restriction

33
Q

What are the risk factors for preserved ejection fraction heart failure?

A

Risks factors are more common in the elderly, females and higher prevalence of hypertension, obesity, AFib, COPD and anaemia.

34
Q

What is the pathophysiology of preserved ejection fraction?

A

Impaired ventricular relaxation which results in passive ventricular filling due to increased ventricular stiffness. This increases the end-diastolic pressure of the left ventircle and pulmonary venous pressure that results in dyspnoea and pulmonary oedema. Typically, there is a non-dilated left ventircle and concentric hypertrophy due to pressure overload.

35
Q

What is the management of Preserved ejection fraction heart failure?

A

Intravenous loop Diuretics for symptomatic relief
Aggressive treatment of hypertension with ACE inhibitors/ARBs and beta blockers
Restoration of sinus rhythm and coronary revascularisation

36
Q

What are clinical features of left-sided heart failure?

A
  • Fatigue
  • Oliguria
  • Palpitations
  • Syncope
  • Angina
37
Q

What causes acute heart failure?

A
  • Myocardial infarction
  • Acute valvulopathy
  • Arrhythmias
  • Pulmonary embolism
38
Q

What are clinical signs of acute heart failure?

A
  • Cardiogenic shock, hypotension, poulmonary oedema causing SOB, chest pain and swelling of peripheries causing raised JVP.
    *Dyspnoea
  • Orthopnea
  • Paroxysmal nocturnal dyspnoea
  • Raised JVP
  • Ascites
39
Q

What are the examination findings for acute heart failure?

A

*Crepitations on auscultations due to pulmonary oedema or decreased breath sounds due to pleural effusion
*S3 heart sound due to rapid ventricular filling with dilated cardiomyopathy
*Apex beat displaced
*JVP distention
*Hepatojugualr reflux
*Ascites
*Hypotension and tachycardia as a compensatory mechanism for reduced ventricular function

40
Q

What investigations are used for heart failure?

A
  • 12 lead ECG
  • FBC
  • CXR
  • Echocardiogram
41
Q

What is pro-BNP?

A

Pro-BNP is an inactive peptide released with active BNP hormone
Doppler echocardiogram to investigate cardiac aboramilities

42
Q

What is the management of acute heart failure?

A

*Initial treatment is an Intravenous loop diuretic such as furosemide, bumetanide or torasemide is ideal, even for hypotension patients to relieve congestive symptoms and fluid retention -> Monitor renal function, weight and urine output. It causes activation of RAAS so ACEi should be started

*Oxygen therapy

*Invasive ventilation for severe dyspnoea with pulmonary oedema, respiratory failure or reduced consciousness

*ACE inhibitor and aldosterone antagonist for acute heart failure

43
Q

What are the investigations for chronic heart failure?

A

Assess fluid status, cardiac rhythm, cognitive status and renal function should
Measure BNP and pro-BNP-> higher the level, the worse the prognosis and above 2,000 ng/litre
Transthoracic echocardiograph to examine valves and detect heart shunts
Cardiac MRI
12 lead ECG
FBC for renal, thyroid and liver function, HbA1c
Urinalysis
Peak flow
Transthoracic echocardiograph

44
Q

Which patients typically have low serum natriuretic peptides?

A

Obese individuals
African background
Patients on diuretics beta blockers, ARBs and ACE

45
Q

Which patients have high levels of serum natriuretic peptide?

A

Age over 70
Hypoxaemia from pulmonary embolism
Renal dysfunction
Sepsis
COPD
Liver cirrhosis
Left ventricular hypertrophy

46
Q

What is the use of trans thoracic echocardiograph?

A

Transthoracic echocardiograph may reveal atrial septal defects, valvular pathology, pericardial disease, ischaemic heart disease, hypertrophic cardiomyopathy, pulmonary hypertension or thrombus.

47
Q

What is the role of inotropic drugs in heart failure?

A

To increase the contractility of the heart-> B1 agonist that are anti-vasopressors and reduce after load

48
Q

What are neprilysin inhibitors?

A

Neprilysin inhibitor which prevents the breakdown of natriuretic peptides that promote the antagonism of RAAS for vasodilation, reduced sympathetic tone and reduced aldosterone

49
Q

What should be avoided when using neprilysin inhibitors?

A

ACE inhibitors due to risk of increased bradykinin.

50
Q

When should ACE inhibtiors be avoided?

A

AVOID WITH ANGIOEDEMA, HYPERKALEMIA, HIGH CREATININE OR AORTIC VALVE STENOSIS
Use of neprilysin inhibitors

51
Q

Which AR locker drugs are ideal in heart failure?

A

candesertan and valsartan

52
Q

How do SGLT2 inhibitors improve heart failure?

A

SGLT2 inhibitors reduce preload and after load to prevent cardiac fibrosis

53
Q

How do phosphodiesterase inhibitors work in heart failure?

A

Phosphodiesterase inhibitors prevent the breakdown of cyclic AMP to have inotropic and peripheral vasodilaing effects and reduce peripheral vascular rest.

54
Q

What are common SGLT2 inhibitors used in heart failure management?

A
  • Dapagliflozin
  • Empagliflozin
55
Q

Which drug is reccomended for hypertension in severe heart failure?

A

hydrosalazine are direct vasodilators to treat hypertension. It can improve exercise intolerance however contraindications are symptomatic hypotension, lupus syndrome and severe renal impairment.

56
Q

how does the cardiac cycle affect blood supply?

A

The coronary arteries fill during diastole to supply blood to the heart; in systole, the cardiac arterioles are constricted by the force of the myocardium contracting. However, if heart rate increases, time during diastole decreases, which becomes an issue with tachyarrythmias even with normal coronary arteries. This is worsened if the patient has anaemia and pre-existing CAD.

57
Q

Where does ischaemia begin?

A

The subendocardium has little blood supply at peak systole, which makes it vulnerable to ischaemia. Infarction begins in the subendocardium and extends towards the epicardium.

58
Q

What are the contraindications for beta blockers?

A
  • Bradycardia
  • Symptomatic hypotension
  • Issues with asthma
  • Sexual dysfunction
59
Q

What is the effect of diuretics in heart failure?

A

Provide symptomatic relief but only mineralocorticoid antagonists provide prognostic benefit.

60
Q

What is the significance of Pouiselle’s law in heart failure?

A

Reduced diameterOf blood vessels increases resistance by 16 fold.

61
Q

What is the typical blood supply for the inferior wall of the heart?

A

Majority by the posterior descending artery and a minority by circumflex.

62
Q

What is heart transplantation contraindicated in?

A
  • Persistent alcohol/drug abuse
  • Cancer with less than 5 years follow-up
  • Systemic multi-organ involvement disease
63
Q

What is a clinical feature of acute heart failure?

A

Cardiogenic shock.

64
Q

What can cause myocardial ischaemia during peak systole?

A

Vulnerability of the subendocardium.

65
Q

What is the typical management for heart failure with normal ejection fraction?

A
  • Management of hypertension
  • Management of diabetes
  • Diuretics for fluid overload
66
Q

Which parasitic disease can cause heart failure?

A

Chagas’ disease is an infection caused by the parasite trypanosomiasis Cruz which causes inflammation of the myocardium producing fibrosis and remodelling, resulting in dilated cardiomyopathy with heart failure and reduced ejection fraction.

67
Q

What worsens heart failure?

A

Heart failure can be worsened with poor diet high in salt and fats, smoking, cocaine and heavy alcohol use
Lung disease, non-compliance, renal dysfunction, anaemia, pulmonary embolus
NSAIDs like.Aspirin due to impairing renal function and leading to water and sodium retention
Infections such as HIV
Calcium channel blockers for systolic heart failure

68
Q

What is CRT?

A

CRT is cardiac re synchronisation therapy, ideally with a biventricular pacemaker,

69
Q

What is CRT-P?

A

CRT-P is a three lead pacemaker used to treat heart failure with a malignant tachyarrythmia

70
Q

What is CRT-D?

A

CRT-D invovles the use of a pacemaker and implantable cardioevrter defibrillator (ICD) for those with risk of sudden cardiac death, for patients with bradycardia or malignant tachyarrythmia. There is a greater risk with ICD because the lead is against the right ventricle, which has a thinner wall.

71
Q

What are the risks with CRT?

A

Risks of CRT are infection, haematoma, collapsed lung and hole in heart chamber and pneumothorax.

72
Q

What is AAI?

A

AAI is a single lead device which inhibits atrial impulses by sensing the atrial rate when required.

73
Q

What is VVI?

A

VVI is a single lead device and pacemaker which inhibits ventricular impulses by sensing the atrial rate when required.

74
Q

What is DDI?

A

DDI is a single lead device and pacemaker which inhibits atria and ventricular impulses by sensing abnormal pulses.

Year 3 (38 decks)

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