Heart Failure Flashcards

1
Q

Define heart failure

A

A progressive clinical syndrome resulting from a structural and/or function abnormality that results in an insufficient cardiac output and/or raised intracardiac pressure at exercise and/or rest

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2
Q

What are the different categories of heart failure based on heart function?

A

HFrEF - EF less or equal to 50%
HFmrEF - EF 41 to 49%
HFpEF - EF greater than or equal to 50%.

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3
Q

What is the key physiology of HF with a reduced ejection fraction?

A

Left ventricle is weakened
Results in poor contractility
Reduced SV-> red CO
This activates compensatory mechanisms such as RAAS/sympathetic system
This can increase preload and afterload - initially compensates, eventually inc workload becomes pathological,

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4
Q

What is the key physiology of heart failure with a preserved ejection fraction?

A

Normal contractility
Impaired relaxation leading to impaired ventricular filling during diastole (diastole dysfuncatoin)
Preserved ejection fraction but reduced SV (due to reduced EDV)
This leads to lower cardiac output and increased filling pressures.

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5
Q

What are the three kay factors affecting heart function?

A

Preload (EDV) - amount in LV before contraction
Afterload (SVR) - resistance/force LV works against to push blood out of the heart - vol in systemic circulation and level of bv constriction
Contractility.

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6
Q

What is the basic pathophysiology underpinning heart failure?

A
  1. damage to mycocardium/heart funcation - leads to reduced cardiac output
  2. Actives compensatory mechanisms of RAAS (red renal perfusion) and SANS (hypotensive)
  3. These compensatory mechanisms are initially beneficial then becomes maladaptive
  4. Result in inc SVR, inc HR, in contractility inc Na+ and water retention -> inc venous return in theory in CO
  5. inc afterload and inc preload
  6. However, increased cardiac work, leads to increased energy consumption
  7. Leads to structural remodelling/myocyte damage of the heart, exacerbates functional impairement
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7
Q

How does adrenergic activation lead to myocyte damage in HF?

A

Directly by cardiotoxicity
indirect by inc HR/contractility - leading to inc cardiac work

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8
Q

What are the signs/symptoms of right sides heart failure?

A

Elevated JVP, pos hepatojugular reflex
Hepatomegaly - enlarged palpable tender liver, nutmeg liver.
Ascities
Excessive nocturnal urination
Peripheral oedema start in ankles and work up (may also have sacral oedema. present as weight gain)
Reduced exercise tolerance
May present with tachycardia and hypertension

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9
Q

What are the signs and symptoms of left-sided heart failure?

A

Pulmonary oedema/congestion = SOB, PND, orthopnoea, basal crackles on auscultation, dull on percussion (indicates effusion)
Reduced exercise tolerance, chronic cough
May present with tachycardia and hypertension

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10
Q

What are the modifiable risk factors for Heart failure?

A

HTN
Smoking
Obesity
Sedentary lifestyle
Cocaine use
Heavy alcohol use

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11
Q

What are the non-modifiable risk factors for heart failure?

A

Age
Sex = male
Family history (congenital cardiomyopathies) - particualrly sudden cardiac death in below <60yrs
Serious lung/heart conditions - COPD
Black and African American.
Thyroid abnormalities.

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12
Q

What are the three main causes of heart failure?

A
  1. Ischemic heart disease (35-40%)
  2. Cardiomyopathy-dilated (30-34%)
  3. HTN (12-20%)
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13
Q

What pathophysiological changes may occur in Heart Failure?

A

Ventricular Dilation
Myocyte hypertrophy
Increased collagen synthesis
Altered myosin gene expression
Altered sarcoplasmic Ca2+ ATP density
Increased ANP secretion
Salt and water retention
Sympathetic stimulation
Peripheral vaosconstrication.

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14
Q

What bedside investigation should be done for suspected heart failure?
What results would you expect to see?

A

ECG - left/right venetricular hypertrophy, ACS
Obs - high HR, high RR, low O2 sats, temp - may be normal, high BP
Resp exam - basal crackles, peripheral oedema, sacral odema
Cardio exam - gallop rhythm, raised JVP, displaced apex beat, ventricular heave. murmurs

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15
Q

What bloods should you do for suspected heart failure?
What would you expect to see?

A

FBC - check for anemia exaggerating symptoms
LFTs
U&Es - baseline for before drug treatment
CRP
troponin - elevated
BNP - elevated
Thyroid function
HbA1C
Lipid Profile
Cardiomyopathy screen

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16
Q

What imaging investigations should be done for suspected heart failure?
What should you expect to see?

A

CXR - cardiomegaly
Echo/stress echo - measure EF, changes in structure
Lung function test - exclude lung pathology
Nuclear cardiology
Cardiac MRI - myocardial fibrosis, amyloidosis, myocarditis ect
Coronary angiogram
Cardiac biospy
Cardiopulmonary execsise testing
Ambulatoragy 24hrs ECG.

17
Q

What are the three key diagnostic tests in heart failure?

A

NTproBNP
CXR
Echo
ECG

18
Q

What plan should be taken based on the NT-pro-BNP level for patients with suspected heart failure?

A

NT-pro-BNP above 2000ng/L refer urgently to specialist for 2ww echo
400-2000ng/L specialist and each within 6 weeks
less than 400 ng/L HF is less likely, discuss with speciality is suspicion persists.

19
Q

What are the different severity/functional ratings of breathlesslness/symptoms related to heart failure?
NYHA classification

A

symptoms = SOB, fatigue or palpitations
Class 1 - no limitation on activity
Class 2 - comofortable at rest but symptomatic with ordinary activities
Class 3 - comfortable at rest but symptomatic with any activity
Class 4 - symptomatic at rest.

20
Q

What are the five principles of management for heart failure?

A

RAMPS
Refer to cardiology
Advise them about the conditions
Medical treatment
Procedural or surgical interventions
Specialist heart failure MDT input such as heart failure specialist nurses.

20
Q

What conservative management should be given for heart failure?

A

Referal to cardiology
Heart failure follow up (community) and liason during hospital admission.
Weight management
Flu, covid and pneumococcal vaccines
Stop smoking
Reduce alcohol intake
Salt + fluid restriction
Optimise treatment of co-morbidities
Written care plan
Cardiac rehabilitation (personalised exercise program)

21
Q

What is the first-line medical treatment of chronic heart failure?

A

ABAL

ACE inhibitor - ramipril - may use ARB instead if not tolerated or valvular heart disease.
Beta blocker - bisporolol
Aldosterone antagonist (if A and B not controlled) spironolcatone or eplernone, not if reduced ejection fraction
Loop diuretics - furosemide or butmetanide.

22
Q

Why must U&Es be monitored in a patient being treated for heart failure?

A

Diuretics, ACEi and Aldosterone antagonists can cause electrolyte disturbance - hyperkalemia (can be fatal)
Risk of renal dysfuncation

23
Q

What additional specialist medical treatment may be used in patients with heart failure?

A

SGLT2 inhibitor (dapagliflozin)
Sacubitril with valsartan (ARNI)
Ivabradine (funny current channel inhibitor)
Hydralazine with a nitrate (reduce Ca2+ in the smooth muscle)
Digoxin (Sodium Potassium ATPase inhibitor)

24
Q

What surgical interventions may be considered in a patient with heart failure?

A

Implantable cardioverter defibrillators - monitor heart, apply defib shock to return sinus rhythm if enter shockable rhythm (commonly for patients with previous V.tach or ventricular fibrillation)
Cardiac resynchronization therapy - EJ <35%, synchronise contraction in RA, RV and LV to optimse heart function
Heart transplant - in suitable patients with severe disease.
Valve disease repair
Coronary stenting or bypass

25
Q

What is the key cardiac physiology?

A

Pulmonary circulation – low pressure system taking deoxygenated blood from the body, through the right heart, to the lungs to oxygenate
Systemic circulation- high pressure system to take oxygenated blood from the left heart to the body to oxygenate cells
Left ventricle wall 3x thicker than right for this reason

26
Q

Describe what happens in systole

A

Atrial relaxation + ventricular contraction
Semilunar valves (aortic + pulmonary) open
Blood pushed out of ventricles and out of the heart under high pressure

27
Q

Describe what happens in diastole

A

Atrial contraction + ventricular relaxation
Atrioventricular valves (mitral + tricuspid) open
Blood pushed out of atria under low pressure to fill ventricles

28
Q

Define cardiac ouput

A

Litres of blood pumped by the heart per minute (L/min)
HR*SV

29
Q

What is the Frank Starling Mechanism of the heart?

A

larger venous return -> larger LV myocrdial strecth -> inc LV contractility -> higher cardiac ouput

30
Q

What type of heart failure does AF typically lead to?

A

HFrEF
Often due to difficuluties with ventricular filling and contraction

31
Q

What is the basic pathophysiology underpinning left sided heart failure?

A

Impaired LV funcation
Backlog of blood waiting to be pumped from the heart
Increased blood volume and pressure in the LA, pulmonary veins and lungs.
Leakage of fluid into lungs and surrounding tissues
Pulmonary oedema and associated symptoms

32
Q

What is the basic pathophysiology of right sided heart failure?

A

Right hear strain
Backlog of and increaed volume of blood throughout the body
Fluid leaks into peripheral tissues
Peripheral oedema + associated symptoms

33
Q

What are the five different categories of causes of heart failure?

A

Ischaemic heart disease
HTN
Cardiomyopathies
Valvular heart disease e.g aortic stenosis
Arrhythmias (atrial fibrillation)

34
Q

What is the gold standard tool for assessing cardiac function?

A

Cardiac MRI - although rarely used in clinical practice, only if echo images are insufficient.

35
Q

What are the signs of heart faillure on a CXR?

A

Alveolar oedema (bat wing opacification)
Kerley B lines
Cardiomegaly
Dilated Upper lobe vessels
Pleural effusions

(ABCDE)

36
Q

What is the acute management for heart failure?

A

High dose diurectics
Fluid restriction
Daily weight
Daily U&Es

37
Q

What is the purppse of the different drugs used in heart failure? (ABAL)

A

ACEi - improve ventricular function and reduce mortality
Beta blocker - reduce HR/myocardium O2 demand/RAAS activation
ARB - sodium diuresis to decrease afterload
Loop diuretic - symptomatic relief from fluid overload

38
Q
A