Heart Failure Flashcards

1
Q

What is heart failure?

A

HF is a clinical syndrome with current or prior symptoms and signs caused by a structural and/or functional cardiac abnormality and corroborated by at least on of the following:

  • Elevated natriuretic peptide levels
  • Objective evidence of cardiogenic pulmonary or systemic congestion by diagnostic modalities such as imaging or hemodynamic measurement at rest or with provocation
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2
Q

Heart failure with reduced EF (HFrEF)

  • Ejection fraction
  • Features
  • Causes
A

EF <40% (systolic HF: inability of ventricle to contract normally)

Causes:

  • Ischemic heart disease, AMI
  • Cardiomyopathy
  • Mitral regurgitation

Features:

  • LV dilatation
  • Globular shape
  • Systolic LV dysfunction
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3
Q

Heart failure with preserved EF (HFpEF)

  • Ejection fraction
  • Features
  • Causes
A

EF > 50% (diastolic HF: inability of ventricle to relax normally)

Features

  • Normal cavity size
  • Concentric hypertrophy
  • Diastolic dysfunction
  • Enlarged left atrium

Causes

  • Constrictive pericarditis
  • Cardiac tamponade
  • Restrictive cardiomyopathy
  • Hypertension
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4
Q

Heart failure with preserved EF (borderline)

- Ejection fraction

A

EF 41-49% aka. heart failure with mid-range EF (HFmrEF)

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5
Q

What is the Framingham diagnostic criteria for heart failure?

A

2 major criteria OR one major + 2 minor criteria

Major criteria

  • Acute pulmonary edema
  • Cardiomegaly
  • Hepatojugular reflex
  • Neck vein distension
  • Paroxysmal nocturnal dyspnea or orthopnea
  • Rales
  • 3rd heart sound gallop

Minor criteria

  • ankle oedema
  • dypsnea on exertion
  • hepatomegaly
  • nocturnal cough
  • pleural effusion
  • tachycardia (>120 bpm)
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6
Q

What is the NYHA classification of heart failure? How does it affect treatment?

A
  1. Class I: no limitation
  2. Class II: slight limitation (comfortable at rest, ordinary activity results in fatigue, dyspnea, angina)
  3. Class III: marked limitation (comfortable at rest, less than ordinary activity lead to symptoms)
  4. Class IV: Inability to carry out any physical activity without discomfort, symptoms at rest.

NYHA class I/II: Focus on Prevention

  • Prevent harmful ventricular remodeling
  • Forestall development of symptoms

NYHA class III/IV: Focus on Treatment

  • Ameliorate symptoms if present
  • Reduce mortality
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7
Q

What is the ACC/AHA classification of heart failure?

A

A: High risk of developing heart failure
- HTN, CAD, DM, FHx cardiomyopathy

B: Asymptomatic heart failure
- Previous AMI, LV systolic dysfunction, asymptomatic valvular dz

C: Symptomatic heart failure (NYHA II- III)
- Known structural heart disease, SOB and fatigue, reduced exercise tolerance

D: Refractory end-stage heart failure
- Marked symptoms at rest despite appropriate medical therapy

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8
Q

What are the signs suggestive of heart failure?

A

More specific

  • Elevated JVP
  • Hepatojugular reflux
  • 3rd heart sound
  • Laterally displaced apex

Less specific

  • Edema (ankle, sacral, scrotal)
  • Pulmonary crepitations
  • Reduced breath sounds
  • Tachycardia
  • Irregular pulse
  • Tachypnoea (>16/min)
  • Hepatomegaly
  • Ascites
  • Cachexia
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9
Q

What are the causes of right heart failure?

A

Typically, due to pul. pathology 🡪 HPV 🡪 ↑ Pulmonary Resistance 🡪 Cor Pulmonale

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10
Q

What are the investigations conducted for heart failure?

A
  1. Blood tests
    - FBC, Renal Panel, LFTs, TFTs 🡪 to assess organ impairment
    - BNP >100ng/L (negative predictive marker)
    - Trops to elucidate ppt cause
    - Iron study (ferritin + fe saturation –> associated with morbidity and mortality)
  2. Chest X-ray (ABCDE)
    - Alveolar oedema (Bat wings)
    - Kerley B lines
    - Cardiomegaly
    - Dilated prominent upper lobe vessels
    - Pleural Effusion – Effusion from HF does NOT require drainage!
  3. ECG
    - LV hypertrophy
    - Arrhythmias (AF, SVT)
    - Q waves → etiology of the heart failure (past MIs)
  4. Echocardiography (mandatory for confirming diagnosis!)
    - Look for cause: Valvular pathology, ASD/VSD, IHD, HCM
    - Confirm the presence of LV dysfunction and assess severity
  5. Right heart catheter (gold standard)
  6. Lung US: to scan lung fields (particularly at the lung bases)
  7. US: to look at IVC (> 2.1 cm → dilated IVC), surrogate for volume status
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11
Q

What are the common causes of heart failure?

A
  • IHD***
  • Hypertension
  • Valvular heart disease
  • Idiopathic dilated cardiomyopathy
  • Alcohol
  • HIV (ischemia via accelerated atherosclerosis or viral induced cardiomyopathy)
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12
Q

What are the causes of acute decompensation in heart failure patients?

A
  • Non-compliance with drugs or diet***
  • Cardiac ischemia
  • Inadequate pre-treatment
  • Arrhythmia: atrial fibrillation
  • Miscellaneous factors: drugs (NSAIDs, verapamil, diltiazem, beta blockers), thyroid, PE, concurrent infections, pneumonia, influenza
  • Uncontrolled HTN
  • No definite factor
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13
Q

What are the goals of treatment of heart failure?

A

1) Identify and correct underlying condition causing heart failure
2) Elimination of the precipitating cause

3) Management of heart failure symptoms
- Treatment of pulmonary and systemic vascular congestion by sodium restriction and diuretics.
- Measures to increase forward cardiac output and perfusion of vital organs through the use of vasodilators and positive inotropic drugs

4) Modulation of the neurohormonal response to prevent adverse ventricular remodelling in order to slow the progression of LV dysfunction
5) Prolongation of long term survival

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14
Q

What is the acute management of heart failure?

A
  • Close monitoring
  • Maintain O2

• Stabilize haemodynamics:
- Effusion from HF does NOT require drainage!

1) Inotropes as needed
- First line: Dobutamine (Beta-1 Adrenergic Receptor Agonist –> Increase SV, stroke work and thus CO
- Noradrenaline (Alpha-1 Agonist, weaker Beta-1 agonist): vasoconstrictor, used in the hypotensive patients

2) Nitrates (IV GTN)
- IV GTN (0 - 300 mcg/kg/min): first line when patients are very breathless, onset 15 minutes

3) ACE-Inhibitor / ARB
• IV Captopril, Enalapril, Lisinopril
• Potent vasodilator
• Counters the neurohormonal response in HF patients
• Used in stabilised pts (oral therapy
• Beware if renal function is impaired or potassium levels elevated

4) Diuretics
• First line: IV Frusemide (loop diuretic)
• Second line: Hydrochlorothiazide (works at DCT)

Invasive measures
• Intra-aortic balloon pump (IABP)
• Extracorporeal membrane oxygenation (ECMO)

Call senior!

B-CONVINCED trial: b-blockers should not be initiated during ADHF episodes if the patient has never been on this but safe to continue on this if patient has been chronically on beta-blockers

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15
Q

What is the non pharmacological management of chronic heart failure?

A

Patient education

  • Symptoms: Look out for oedema, weight gain (>2kg in 3 days), orthopnoea, coughing when lying down
  • Side effects of medications: Importance of drug titration
  • Carer education
  • Salt restriction (2 to 3g /day) 🡪 actually more important than fluid restriction!
  • Fluid restriction (1.5 to 2L/day)
  • Smoking cessation and restriction/abstinence from alcohol
  • Exercise training and weight loss
  • Immunisation against pneumococcus and influenza
  • Screening for psychological issues
  • Screening for sleep disorders incl. OSA → needs to be treated to prevent readmission
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16
Q

What is the pharmacological management for chronic heart failure patients with reduced ejection fraction?

A

[Mortality benefit]

1) ACE-I
• Commonly used : Enalapril, Lisinopril, Captopril
• Contraindicated in pts with CKD / ARF; Bilateral RAS; HyperK
• Reduces Fibrosis and -ve remodeling

2) B-blockers (CMB):
• Carvedilol, metoprolol, bisoprolol
• Initiate AFTER starting Diuretics & ACE-I; when pt is no longer in cardiogenic shock
• C/I: ABCD – COPD, Asthma, Heart Block / Bradydysrhythmias, Decompensated HF

3) Aldosterone antagonist:
• Spironolactone, eplerenone

4) ARNI: Valsartan + Sacubitril
5) SGLT2-i

[Morbidity reducing]

1) Hydralazine/isosorbide dinitrate: if creatinine does not allow use for ACE-I or ARB
2) Ivabradine used when EF reduced AND patient in sinus rhythm AND max dose of b-blockers AND HR >70
3) Digoxin used when patient is very symptomatic, fast AF
4) IV iron replacement

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17
Q

What is the surgical management of heart failure and what are the indications?

A

Implantable cardiac defibrillator (ICD)
- Purpose: Secondary prevention for significant ventricular arrhythmia

Cardiac Resynchronisation therapy (CRT)

18
Q

What are the features of end stage heart failure?

A
  • Repeated >2 hospitalisation for HF in past year
  • Progressive deterioration of renal function
  • Weight loss without other cause
  • Intolerance to ACE-I / beta-blockers
  • Frequent systolic BP<90mmHg
  • Persistent dyspnea with dressing of bathing requiring rest
  • Inability to walk 1 block on level ground
  • Recent need to escalate diuretics, often reaching daily frusemide doses >160mg/day
  • Na<133mEq/L
  • Frequent ICD shocks
19
Q

What is the management of heart failure?

A
  • Long term inotropes –> dobutamine, levosimendan
  • Ventricular assist device
  • Heart transplant
  • Palliative management
20
Q

Carbonic anhydrase inhibitors

  • examples
  • MOA
A

Acetazolamide

Inhibition of proximal convoluted tubule Na bicarbonate reabsorption

21
Q

Loop diuretics

  • examples
  • MOA
  • side effects
A

Furosemide, Bumetanide, Tosemide

Inhibition of Na/ K/2Cl cotransporter in the thick ascending loop

S/E: hypokalemia, renal impairment 🡪 hence supplement w/ SpanK

22
Q

Thiazide type diuretics

  • examples
  • MOA
A

Hydrochlorothiazide, Metolazone

Inhibition of Na/Cl contransporter in distal convoluted tubule

23
Q

Potassium sparing diuretics

  • examples
  • MOA
A

Amilloride, Triamterene

Inhibition of aldosterone responsive epithelial Na Channel (ENaC) in distal nephron + collecting tubule

24
Q

Aldosterone antagonists

  • examples
  • MOA
  • Side effects?
A

Spironolactone, Eplerenone

Inhibition of aldosterone receptors + collecting tubule, reducing Na channel and Na/K ATPase

Side Effect

  • Spironolactone – gynecomastia, erectile dysfunction
  • Both – Hyperkalaemia
25
Q

Vasopressin antagonists

  • examples
  • MOA
A

Inhibition of V2 receptors in distal nephron + collecting tubule, reducing aq (water) channel density

Conlvaptan, Tolvaptan

26
Q

Vasodilators

  • Venodilators (decrease preload) examples
  • mixed examples
  • Arteriolar dilators (decrease afterload) examples
A

Venodilators
- nitrates

Mixed

  • nitroprusside
  • ACEI
  • ARB
  • a adrenergic blockers
  • a central agonists
  • nesiritide

arteriolar dilators

  • hydralazine
  • minoxidil
  • ca2+ channel blockers
27
Q

Inotropes

  • examples
  • vehicle given in
  • indications
  • side effects
  • precautions
  • contraindications
A

Include Dopamine(beta 1,2 and alpha), Dobutamine(beta only), Noradrenaline (beta 1 and alpha), Adrenaline(B1/2 and alpha), Phenylephrine (alpha 1 only)

Only can be given Intravenously

Indications – Acute on chronic refractory heart failure, severe acute myocardial failure, cardiogenic shock

Side effects – Hypotension, arrhythmias, tachycardia

Precautions – Close monitoring of hemodynamics. Check potassium levels to minimize arrhythymias

Contraindications – Ventricular arrhythmias, phaeochromocytoma

Dopamine to use with care in aortic stenosis

Noradrenaline/Adrenaline for septic shock (vasodilatation in septic shock)

28
Q

What is the MOA of digoxin?

A

1) Inotropic Effect on myocardial cells
Sodium pump inhibited -> Increase in intracellular sodium -> Calcium influx -> Increased myocardial contractility (Positive inotropy)

2) Parasympathetic activation -> Increase vagal tone -> Slower AV conduction and Prolongation of AV refractory period 🡪 reduced HR
3) Sympathetic inhibition
4) Inhibition of renin release due to decreased activity of renal sodium pump with a natriuretic effect

29
Q

In what groups of patients should use of digoxin be cautioned/ contraindicated ?

A

C/I: Cor Pulmonale (right sided failure without left sided failure or AF) or WPW

Caution: in renal failure and small sized patients

  • In renal failure 🡪 reduced Vd 🡪 require renal dose adjustment!
  • In small lean body mass 🡪 less skeletal muscle 🡪 less Digoxin binds to Skeletal Muscles and more binds to Cardiomyocytes
30
Q

What are calcium sensitizers?

A

Include Levosimendan

Sensitize the contractile receptors to the prevailing level of calcium

Long acting

Very expensive

31
Q

What is the precaution for sodium nitroprusside?

A

Nitroprusside is a donor of nitric oxide that vasodilates by formation of cyclic GMP in vascular tissue

Toxicity in liver and renal failure due to decreased cyanide metabolism and excretion of end products.

32
Q

What are the features and causes of a diastolic HF pattern?

A

Diastolic HF Pattern
- Relaxation & Filling dysfunction
🡪 High LVEDP & Normal/Low LVEDV

Usually, EF > 50% (i.e. HF w/ preserved EF)

Features:

  • Normal cavity size
  • Concentric hypertrophy
  • Enlarged left atrium

Causes:

  • Constrictive pericarditis
  • Hypertrophic Cardiomyopathy
  • Restrictive cardiomyopathy
33
Q

What are the features and causes of a systolic HF pattern?

A
  • Contractile Dysfunction
  • Usually, EF < 40% (i.e. HF w/ reduced EF)

Features:

  • LV dilatation
  • Eccentric Hypertrophy
  • Globular shape

Causes:

  • Dilated Cardiomyopathy
  • Ischemic heart disease, AMI
  • Mitral/Tricuspid regurgitation
  • Long Standing HTN
34
Q

What is high output heart failure and why does it occur?

A

When the body requires MORE than what the heart can deliver despite a NORMAL FUNCTIONING HEART

Causes HF because

  • Fits in w/ the definition of HF as there is malperfusion of organs
  • Eventually exhausts the heart causing cardiomyopathy

Eg: Thyrotoxicosis

Eg: Shunting in AVF -> too much blood bypasses organs and travel from A to V -> starving organs of blood -> causes heart to pump faster & harder

35
Q

What are the signs and symptoms of acute heart failure? What is the relevant management?

A

S&S varies depending on Volume Overload OR Low CO OR Both

Acute HF is classified into Forrest Haemodynamic Subsets

Cold & Wet VS Wet & Warm VS Dry & Cold

Volume Overload = Wet; Characterised by:

  • Acute Pulmonary Edema
  • Elevated JVP
  • Pedal Edema
  • Mx: Nitrates (C/I in RHF), ACE-I, Diuretics

Low Cardiac Output = Cold; Characterised by:

  • Haemodynamic Compromise (Cardiogenic Shock)
  • Cold and Clammy peripheries
  • Mx: Aim to ↑CO via inotropes: Dobutamine
36
Q

What is the relevant history to ask in a patient with heart failure?

A

Typical Symptoms

  • Dyspnoea, Cough (+/- pink, frothy sputum from APO)
  • Orthopnoea: “how many pillows do you need when you sleep?”, “do you feel breathless when lying down?”
  • Paroxysmal Nocturnal dyspnoea: “do you wake up at night feeling breathless?”
  • Recued Effort Tolerance: “how many bus stops before you feel tired?”
  • Ankle Swelling

Atypical Symptoms

  • Wheeze
  • Weight Gain (>2kg/week) due to water retention
  • Bloatedness, LOA
  • Palpitations
  • Syncope

Do you have any history of heart conditions? Previous Strokes?

Do you smoke? Metabolic Risk Factors?

AETIOLOGY of HF: Infection, Infarction, Indiscretion (fluid / medication)

37
Q

What is the relevant physical examination to perform in a patient with heart failure?

A
  • Elevated JVP, +ve Hepatojugular Reflux
  • Displaced Apex Beat
  • Pedal Edema, Sacral Edema
  • Bilateral, Bibasal Coarse Inspiratory Crepitations
  • Tachypnoea
  • +/- Hepatomegaly, Ascites

Note: Depending on aetiology of murmur

  • +/- Palpitations and arrhythmia
  • +/- Murmurs
38
Q

Ivabradine

  • Indications
  • MOA
  • Side effects
A

Indicated in maximum tolerated dose of beta blocker OR C/I to beta blocker use

Sensitizes contractile receptors to the prevailing level of calcium 🡪 increases contractility

Concurrent treatment should include ACEI or ARB and spironolactone

Targets the funny channel, rate control without affecting BP

Side effect: blurring of vision

Very expensive ☹

39
Q

What are the potential causes of elevated natriuretic peptide (cardiac & non cardiac)?

A

Cardiac

  • LV dysfunction
  • Acute coronary syndrome
  • Heart muscle disease including LVH
  • Valvular heart disease
  • Pericardial disease: constriction and tamponade
  • Atrial fibrillation, atrial flutter
  • Myocarditis
  • Cardiac surgery
  • Cardioversion
  • Toxic metabolic myocardial insults, including cancer chemotherapy

Non cardiac

  • Advancing age
  • Anemia
  • Renal failure
  • Pulmonary: OSA, severe pneumonia
  • Pulmonary hypertension
  • Critical illness
  • High output states: sepsis, cirrhosis, hyperthyroidism
  • Severe burns
  • Pulmonary embolism
40
Q

What are the causes of diseased myocardium?

  • Toxins
  • Infection
  • Inflammatory conditions
  • Infiltrative causes
  • Metabolic
  • Genetic
A

Toxins: Alcohol, cocaine, amphetamine, anabolic steroids. Anthracycline, interferons monoclonal antibodies, NSAIDS

Infection: Bacteria, viruses (HIV/AIDS), parasites (Chagas Disease)

Inflammatory conditions: Lymphocytic/giant cell myocarditis, Graves, RA, CTD, e.g. SLE, eosinophilic myocarditis

Infiltrative : Amyloidosis, sarcoidosis, haemochromatosis

Metabolic: Graves, acromegaly, GH deficiency, hypercortisolism, Conn’s
Addison’s, obesity, anorexia, malignancy

Genetic: Hypertrophic cardiomyopathy, DCM, LV non-compaction, ARVC, muscular dystrophies

41
Q

What is the stages in the development and progression of heart failure?

A

Stage A: At risk for heart failure

  • without current or prior symptoms or signs of HF
  • without structural biomarkers, or genetic markers or heart diseases

Stage B: Pre heart failure

  • Parents without current or prior symptoms or signs of HF but evidence of one of the following
    1) Structural heart disease
    2) Abnormal cardiac function
    3) Elevated natriuretic peptide levels/ elevated cardiac troponin levels in the setting of exposure to cardiotoxins

Stage C: Heart failure
- Parents with current or prior symptoms or signs of HF caused by structural and/ or functional cardiac abnormality

Stage D:

  • Severe symptoms and/ or signs of HF at rest, recurrent hospitalizations despite GDT, refractory or intolerant to GDMT
  • Requiring advanced therapies such as transplant, mechanical or circulatory support, or palliative care