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Year 3 Semester 1 > Heart failure > Flashcards

Heart failure Flashcards

1
Q

Definition of heart failure + 3 categories of ejection fraction

A

Condition in which heart is unable to generate cardiac output sufficient to meet demands of body

  • Due to an inherited or acquired abnormality of cardiac structure and/or function
  • Commonly categorized into 3 broad groups
  • HF with reduced ejection fraction (HFrEF = systolic failure): LVEF <40%
  • HF with mildly reduced ejection fraction: LVEF = 40-50%
  • HF with preserved ejection fraction (HFpEF = diastolic failure): LVEF > 50%
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2
Q

Epidemiology/RF of HF

A
  • Hx of MI
  • Diabetes mellitus
  • Dyslipidaemia
  • African/hispanic
  • Old age (65+)
  • Male sex
  • Hypertension
  • Left ventricular dysfunction
  • Cocaine abuse
  • Exposure to cardiotoxic agents
  • Renal insufficiency
  • Valvular heart disease
  • Sleep apnoea
  • Family history of heart failure
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3
Q

Precipitants of HF (HEART FIALED)

A 
Hypertension (common) 
Endocarditis/environment (e.g.heatwave) 
Anaemia
Rheumatic heart disease and other valvular disease
Thyrotoxicosis
Failure to take meds (very common) 
Arrhythmia (common) 
Infection/Ischemia/Infarction (common) 
Lung problems (PE, pneumonia, COPD) 
Endocrine (pheochromocytoma, hyperaldosteronism)
Dietary indiscretions (common)
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4
Q

Afterload + Preload?

A

Afterload = Sqeeze
- pressure that the heart needs to exert to eject blood during systole

Preload = Stretch
- EDV –> volume of blood in ventricle after diastole –> stretch

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5
Q

Systolic Failure (HFrEF) mechanism

A

Contractility problem “pump dysfunction”

  • -> dec. contractility
  • -> systolic ventricular dysfunction
  • -> dec. stroke volume
  • -> dec. LV ejection fraction (LVEF)
  • -> dec. CO (not enough blood pumped to circulation)
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6
Q

Causes of Systolic HF

A
  1. Ischaemia due to MI –> cardiac tissue damage
  2. Dilated cardiomyopathy (dilated & weakened ventricles)
  3. Long standing hypertension
  4. Cardiac arrhythmias
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7
Q

Diastolic Failure (HFpEF) mechanism

A

Very stiff ventricles / cannot relax normally
–> dec. ventricular compliance –> diastolic ventricular dysfunction –> red. ventricular filling + inc. diastolic pressure –> normal SV but dec. preload (abnormal filling) –> dec. CO with normal ejection fraction

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8
Q

Causes of Diastolic HF

A

Increased stiffness of ventricles

  • ventricular hypertrophy
  • long standing hypertension, AS, hypertrophic cardiomyopathy
  • restrictive cardiomyopathy

Impaired relaxation of ventricle

  • constrictive pericarditis
  • pericardial tamponade
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9
Q

Left-sided HF (HFrEF):

- afterload & preload

A

Increased left ventricular afterload:

  • increased mean aortic pressure; (e.g., arterial hypertension)
  • outflow obstruction (e.g., aortic stenosis)

Increased left ventricular preload:
- left ventricular volume overload (e.g., backflow into the left ventricle caused by aortic insufficiency)

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10
Q

Right-sided HF (HFpEF):

- afterload & preload

A

Increased right ventricular afterload:
- increase in pulmonary artery pressure (e.g., pulmonary hypertension)

Increased right ventricular preload:
- right ventricular volume overload (e.g., tricuspid valve regurgitation, left-to-right shunt)

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11
Q

Left sided vs Right sided

Symptoms

A

Left:

  • cough (frothy pink sputum)
  • PND, orthopnoea
  • crackles/rales

Right:

  • nocturia
  • peripheral oedema (swelling of ankles)
  • Jaundice
  • abdominal discomfort
  • anorexia/nausea (GIT oedema)

Common:

  • dyspnoea
  • fatigue
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12
Q

Left sided vs Right sided

Signs

A

Left:

  • Bilateral basilar crackles
  • displaced apex beat laterally (beyond MCL)

Right:

  • elevated JVP
  • hepatojugular reflux
  • hepatosplenomegaly

Common:

  • Anaemic signs (pallor)
  • poor peripheral perfusion/cyanosis
  • reduced exercise tolerance
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13
Q

Approach in patient with suspected heart failure

A

Initial assesses (EUC, LFT, CBC, ECG, CXR)

  • ->
  • Echo (HF diagnosed)
  • BNP or NT-proBNP (uncertain diagnosis –> high then echo)
  • -> confirm HF + EF status
  • -> Management according to:
  • HFrEF
  • HFpEF
  • valvular, pericardial or congenital

+ Underlying causes

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14
Q

Diagnosis of HF (investigations)

A

Left:

  • inc. BNP/NT-proBNP
  • CXR: cardiomegaly, pulmonary vascular congestion, enlargement of LA/ventricle/pulmonary arteries
  • Echo: LV hypertrophy with eccentric remodelling, LA enlargement

Right:

  • inc. BNP/NT-proBNP
  • LFT: inc. serum total bilirubin & aminotransferase (congestive hepatopathy), elevated AST, ALT & LDH, hypoalbuminemia (cardiac cirrhosis in long standing)
  • CXR: cardiomegaly, pulmonary vascular congestion, enlargement of RA/ventricle/pulmonary
  • Echo: evaluate RV size, function + detect haemodynamic alterations
  • MRI: myocardial tissue, ventricular volume, muscle damage
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15
Q

Imaging for HF

A

Transoesophageal:
- only for emergency (aortic dissection)

Transthoracic Echo:
- assess cardiac structure & systolic/diastolic function of both ventricles
(results = see next card)

CXR:

  • changes to the cardiac silhouette
  • boot-shaped heart on PA view –> RV enlargement
  • Alveolar oedema, Kelley B lines, Cardiomegaly, dilation of prominent pulmonary blood vessels, effusion (costodiaphragmatic recess = blunting of costophrenic angles)
      • Kerley B lines
      • dilation
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16
Q

Transthoracic echo looks at:

A

Systolic HF: depressed & dilated L&/R ventricle with low EF

Diastolic HF: normal LVEF but LV hypertrophy & abnormal diastolic filling patterns

Pulmonary hypertension
Pericardial/Pleural effusion
Complications: MR, LA enlargement

17
Q

HF on CXR: ABCDE

A

Alveolar oedema
Kelley B lines
Cardiomegaly
Dilation of prominent pulmonary blood vessels
Effusion –> (costodiaphragmatic recess = blunting of costophrenic angles)

18
Q

Investigations list for CHF

A 
Echo
ECG
EUC
LFT
Troponin
CXR
D-dimer
HbA1c (DM)
BNP
ABG
CBE
19
Q

Immediate management for Pulmonary oedema

A

ABCDE + POND +/- morphine
ABCDE:
- Airways (ensure latency, give O2, position patient)
- Breathing (assess rate & rhythm, attach pulse oximetry)
- Circulation (cyanosis, temperature, capillary refill, pulse, auscultation, obtain IV, ABG, ECG, BP)
- Disability
- Exposure

POND:

  • Positive pressure/position:
    • continuous positive airway pressure –> dec. preload & need for ventilation when appropriate, sit patient up with legs hanging down unless patient is hypotensive
  • Oxygenation
  • Nitrates: smooth muscle relaxation –> venous dilation –> preload reduction
  • Diuretics –> furosemide IV/intramuscular

Morphine:
- used traditionally as it reduces dyspnoea secondary to its effects on ventilation resulting in reduced preload (this mech is considered to be less clear now).
- it also plays a role in reduced SNS activity and reduced anxiety and distress
BUT number of side effects
- acute pulmonary oedema (respiratory & CNS depression, reduced CO, and hypotension)
- may be a significant factor in increased ICU admissions & higher mortality rate

20
Q

Furosemide Electrolyte changes + why

A

furosemide blocks Na/K/Cl transporter in the loop of Henle –> results in more sodium making its way to the distal convoluted tubule –> kidney senses this then tries to retain sodium –> swapping sodium for potassium and hydrogen ions –> hypokalaemia & alkalosis

21
Q

HF Management (non-pharm)

A

Physical activity, diet, smoking, alcohol, coffee (can exacerbate arrhythmia by HR,BP), smoking, fluid management, vaccination, travel (PE)

22
Q

HF Management (Pharm)

A

ACE-i

Cardio selective beta-blockers –> reduce mortality and risk of hospitalisation

Potassium-sparing/aldosterone antagonists diuretics

SGLT2 (cannot be used with ACE/ARB)

ARNI (angiotensin receptor nephrilysin inhibitor) - cannot be used with ACE/ARB

22
Q

HF Management (Pharm)

A

ACE-i

Cardio selective beta-blockers –> reduce mortality and risk of hospitalisation

Potassium-sparing/aldosterone antagonists diuretics

SGLT2 (cannot be used with ACE/ARB)

ARNI (angiotensin receptor nephrilysin inhibitor) - cannot be used with ACE/ARB

23
Q

Decompensation

A
  1. Forward failure:
    - red. CO –> poor organ perfusion –> organ dysfunction (hypotension, renal dysfunction)
  2. Backward failure:
    - LV –> inc. LV volumes or pressure –> blood backup into lungs –> inc pulmonary capillary pressure –> cardiogenic pulmonary oedema (orthopnoea) & inc. pulmonary artery pressure
24
Q

HF Compensatory mechanism (neurohumoral responses)

A
  1. SNS activation
    Reduced CO -> low BP -> baroreceptors in the aortic arch and carotid sinus signal the brain -> release hormones that act on beta-1 receptors (inc HR and contractility) and alpha 2 receptors (vasoconstriction of arteries) -> inc cardiac contractility and TPR -> maintain BP and end-organ perfusion (kidney)
  2. RAAS activation
    reduced CO -> hypoperfusion of kidneys -> macula dense cells detect low NA+/BP -> afferent artery dilation and renin secretion (release angiotensin 2 stimulate efferent artery constriction) –> inc renal perfusion and GFR
    - inc. ADH release –> H20 retention in DCT & collecting duct
    - aldosterone release –> act on collecting duct –> inc. Na,Cl reabsorption and water follows –> fluid and salt retention –> inc. preload
  3. ANP & BNP release
    ANP: release from atrium in response to excess volume from atrial stretch
    BNP: release from atrium in response to ventricular stretch
    Both have diuretic, hypotensive effects by increasing excretion of salt and water (counteract RAAS)
  4. Endothelin
    Released from vascular endothelium
    - Vasoconstriction
    - Inc sensitivity of the heart to calcium to promote contractility

Year 3 Semester 1 (2 decks)

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