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Week 5 - Cardiology > Heart Failure & Therapeutics > Flashcards

Heart Failure & Therapeutics Flashcards

1
Q

Define heart failure [3]

A

failure of the heart to pump blood (oxygen) at a rate sufficient to meet the metabolic requirements of the tissues [1]

caused by an abnormality of any aspect of cardiac function [1] & with adequate cardiac filling pressure

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2
Q

Heart failure is characterised by what kind of haemodynamic changes? [2]

A

systemic vasoconstriction

neurohumoral activation

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3
Q

What are the common causes of heart failure? [5]

A
  1. coronary artery disease (MI)
  2. hypertension
  3. idiopathic
  4. toxins (alcohol/chemotherapy)
  5. genetic
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4
Q

What are the less common causes of heart failure? [8]

A
  1. valve disease
  2. infections (viral, Chagas)
  3. congenital heart disease
  4. haemochoromatosis
  5. amyloid disease
  6. thyroid disease
  7. pericardial disease, e.g. TB
  8. endocardial disease
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5
Q

Name the 4 main types of heart failure

A
  1. reduced ejection fraction heart failure (HF-REF) “systolic HF”
  2. chronic congestive HF
  3. perserved ejection fraction heart failure (HF-PEF) “diastolic I-IF”
  4. acute “decompensated”
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6
Q

What are the typical features of HF-REF? [3]

  • hint:
    • who gets it?
    • aetiology?
A

young, males often get it

often caused by coronary aetiology

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7
Q

What are the typical features of chronic congestive HF? [2]

A

present for a period of time

may have been acute or may become acute

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8
Q

What are the typical features of HF-PEF? [3]

  • hint
    • who gets it?
    • aetiology?
A

older, females often get it

hypertensive aetiology

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9
Q

What are the typical features of acute decompensated HF? [3]

A

usually admitted to hospital

worsening of chronic or de novo

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10
Q

Explain the pathophysiology of heart failure [11]

A
  1. myocardial injury occurs
  2. results in left ventricular systolic dysfunction
  3. perceived reduction in circulating volume and pressure
  4. neurohumoral activation -> compensatory mechanisms
    • SNS (sympathetic nervous system)
    • RAAS (renin-angiotensin-aldosterone system)
    • ET, AVP etc. (endothelin, arginine vasopressin)
    • natriuretic peptides (ANP/BNP)
  5. these compensatory mechanisms become maladaptive over time leading to worsening of HF
  6. systemic vasoconstriction and renal sodium & water retention occurs
  7. leads to further left ventricular systolic dysfunction (essentially a vicious cycle)
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11
Q

What are the symptoms of heart failure? [7]

A
  1. dyspnoea
  2. orthopnoea
  3. paroxysmal nocturnal dyspnoea (PND)
  4. cough
  5. ascites (swelling in abdomen)
  6. ankle & leg swelling
  7. fatigue
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12
Q

What is dyspnoea? [1]

A

shortness of breath

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13
Q

What is orthopnoea? [1]

A

shortness of breath when lying down

  • patients often say that they have to sleep with several pillows
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14
Q

What is paroxysmal nocturnal dyspnoea (PND)? [1]

A

severe shortness of breath and cough at night

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15
Q

What are the signs of heart failure? [6]

A
  1. peripheral oedema (ankles, legs, sacrum, abdomen)
  2. elevated JVP
  3. third heart sound
  4. displaced apex beat (cardiomegaly)
  5. pulmonary oedema (lung crackles)
  6. pleural effusion
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16
Q

What does NYHA classification describe? [1]

A

describes how functionally limited the patient is by their heart failure (most patients are class 2)

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17
Q

Describe the features of NYHA Class 1 of heart failure [3]

A
  1. no symptoms
  2. no limitation in ordinary physical activity
    • shortness of breath when walking, climbing stairs etc.
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18
Q

Describe the features of NYHA Class II heart failure? [2]

A
  1. mild shortness of breath and/or angina
  2. slight limitation during ordinary activity
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19
Q

Describe the features of NYHA Class III heart failure? [2]

A
  1. marked limitation in activity due to symptoms, even during less-than-ordinary activity (e.g. short walking distances [20-100m])
  2. comfortable only at rest
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20
Q

Describe the features of NYHA Class IV heart failure? [3]

A
  1. severe limitations
  2. experiences symptoms even while at rest
  3. most bedbound patients
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21
Q

Name the investigations done on all patients [6]

A
  1. ECG
  2. CXR (chest x-ray)
  3. echocardiogram
  4. blood chemistry
  5. haematology
  6. natriuretic peptides (BNP/NT-proBNP)
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22
Q

What features are you looking for on ECG when investigating heart failure? [5]

A
  1. evidence of myocardial infarction (MI)
  2. evidence of left ventricular hypertrophy
  3. rhythm
  4. rate
  5. QRS duration
23
Q

What are you looking for on chest x-ray when investigating heart failure? [2]

A

to exclude lung pathology and pulmonary oedema

24
Q

What does an echocardiogram assess? [3]

A
  1. chamber size
  2. systolic and diastolic function
  3. valves
25
What aspects of blood chemistry would you assess when investigating heart failure? [8]
1. FBC (full blood count) 2. U&Es (urea & electrolytes) - assessing kidney function 3. fasting blood glucose 4. urinalysis 5. thyroid function test 6. LFTs 7. urate 8. creatinine
26
If there is **low BNP** (or NT-proBNP) and **normal ECG**, how should you proceed with the investigation? [2]
1. heart failure is **excluded** 2. consider alternative cause for symptoms
27
If there is **raised BNP** (or NT-proBNP) or **abnormal ECG**, how should you proceed with your investigation? [3]
1. heart failure **possible** 2. refer for **echocardiography** 3. do ECG (if not already done) * to determine cause of HF and future management decisions
28
Name the investigations done on **selected** patients [5]
1. coronary angiography 2. exercise test 3. ambulatory ECG monitoring 4. myocardial biopsy * to identify viral causes 5. genetic testing
29
Describe the SIGN guidelines for treatment of heart failure
see image
30
What are diuretics used to treat? [2]
pulmonary oedema peripheral oedema
31
Describe the basic steps involved in RAAS [6]
1. angiotensinogen is produced by the liver 2. angiotensinogen is converted into angiotensin I * by renin (which is produced in the kidney) 3. angiotensin I is then converted into angiotensin II * by ACE (which is produced in the lungs in response to low circulating volume) 4. angiotensin II has several effects on: * blood vessels * heart * kidney * adrenal glands * brain
32
What are the effects of RAAS on blood vessels? [4]
1. vasoconstriction 2. smooth muscle cell hypertrophy 3. inflammatory cytokines 4. endothelin secretion
33
What are the effects of RAAS on the kidney? [3]
1. sodium and water retention 2. efferent arteriolar vasocontriction 3. glomerular and interstitial fibrosis
34
What are the effects of RAAS on the heart? [5]
1. cellular hypertrophy 2. myocyte apoptosis 3. myocardial fibrosis 4. inflammatory cytokines 5. coronary vasoconstriction
35
What are the effects of RAAS on the adrenal glands? [1]
1. aldosterone secretion
36
What are the effects of RAAS on the brain? [2]
1. vasopressin secretion 2. sympathetic activation
37
Describe the mechanism of action of ACE inhibitors and how does the main side effect of the drug occur? [5]
1. Dilates arteries and veins by blocking angiotensin II formation and inhibiting bradykinin metabolism. * This vasodilation reduces arterial pressure, preload and afterload on the heart. * By blocking breakdown of bradykinin, this increases which is responsible for a troublesome side effect of ACE inhibitors, namely, a dry cough 2. Downregulates sympathetic adrenergic activity by blocking the facilitating effects of angiotensin II on sympathetic nerve release and reuptake of norepinephrine. 3. Promote renal excretion of sodium and water (natriuretic and diuretic effects) by blocking the effects of angiotensin II in the kidney and by blocking angiotensin II stimulation of aldosterone secretion. This reduces blood volume, venous pressure and arterial pressure. 4. Inhibit cardiac and vascular remodelling associated with chronic hypertension, heart failure and MI
38
Describe the mechanism of action of beta blockers [1]
Inhibits sympathetic stimulation in the heart and vascular smooth muscle
39
If a patient is intolerant to ACE inhibitor due to a cough, what is the alternative (including drug name)? [2]
Angiotensin Receptor Blocker (ARB) also known as Angiotenisn Receptor Neprilysin Inhibition (ARNI) Drug name: combination drug: **sacubitril/valsartan**
40
What are natriuretic peptides? [2]
1. peptides that stimulated diuresis (increased urine production) and vasodilatation 2. act on kidney tubules to promote excretion of sodium (natriuresis) and water
41
Give 5 examples of natriuretic peptides [5]
1. bradykinin (BK) 2. adrenomedullin (ADM) 3. substance P 4. vasoactive intestinal peptide (VIP) 5. calcitonin gene-related peptide (CGRP)
42
What is neprilysin?
enzyme that degrades natriuretic and other vasoactive peptides
43
Why would you want to inhibit neprilysin? [1] (mechanism of action of ARNI)
by inhibiting neprilysin, this prevents the degradation of natriuretic peptides allowing them to function properly, which helps to treat heart failure
44
Why should you **avoid** giving ARNI **with** an ACE inhibitor? [3]
Associated with risk of **angioedema** * Probably due to concurrent inhibition of at least 2 pathways involved in the degradation of bradykinin and substance P, which are the major effectors of angioedema * Bradykinin is inactivated primarily by ACE, but also by neprilysin and aminopeptidase P (APP), while substance P is inactivated by ACE, neprilysin and dipeptidyl peptidase IV
45
What is angioedema? [1]
Rapid swelling of the area beneath the skin or mucosa
46
Describe the mechanism of action of SGLT2 inhibitors [3]
1. SGLT2 inhibitors cause afferent arteriolar constriction 2. Results in: * Diuresis * Natriuresis * Glycosuria * ↓ Proteinuria 3. Leads to ↓ preload and ↓ LV wall stress
47
Explain how a implantable cardioverter defibrillator (ICD) works [5]
1. Placed under the skin to monitor heart rate & rhythm, with thin wires connecting it to the heart 2. If an ICD notices a dangerous heart rhythm, it can deliver one or more of the following treatments: * **Pacing** → series of low-voltage electrical impulses (paced beats) at a fast rate to try and correct the heart rhythm * **Cardioversion** → one or more small electric shocks to try and restore the heart to a normal rhythm * **Defibrillation** → one or more larger electric shocks to try and restore the heart to a normal rhythm
48
Explain how cardiac resynchronisation therapy (CRT) works [4]
1. A therapy that is sometimes required to maximise the pumping function of the heart in patients with underlying poor ventricular function, for example, patients with heart failure. 2. The two ventricles often become uncoordinated, making the heart less efficient. 3. A normal pacemaker only has wires (leads) in the right side of the heart. CRT requires an extra wire to be placed into the left ventricle to enable both sides to beat together (resynchronisation). 4. Making the lower chambers of the heart work together can improve the overall function of the heart as a pump and reduce the symptoms of breathlessness and fatigue.
49
What is CRT-P? [1]
CRT with pacemaker
50
What is CRP-D? [1]
CRT with defibrillator
51
What is **ivabradine** and describe its mechanism of action [3]
Ivabradine is a sinus node inhibitor Selectively inhibits the pacemaker If current in a dose-dependent manner. Blocking this channel reduces cardiac pacemaker activity, selectively slowing the heart rate and allowing more time for blood to flow to the myocardium
52
What are the features of congestion? [7]
1. pulmonary congestion 2. orthopnoea/paroxysmal nocturnal dyspnoea 3. peripheral (bilateral) oedema 4. jugular venous dilatation 5. congested hepatomegaly 6. gut congestion, ascites 7. hepatojugular reflux
53
What are the features of hypoperfusion? [5]
1. cold sweated extremities 2. oliguria (peeing less than normal) 3. mental confusion 4. dizziness 5. narrow pulse pressure
54
Describe the guidelines in managing a patient with acute heart failure

Week 5 - Cardiology (12 decks)

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