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My MRCP > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

Pathophysiology of Heart Failure

Mechanisms of heart failure [3]

A

Systolic and diastolic failure
Left and right failure
High and low output failure

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2
Q

Explain systolic vs diastolic heart failure but note that they usually co-exist

A 
Systolic Heart Failure EF low
- Decreased pumping / CO and fluid backs up
- Eg IHD, MI, cardiomyopathy
Diastolic - preserved EF
- Hypertrophy so doesn't fill or relax 
- Fluid back up
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3
Q

Explain the difference between Left and Right sided Heart Failure

A
  • Left sided failure:
  • Ax: IHD, valvular heart disease
  • Regurgitation of blood into lungs > pulmonary congestion, hypertension
    -Caused by poor systolic function > decreased pulses
  • Right sided failure:
  • Ax: LVF, pulmonary stenosis, cor pulmonale
  • Less blood goes to lungs
  • Blood backs up to body tissues causing edema
    Right-sided heart failure generally develops as a result of advanced left-sided heart failure
  • Congestive cardiac failure: left and right failure
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4
Q

Describe low [4] and high [3] output failure

A

Low output failure

  • cardiac output reduced, normally increases with exertion
  • Pump failure
  • Excessive preload
  • Chronic excessive after load

High output failure (rare)

  • output normal or increased due to increased body requirements
  • but CO can’t meet these requirements
  • Anaemia, pregnancy, Paget’s disease, AV malformation
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5
Q

Causes of low output failure:
Pump failure [3]
Excessive preload [2]
Chronic excessive after load [2]

A
  1. Pump failure:
    - systolic and/or diastolic failure
    - reduced heart rate (post-MI, heart block, beta blockers), negatively ionotropic drugs (anti-arrhythmic agents)
  2. Excessive preload:
    - mitral regurgitation
    - fluid overload (NSAIDs causing excessive fluid retention, normal heart but renal impairment or fluids running too fast)
  3. Chronic excessive afterload:
    - aortic stenosis, hypertension
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6
Q

Presentation of RHF [6] and LHF [6]

A

RHF:

  • JVP elevated
  • peripheral oedema (sacrum, thighs, abdo wall), ascites
  • nausea, anorexia
  • venous engorgement
  • neck and face pulsation (tricuspid regurgitation)
  • epistaxis

LHF:

  • SOB, orthopnoea, PND, nocturnal cough (pink frothy sputum)
  • wheeze (cardiac asthma)
  • RV heave
  • poor exercise tolerance
  • fatigue
  • weight loss (cardiac cachexia; can be masked by “weight gain” due to oedema)
  • muscle wasting
  • cool peripheries, cyanosis
  • displaced apex beat
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7
Q

Investigations for heart failure [4]

A

N-terminal pro B type natriuretic peptide
TFTs- thyrotoxicosis may mimic HF, Haematinics
ECG
TTE
CXR

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8
Q

B-type natriuretic peptide (BNP) is a hormone produced mainly by the left ventricular myocardium in response to strain. Very high levels are associated with a poor prognosis.

A

high (2000ng/L) = TTE in 2w
Natriuretic peptides are non-specific but
very sensitive and so a normal level virtually
excludes heart failure.

2. raised (400-2000ng/L) = TTE in 6w

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9
Q

HF

Findings on ECG

A

Ischemic changes
Ventricular hypertrophy
- RVH = tall R wave in V1, deep S wave in V6
- LVH = deep S wave in V1, tall R wave in V6

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10
Q

TTE uses in ix heart failure [3]

CXR [5]

A
  • TTE: identify valve disease, systolic and diastolic ventricular function and cardiac shunts
  • CXR: ABCDE =
    Alveolar oedema (bat’s wings)
    Kerley B lines (interstitial oedema)
    Cardiomegaly
    Dilated prominent upper lobe vessels
    Pleural Effusion
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11
Q

Diagnostic criteria for HF

A

Framingham criteria for congestive cardiac failure

>2 major OR 1 major and 2 minor

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12
Q

What is part of the Framingham MAJOR criteria [9]

A

 PND
 Bibasal crackles
 Neck vein distension
 Hepatojugular reflux
 Acute pulmonary oedema
 S3 gallop
 Cardiomegaly (cardiothoracic ratio >50% on CXR)
 Increased CVP (>16cmH2O in right atrium)
 Weight loss >4.5kg in 5d in response to mx

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13
Q

What is part of the Framingham MINOR criteria [7]

A 
	Bilateral ankle oedema 
	Nocturnal cough 
	SOB on ordinary exertion 
	Hepatomegaly 
	Tachycardia (>120bpm)
	Pleural effusion
	Decrease in VC of 1/3 of maximum recorded
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14
Q

Increased BNP [12]

A 
Age
LVH, Ischaemia, Valve
Tachycardia, Overload
Hyperaemia inc PE
Low GFR, CKD
Sepsis
COPD
DM
Liver cirrhosis
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15
Q

What causes decreased BNP [4]

A

Obesity
ACEI
BB
Diuretic / aldosterone antagonist

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16
Q

What is the New York classification of HF

A

Class 1 = no limitation
Class 2 = mild limitation to exercise, none at rest
Class 3 = moderate limitation, not at rest
Class 4 = severe limitation at rest

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17
Q

Management modalities of HF [5]

A

Lifestyle modification
Vaccination
Monitoring
Rx
Definitive treatment

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18
Q

Mx HF: Lifestyle mods [4], Vaccination [2]

A

Lifestyle modification:
- Cardiac rehab
- Smoking cessation, reduce alcohol
- Salt and fluid moderation
- Avoid NSAIDs
Vaccination:
- annual influenza
- and one off pneumococcal vaccination (need 5y booster if asplenia or CKD)

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19
Q

Mx HF: monitoring, definitive

A
  • Monitoring: effective mx lowers BNP levels

* Cardiac transplantation: severe refractory symptoms or refractory cardiogenic shock

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20
Q

Acute heart failure

Etiology: describe two groups and their causes

A
  1. Acute on chronic HF: precipitated by ACS, hypertensive crisis, acute arrhythmia, valvular disease
  2. De-novo acute HF: viral myopathy, toxins , valve dysfunction
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21
Q

Signs of Acute heart failure [8]

A
  • distress, pallor, sweating, sitting forward
  • cyanosis, tachycardia
  • pulsus alterans
  • elevated JVP
  • displaced apex beat
  • bibasal crackles, wheeze
  • S3 heart sound (gallop rhythm),
  • BP usually normal*
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22
Q

What causes severe pulmonary oedema [6]

A

LVF post MI or IHD
Valve disease
HF
ARDS any cause
Fluid overload
Neurogenic
Infection

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23
Q

What causes peripheral oedema [6]

A 
Heart failure = most common
Cellulitis
DVT
Lack of mobility
Chronic venous insuffinecy 
Lymphoedema
24
Q

Initial management of acute heart failure [8]

A 
Stop fluids
Sit patient up 
100% O2 if sats <96 but careful in COPD 
IV access, bloods: FBC U&E, CRP, ABG, *BNP, troponin
ECG (MI, arythmias)
IVFurosemide 40-80mg
IV Diamorphine 1.25mg-5mg slowly
GTN 2 puffs sublingual (unless SBP<90)
25
Q

Management of hypertension in acute heart failure [4]

A

o SBP >100: start ISOSORBIDE DINITRATE infusion (keep SBP>90)
 Echocardiogram: identify underlying cause

o SBP <100: treat for cardiogenic shock and refer to ICU

26
Q

Mx of cardiogenic shock [6]

A 
IV Opiates - act as vasodilator 
Vasodilator
Inotropes - NA (often need CCU / ITU) 
NIV - CPAP
Ultra filtration
Mechanical circulatory assistance
27
Q

Subsequent mx for acute heart failure [4]

A
  • aim for weight loss of 0.5kg/day
  • repeat CXR
  • treat as CHF
  • ‘Cardiac resynchronisation therapy’
    consider for biventricular pacing or cardiac transplantation
28
Q

You’ve given isosorbide nitrate for patient in acute heart failure SBP >100. However she continues to worsen, what do you do? [3]

A

Worsening symptoms:

  • more FUROSEMIDE
  • CPAP (recruits more alveoli and drives fluid back into vasculature)
  • NITRATES
29
Q

What is Cor Pulmonale

A

Cor pulmonale is defined as an alteration in the structure and function of the right ventricle (RV) of the heart caused by a primary disorder of the respiratory system.

30
Q

Causes of cor pulmonale [4]

A

Interstitial lung disease
PE
CF
Pulmonary hypertension

31
Q

Two groups of drugs used in heart failure therapy?

A

Diuretics

Drugs that reduce ejection fraction

32
Q

Chronic heart failure: drug management
reduced EF

A
  1. ACEI
  2. BB
  3. Mineralocorticoid receptor antagonist or aldosterone antagonist or dapagliflozin (SGLT-2 inhibitors)
  4. Ivabradine
  5. Digoxin
    Sacubitril valsartan (angiotensin receptor neprilysin inhibitor)
33
Q

What drugs improve survival [3]

What drugs improve symptoms and survival [2]

A

Improve survival only:
BB
Ivabradine
Vasodilator

Improve symptoms and survival:
ACEI / ARB (but not if EF normal)
Spirnolactone

34
Q

Loop diuretics
MOA
Eg [2]

A

Loop of Henle - ascending
Inhibit Na-K-Cl
Furosemide - rapid IV
Bumetanide - slower use in older people

35
Q

What do you do if resistant to loop

Eg [2]

A

Use with thiazide (inhibit reabsorption of Na at DCT)
Don’t leave on for too long
Indapamide / BDZ

36
Q

What are adverse effects of loop diuretics? [7]

A

Dehydration, Dizzy, Hypotension
Metabolic disturbances: low K, Ca, Na, Cl
Hypochloraemic alkalosis
Gout
Impaired glucose tolerance
Renal failure due to dehydration, Uraemia
Ototoxicity

37
Q

What do BB do [3]

Eg [2]

A

Block sympathetic hormonal changes in HF
Can precipitate deterioration
Only use by specalist when other therapy has been tried
BISOPROLOL or CARVEDILOL

38
Q

When are BB CI [4]

A

Asthma
Hypotension
AV block
Verapamil - rate-liming CCB

39
Q

When is morphine indicated [2]
MOA
SE

A

Anxious
Use if restless and distressed
Vasodilator as reduced sympathetic drive
Can cause respiratory depression

40
Q

What does Ivabradine do [2] and criteria of use

A

Inhibitor of SA Node
Does not modify contractility
Must be on standard therapy, including BB and HR >75, left ventricular fraction < 35%

41
Q

What does digoxin do?

A

Inotrope properties
Enhance cardiac function by increasing availability of cardiac
Use if still symptomatic on therapy
Strong indication for its use in AF

42
Q

What are affects of digoxin [2] and how do you monitor

A

Arrythmia
Confusion
U+E - particularly K (if low = more toxic)

43
Q

What are vasodilators

MOA

A

Hydralazine
Nitrate - isosorbide denitrate

MOA: Reduce preload and after load
Use if intolerant to ACEI

44
Q

What does ACEI do for heart failure

A

Prevents conversion of angiotensin I to II

Reduce preload and after load

45
Q

What do you do if K >6

A

Stop ACEI immediate

46
Q

What does (Sacubitril) do

A

Prevent metabolism of ANP and BNP
* should be initiated following ACEi or ARB wash-out period

47
Q

What anti-coagulant and when are they indicated?

A

DOAC or warfarin

If in AF

48
Q

What do you do if spironolactone not tolerated

A

Eplerenone if not tolerated or if had MI

Aldosterone antagonist

49
Q

What are SE of spironolactone [3]

A

Gynaecomastia
HyperK
Renal failure

50
Q

What do diuretics interact with [5]

A

NSAID
Anti-hypertensives = hypo
Vancomycin
Lithium
Aminoglycosides

51
Q

What does morphine do in pulmonary oedema

A

Reduce preload

52
Q

Acute management [8]

A

oxygen
IV loop diuretics
opiates
vasodilators
inotropic agents
CPAP
ultrafiltration
mechanical circulatory assistance: e.g. intra-aortic balloon counterpulsation or ventricular assist devices

53
Q

First line treatment [4]

A
  1. ACEi and a BB (start one at a time) ACE-inhibitors and beta-blockers have no effect on mortality in heart failure with preserved ejection fraction
  2. Diuretics for fluid overload
  3. Offer annual influenza vaccine
  4. Offer one off pneumococcal vaccine
54
Q

Sacubitril-valsartan indications [2]

A

In heart failure with reduced ejection fraction who are symptomatic on ACEi or ARB
Initiate following ACEi or ARB washout period

55
Q

When is cardiac resynchronisation therapy indicated in heart failure?

A

Cardiac resynchronisation therapy (CRT) uses a pacemaker that can stimulate the left ventricle. This is a very effective means of improving HF, particularly where there is sinus rhythm and LBBB.
Combining an ICD with a cardiac resynchronisation therapy-pacemaker (CRT-P) results in a cardiac resynchronisation therapy defibrillator (CRT-D).

56
Q

Medication that may exacerbate heart failure [6]

A

thiazolidinediones- pioglitazone is contraindicated as it causes fluid retention
verapamil - negative inotropic effect
NSAIDs/glucocorticoids- should be used with caution as they cause fluid retention
low-dose aspirin is an exception - many patients will have coexistent cardiovascular disease and the benefits of taking aspirin easily outweigh the risks
class I antiarrhythmics
flecainide (negative inotropic and proarrhythmic effect)
alpha blockers like doxazosin or tamsulosin

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