Heart failure Flashcards

1
Q

Whcih side heart failure causes JVP raise?

A

Right

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2
Q

Which side heart failure causes pulmonary congestion?

A

left

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3
Q

How does Pulmonary hypertension cause cor pulmonale?

A

Increased pressure in pulmonary circulation -> R ventricle working harder -> hypertrophy -> failure

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4
Q

Bloods before start a statin:

A

Non fasting lipid profile

Liver function tests

Renal function - eGFR

HBA1c

Creatinine kinase if persistent muscle pain

TSH if dyslipidemia present

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5
Q

Which sputum is suggestive of HF?

A

Pink, frothy

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6
Q

Cardiac causes chronic HF

A

IHD
Arrhytmias
Valvular or congenital HD (ASD,VSD)
Myocarditis/pericarditis
Cardiomyopathy
Perciardial effusion, cardiac tamponade etc

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7
Q

What drugs can cause HF?

A

Negative inotropes eg beta blockers
Fluid retaining properties - steroids, NSAIDs
alcohol
Chemotherapy

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8
Q

What increases in metabolic demand can cause HF?

A

Pregnancy
hyperthyroidism/thryotoxicsosi
Anaemia
Liver failure
BeriBeri - thiamine deficiency
Pagets disease

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9
Q

What are the three features of Becks triad?

A

Jugular vein distension
Low BP
Muffled heart sounds

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10
Q

What does Becks triad indicate?

A

Cardiac tamponade

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11
Q

Signs of HF on CXR

A

Pulm oedema
Cardiomegaly

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12
Q

What positive test on bloods indicates HF?

A

Raised pro-Brain Naturietic peptide

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13
Q

When is BNP released? What does it do?

A

Released by myocardium when under tension, cleaved into BNP and pro. Increases diuresis and blocks RAS system

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14
Q

Indications for ECHO

A

Septal defects
Valve function
When its hard to visulaise eg tamponade, endocarditis, pericarditis
Heart function eg pre-op, before cardiotoxic chemo
Emergency - unstable nedocarditis, aortic dissection

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15
Q

What criteria is used to classify heart failure?

A

New York Heart Association classification

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16
Q

What does II stage NYHA mean?

A

Slight limitation physical activity, comfortable at rest. Ordinary physcial activity results in fatigue, palpitation, dyspnoea

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17
Q

What is the difference between III and IV NYHA HF classification?

A

Marked limitation of physical activity vs unable to carry on any physical activity without discomfort.
Comfy at rest vs symptoms HF at rest. Less than ordinary activity causes fatigue palpitation or dyspnoea in stage III, any physical activity increases discomfort in stage 4

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18
Q

Stage I of NYHA HF criteria

A

No limitation physical activity
Ordianry activity doesnt cause undue symptoms

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19
Q

Two other stagings of HF

A

Canadian CVS society grading of angina pectoris
European Heart Rhythm association score of AF

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20
Q

What levels of BNP rule out HF?

A

BNP less than 100ng/L
NT-proBNP < 300ng/litre

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21
Q

What investigation shouldbe done next with new suspected AF with raised BNP levels?

A

Transthoracic doppler 2D ECHO
Consider with people presenting with sus acute HF within 48 hours of admission

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22
Q

When should a HF patinet not be on beta blockers

A

HR under 50
2 or 3 degree Aventricular block
Sick sinus syndrome
Shock

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23
Q

When do you start a beta blocker in people with acute heart failure due to LV systolic dysfunction in hospital

A

When condition stabilised eg IV diuretics no longer needed 48 hours before

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24
Q

What to start in patients with acute HF and reduced LV ejection fraction in hopsital

A

ACE i and aldosterone antagonist

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25
Q

Immediate treatment for acute AF

A

IV diuretic with bolus or infusion
Higher dose if already taking

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26
Q

What important to monitor in diuretic therapt

A

Renal fucntion
Weight
Urine output

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27
Q

When are nitrates offered in acute HF?

A

Concomittant MI, severe HPTN, regurgitant aortic or mitral valve disease, monitor BP closely

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28
Q

When do you consider inotropes or vasopressors in acute HF?

A

Acute HF and potentially reversible cardiogenic shock

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29
Q

When to consider invasive ventialtion in acute heart failure?

A

Leading to or complicated by respiratory failure or reduced consciousness or physical exhaustion

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30
Q

When to refer 2 week pathway vs 6 week pathway for ECHO for suspected HF

A

2 week - above 2000 ng/litre NT-proBNP
6 week - 400-2000 ng/L
Because high levels of NTproBNP are associated with poor prognosis

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31
Q

What are other causes that could -> high BNP levels

A

Over 70
LVH
Ischaemia
Tachycarida
RV overload
Hypoxaemia (incl PE)
Renal dysfunction (eGFR <60)
Sepsis
COPD
Diabetes
Cirrhosis

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32
Q

What do ECHO to look for

A

Exclude valve disease, assess systolic and diastolic function of L ventricle and detect intracardiac shunts

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33
Q

What can reduce levels of serum natiuretic peptide?

A

Obesity
African /african-caribbean family background
Diuretic treatemtn
ACEis
Betablockers
ARBs
Mineralcorticoid receptor antagonists

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34
Q

What need to do for HF diagnosis

A

ECHO
CXR
Bloods:
-FBC
-U+Es
-Thyroid function profile
-LFTs
-Lipid profle
-HbA1c
Urinalysis
Peak flow or spirometry
If confirmed and unsure why,m investigate cause

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35
Q

First line treatment for chronic HF and reduced ejection fraction

A

ACEi (start low and tirate up)
and a beta blocker
Diuretics for fluid retention

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36
Q

2nd line for HF and reduced ejection fraction if still have symptoms after ACEi and beta blocker

A

Mineralcorticoid receptor antagonists

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37
Q

What to monitor with MRA

A

Serum sodium and potassium
Renal function
Before and after start and after each dose uncrement
Blood pressure
Monthly for 3 months then every 6 months

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38
Q

When is Ivabradine used in HF?

A

NYHA II to IV
AND
Sinus rhythm, HR 75BPM +
AND In combo with standard therapu - ACE is, beta blockers, aldosterone antafonists, or when beta blocker therapy contraindicated
AND with LV ejection fraction <35%

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39
Q

How long is the stabilisation period before ivabradine initiated?

A

4 weeks

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40
Q

When to use sacubitril valsartan

A

NYHA II to IV
AND LV ejection fraciton under 35%
Already taking ACEi or ARBs

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41
Q

What drug can be used for peope of afro caribbean family origin and mod to sev HF with reduced ejection fraction

A

Hydralazine + nitrate

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42
Q

When is digoxin initiated?

A

Worsening or severe HF with reduced ejection fraction despite first line treatment HF.

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43
Q

What are people with CKD and chronic HF may prone to on the first line medications?

A

Hyperkalemia

44
Q

Other drugs used inHF

A

Amiodarone
Diuretics

45
Q

What CCB should be avoided in HF with reduced ejection fraciton?

A

Verapamil, diltiazem, Short acting dihydropyridine agents

46
Q

Lifestyle advice for HF

A

Cut out smoking and alcohol
DVLA
aIR TRAVEL
Fluid restriction for dilutational hyponatremia
Reduce if high intake of salt or fluids.
Cardiac rehabilitation unless unstable

47
Q

What should chronic HF patients be monitored for?

A

6 monhtlya clinical assessment of functional capacity, fluid status, cardiac rhythm
(minimum of examining the pulse), cognitive status and nutritional status
* a review of medication, including need for changes and possible side effects
* an assessment of renal function.
Serum potassium esp important if on digoxin or MRA

48
Q

Whenh is cardiac transplant considered?

A

Severe refractory symptoms or refractory cardiogenic shock

49
Q

Symptoms of L sided HF

A

Breathlessness
Cough
Cardiac wheeze
Orthopnea + PND
Bilateral crepitations in lower zones
Pleural effusion
Gallop rhythm - S3
Pitting oedema

50
Q

R sided HF symptoms

A

Peripheral oedema
Ascites
Raised JVP
Hepatomegaly

51
Q

List as many causes of R sided HF as can

A

Sleep apnoea
COPD
Chronic TE puomonary disease
Cystic fibrosis
Interstitial lung disease
Kyphoscoliosis
Pneumoconicosis
Primary/secondary pulmonary HPTN
Pulmonary vascualr disease

52
Q

signs of general Heat failure

A

Hypotension
Tachycardia
Gallop rhythm - presence S3,S4
Displaced apex

53
Q

When is a heart failure considered to have reduced ejection fraction?

A

less than 40%

54
Q

Is there systolic or diastolic dysfunction in HF with reduced ejection fraction

A

Systolic

55
Q

What conditions cause increased metabolic demand that can lead to HF?

A

Pregnancy
Hyperthyroidism
Anaemia

56
Q

Changes in CXR in HF

A

Cardiomegaly
Upper lobe diversion
Alveolar oedema
Kerley B lines
Pleural effusions

57
Q

Why is there fluid accumulation in heart failure?

A

Neuro-hormonal activation -> impaired regulation of sodium excretion through kidneys
Sodium and fluid accumulation. Glycosaminoglycan networks become dysfunctional in buffering this, also organ dysfunction affecting kidneys

58
Q

What neuro hormonal systems are affected in heart failure?

A

RAAS
Arginine-vasopressin system
Sympathetic nervous system

59
Q

When does tissue oedema occur?

A

When the transudation from capillaries into the interstitium exceeds the maximal drainage of the lymphatic system due to increased transcapillary hydrostatic gradient, decreased oncotic pressure gradient and increased interstitial compliance

60
Q

What cardiac complications arise from congestion?

A

S3, JVP, + hepatojugular reflux
Functional mitral and tricuspid regurgitiation
Elevated BNPs

61
Q

What resp complications arise from congestion?

A

PLeural effusion
Dyspnoea, orthopnea, PND
Rales, crackles, wheeze, tachypoea, hypoxia

62
Q

Congested lungs on ultrasound appearance

A

B-lines/comets

63
Q

Complications for kidney from congestion

A

Decreased urine output
Elevated creatinine levels
Hyponatremia

64
Q

Complications for liver from congestion

A

RUQ discomfort
Hepatomegaly
jaundice
Elevated parameters of cholestasis

65
Q

Bowel complications from congestion

A

N+V
Abdo pain
Ascites
Increased abdominal pressure
Cachexia

66
Q

Treatments chronic HF

A
  • ACEi and B blockers
  • SGLT2 inhibitors - dapagliflozin
  • Aldosterone antagonists eg epleronone
  • Control of risk factors - statins, smoking cessation, alcohol etc
67
Q

Acute Heart failure stepwise management

A

Sit patient up
High flow oxygen
IV furosemide
Diamorphone + anti-emetic
BP stable then consider GTN spray
Catheterisation to monitor urine output
Treat underlying causes
Consider CPAP
If BP low consider ITU + inotropes eg IV dobutamine

68
Q

Treatment for cardiogenic shock

A

inotropes eg IV dobutamine

69
Q

Immunisation in HF

A

Annual flu and covid
Single pneumococcal vaccine

70
Q

Which NYHA classes can fly without oxygen?

A

I + II

71
Q

Drugs that reduce mortality vs symptomatic relief

A

Mortality -
-ACEis/ARBS
-Beta blockers
-Spirinolactone
-Hydralazine with nitrates

Symptomatic
-Loop or thiazide like diuretics
-Digoxin
-Ivabradine

72
Q

Ivabradine indications

A

treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Lowers HR and therefore increase flow to myocardium

73
Q

Why use ivabradine over CCBs and Beta blockers

A

Ivabradine acts directly on funny channels in the SA node to lower HR, but no negative ionotropic side effects

74
Q

When are negative inotropes helpful?

A

keep your heart muscles from working too hard by beating with less force. This is helpful when you have high blood pressure, chest pain, an abnormal heart rhythm or a disease like hypertrophic cardiomyopathy.

75
Q

What drugs are negative inotropes?

A

beta-blockers, calcium antagonists, and antiarrhythmics

76
Q

Signs of HF on CXR

A

Alveolar oedema - bats wings
Kerley B lines - interstitial oedema
Pleural effusion
Prominent upper lobe vessels - Antlers sign
Cardiomegaly

77
Q

Investgiations for HF

A

Bloods - FBC, U+Es, LFTs, TFTs, lipid profile, BNP or pro-BNP
Urinalysis
CXR
ECG
ECHO
Lung function tests
Cardiac MRI - gold standard for ventricular volumes, mass and wall motion

78
Q

Resp causes of HF

A

COPD
Obstructive sleep anoea
PE

79
Q

How is cardiac output maintatined inHF?

A

Increasing stroke volume, HR, ventricular remodelling -> increased wall thickness

80
Q

How is MAP maintained in HF?

A

Activation of sympathetic, RAAS

81
Q

How do compensatory mechanisms damage the heart?

A

Sodiy=um/water retention and vasoconstriction from SNS and RAAS activation cause increased preload and afterload, causing increased cardiac workload and myocyte damage -> decreased cardiac input, further activating those systems

82
Q

Why do BNP before take for ECHO even though its not specific to HF?

A

Because its very sensitive so if there is a low level you can rule out HF

83
Q

Cardiac terminology explanation

A
  • CO = SV x HR
    • CO = blood pumped per min
    • SV = ml blood per contraction pumped
  • Preload = blood filling up ventricle. eg end diastolic volume. Affected by
    • Venous return
    • Fluid volume in body
    • Atria contractility → ventricles
  • Afterload - pressure required to pump blood into arteries
    • BP
    • Atherosclerosis
    • Aortic stenosis
  • Contractility - ability heart to contract and pump out blood during systole
      • inotropes eg epinephrine increase
      • inotropes eg beta blockers, CCBs decrease
  • Ejection fraction - % ventricular blood pumped out per contraction
    • Normal = 50-70%
84
Q

Causes of reduced ejection fraction

A

Coronary HD
Muscle damage after MI
DCM
HPTN

85
Q

Causes of HF w preservef EF

A

Anything that effects the filling of ventricle and the ability of the wall to stretch

Common -

  • HPTN
  • CAD
  • Diabtets

Rare

  • Hpertrophic CM
  • Infiltrative diseases eg amyloidosis, sarcoidosis
86
Q

Bloods for oedema

A
  • U+Es + LFTs
  • Albumin - reduced synthesis (liver) or increased excretion (kidney)
  • FBC - anaemia
  • Thyroid profile
    • Hypothyroidism → oedema and fatigue
  • Pro-BNP> 400 = HF
87
Q

Signs of palleation with HF

A

Frequent hospital admissions for decompensations or comorbid conditions
Symptoms refractory to optimal med treatment
Poor QOL + dependent for all ADLs

Others:
- Poor response to treatment and severe breathlessness at rest (New York Heart Association class IV).
- Presence of cardiac cachexia.
- Low serum albumin.
- Progressive deterioration in estimated glomerular filtration rate (eGFR) and hypotension limiting the use of drug treatments.
- Acute deterioration and increasingly frequent hospital admissions from comorbid conditions (such as a chest infection).
- Poor quality of life and dependence on others for most activities of daily living.
- People who are clinically judged to be close to the end of life.

88
Q

Symtpoms of end stage HF

A
  • Pain
  • SOB
  • persistent cough
  • fatigue
  • Limited physical actiity
  • Depression and anxiety
  • Loos of appetite and nausea
  • Oedema
  • Insomnia
  • Cognitive impairment
89
Q

What do if proBNP >400

A

ECHO and specialist assessment within 6 weeks

90
Q

What do if proBNP >2000

A

Urgent review within 2 weeks

91
Q

NYHA scoring

A

Class I - no limitation of physical activity
II - slight reduction in physical activity -> faigue, palpitation, SOB
III - marked limitation of activity. Less than ordinary physical acitvity -> fatigue, palpitation or dyspnoea
IV - Unable to do any physical activity without discomfort. Symtpoms of HF at rest.

92
Q

Lifestyle for chronic HF

A
  • Salt reduction (reduce sodium and water retention)
    • Strict fluid restrictions only neessary when acute decompesnation or sever dilutional hyponatremia
  • Smoking cessation
  • Annual flu and pneumonia vaccines
  • Tracking weight
  • Exercise
93
Q

1st line for HF w preserved EF

A

Manage comorbidities eg HPTN, AF, IHD, DM
Exercise based cardiac rehab
If symptoms persist - hydralazine + nitrate
Digoxin for symptoms

94
Q

1st line for HF w reduced EF

A

ACEi + BB + MRA
ARB if ACEi intolerant
Hydralazine and nitrate if intolerant to both

95
Q

2nd line for HF w reduced EF

A

ACEi/ARB -> sacubitril valsartan if <35% EF
+ ivabradine for sinus rhtyhm if HR >75 and EF <35%

96
Q

What is sacubatril valsartan

A

angiotensin receptor-neprilysin inhibitor - ARNI

97
Q

Physiology of HF meds how worj

A
  • ACEis → minimise RAS system (and therefore excess fuid and sodium retenrion), reduces preload and afterload
  • Beta blockers - slow HR allow more ventricular filling and greater contractility
  • Nitrates reduce vasocnstriction and therefpre afterload
  • Diuretics and ladosterone antagonists - reduce sodium and water retention, therefore reduce preload
98
Q

When use ICD in HF

A

LCSD and EF <35%
ICD detect fatal rhtyhms, pace and defib

99
Q

When is ICD innapropriate HF

A

v severe disease or severe comorbidities, palleative in next year

100
Q

What is cardiac resynchronisation therapy used in in HF

A

Poor ventricular contraction
>150ms and LBBB
Prolonged QRS
SystolicHF
Mod/sev symptoms
- to improve morbidity, mortality and reduce exacerbations.
- With or without a defib (CRT

101
Q

Heart transplants in HF

A
  • Low donor availability and high risk
  • Strong immunosupression required
  • LC assist device used to keep patient alive/optimise before transplant. Physically pumps blood from heart.
102
Q

Medical anagement of acute HF

A
  • Clearly identified trigger should be treated
  • Oxygen if hypoxic
  • Position sat upright
  • Loop diuretics if fluid overload - IV furosemide _ monitor renal function
  • Inotropes/vasopressors if unstable.hypovolaemix
103
Q

Causes of HF decompensation

A
  • ACS - MI
  • Tachyarrhytmia eg AF
  • PE
  • Severe HPTN
  • Infection
  • Drugs eg NSAIDs, steroids
  • Renal insufficiency
  • Not taking meds or folloing dietary requirements
104
Q

Signs of HF decompensation

A
  • Bi basal coarse crackles
  • Raised JVP (raised central venous pressure)
  • Peripheral oedema
  • Wheeze, S3 heart sound, ascites, poor perfusion
105
Q

Warm/cold vs wet/dry HF

A
  • Warm = normal perfusion
  • Cold = cold peripheries, prolonged CRT, reduced urine output
  • Wet - pulmonayr/peripheral oedema, raised JVP
  • Dry - normal/not congested
  • Warm and wet
    • Perfused but congested
    • Fluid overload
    • Diuretics/vasodilators
  • Warm and dry
    • Compensated
    • Optimise meds and treat triggers
  • Cold and dry (least common)
    • Poorly perfused but not congested
    • Hypovolaemic shock
    • Consider fluid bolus/inotropes
  • Cold and wet
    • Poorly perfused and congested
    • Cardiogenic shock
    • Consider diuretics if BP>90
    • Vasopressors/inotropes
    • Worst prognosis
106
Q

Acute HF management

A
  1. ASSESS A to E
  2. Bedside:
  3. Obs
    1. ECG - Arrhytmias OR MI
  4. Bloods
    1. FBC
    2. U+Es
    3. LFTs
    4. NT-proBNP
    5. Troponin if sus ACS
    6. Consider d-dimer if sus PE
  5. Imaging
    1. CXR
    2. ECH0 - urgent if HF new of EF not known