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DAQ 1 revision Case 1-4 > HF > Flashcards

HF Flashcards

1
Q

Risk factors of HF

A

ACS especially MI, hypertension, DM, valvular diseases, smoking, obesity, thyroid diseases

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2
Q

Differentials for dyspnoea with/without chest pain

A

HF/ HF exacerbation
(PND better as slow fluid buildup, orthopnoea, nocturia, ankle oedema )
COPD exacerbation
Anaemia
(iron-deficiency, chronic disease, B12 deficiency)
Lung cancer
Pneumothorax
(young male, chest pain on inspiration, acute onset)

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3
Q

What is ejection fraction, afterload, preload?

A

Ejection fraction: percentage of the blood leaving the heart each time it contracts

Afterload/squeeze: the amount of pressure the heart must contract against to eject blood after systole

Preload/stretch: the amount of sarcomere stretches at the end of ventricular filling during diastole

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4
Q

What is the pathology of LHF?

A

MI → dec. aerobic respiration → dec. ATP → dec. function of myocardium → dec. contractility → inc. amount of blood retained in heart after systole → over time, inc. preload → ventricular remodelling → left ventricular dilation (eccentric hypertrophy)

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5
Q

What is the pathology of RHF?

A

thin walls –> accept a range of volume BUT sensitive to pressure

secondary to LHF due to inc afterload

cor pulmonale due to COPD

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6
Q

Symptoms

RHF vs LHF

A

LHF –> pulmonary circulation
orthopnoea

RHF --> systematic circulation
peripheral oedema
abdominal discomfort
PND
(fluid from peripheral oedema is drained via veins causing congestion)
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7
Q

Signs

RHF vs LHF

A

LHF
basal crackles
displaced apex beat

RHF 
peripheral oedema
raised JVP
ascites
hepatosplenomegaly
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8
Q

Signs/symptoms for HF in general

A

Symptoms

  • Fatigue, dizziness
  • Impaired urine output (renal hypoperfusion)

Signs

  • Hypotension, tachycardia
  • Cool/cyanosed peripheries
  • Slow capillary refill
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9
Q

Precipitant of symptomatic exacerbations

A 
HEART FAILED
HYPERTENSION
endocarditis
anaemia
rheumatic heart disease
Thyrotoxicosis
FAILURE TO TAKE MED
arrhythmia
Infarction/ischaemia/infection
Lung problems (COPE, pneumonia)
Endocrine
DIETARY: salt intake, fluid overload
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10
Q

What is systolic HFrEF?

Pathology?

A

Inability of ventricle to contract normally –> dec CO, SV –> dec EF <50%

  • impairment of ventricular contractility: ACS
  • inc afterload: hypertension, AS
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11
Q

What is diastolic HFpEF?

Pathology?

A

Inability of ventricle to relax and fill normally –> inc filling pressure EF >50%
- impaired ventricular relaxation/filling
ageing, tamponade

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12
Q

Diagnostic features of HFrEF

A

S3 (post S2) –> rapid ventricular filling in systole
displaced apex beat
dull percussion note over bases –> pleural effusion

investigations

  • CXR: cardiothoracic ratio > 0.5
  • previous infarcts, deformed valves
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13
Q

Diagnostic features of HFpEF

A

S4 (before S1): hard contraction of atrium in diastole

normal size heart on CXR

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14
Q

Complications of HF

A
  • Sudden cardiac death (1/3 of death in HF)
  • Anaemia
    Chronic kidney failure: hypoperfusion –> drop in EPO production –> few RBC
  • Cardiorenal syndrome
    Systolic: reduced CO  hypoperfusion  prerenal kidney failure
  • Arrhythmia
  • Stroke (Blood stasis in dilated chambers)
  • Hepatic congestions (receive 25% of CO –> hepatic hypoxia)
    Inc ALT/AST, inc bilirubin, abdo discomfort
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15
Q

Investigations for HF

A

CBE

  • Anaemia (resulting from hypoperfusion of kidney)
  • Infection that exacerbates HF decompensation
Cardiac markers (TO RULE OUT MI)
-	Troponin T

ECG
- Previous MI –> infarcted area shows pathological Q wave, inverted T
- LV hypertrophy –> left axis deviation
EUC
- Sodium: dilutional hyponatremia
- Potassium: HyperK (impaired renal), hypoK (diuretics)
- GFR

LFT
- Inc ALT/AST, inc bilirubin –> RHF

Chest X-ray

  • Pulmonary oedema (bat wings)
  • Kerley B line (interstitial oedema) –> short linear markings at lung bases
  • Cardiomegaly
  • Dilated pulmonary vessels
  • Effusions (blunting of costo-diaphragmatic recess)
  • Thickening of fissures

Echo
systolic/diastolic function, valves, wall thickness, wall motion abnormalities
- transthoracic
transesophageal (invasive, emergency situations such as aortic dissection)

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16
Q

Approach for diagnosing HF

A

initial assessment
- EUC, LFT, CBE, ECG, CXR
HF diagnosed
echocardiogram to confirm HFrEF, HFpEF, valvular diseases

17
Q

Management of acute pulmonary oedema as HF exacerbation

A

ABCDE + POND
Position: sit up, positive airway
- reduce V/Q mismatch, assist work of breathing
Oxygen (92-96% target)
Nitrates
- Smooth muscle relaxation –> venous dilation –> preload reduction
Diuretics (frusemide)
- Evidence of fluid overload  pulmonary oedema

18
Q

Behavioural management of HF

A
  • Physical activity: physio, walking, light weightlifting
    Avoid exercise preventing normal talking
  • Diet changes
    Reduce sodium intake (3g max/day)
    High fibre diet: constipation is common due to gut hypoperfusion
  • Fluid management: fluid overload causes acute decompensation
  • Weight diary: every morning, same time and same clothes
    Restricted to 1.5L per day
    Weight gain or loss >2kg within 3 days  seek help
  • Alcohol + caffeine
    Limit to 1-2 standard drinks/day
    Caffeine can exacerbate arrhythmia  inc HR/BP
  • Smoking cessation
  • Vaccination
    Inc risk of especially resp infections  causes acute decompensation
    Influenza and pneumococcal vaccinations!
  • Travel
    Inc risk of DVT
19
Q

Approach to pharmacological management of HFpEF

A

No proven pharm

Treat associated underlying diseases

20
Q

Approach to pharmacological management of HFrEF

A

reduce mortality: ACEi/ARB + beta blockers + potassium sparing diuretics

ACEi 
ARB (not effective as ACEi, use in patients with absolute contraindications of ACEi and severe side effects)
loop diuretics
cardio selective beta blockers
potassium sparing diuretics

Repeat echo in 3-6 months to check efficacy of the medication If EF still < 40%, use SGLT2/ARNI instead of ACEi/ARB
SGLT2/ARNI CANNOT BE USED WITH ACE/ARB SO STOP ACE/ARB
ARNI: wait at least 36 hours after stoping ACE/ARB

21
Q

MOA and side effect of ACEi

A

By blocking ACE enzymes, it prevents Angiotensin II formation and inhibit bradykinin breakdown –> reduce angiotensin II-induced vasoconstriction and sodium/fluid retention –> reduce preload and afterload

absolute contraindication

  • history of intolerance
  • history of hereditary/idiopathic angioedema
  • pregnancy
  • renal artery stenosis

Relative contraindication

  • Hypotension < 90
  • Hyperkalaemia > 6
  • Renal impairment

side effect

  • dry cough
  • angioedema (swelling of tongue, face, throat)
  • hyperkalaemia inhibiting aldosterone –> arrythmia
22
Q

MOA and side effect of angiotensin II receptor blockers

ARB - sartan

A

used if ACEi is not tolerated
Competitively inhibit binding of angiotensin II –> reduce angiotensin II-induced vasoconstriction and sodium retention
Do not act on bradykinin

side effect
- hyperkalaemia inhibiting aldosterone –> arrythmia

23
Q

MOA and side effect of loop diuretics (furosemide)

A

Act on luminal Na+/K+/2Cl- co-transporters in ascending loop of Henle –> sodium, potassium, chloride loss in urine

Dramatic diuresis: incontinence, nocturia, polyuria, high urea
Postural hypotension
Monitor Hyponatremia and hypokalaemia alkalosis
- Dehydration from excessive fluid loss (hydrogen ion loss  alkalosis)
- Hypokalaemia alkalosis: As a result of excessive sodium loss, kidney tubules try to compensate sodium loss by losing potassium and hydrogen ions
- Hypotension from excessive fluid loss  renal function

24
Q

MOA and side effect of cardio selective beta blockers

A

Competitively blocks beta receptors in heart –> reduce contractility, bronchi relaxation, relax SMC of arteries
Do not use beta blockers during decompensation – the patient is already fluid overload, so reducing cardiac contractility would be detrimental, wait until stabilise

reduce mortality and risk of hospitalisation

25
Q

MOA and side effect of SGLT2

A

Inhibits sodium-glucose co-transporter, reducing glucose reabsorption in kidney and increasing excretion in urine
Associated with fewer exacerbation of HF, reduced BP & lipids

Side effect
Polyuria, increased frequency, polydipsia
Risk of UTI, dehydration
Euglycemic ketoacidosis

26
Q

MOA and side effect of potassium sparing diuretics/aldosterone antagonists

A

Inhibit sodium absorption in the distal tubule by antagonising aldosterone, increasing sodium and water excretion and reducing potassium excretion
they are weak diuretics

hyperkalaemia, hyponatraemia, hypochloraemia (especially when combined with thiazide diuretics)

DAQ 1 revision Case 1-4 (5 decks)

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