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Cardiovascular system > Lecture 19- Heart failure investigations management > Flashcards

Lecture 19- Heart failure investigations management Flashcards

1
Q

how many classes of heart failure

A

4

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2
Q
  • Class I
    *
A

No symptomatic limitation of physical activity

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3
Q
  • Class II
    *
A
  • Slight limitation of physical activity
  • Ordinary physical activity results in symptoms
  • No symptoms at rest
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4
Q
  • Class III
A
  • Marked limitation of physical activity
  • Less than ordinary physical activity results in symptoms
  • No symptoms at rest
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5
Q
  • Class IV
A
  • Inability to carry out any physical activity without symptoms
  • May have symptoms at rest
  • Discomfort increases with any degree of PA
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6
Q

questions you ask

A
  1. Does the patient have heart failure?
  2. What sort of heart failure does the patient have?
  3. What is causing heart failure?
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7
Q
  1. Does the patient have heart failure?
A
  • History and clinical examination?
  • Differential diagnosis?
    • E.g. just unfit i.e. maybe just retired from a very active job and started doing less activity.. breathlessness
    • Anaemia?
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8
Q
  1. What sort of heart failure does the patient have?
A
  • Left ventricular systolic dysfunction
  • Heart failure with a preserved ejection fraction
  • Valvular / structural (e.g. VSD) heart failure
  • Right ventricular failure
  • High output cardiac failure
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9
Q
  1. What is causing heart failure?
A

a. IHD?
b. HBP?
c. Viral?

​

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10
Q

management of heart failure can be

A

symptomatic treatment or prognostic treatment

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11
Q

example of symptomatic treatmetn1

A

furosemide

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12
Q

what is prognotstic treatment

A

b[provide better outcomes- left ventricular systolic dysfunction (LVSD) only

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13
Q

example of prognostic treatment

A

o Cardiac rehab/ community heart failure team

o ACE/Angiotensin receptor blockers (ARBs)

o Beta blocker

o MRA (spironolactone)

o Sacubitril valsartan

o ICD/ biventricular pacemaker

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14
Q

Case 1: Patient history

A

· 35 year old male

· Married with 3 kids

· Progressive SOB (shortness of breath) 1 month

· Sudden onset severe SOB

· No peripheral oedema (must be left sided)

· No significant PMH

· No medications

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15
Q

Case 1: patient signs

A

· Temp 36.8

· Pulse 130

· BP 170/70mmHg

· Loud heart murmur

· RR40

· pO2 91% (hypoxic)

· Profuse bilateral crepitations (can hear pulmonary oedema)

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16
Q

investigations

A

ECG, CXR, transthoracic echocardiogram

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17
Q

Case 1: ECG shows

A
  • Fast atrial fibrillation

o May have caused decompensation

o Tachycardia may be due to pulmonary oedema- priority is to treat this

o Rate control challenging, beta blockers may make acute heart failure worse

o Anticoagulants

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18
Q

Transthoracic echocardiogram used to see

A

o Mitral regurgitation

o Aortic stenosis

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19
Q

treatment for:

o Mitral regurgitation

o Aortic stenosis

A

o Surgical fixation?

o Furosemide

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20
Q

furosemide

A
  • Venodilatory effect immediate
  • Onset diuretic action 30 minutes peaking 60-90 minutes
  • Higher doses required in renal failure
  • Monitoring is key:

· HR, BP, RR, pO2%, CXR

· Fluid balance, hourly urine output

· Daily weights (1kg weight loss per day- loss of water)

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21
Q

Case 1: CXR shows

A
  • Cardiomegaly

o Cardiothoracic ratio >50%

  • Upper lobe diversion
  • Fluid in the fissure
  • Pleural effusions
  • Kerley B lines
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22
Q
A
23
Q

Case 1: what to do?

A
  • Recognise as emergency
  • ABCDE
  • Immediate treatment:
    • Furosemide 80mg stat (NOW)
      • Should help relieve pulmonary oedema
    • O2 (for low pO2)
    • Highly likely to require respiratory support (phone respiratory)
      • CPAP
    • Second line IV nitrate (GTN), IV morphine
24
Q

Case 2: patient history

A
  • 65 year old female
  • NYHA III 2 weeks
  • Orthopnoea and PND
    • Paroxysmal nocturnal dyspnea (PND) is a sensation of shortness of breath that awakens the patient, often after 1 or 2 hours of sleep, and is usually relieved in the upright position.
  • Baseline NYHA I
  • MI 5 years ago
  • Aspirin 75mg od
  • Atorvastatin 80mg od
25
Q

Case 2: patient signs

A
  • Apyrexial (without fever)
  • Pulse 70
  • BP 100/60 mmHg
  • Normal heart sounds
  • Bibasal crepitations
26
Q

case 2: ECG shows

A

LBBB

27
Q

case 2: CXR

A

mild congestion

28
Q

case 2:

A

BNP 2000

29
Q

case 2: immeditate treatment

A
  • Furosemide 40mg od
  • Urgent referral to specialist
30
Q

case 2: further investigaton

A

tra nsthroacic echocardiogram- severe LV impairment

31
Q

case 2: prognostic treatment

A
  • ACE? ARB
  • Beta blocker?
  • Mineralocorticoids steroid
32
Q

case 2: key history question

A
  • Recent viral illness
  • Anabolic steroids
  • ETOH (alcohol)
  • Smoking and Family history
33
Q

case 2: ECG results

A
  • Lack of synchronisation of ventricles
  • She would benefit from a biventricular pace maker
34
Q

Case 2: blood tests

A
  • NTpro-BNP
  • FBC
  • U&E
  • clotting
  • thryodi function and Vitamin D level
  • CRP
35
Q

NTpro-BNP

A

o Natriuretic peptide: released in response to atrial/ ventricular stretch due to fluid overload

  • Natriuretic peptides are hormones with diuretic and vasodilator effects, mainly secreted in the left ventricle as a mechanism to compensate for pressure overload

o Normal range varies with age/gender

o Atrial fibrillation can trible BNP/ NTpro-BNP

36
Q

FBC

A

o Patients with heart failure are often anaemic

  • Anaemia of chronic disease
  • MAHA

o Anaemia might explain symptoms

37
Q

U & E

A

o Renal function often deteriorates in heart failure

o Na/K levels important for medications

38
Q

clotting

A

o Important if considering anticoagulation

39
Q
A
40
Q

Thyroid function, vitamin D level

A

o Alternate explanation for symptoms

41
Q

CRP

A

look for infection/ inflammation

42
Q

Natriuretic peptides

A

· Hormone released in response to atrial/ventricular stretch due to fluid overload

· Negative predictive value 97%

· Normal range varies with age / gender

· Atrial fibrillation can triple BNP / NTpro-BNP

43
Q

Effects of ANP and BNP

A
  • increased:
    • natriuresis
    • diuresis
    • vasodilitation
  • decreased
    • RAAS activity
44
Q
A
45
Q
  • Early compensatory mechanism to improve CO:
A

o Cardiac contractility

o Arterial and venous vasoconstriction

o Tachycardia

46
Q

long-term deleterious effects:

A

o β-adrenergic receptors are down-regulated / uncoupled

o Noradrenaline

  • Induces cardiac hypertrophy / myocyte apoptosis and necrosis via α- receptors
  • Induce up-regulation of the RAAS
  • Reduction in heart rate variability (reduced paraSNS and increased SNS)
47
Q

B blockers: physiological effects in heart failure

A

Can reduce all-cause mortality

  1. Reduce heart rate (cardiac beta receptor)
  2. Reduce BP (reduce CO)
  3. 1+ 2= reduced myocardial oxygen demand
  4. Reduce mobilisation of glycogen
  5. Negate unwanted effects of catecholamines
48
Q

however take care of B blocker becasue

A

failing myocardium may be dependent on heart rate

  • Initiate at low dose
  • Titrate slowly
  • May need to alter concomitant medication (e.g. diuretics)
49
Q

you can treat the RAAS system with

A
  • ACEi
  • ARB
50
Q

spironolactone

A

aldosterone receptor antagonists

51
Q

how does aldosterone receptor antagonists- spironolactone- work

A
  • Potassium-sparing diuretic that prevents your body from absorbing too much salt and keeps potassium levels from getting too low
  • Used to treat:

o Heart failure

o High BP

o Hypokalaemia

52
Q

when is spironolactone used

A

When despite of ACEi and /ARB therapy aldosterone conc returns to normal

53
Q

Biventricular pacemaker and defibrillator

A

causes your heart to beat. A biventricular pacemaker is a special type of pacemaker that paces both sides of the lower chambers of the heart (the right and left ventricles) to help treat heart failure. This type of pacing is called “biventricular pacing,” and the therapy provided by biventricular pacing is called cardiac resynchronization therapy. A biventricular pacemaker and ICD help keep the heart pumping in a more normal way. The pacemaker device keeps the heart from beating too slowly. It tries to restore the normal squeezing pattern of the heart. This is called resynchronization pacing. This can lead to more efficient and stronger heart contraction. The ICD part of the device detects dangerously fast heart rhythms and stops them. If the device detects an abnormally fast heartbeat that can cause cardiac arrest, it will send a “shock” to the heart. The shock stops this dangerous heart rhythm and restores a normal heartbeat.

Cardiovascular system (30 decks)

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