Heart Failure Investogation Flashcards

1
Q

What are the 2 key questions in investigation heart failure

A

Two Key Questions:
1. Does the patient have heart failure?
– What has the history / clinical examination
told you?
– Differential diagnosis?
2. Why does the patient have heart failure?
– Ischaemia v. non ischaemia

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2
Q

What is the NYHA functional classification of the progression of heart failure

A

• Class I
– No symptomatic limitation of physical activity

• Class II
– Slight limitation of physical activity
– Ordinary physical activity results in symptoms
– No symptoms at rest

• Class III
– Marked limitation of physical activity
– Less than ordinary physical activity results in symptoms
– No symptoms at rest

• Class IV
– Inability to carry out any physical activity without symptoms
– May have symptoms at rest
– Discomfort increases with any degree of physical activity

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3
Q

What investigations should be carried out

A
• Baseline blood tests:
– Full blood count - anaemia is indicative
– Electrolytes and renal function
– Glucose / HbA1C
– Lipid profile 

• Specialist blood test:
– BNP (Brain Natriuretic Peptide)

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4
Q

What are natriuretic peptides?

A

-

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5
Q

What does BNP indicate?

A

LV sits. Dysfunction + LV Diast. Ysfuncion, valvular dysfunctio, RV dysfunction

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6
Q

What does teh ECG look like in heart failure?

A

See slide for eg

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7
Q

Describe a chest x ray example in eras failure

A

See slide

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8
Q

Wha rare other tests to undertake

A

Other ‘tests’ – answering 2nd question - is it something else?
• Thyroid function tests • Viral titres • Specialist cardiac imaging e.g. MRI • Coronary angiography

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9
Q

Define starlings law

A

The force developed in a muscle fibre
depends on the degree to which the fibre
is stretched

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10
Q

Describe teh management of acute heart failure

A
Management of acute heart failure
• Admit to hospital! 
• Oxygen 
• Intravenous loop-diuretic (furosemide)
• Heparin (to prevent DVT) 
• Patient may require:
– Additional ventilator support (CPAP)
– Intravenous ‘nitrates’ 
– preload reduction +/-
coronary vasodilation
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11
Q

Describe the action of furosemide

A

Reduce fluid, reduce end diastolic pressure, back up curve (see slide) - if its overdone, CO will get worse
• Has an immediate venodilatory effect - improves CO - within 5 min
• Onset of diuretic action within 30 minutes
• Peak action about 60-90 minutes
• Higher dose required in renal failure
• Monitoring is key:
– Patient observations PR, RR, BP and O2 Sats.
– Urine output! - if not enough, haven’t given enough
Ppl with renal failure - only drug which u give a higher dose - drug needs to get acros glomerulus to have action

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12
Q

What are the key principles in the management of heart failure

A
• Correct underlying cause 
• Non-pharmacological measures 
• Pharmacological therapy
1. Symptomatic improvement
2. Delay progression of heart failure
3. Reduce mortality 
• Treat complications/associated
conditions/cardiovascular risk factors
– Eg. arrhythmias
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13
Q

Describe the neurohormonal activation

A

• Sympathetic Nervous System
• Renin-Angiotensin-Aldosterone System
Concentrate on first 2

  • Natriuretic Hormones
  • Anti-Diuretic Hormone
  • Endothelin
  • Prostaglandins / Nitric Oxide
  • Kallikrien System
  • Tissue Necrosis Factor - a
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14
Q

Descrbe the sympathetic activation on heat failure

A

See slide

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15
Q

Describe the effect of the sympathetic nervous system in heart failure

A

• Baroreceptor-mediated response
• Early compensatory mechanism to improve CO:
– Cardiac contractility
– Arterial and venous vasoconstriction
– Tachycardia
• However long-term deleterious effects:
– β-adrenergic receptors are down-regulated / uncoupled
– 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)

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16
Q

What are the physiological effects of beta blockers in heart failure

A
  1. Reduce heart rate (cardiac beta receptor)
  2. Reduce BP (…..reduce cardiac output) 1+2 -> Reduced myocardial oxygen demand
  3. Reduce mobilisation of glycogen
  4. Negate unwanted effects of catecholamines
17
Q

How to beta blockers affect mortality

A

See slide

18
Q

How should b blockers be administered

A

• Care !
• Failing myocardium dependent on heart
rate
• Initiate at low dose
• Titrate slowly
• May have to alter concomitant medication (e.g. diuretic)
Wait until patient is stable. Start low and then uptitrate

19
Q

Describe the raas system in heart failure

A

See slide

20
Q

How is the raas system targeted for treating heart failure

A

ACE inhibitors - affect ACE - prevent 70% of angiotensin I-> angiotensin II

Angiotensin R blockers - block the angiotensin 2 from acting on its receptors to reduce effects

Giving one or the other had same clinical impact as giving birth

21
Q

Describe the current management of heart failure

A

See slide

22
Q

What is the role of aldosterone receptor antagonists.and gove an example

A

Role of Aldosterone Receptor Antagonists SPIRONOLACTONE
• In spite of ACE inhibitor / ARB therapy,
aldosterone concentration returns to normal
• Aldosterone “escape”
Raising potassium?
Direct benefit - preventing toxicity to heart itself
Add on treatment
See slide

23
Q

Describe intervention for heart failure

A
Intervention
– Treat underlying cause
   - Valve surgery
   - Revascularisation 
– Heart Transplantation 
– Mechanical assist devices

Implantable Pacemakers
– Biventricular Pacing

Implantable Defibrillators

24
Q

What are lifestyle modifications for heart failure

A
 Lifestyle Modification
– Reduce salt
– reduce Alcohol
– increase Aerobic exercise
– reduce BP