Heart Failure Investogation Flashcards
What are the 2 key questions in investigation heart failure
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
What is the NYHA functional classification of the progression of heart failure
• 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
What investigations should be carried out
• Baseline blood tests: – Full blood count - anaemia is indicative – Electrolytes and renal function – Glucose / HbA1C – Lipid profile
• Specialist blood test:
– BNP (Brain Natriuretic Peptide)
What are natriuretic peptides?
-
What does BNP indicate?
LV sits. Dysfunction + LV Diast. Ysfuncion, valvular dysfunctio, RV dysfunction
What does teh ECG look like in heart failure?
See slide for eg
Describe a chest x ray example in eras failure
See slide
Wha rare other tests to undertake
Other ‘tests’ – answering 2nd question - is it something else?
• Thyroid function tests • Viral titres • Specialist cardiac imaging e.g. MRI • Coronary angiography
Define starlings law
The force developed in a muscle fibre
depends on the degree to which the fibre
is stretched
Describe teh management of acute heart failure
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
Describe the action of furosemide
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
What are the key principles in the management of heart failure
• 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
Describe the neurohormonal activation
• 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
Descrbe the sympathetic activation on heat failure
See slide
Describe the effect of the sympathetic nervous system in heart failure
• 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)
What are the physiological effects of beta blockers in heart failure
- Reduce heart rate (cardiac beta receptor)
- Reduce BP (…..reduce cardiac output) 1+2 -> Reduced myocardial oxygen demand
- Reduce mobilisation of glycogen
- Negate unwanted effects of catecholamines
How to beta blockers affect mortality
See slide
How should b blockers be administered
• 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
Describe the raas system in heart failure
See slide
How is the raas system targeted for treating heart failure
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
Describe the current management of heart failure
See slide
What is the role of aldosterone receptor antagonists.and gove an example
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
Describe intervention for heart failure
Intervention – Treat underlying cause - Valve surgery - Revascularisation – Heart Transplantation – Mechanical assist devices
Implantable Pacemakers
– Biventricular Pacing
Implantable Defibrillators
What are lifestyle modifications for heart failure
Lifestyle Modification – Reduce salt – reduce Alcohol – increase Aerobic exercise – reduce BP
