Heart Failure Flashcards
Life Expectancy from heart failure diagnosis:
- 5 year mortality: 50%
- <1 year for advanced HF
3 Clinical Syndromes of Heart Failure:
- chronic heart failure: peripheral oedema
- acute heart failure: pulmonary oedema
- cardiogenic shock: low BP <90mmHg
LV systolic heart failure:
- LV weakness +- dilation/thinning
- due to:
- IHD (acute MI or chronic ischaemia) c.70%
- Hypertension
- Inherited (autosomal dominant)
- Alcohol excess
- Post viral
- Toxins (eg chemotherapy drugs)
- Metabolic (eg hypothyroid, iron overload,
thiamine deficiency)
- Unknown cause (‘idiopathic’)
How can we measure LV function:
- no single perfect measure
- LV function depends on loading: preload = venous
return, afterload = blood pressure) - LV contractility measurement should be independent
of loading: isovolumic dP/dt, end-systolic elastance (
difficult to measure) - LV ejection fraction
Ejection fraction =
Stoke Volume =
stroke volume/ end-diastolic volume
end-diastolic volume - end-systolic volume
Systolic Heart Failure - Haemodynamics:
- decreased LV contractility (WEAK): reduced stroke
volume - increased LV diastolic pressure
- increased LV end diastolic volume (DILATED)
- reduced LV ejection fraction: systolic heart failure =
Left ventricular ejection fraction <40%, normal LVEF = 55-70%
Signs and symptoms of systolic heart failure occur at what %
<40% of left ventricular ejection fraction
Heart Failure pathophysiology:
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right and left sided heart failure can occur independently
Heart Failure Symptoms:
- breathlessness: exertional, orthopnoea, paroxysmal
nocturnal dysponea - fatigue
- leg swelling
How do we classify heart failure?
- NYHA, New York Heart Association severity
classification - class 1 = asymptomatic
- class 2 = mild symptoms with day to day activities
- class 3 = moderate symptoms with minor exertion
- class 4 = symptoms at rest
The patient with heart failure diagram
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Signs of Heart Failure:
- elevated JVP = right atrial pressure
- oedema: ankles, shins, thighs, genitals, trunk, ascites,
pleural effusion - Lung Crackles (Inspiration, Bases):
- low volume pulse, low BP
- tachycardia, increased RR
- displaced apex beat
- murmur (functional MR (mitral regurgitation)
- liver enlargement (hepatomegaly) (tender right
quadrant) (mildly low liver function)
Ascites
swelling in abdomen
Heart Failure Investigations:
- ECG
- BNP = brain natriuretic peptide
- echocardiogram
- cardiac MRI
- cardiac catherterisation
ECG in heart failure:
- rarely normal in patients with heart failure
- tall complexes = LV hypertrophy
- broad complexes = left bundle branch block
- T wave inversion
BNP in heart failure:
- brain natriuretic peptide (blood test)
- released by the left atrium (LA), in response to
increased LA pressure - sensitive for HF, therefore used as a screening test
- not specific
Investigations 1 diagram
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Echocardiogram in heart failure:
- LV dimensions/functions
- LV ejection fraction
- estimate intra-cardiac pressuresnnbfb
Cardiac MRI in heart failure:
- LV dimensions/function
- LV ejection fraction
- characterise myocardial pathology
Cardiac Catheterisation:
- LV dimensions/function
- direct measurement of intra-cardiac
pressures - coronary angiography
Left Sided Heart Failure:
- acute presentation (MI)
- elevated left heart pressures transmitted
back to the pulmonary capillaries - pulmonary oedema occurs when
pulmonary capillary pressure >25mmHg,
serum albumin = c.25g/L - in the most extreme cases, unable to
maintain cardiac output: CARDIOGENIC
SHOCK:
- cold, clammy
- thready pulse
- SBP <90mmHg
Right Heart Failure Mechanisms:
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- decreased left ventricular contractility,
which increases PA pressure, which
increases RV pressure, which increases RA
pressure leading to peripheral oedema
Left Heart Failure Mechanisms:
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- decreased LV contractility, which increases
left ventricular end diastolic pressure,
which increases left atrial pressure
- which increases pulmonary venous
pressure
Right Sided Heart Failure:
- chronic presentation
- most commonly due to left hearted
disease - elevated left heart pressures BUT
- LA dilates and LA/PV pressure <25mmHg
- pressure transmitted back to
PA,RV,RA,SVC/IVC:
- elevated JVP
- leg oedema
- pleural effusion/ ascites
Cor Pulmonale:
- is
- caused by
- results in
- right sided heart failure due to chronic lung
disease - many causes: COPD, lung fibrosis,
pulmonary hypertension - elevated pulmonary artery pressures
- pressure transmitted back to RV, RA,
SVC/IVC: high JVP, leg oedema, pleural
effusions/ ascites
Preload diagram
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- preload is important, degree of preload is
important to make sure the heart is
stretched enough
- but if preload is too high, increases cardiac
output because increased venous return to
the heart
Renin-Angiotensin-Aldosterone System
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Neuro-endocrine activation in heart failure:
- low cardiac output activates
- mechanisms
- results/consequences
- low cardiac output activates:
- RAAS
- Reduced renal perfusion
- by multiple mechanisms:
- low BP
- low NaCl delivery to kidneys (macula
densa cells in the DCT) - sympathetic division
- increases preload, increased cardiac
output but - oedema/ascites/pleural effusion
- increased afterload: angiotensin mediated
vasoconstriction
RAAS activation diagram
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RAAS activation 2 diagram
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Sympathetic Activation in the heart:
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- sympathetic activation is meant to restore
the patient back to normal
- if over activated , heart becomes weak and
tired
- increases heart rate (beta 1 receptors
activated) and hence increases contractile
force
- short term: increases cardiac output
- long term: worsens heart failure (flogging a
dead horse)
Diastolic Heart Failure:
- due to prolonged sympathetic activation
- heart failure but LV systolic function is
GOOD: HFpEF = heart failure with
preserved ejection fraction - chronic heart failure syndrome but:
- normal LV volume
- LV ejection fraction >40% - due to increased LV stiffness, hence
reduced compliance - causes same cascade of increased
pressures - LV dilation
Sympathetic activation and the arterial system:
- vasoconstriction (alpha 1)
- increases systemic vascular resistance
(SVR) - increases afterload
- in the short term: maintains arterial blood
pressure - long term: increases workload on already
weakened heart (making dying horse run
uphill)
Diastolic Heart Failure Mechanisms:
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- LV stiffness increases, increases LA
pressure, which increases pulmonary
venous pressure causing pulmonary
oedema, if prolonged can increase pressure on RV, RA, PA
Therapeutic targets of chronic heart failure:
- fluid retention: loop diuretic (furosemide)
- angiotensin II production: ACE inhibitor
(ramipril) - Angiotensin II receptors: Angiotensin
receptor inhibitor
(Losarten) - Aldosterone antagonists: Spironolactone
- Sympathetic system: beta blockers
(bisprolol)
LV diastolic failure is commonly seen in
elderly patients
hypertension, diabetes, atrial fibrillation
LV diastolic heart failure is classified as a ——– cardiomyopathy
restrictive
LV diastolic heart failure aetiology:
- amyloid heart disease
- sarcoidosis
- severe LV hypertrophy: hypertension,
hypertrophic cardiomyopathy
Chronic heart failure: advanced therapeutics: Fluid Retention:
- Dapaglifozin:
- SGLT-2 inhibitors
- reduces glucose reabsorption in the kidney
- osmotic diuresis
- Neprilysin inhibitors:
- sacubatril usually used with an angiotensin
antagonist (Valsartan) - I(small f) inhibitor: Ivabradine
Acute Heart Failure Management:
PODMAN
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