Heart Failure Flashcards
Pathophysiology of Heart Failure
Mechanisms of heart failure [3]
Systolic and diastolic failure
Left and right failure
High and low output failure
Explain systolic vs diastolic heart failure but note that they usually co-exist
Systolic Heart Failure EF low - Decreased pumping / CO and fluid backs up - Eg IHD, MI, cardiomyopathy Diastolic - preserved EF - Hypertrophy so doesn't fill or relax - Fluid back up
Explain the difference between Left and Right sided Heart Failure
- Left sided failure:
- Ax: IHD, valvular heart disease
- Regurgitation of blood into lungs > pulmonary congestion, hypertension
-Caused by poor systolic function > decreased pulses - Right sided failure:
- Ax: LVF, pulmonary stenosis, cor pulmonale
- Less blood goes to lungs
- Blood backs up to body tissues causing edema
Right-sided heart failure generally develops as a result of advanced left-sided heart failure - Congestive cardiac failure: left and right failure
Describe low [4] and high [3] output failure
Low output failure
- cardiac output reduced, normally increases with exertion
- Pump failure
- Excessive preload
- Chronic excessive after load
High output failure (rare)
- output normal or increased due to increased body requirements
- but CO can’t meet these requirements
- Anaemia, pregnancy, Paget’s disease, AV malformation
Causes of low output failure:
Pump failure [3]
Excessive preload [2]
Chronic excessive after load [2]
- Pump failure:
- systolic and/or diastolic failure
- reduced heart rate (post-MI, heart block, beta blockers), negatively ionotropic drugs (anti-arrhythmic agents) - Excessive preload:
- mitral regurgitation
- fluid overload (NSAIDs causing excessive fluid retention, normal heart but renal impairment or fluids running too fast) - Chronic excessive afterload:
- aortic stenosis, hypertension
Presentation of RHF [6] and LHF [6]
RHF:
- JVP elevated
- peripheral oedema (sacrum, thighs, abdo wall), ascites
- nausea, anorexia
- venous engorgement
- neck and face pulsation (tricuspid regurgitation)
- epistaxis
LHF:
- SOB, orthopnoea, PND, nocturnal cough (pink frothy sputum)
- wheeze (cardiac asthma)
- RV heave
- poor exercise tolerance
- fatigue
- weight loss (cardiac cachexia; can be masked by “weight gain” due to oedema)
- muscle wasting
- cool peripheries, cyanosis
- displaced apex beat
Investigations for heart failure [4]
N-terminal pro B type natriuretic peptide
TFTs- thyrotoxicosis may mimic HF, Haematinics
ECG
TTE
CXR
B-type natriuretic peptide (BNP) is a hormone produced mainly by the left ventricular myocardium in response to strain. Very high levels are associated with a poor prognosis.
high (2000ng/L) = TTE in 2w
Natriuretic peptides are non-specific but
very sensitive and so a normal level virtually
excludes heart failure.
2. raised (400-2000ng/L) = TTE in 6w
HF
Findings on ECG
Ischemic changes
Ventricular hypertrophy
- RVH = tall R wave in V1, deep S wave in V6
- LVH = deep S wave in V1, tall R wave in V6
TTE uses in ix heart failure [3]
CXR [5]
- TTE: identify valve disease, systolic and diastolic ventricular function and cardiac shunts
- CXR: ABCDE =
Alveolar oedema (bat’s wings)
Kerley B lines (interstitial oedema)
Cardiomegaly
Dilated prominent upper lobe vessels
Pleural Effusion
Diagnostic criteria for HF
Framingham criteria for congestive cardiac failure
>2 major OR 1 major and 2 minor
What is part of the Framingham MAJOR criteria [9]
PND
Bibasal crackles
Neck vein distension
Hepatojugular reflux
Acute pulmonary oedema
S3 gallop
Cardiomegaly (cardiothoracic ratio >50% on CXR)
Increased CVP (>16cmH2O in right atrium)
Weight loss >4.5kg in 5d in response to mx
What is part of the Framingham MINOR criteria [7]
Bilateral ankle oedema Nocturnal cough SOB on ordinary exertion Hepatomegaly Tachycardia (>120bpm) Pleural effusion Decrease in VC of 1/3 of maximum recorded
Increased BNP [12]
Age LVH, Ischaemia, Valve Tachycardia, Overload Hyperaemia inc PE Low GFR, CKD Sepsis COPD DM Liver cirrhosis
What causes decreased BNP [4]
Obesity
ACEI
BB
Diuretic / aldosterone antagonist
What is the New York classification of HF
Class 1 = no limitation
Class 2 = mild limitation to exercise, none at rest
Class 3 = moderate limitation, not at rest
Class 4 = severe limitation at rest
Management modalities of HF [5]
Lifestyle modification
Vaccination
Monitoring
Rx
Definitive treatment
Mx HF: Lifestyle mods [4], Vaccination [2]
Lifestyle modification:
- Cardiac rehab
- Smoking cessation, reduce alcohol
- Salt and fluid moderation
- Avoid NSAIDs
Vaccination:
- annual influenza
- and one off pneumococcal vaccination (need 5y booster if asplenia or CKD)
Mx HF: monitoring, definitive
- Monitoring: effective mx lowers BNP levels
* Cardiac transplantation: severe refractory symptoms or refractory cardiogenic shock
Acute heart failure
Etiology: describe two groups and their causes
- Acute on chronic HF: precipitated by ACS, hypertensive crisis, acute arrhythmia, valvular disease
- De-novo acute HF: viral myopathy, toxins , valve dysfunction
Signs of Acute heart failure [8]
- distress, pallor, sweating, sitting forward
- cyanosis, tachycardia
- pulsus alterans
- elevated JVP
- displaced apex beat
- bibasal crackles, wheeze
- S3 heart sound (gallop rhythm),
- BP usually normal*
What causes severe pulmonary oedema [6]
LVF post MI or IHD
Valve disease
HF
ARDS any cause
Fluid overload
Neurogenic
Infection
What causes peripheral oedema [6]
Heart failure = most common Cellulitis DVT Lack of mobility Chronic venous insuffinecy Lymphoedema
Initial management of acute heart failure [8]
Stop fluids Sit patient up 100% O2 if sats <96 but careful in COPD IV access, bloods: FBC U&E, CRP, ABG, *BNP, troponin ECG (MI, arythmias) IVFurosemide 40-80mg IV Diamorphine 1.25mg-5mg slowly GTN 2 puffs sublingual (unless SBP<90)
