Chronic Heart Failure Flashcards
What are the 2 types of dysfunction which can be present in HF? What are the associated precipitating events?
Systolic dysfunction= impaired LV contraction -decreased CO -EF< 40% Causes: -IHD -MI -Cardiomyopathy
Diastolic dysfunction= impaired LV relaxation due to stiffening -increased filling pressures -EF> 50%== HFpEF (heart failure with preserved ejection fraction) Causes: -ventricular hypertrophy -constrictive pericarditis -tamponade -restrictive cardiomyopathy
Both lead to state of chronic back pressure
How does the heart try to compensate for the dysfunction present in HF to try and maintain CO?
Dilation
Hypertrophy
Increased HR via Ad
RAAS activated
ANP released to decreased BP via diuresis
What are the causes of LVF?
IHD
Valvular heart disease- aortic stenosis
MI
Cardiomyopathy
Hypertension
Arrthymias i.e AF
How is someone with LVF likely to present?
SOB- worse on exertion i.e. poor exercise tolerance
Fatigue
Cough- producing frothy white/pink sputum
Orthopnoea- ask number of pillows require
PND (paroxysmal nocturnal dyspnoea)
Wheeze= cardiac asthma (bronchiole wall thickening due to increased back pressure into bronchiole veins via LA
Peripheral oedema
Why do people with LVF produce frothy white/pink sputum?
Increased pressure in LA causes increased back pressure across pulmonary veins and capillaries. The fenestrated capillaries in lungs are prone to bursting with increased pressure which leads to small amount of blood accumulating in the alveoli
What is paroxysmal nocturnal dyspnoea (PND) and why does it occur in people with HF?
Waking up in night with acute SOB, cough and wheeze
Fluid accumulates across large surface area of lungs when person lies flats= reduces area of lung able to work effectively
Resp centre becomes less responsive to resp rate and effort during sleep so person can develop more significant hypoxia before being woken up
Decreased adrenaline circulating when sleeping meaning myocardium is more relaxed= reduces CO
How is HF diagnosed?
Clinical diagnoses= evidence of signs and symptoms inline with HF
BNP blood test = elevated
-released in response to volume expansion and increased wall stress of cardiac myocytes
ECG= can indicate the cause i.e. historic MI or hypertrophy
CXR
Echocardiogram
-can assess the ejection fracture to differentiate between the different forms of HF
What is the first line medical treatment for HF? What are the aims of this treatment?
ABAL
ACEi= ramipril
- considered in all LV systolic dysfunction
- ARB can be used if patient has problem with cough
Betablocker= bisoprolol/carvedilol
-start slow and go slow (want to be cautious with changes in dosage )
Aldosterone antagonist= spironolactone (when A+B not controlling)
Loop diuretic= furosemide (improves symptoms)
Aim:
-decrease cardiac work but decreasing the rate of the heart with beta-blockers and by decreasing the afterload by removing any excess retained fluid
Why do U+Es need to be closely monitored in HF patients?
ACEi and aldosterone antagonists can lead to electrolyte disturbances
What signs on examination would be indicative of HF?
Cold peripheries/cyanosis Narrow pulse pressure Peripheral oedema Displaced apex beat due to LV dilation RV heave= pulmonary hypertension Murmurs associated with valve disease
What ECG changes can be found in HF?
Prolonged QRS
Left axis deviation= due to associated LV hypertrophy
Left ventricular hypertrophy= increased height of QRS complexes (>25 combined)
LBBB
What signs on CXR would indicated HF?
A= alveolar oedema (looks like bat wings)
B= Kerley B lines due to interstitial oedema
C= cardiomegaly (globular heart)
D= dilated prominent upper lobes veins (upper lobe diversion)
E= pleural effusion
What does low-output mean in context of HF? What are the causes of low-output heart failure?
Decreased CO without ability to increase CO with normal exertion
Excessive preload
- mitral regurgitation
- fluid overload i.e renal failure
Pump failure
- systolic +/- diastolic HF
- decreased HR when on beta blockers or post-MI
- negative ionotropic antiarrhythmics
Chronic excessive afterload
- aortic stenosis
- hypertension
What is the different consequences for excessive preload and excessive afterload on heart failure?
Preload= ventricular dilatation
-leads to exacerbation of pump failure
Afterload= ventricular hypertrophy
-leads to stiffening of ventricle wall which leads to diastolic dysfunction
When is digoxin used in treatment of heart failure?
In patients with LVSD who are still symptomatic after treatment with ACEi and beta blockers or in patients who have AF
Where is BNP secreted from and what is it’s role? Why is it investigated in suspected HF? What is the diagnostic criteria for BNP?
Secreted by ventricular myocardium (secretion closely related to ventricular pressure)
Role:
- increase GFR and decreased renal absorption of Na+ which reduces the preload
- relaxation of SM to decreased preload
Sensitive bio-marker to distinguish heart failure from the other possible causes of dyspnoea
>100ng/L= indicates HF <50ng/L= “rules out” HF
Apart from heart failure, what other conditions can cause a rise in BNP?
Tachycardia Cardiac ischaemia COPD PE Renal disease Sepsis Diabetes Hepatic cirrhosis
Why is it important to monitor Hb levels in HF patients?
Need to determine if have anaemia:
- anaemia can induce high output state which can exacerbate HF
- associated with high mortality if untreated/managed
TX:
-iron infusion
How is the management of HF adjusted when patient has CKD?
Need to change form which diuretics administered to reduce the strain on the kidneys:
-move from oral furosemide to infusion
How is ARNI used in HF alongside the 1st line treatment (ABAL)? What are the possible SE?
ARNI= Entresto= contains 2 active components= Valsartan + Sacubitril
- valsartan= angiotensin blockers
- sacubitril= neprilysin inhibitor= prevents the breakdown of natriuretic peptides (BNP) (i.e. inhibits normal action of neprilysin) = increases Na+ and H2) excretion to reduce blood volume and reduce blood pressure
Therefore= decreases strain on heart
Use:
-used in chronic HF with reduced ejection fraction or NYHA II, III, IV
SE:
- renal impairment
- hypotension
How can SGTL2 drugs be used in HF management along side 1st line treatment?
Have been found to decreased mortality of HF patients
- block glucose reabsorption in PCT
- glucose absorption paired with sodium absorption so decreasing glucose absorption leads to increased sodium excretion which can lead to increased water loss= can act to lower BP and decreases strain on heart
What is the NYHA scoring system used in HF?
New York Heart Association classification of severity of chronic HF
I= no physical limitation of ADL II= slight limitation of ADL i.e. mild SOB when walking III= marked limitation in ADL i.e. breathless when getting dressed, cleaning, putting the bins out IV= breathless at rest
What is CRT and what role does it have in management HF?
Cardio re-synchronisation therapy
Used in patients with left ventricular systole dysfunction= the dysfunction in contraction can lead to symptoms such as breathlessness (patients with congestive HF)
It is placed in the coronary sinus in HF
