Clinical management of heart failure Flashcards
To maintain normal cardiac function it is required to have adequate:
- Myocardial contractility
- Effective blood supply
- Effective conduction system
- Effective valve function
What is heart failure
- Clinical syndrome characterised by typical symptoms (e.g., breathlessness and fatigue)
- May be accompanied by signs (e.g., elevated Jugular Venous Pressure, pulmonary crackles and peripheral oedema)
- Caused by a structural and/ or functional cardiac abnormality
- Resulting in reduced cardiac output and/or elevated intracardiac pressures at rest or during stress.
Pathophysiology of heart failure involves changes in:
- cardiac function
- neurohormonal status
- systemic vascular function
- blood volume
- integration of cardiac and vascular changes
These can be seen as compensatory changes to help maintain CO (by the Starling mechanism of the heart) and arterial B pressure (by systemic vasoconstriction).
Over a long time these changes can worsen cardiac function. Therefore some of the best treatments for HF control these changes e.g., diuretics, vasodilators
Compensatory mechanisms during heart failure
Cardiac
- Frank-stalring mechanism
- chronic ventricular dilation or hypertrophy
- tachycardia
Autonomic nerves
- Increased sympathetic adrenergic activity (ßR’s activated by NE elevate cAMP- decrease contractility in sm muscle but increases it in cardiac)
- Reduced vagal activity of the heart (parasympathetic action on heart)
Hormones
- RAAs system
- ADH
- Circulating catecholamines (e.g,. adrenaline)
- Natriuretic peptides
What is the change in cardiac function seen in HF?
decreased CO duie to decreased SV.
how can the neurohormonal changes result in pathology
can aggravate heart failure by:
- increasing ventricular afterload (which depresses stroke volume)
- increasing preload to the point where pulmonary or systemic congestion and edema occur
therefore attenuating these changes can help in heart failure e.g.,
- beta blockers decrease excessive symp activity in the heart
- ACE inhibitors, AngR blockers and aldosterone R antagonists
What are the 2 reasons that stroke volume may change in HF?
1) systolic dysfunction results from:
a) loss of intrinsic inotropy (contractility) - caused by alterations in signal transduction mechanisms responsible for regulating inotropy
b) loss of viable contracting muscle following acute myocardial infarction
2) Diastolic dysfunction (vent less compliant so doesn’t fill as it should– less ejection – starling’s law)
Both dysfunctions result in a greater EDV– Starling’s law of the heart (stretches walls, more cross bridges, stroke volume???)
Therapeutic interventions to improve cardiac function include
use of cardiostimulatory drugs (B2 agonists and digitalis) that stimulate HR and contractility
and
use of vasodilators to reduce ventricular afterload (average arterial pressure- pressure vents must overcome to eject blood)
What are the neurohormonal responses to HF (patho)
- Activation of sympathetic nerves and the renin-angiotensin-aldosterone system and
- increased release of ADH and ANP
What are the net changes casued by the neurohormonal changes?
They all have the target of keeping organs perfused in face of decreased CO
- arterial vasoconstriction (maintain arterial pressure)
- venous constriction (maintain venous pressure)
- increased blood volume (increase ventricular filling- EDV- starling’s- increase SV)
How does blood volume change in heart failure
compensatory increase in BV to increase ventricular preload and thereby increase SV by Starlings law of the heart:
Reduced renal perfusion (symp constriction of afferent renal a) results in decreased urine output and retention of fluid
combination of reduced renal perfusion and sympathetic activation of the kidneys stimulates the release of renin, thereby activating the renin-angiotensin system
increase in circulating ADH
why can the blood volume change become pathological
raises venous pressures leading to pulmonary and systemic oedema
When edema occurs in the lungs, this can result in exertional dyspnea (shortness of breath during exertion). Therefore, most patients in heart failure are treated with diuretic drugs to reduce blood volume and venous pressures in order to reduce edema.
Which sided heart failure results in congetsion of the pulmonary vascualr system and pleural effusions
left
causes of heart failure
- Arrythmias
- Cardiotoxins (e.g., chemotherapy, alcohol, illicit drugs)
- Congenital heart disease
- Genetic cardiomyopathies (e.g. dilated or hypertrophic cardiomyopathies)
- Hypertensive heart disease
- Infection (e.g. myocarditis, infective endocarditis)
- Ischaemic heart disease
- Lung disease
- Pregnancy
- Thyroid disease/ anaemia
- Valvular heart disease
3 most common causes of heart failure
- Ischaemic heart disease
- MI
- Angina
irreversible causes of heart failure
Ischaemic heart disease
Lung disease
Congenital heart disease
Genetic cardiomyopathies (e.g. dilated or hypertrophic cardiomyopathies)
Hypertensive heart disease
relevence of cardiac remodelling
hypertrophy of myocardium in an effort to increase contractility
how does valve disease lead to HF
Valves can either be stenotic: stiff and struggle to open restricting blood flow through them
Or regurgative- leaky and don’t close properly blood flows back through them when they’re closed.
Both affect the functioning of the heart.
what are the 3 kinds of cardiomyopathy
cardiomyopathy is a general term for disease of the myocardium
types:
- Hypertrophic- muscle of the ventricles become thickened, reducing the volume that the ventricles can hold and the amount it can force out during systole. This often doesn’t cause a change in ejection fraction.
- Restrictive- muscle walls become more fibrous and don’t move in the same way, a;tered filling and ejection- variable EF depending on ratio.
- Dilated- muscle walls are thin and stretched, holding a larger volume but without the muscle capacity to force the blood out during diastole and hence a reduced EF.
What is ejection fraction?
- the ratio of the amount of blood that can be forced out in a single contraction as a proportion of the volume it can hold. In this case smaller volume and smaller output but normal EF.
Extremely important in determining the treatment options for heart failure.
HF w reduced EF it is <40%
HF w mid-range EF is 41-49%
HF w preserved EF is 55-70%
what is the most common arrhythmia
atrial fibrillation
Symptoms of CHF
- breathlessness
- orthopnea- struggle to breathe when lying down
- paroxysmal nocturnal dyspnoea (attack of severe shortness of breath and coughing that generally occurs at night)
- reduced exercise tolerance
- fatigue, tiredness, increased time to recover after exercise
- ankle swelling
Signs of CHF
Specific:
- Elevated jugular venous pressure
- Hepatojugular reflux
- Third heart sound (gallop rhythm)
- Laterally displaced apical impulse
Less specific:
- Weight gain
- Tachycardia
- Ascites
- Hepatomegaly
- Peripheral oedema
- Tachypnoea
Relevance of BNP in diagnosing CHF
Investigations for diagnosing HF
- CXR
- ECG
- FBC
- U&Es
- LFTs
- TFTs
- BNP
- Peak flow, spirometry
- Echocardiogram is gold standard. it is a type of ultrasound
Types of heart failure
- HFrEF- reduced (EF< 40)
- HFpEF- preserved
- HFmrEF- mid range (EF>70?)
- Systolic dysfunction
- Diastolic dysfunction
- Left
- Right
- Cor pulmonale- remodelling of the right side of the heart accompanied by functional changes due to pulmonary hypertension. Often stems from left sided heart failure.
- Low output- low CO output, end organ hypoperfusion e.g., tachy and brady cardias + impairment of left ventricle
- High output- normally functioning heart cannot keep up w increased demands from organs e.g., pregnancy, anaemia
- Valvular-
- Arrhythmic- arrhythmias exacerbate heart failure symptoms
treatment options list
- manage comorbidities e.g., hypertension, atrial fib, ischaemic heart disease
- Offer a personalised exercised based cardiac rehab
- Medication: ACEI, ßB, ARB if intolerant to ACEI, consider hydralizine and ARB, perhaps sacubitril, valsartan, ivabradine, digoxin
medical treatments
see pharmacology lecture
start with ACE I (enalapril) and ARB (angiotensin receptor blocker) (valsartan)
then ßB (atenolol), MRA (minerlocorticoid receptor antagonist) (spiroronalactone)
ivabradine, SGLT2 inhibs (Dapagliflozin)
Non-pharmacological management
- Cardiac Resynchronisation Therapy (CRT pacing)
- Implantable Cardioverter Defibrillator (ICD)
- Left Ventricular Assist Device (LVAD)
- Bridge to transplant
- Heart transplant
- Abstinence
- Salt restrictions
- Fluid restrictions
- Heart failure rehab
- This is recommended to all HF patient and aims on improving symptoms.
Disease trajectory
- Difficult to predict
- Frequent admissions
- Poor QoL
- Depression/ anxiety
- Palliative care/ timings
