U12C4 Heart Failure Flashcards
What is the NYHA (New York heart association) functional classification?
I. No limitation of physical activity. Ordinary physical activity does not cause undue fatigue, palpitation, dyspnoea.
II. Slight limitation of physical activity. Comfortable at rest. Ordinary physical activity results in fatigue, palpitation, dyspnoea.
III. Marked limitation of physical activity. Comfortable at rest. Less than ordinary activity causes fatigue, palpitation, or dyspnoea.
IV. Unable to carry on any physical activity without discomfort. Symptoms of heart failure at rest. If any physical activity is undertaken, discomfort increases.
Left vs right heart failure
What is the management of CHF?
What is the diagnosis of CHF?
-Chest X-ray: Look for cardiomegaly (>0.5), pulmonary congestion with upper lobe diversion, fluid in fissures, Kerley B lines and pulmonary oedema.
- ECG: Identify ischaemia (pathological Q waves), ventricular hypertrophy or arrhythmia (lack of P waves – A fib)
- Echocardiography: Assess cardiac chamber dimension, systolic and diastolic function, regional wall motion abnormalities, valvular disease and cardiomyopathies.
- Nuclear cardiology: Radionucleotide angiography (RNA) can quantify ventricular ejection fraction; SPECT or PET can demonstrate myocardial ischaemia and viability in dysfunctional myocardium.
- Cardiac MRI (CMR): Assess cardiac structure and function and viability in dysfunctional myocardium with the use of dobutamine for contractile reserve or with gadolinium for delayed enhancement (‘infarct imaging’).
- Cardiac catheterization: Diagnosis of ischaemic HF (and suitability for revascularization) and for measurement of pulmonary artery pressure, left atrial (wedge) pressure, left ventricular end-diastolic pressure.
- Cardiac biopsy: This is used for diagnosis of cardiomyopathies, such as amyloid, and for follow-up of transplanted patients to assess rejection.
- Cardiopulmonary exercise testing: Peak oxygen consumption (VO2) is predictive of hospital admission and death in heart failure. A 6-minute exercise walk is an alternative.
- Ambulatory 24-hour ECG monitoring (Holter): This is used in patients with suspected arrhythmia and may be employed in those with severe heart failure or inherited cardiomyopathy to determine whether a defibrillator is appropriate (non-sustained ventricular
tachycardia).
- Stress echocardiography: Assess viability in dysfunctional myocardium – dobutamine identifies contractile reserve in stunned or hibernating myocardium.
What is heart failure?
- Clinical syndrome
- Characterised by typical symptoms (e.g. breathlessness and fatigue)
- 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 a reduced cardiac output
What are the causes and risk factors of heart failure?
- Ischaemic heart disease
- Lung disease
- Congenital heart disease
- Genetic cardiomyopathies
- Hypertensive heart disease
- Arrhythmias
- Cardiotoxins
- Thyroid disease / Anaemia
- Infection
- Pregnancy
- Valvular heart disease
- Older age – means you are more likely to have a prior mentioned condition which causes HF AND with progressing age myocardial systolic (lowered contractility) & diastolic (cardiac stiffness) function lowers = dec ability to contract & relax
- FH of HF – genetics which predispose someone to HTN or hypercholesterolaemia (familial hypercholesterolaemia – genes: type 1 LDL-R mutation & type II ApoB mutation) AND families tend to have similar diets so if this is poor this is a risk in itself
- Ethnicity – Black & African American – these individuals may have certain genes which predisposes them to HTN = variants of the GRK4 is linked to impaired Na+ excretion
- Smoking – nicotine increases adrenaline (catecholamine) – which increases platelet aggregation = inc thrombosis = inc resistance to blood flow (TPR) = inc Pa – HTN – which again is a causative factor for heart failure if this HTN is long-term
- Poor diet – high fat diet can cause hyperlipidaemia = risk of atherosclerosis (LDL into tunica intima…)
- Chronic heavy alcohol use – can cause alcoholic cardiomyopathy = fibrosis of myocardium over time = dec contractility – causing ventricular dilation as a compensatory mechanism (direct effect on HF) AND causes HTN by lowering vasodilators such as NO either by inhibiting eNOS or due to oxidative stress on vascular endothelium (indirect effect on HF)
- Illicit drugs – injecting these can cause collapse of veins, bacterial infections of blood vessels & heart valves AND certain drugs (cocaine, amphetamine) are linked to dilated cardiomyopathy AND HTN (stimulant drugs)
- HIV – inflammatory damage to myocardium AND high levels of inflammation promotes a pro-coagulant state (by lowering levels of endogenous anticoagulants & impairing fibrinolysis) = thrombosis = thrombotic complications (HTN – see above)
- Obesity – links to diet & inflammatory state (adipose tissue stimulates release of pro-inflammatory mediators)
- Diabetes – can worsen or inc risk of HF – as hyperglycaemia can damage blood vessels & nerves (& inflammatory & HTN link)
- Anaemia – body tries to compensate for low O2 by inc HR = tachycardia = inc cardiac work
- Hyperthyroidism – cause or worsen cardiac conditions - thyroid hormones upregulate B1 adrenergic recs = inc sensitivity to catecholamines = inc contractility, HR = inc SV = inc CO - so inc myocardial O2 demand –> BUT then in later stages this inc HR causes systolic & diastolic dysfunction (forms of LVHF) -> systolic dysfunction if the inc HR causesinc pressure in ventricles = causing biventricular dilation – which thins the walls of the ventricles (dec contractile state of myocytes) making them weaker - which in turn lowers contractility = dec SV - whereas diastolic dysfunction is where this high HR causes dec diastolic filling of ventricles = dec EDV = dec SV => both of these are reversible by treating tachycardia (tachycardia-induced cardiomyopathy)
- Sleep apnoea – frequent drops in O2 sats whilst sleeping (repeated hypoxemia) = dec O2 delivery to myocardium = overstimulation of symp NS, RAAS = inc HR, contractility = inc Pa = HTN (BP is high during sleep & can be high when awake)
- Pregnancy – systemic vasodilation by inc NO production = ~30% dec in TPR = dec BP (Pa) in 1st trimester & most of 2nd – to compensate for this CO increases during trimester 1 & 2 (by ~40%) by inc SV => this is all to inc blood flow to meet inc metabolic demands of tissuesIn 3rd trimester – BP starts to rise
What are the types of heart failure?
- HFrEF - reduced
- HFpEF – preserved
- HFmrEF – mid range
- Systolic dysfunction
- Diastolic dysfunction
- Left
- Right
- Cor pulmonale
- Low output
- High output
- Valvular
- Arrhythmic
- Cardiomyopathies
What is the pathophysiology of heart failure?
What is the ejection fraction borders for heart failure?
What would BNP levels indicate?
- Elevated natriuretic peptides can be easily measured by readily available blood test
- NT-pro BNP
- Hormone secreted by cardiomyocytes in the ventricles in response to stretching
- Other causes raised levels:
1. Acute renal failure and chronic renal failure.
2. Hypertension (HTN)
3. Pulmonary diseases such as pulmonary hypertension, severe chronic obstructive pulmonary disease (COPD), pneumonia, pulmonary embolism, adult respiratory distress syndrome (ARDS)
What are the non-pharmacological management for heart failure?
- Devices
1. Cardiac Resynchronisation Therapy (CRT pacing)
2. Implantable Cardioverter- Defibrillator (ICD) - Advanced HF therapy – specialist centres
- Left Ventricular Assist Device (LVAD)
- Bridge to transplant
- Heart transplant
- Salt and fluid restrictions
- Hear failure rehab
What are the electrophysiological changes in chronic heart failure?
What is the pathogenesis of left heart failure?
What is the pathogenesis of right heart failure?
What are the signs and symptoms of left heart failure?
What are the signs and symptoms of left vs right heart failure?
What is paroxysmal nocturnal dyspnea?
