Heart failure Flashcards
1
Q
Definition
A
Failure of the heart to pump blood at a rate sufficient to meet the metabolic requirements of the tissues, caused by an abnormality of any aspect of cardiac function and with adequate cardiac filling pressure.
2
Q
Causes of Heart failure
A
- Vascular - (Coronary artery disease, HTN)
- Infective (bacterial, fungal, viral)
- Trauma -
- Autoimmune
- Metabolic - pregnancy, Endocrine disorders (DM, Thyroid disease)
- Infiltrative (amyloidosis, haemochromotosis)
- Neoplastic
- Congenital heart disease
- Drug induced - heroin, cocaine, chemotherapy
75% caused by IHD
3
Q
Pathophysiology
(Neurohumeral)
A
- Initial event (infarction, inflammation, pressure/volume overload) causes myocardial damage, resulting in an increase in myocardial wall stress.
- This is followed by the activation of of multiple neuroendocrine systems :
- SNS
- Improves ventricular function by increasing heart rate and muocardial contractility
- constriction of venous capacitance vessels redistributes flow centrally and the increased venous reutrn to the heart (preload) further augments ventricular function via the starling mechanisms
- Sympathetic stimulation, however, also leads to arteriolar contrction, this increasing the afterload which would eventually reduce cardiac output
- RAAS
- The fall in CO and increased sympathetic tone lead to diminshed renal perfusion, activation of the RAAS and hence increased fluid retention
- Salt and water retention further increases venous pressure and maintains stroke volume by the starlng mechanism
- as salt and water increases peripheral and pulmonary congestion causes oedema and contritues to dyspnoea.
- angiotensin II also causes arteriolar contruction,t thus increases the afterload and work of the heart
-
Natruretic peptides
- there are release from the atria (ANP), ventricles (BNP) and vascular endothelium (c-type peptide)
- the have diuretic, natriretic and hypotensice proerties
- the effect of their action may present a beneficial albeit inadequate, compensatory response leading to reduced cardiac load (preload and afterload)
- ADH
- Also known as vasopressin
- released from hypothalamus
- triggered by low CO
- Also stimulate by AT II
- ehances water reabsorption by the kidneys
- Promotes water retention
4
Q
Pathophysiology
(ventricular dilation and ventricular remodelling)
A
Ventricular dilation
- myocardial failure leads to a reduction of the volume of bloood ejected with each heartbeat, and thus an increase in the volume of blood remaining after systole.
- the increased diastolic volume stretches the myocardial fibres and as starling law would suggest, myocardial contraction is restored
- once heart failure is established, the compensatory effects of cardiac dilation become limited by the flattened contour of starlings
- eventially the increased venous pressure contributes to the development of pulmonary and peripheral oedema
Ventricular remodelling
- Process of hypertrophy, loss of myoctyes and increased interstitial fibrosis which all contribute to progressive and irreversibel pump (contractile) failure.
- the process is multifactorial and includes apoptosis of nyoctyes and changes in cardiac contracile gene expression
5
Q
Clinical symptoms and signs of left heart failure
A
Left side of the heart is responsible for receiving oxygen-rich blood from the lungs and pumping it forward to they systemic circulation. Failure then results in blood to back up into the lungs
Symptoms
- dyspnoea (SOB)
- orthopnoea (SOB when lying flat)
- paroxysmal nocturnal dyspnoea (sudden night time attack of SOB)
- fatigue (respiratory compromise)
- nocturnal cough (pink frothy sputum)
- wheeze (cardiac asthma)
- cold peripheries
- muscle wasting
Signs
- diaphroesis (sweating)
- tachycardia
- pulmonary crackles
- loud P2
- S3 gallop (systolic dysfunction)
- S4 gallop (diastolic dysfunction)
6
Q
Symptoms and signs of right heart failure
A
Right sided heart failure is often caused by pulmonary heart disease (cor pulmonale),difficulites of the pulmonary circulation
Symptoms
- Peripheral oedema (up to thighs, scarum, abdominal wall)
- right upper quadrant discomfort (hepatic enlargement)
Signs
- Jugular venous distention
- hepatomegaly
- peripheral oedema
7
Q
Symptoms NYHA classifcation
A
1- No limitation of PA
- Slight limiation of PA - Symptoms with ordinary levels of exertion (e.g. walking upstairs)
3, Marked limitation of PA - symptoms with minimal levels of exertion (e.g. dressing)
- Symtoms at rest
8
Q
Systolic versus diastolic failure
A
- Systolic failure - inability of the ventricle to contract normally, resulting in decreased cardiac output. Ejection fractoin is <40%. Causes: IHD, MI, cardiomyopathy
- Diastolic failure - inability of the ventricle to relax and fill normally, causing increased filling pressures. EF >50% causes: constrictive pericarditis, tamponade
9
Q
Acute vs Chronic heart failure
A
- acute - used exclusvely to mean new onset acute or decmpensation of chronic heart failure, characterised by pulmonary and/or peripheral oedema
- Chronic - develops progress slowly. Venous congestion is common but arterial pressure is well maintaned until very late
10
Q
Low output vs high output failure
A
-
Low output -cardiac output is decreased and fails to increase normally with exertion
- Pump failure - systolic and or diastolic HF, decreased heart rate (b-blockers, heart block, post MI), negatively inotropic drugs
- Excessive- mitral regurg or fluid overload
-
High output - rare. Here, output is normal or increased in the face of increased needs. Failure occurs when cardiac output fails to meet these needs. It will occur with a normal heart rate, but even earlier if there is heart disease
- anaemia, pregnancy, hyperthyroidism
11
Q
Investigations
A
AIm of investifation is a patient wit symptoms and signs of heart failure is to objectively show evidence of cardiac dysfunction
- Chest X-ray - see next card
- ECG - evidence of underlying cause (arrhytmias, ischaemia, left ventricular hypertrophy in hypertension)
- Bloods - FBC (anaemia exacerbating HF), Liver biochem (alterted due to hepatic congestion), Blood glucose (diabetes), Urea and electrolytes (as a baseline before starting diuretics), Thyroid function (AF), BNP (excludes heart failure)
- Echo- performed in all patients with new onset failure. Assement of ventricular systolic and diastolic dunction, shows regional wall motion abnoramilties and shows the aetiology of heart failure
According to nice if ECG and B-type NP are normal, heart failure is unlikely.If either is abnormal then echo is required
12
Q
CXR signs of heart failure
A
- Alevolar oedema (bat wings)
- Kerley B lines (interstitial oedema)
- Cardiomegaly
- Dilated prominent upper lobe vessels
- Pleural effusions
13
Q
General measures of treatment of chronic heart failure
A
- Education fo patients and family
- Physical activity: reduce during exacerbations to reduce work of the heart (encourage low level 20-30 mins walks 3-5 times a week)
- diet and social: weight reduction, no added salt, avoid alcohol, stop smoking)
- Vaccinate against pneumoccal disease and influenza
- correct aggravating factors e.g arrhythmias, anaemia, hypertension
- Driving: unrestricted, except symptomatic heart failure disqualifies large lorries and buses
- Sexual activity: tell patient on nitrates not to take phosphodiesterase type 5 inhibitors
14
Q
Pharmacological management of heart failure
A
- Ace Inhibitor - Improves symptoms and prolongs life - increase sodium and water excretion by reducing afterload
- B-blockers - (carvediol) - decreases moratlity (start low and go slow) - block chronically activated sympatehtic acitivuty
- Vasodilators - Combination of hydralazine and isosorbide dinitrate should be used if intolerant of ACE-I
- Diuretics - Give loop to reliver symptoms - Furosemide 40mg/24h PO. Increase dose as necessary and add K+ sparing diuretic (spironolactone) If K+<3.2 mmol/L
- Digoxin - indicated in patient with heart failure and atrial fib
15
Q
Non-pharmacological treatment in selected cases
A
- Revascularisation (CABG) - CAD is the most common cause of ehart failure
- cardiac resyncrhoization - improves co-ordination of atrial and ventricles
- implantable cardoverter defibrillator
- replacement of diseased valves
