Cardiology 2 Flashcards
Heart failure - definition
Cardiac output is inadequate for the body’s requirements – affects 1-3% of the general population.
HF - systolic vs diastolic
- Systolic – inability of the ventricles to contract normally resulting in a reduced cardiac output and an ejection fraction of <40%. Causes – ischaemic heart disease, MI or cardiomyopathy.
- Diastolic – inability of the ventricles to relax normally resulting in increased filling pressure and an ejection fraction of >50%. Causes – constrictive pericarditis, tamponade, restrictive cardiomyopathy or hypertension. (In reality there’s usually a combination of the two types).
HF - left vs right failure
Can occur separately or together as congestive heart failure:
- Left ventricular failure – causes dyspnoea, poor exercise tolerance, fatigue, orthopnoea, paroxysmal nocturnal dyspnoea (PND), nocturnal cough (with or without pink frothy sputum), wheeze (cardiac ‘asthma’), nocturia, cold peripheries, weight loss and muscle wasting.
- Right ventricular failure – can be caused by left ventricular failure, lung disease or pulmonary stenosis. It leads to peripheral oedema (can be up to abdominal wall), ascites, nausea, anorexia, facial engorgement, pulsation in neck and face (tricuspid regurgitation) or epistaxis.
HF - acute vs chronic
- Acute – new onset or decompensation of chronic heart failure – characterised by pulmonary or peripheral oedema.
- Chronic – progresses slowly – venous congestion occurs but arterial pressures well maintained.
HF - low output vs high output
Low output – cardiac output is reduced and fails to increase normally with exertion. Causes:
- Pump failure – systolic or diastolic heart failure, decreased heart rate (e.g. β blockers, heart block or post MI) or negatively inotropic drugs (e.g. most antiarrhythmic drugs).
- Excess preload – mitral regurgitation or fluid overload (e.g. NSAIDs causing retention or fast IVI).
- Chronic excessive afterload – aortic stenosis or hypertension.
High output – despite increased output the heart fails to meet the increased need of the body. Causes – anaemia, pregnancy, hyperthyroidism, Paget’s, beri beri or an AV malformation.
HF - Framingham criteria
Framingham criteria for congestive heart failure – diagnosis requires 2 major or 1 major and 2 minor:
- Major criteria – acute pulmonary oedema, crepitations, paroxysmal nocturnal dyspnoea, neck vein distension, hepatojugular reflex, increased CVP, S3 gallop, cardiomegaly and weight loss.
- Minor criteria – dyspnoea on ordinary exertion, nocturnal cough, pleural effusion, decrease in vital capacity, tachycardia, hepatomegaly and bilateral ankle oedema.
HF - New York Classification
- I – no dyspnoea from ordinary activity.
- II – dyspnoea from ordinary activities.
- III – less than ordinary activity causes dyspnoea.
- IV – dyspnoea is present at rest.
HF - Signs
Exhaustion, cool peripheries, cyanosis, hypotension, narrow pulse pressure, displaced apex (due to LVH), RV heave (due to pulmonary hypertension and RVH), mitral or aortic murmurs or a wheeze.
HF - Investigations
- Bloods – FBC (anaemia or infection), Us and Es (potassium level) and BNP (myocyte damage).
- CXR – A – alveolar oedema (Bat wing appearance), B – Kerley B lines (interstitial oedema), C – cardiomegaly, D – dilated prominent upper lobe vessels (diversion) and E – pleural effusion.
- ECG – may reveal a cause of heart failure e.g. ischaemia, MI or ventricular hypertrophy.
- Echocardiography – may indicate cause e.g. MI or valve disease and level of LV dysfunction.
HF - acute management
- Sit the patient upright and give 100% oxygen.
- Get IV access and get an ECG – identify arrhythmias and treat accordingly.
- Give diamorphine (2.5-5mg) with metoclopramide (10mg).
- Give IV furosemide (40-80mg) - but larger doses required in renal failure.
- GTN 2 puffs or 2 0.3mg tablets sublingual (not if systolic BP <90 mmHg).
- Start IV isosorbide dinitrate infusion (2-10mg/h) if systolic BP >100 mmHg.
- If worsening – give further furosemide (40-80mg), consider ventilation or increase nitrate infusion.
- Once stable – change to oral furosemide and consider addition of bendroflumethiazide (2.5-5mg OD). Patients should also be on an ACE-I, β blocker and spironolactone.
- Consider whether the patient is suitable for biventricular pacing or a cardiac transplant.
HF - chronic management - conservative
Encourage patient to stop smoking, reduce salt intake or optimise weight and nutrition.
HF - chronic management - medical
Treat cause (dysrhythmias or valve disease), treat exacerbating factors (anaemia, thyroid disease, infection, hypertension) and avoid exacerbating factors (NSAIDs, verapamil).
- ACE-I – lisinopril (10mg OD) to relieve symptoms or candesartan (4mg OD) if cough.
- Diuretics – give furosemide (40mg OD) to relieve symptoms and increase as necessary. (Monitor Us and Es and give potassium sparing - spironolactone if K+ is <3.2 mmol/L).
- B blockers – give carvedilol (3.125mg OD and increase slowly) to reduce mortality.
- Spironolactone – if patients are still symptomatic they should be given 25mg PO OD.
- Digoxin – 0.125-0.25mg PO OD can be given but Us and Es should be monitored (K+).
- Vasodilators – If ACEi or ARB are not tolerated hydralazine or a nitrate should be given.
Hypertension - definition
A major risk factor for stroke and MI but usually asymptomatic. Hypertension causes 50% of all vascular deaths and most preventable deaths are in areas without universal screening – primary care task.
- Stage 1 - clinic BP is >140/90 mmHg and subsequent ABPM or HBPM is >135/85 mmHg.
- Stage 2 - clinic BP is >160/100 mmHg and subsequent ABPM or HBPM is >150/95 mmHg.
- Severe - clinic systolic BP is >180 mmHg or clinic diastolic BP is >110 mmHg.
Hypertension - pathophysiology
95% of cases are essential hypertension where a combination of genetic and environmental factors results in a hypertensive phenotype. Causes of secondary hypertension include:
- Renal disease – 75% are caused by intrinsic renal disease e.g. glomerulonephritis, polyarteritis nodosa, systemic sclerosis, chronic pyelonephritis or polycystic kidneys. 25% are caused by renovascular disease e.g. frequently atheromatous and rarely fibromuscular dysplasia.
- Endocrine – Cushing’s or Conn’s, phaeochromocytoma, acromegaly or hyperparathyroidism.
- Others – coarctation, pregnancy, steroids, mono-amine oxidase inhibitors or the OCP.
Malignant hypertension
Refers to severe hypertension e.g. SBP >200mmHg or DBP >130 mmHg with bilateral retinal haemorrhages and exudates with or without papillodema. Symptoms are common – headache ± visual disturbance. It requires urgent treatment as it may precipitate acute renal failure, heart failure or encephalopathy. Untreated 90% die within a year but treated 70% survive 5 years.
