Heart failure, hypertension and Rheumatic fever

Question 2

Heart failure - definition

Answer 2

Cardiac output is inadequate for the body’s requirements – affects 1-3% of the general population.

Question 3

HF - systolic vs diastolic

Answer 3

• 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).

Question 4

HF - left vs right failure

Answer 4

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.

Question 5

HF - acute vs chronic

Answer 5

• 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.

Question 6

HF - low output vs high output

Answer 6

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.

Question 7

HF - Framingham criteria

Answer 7

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.

Question 8

HF - New York Classification

Answer 8

• I – no dyspnoea from ordinary activity.
• II – dyspnoea from ordinary activities.
• III – less than ordinary activity causes dyspnoea.
• IV – dyspnoea is present at rest.

Question 9

HF - Signs

Answer 9

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.

Question 10

HF - Investigations

Answer 10

• 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.

Question 11

HF - acute management

Answer 11

• 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.

Question 12

HF - chronic management - conservative

Answer 12

Encourage patient to stop smoking, reduce salt intake or optimise weight and nutrition.

Question 13

HF - chronic management - medical

Answer 13

Treat cause (dysrhythmias or valve disease), treat exacerbating factors (anaemia, thyroid disease, infection, hypertension) and avoid exacerbating factors (NSAIDs, verapamil).

1. ACE-I – lisinopril (10mg OD) to relieve symptoms or candesartan (4mg OD) if cough.
2. 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)
3. B blockers – give carvedilol (3.125mg OD and increase slowly) to reduce mortality.
4. Spironolactone – if patients are still symptomatic they should be given 25mg PO OD.
5. Digoxin – 0.125-0.25mg PO OD can be given but Us and Es should be monitored (K+).
6. Vasodilators – If ACEi or ARB are not tolerated hydralazine or a nitrate should be given.

Question 14

Hypertension - definition

Answer 14

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.

Question 15

Hypertension - pathophysiology

Answer 15

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.

Question 16

Malignant hypertension

Answer 16

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.

Question 17

Hypertension - signs and symptoms

Answer 17

Usually asymptomatic except in malignant hypertension. Headaches are no more common than in the general population.

There may be signs of underlying disease e.g. renal disease, phaeochromocytoma, radio-femoral delay or weak femoral pulses in coarctation or Cushing’s.

Look for end organ damage – left ventricular hypertrophy, retinopathy and proteinuria.

Question 18

Stages of retinopathy

Answer 18

• I – tortuous arteries with thick shiny walls (copper wiring).
• II – AV nipping (narrowing where vessels cross).
• III – flame haemorrhage and cotton wool spots.
• IV – papilloedema.

Question 19

Hypertension - investigations

Answer 19

• 24 hour ambulatory ECG for diagnosis.
• To quantify overall risk – fasting glucose and cholesterol.
• To look for end organ damage – ECG for LVH or past MI and urine analysis for protein or blood.
• To exclude secondary causes – Us+ Es (K+ down in Conn’s) and Ca+ (up in hyperparathyroidism).
• Special tests – renal ultrasound or arteriography for renal artery stenosis, 24 hour urinary VMA (phaeo), urinary free cortisol, renin, aldosterone and echo.

Question 20

Hypertension - management principles

Answer 20

• Look for and treat underlying cause e.g. renal disease or excessive alcohol consumption.
• Medical therapy - is especially important if BP is persistently >160/100 mmHg, 10 year cardiovascular risk is >20%, existing vascular disease and there’s target organ damage (e.g. of the brain, kidney or retina).
• Treatment goal - <140/85 mmHg or <135/80 in diabetic patients.

Question 21

Hypertension - lifestyle changes

Answer 21

Decrease concomitant risk factors – stop smoking, low fat diet, reduce alcohol and salt diet, increase exercise and reduce weight if patient is obese i.e. BMI is >30.

Question 22

Hypertension - caution with drugs

Answer 22

Don’t use β-blockers in patients with asthma or COPD, ACE inhibitors or angiotensin receptor blockers in pregnancy and thiazide diuretics in patients with gout.

Question 23

Hypertension - management

Answer 23

• Step 1 - start ACEi/ARB if <55 years or CCB or thiazide diuretic if >55 years or of African or Caribbean descent.
• Step 2 - ACEi/ARB with a CCB or ACEi/ARB with a thiazide diuretic.
• Step 3 - ACEi/ARB with a CCB with a thiazide diuretic.
• Step 4 - add further diuretic (spironolactone), alpha blocker (doxazosin) or a beta blocker. Consider referral to a specialist.

Question 24

Hypertension - malignant management

Answer 24

Use oral therapy unless there’s encephalopathy or congestive cardiac failure. The aim is to lower blood pressure over days not hours – avoid sudden drops as cerebral auto-regulation is poor so risk of stroke is increased. PO drugs - atenolol or diltiazem can be used.

• With encephalopathy – insert intra-arterial line and aim to reduce diastolic BP to 110mmHg over 4 hours. Give 40-80mg Furesmide then IV labetalol or IVI of sodium nitroprusside.

Question 25

Rheumatic fever - definition

Answer 25

• A systemic infection that is still common in developing countries. Peak age of onset is 5-15 years of age.
• A pharyngeal infection with group A strep triggers rheumatic fever 2-4 weeks later in the susceptible 2% of the population. Strep antibodies react with valvular tissue and may cause permanent damage.

Question 26

Rheumatic fever - Jones’ criteria

Answer 26

Diagnosis requires evidence of strep infection plus 2 major or 1 major or 2 minor:

• Strep infection – requires positive throat culture (usually negative by time of diagnosis), rapid streptococcal antigen test, elevated or rising streptococcal antibodies or recent scarlet fever.
• Minor criteria – fever, raised CRP or ESR, arthralgia, prolonged PR interval or previous RF.

Question 27

Rheumatic fever - major criteria

Answer 27

CASES:

• Carditis – presents as one of tachycardia, murmur (aortic or mitral regurgitation), pericardial rub, congestive cardiac failure, cardiomegaly and conduction defects.
• Arthritis – a flitting polyarthritis that usually affects larger joints e.g. hips or knees.
• Subcutaneous nodules – small, mobile painless nodules on extensor surfaces and spine.
• Erythema marginatum – red raised edges and clear centres on trunk, thighs and arms.
• Sydenham’s chorea – aka St Vitus’ dance occurs late in 10% = involuntary movements.

Question 28

Rheumatic fever - management

Answer 28

• Bed rest – until the CRP has been normal for 2 weeks (could take up to 3 months to occur).
• Antibiotics – 0.6-1.2g IM benzylpenicillin TDS for 10 days (or erythromycin if there’s an allergy).
• Analgesia – aspirin, NSAIDs or steroids should be given to patients with arthritis or carditis.

Question 29

Rheumatic fever - prognosis

Answer 29

60% with carditis develop rheumatic heart disease (correlated with severity) and valve stenosis – valves affected include mitral in 70%, aortic in 40%, tricuspid in 10% and pulmonary in 2%.