Hospital Based Practice – Chest Pain

Differential Diagnoses.
• As always, one way of thinking about lists is based on systems.
o Cardiovascular.
 Heart.
• Acute coronary syndromes.
• Myocarditis
• Pericarditis
• Left ventricular hypertrophy.
 Vessels.
• Aortic dissection
• Aortic aneurysm.
o Respiratory.
 Pneumothorax.
 Pulmonary Embolism
 Pneumonia
o Gastrointestinal.
 Oesophageal spasm
 GORD
 Peptic ulcer
 Cholecystis.
 Pancreatitis
o Neuromuscular.
 Rib fracture.
 Chostochondritis
 Vertebral collapse compressing nerve.
 Shingles.
o Anxiety.

• The type of pain can tell you a lot about the diagnosis.
o Pleuritic pain.
 Pneumonia
 Pneumothorax
 PE
 Pericarditis.
• Tends to be retrosternal
• Relieved by leaning forwards.
o Crushing/ tightness.
 Angina
 Acute coronary syndromes
• Tends to last longer than angina, and have associated symptoms.
o Burning.
 Oesophagitis
 Shingles.
• Pain often precedes rash
 GORD
 Peptic ulcer disease.
o Tearing.
 Dissecting aortic aneurysm.
• Often interscapular pain.
o Tenderness on palpation.
 Rib fracture.
 Costochondritis
  Shingles.

History of patient with chest pain

• The SOCRATES system will normally give a good idea what the source of the pain is.
• Then questions can be asked about other symptoms and risk factors to confirm.
• Onset and progression.
o Cardiac ischemic pain.
 Develops over a few minutes.
 Aggrevated by.
• Exercise.
• Emotion
• Cold weather.
 Relieved by.
• Rest.
• Nitrates.
o Giving nitrates can be a diagnostic test for ischemic
cardiac pain.
 MI.
• Severe pain
• Often associated nausea, vomiting and sweating.
• Pain not fully resolved with nitrates.
o Pneumothorax/ PE.
 Sudden onset of pleuritic pain.
• Often even down to the level of patients rememebering exactly
what they were doing at the time.
 Associated dyspnoea.

Investigation.
• All chest pain patients should have an ECG and a CXR.
• Other tests depend on history and examination, but it is likely that they may require.
o FBC
o U&E
o Blood glucose
• ECG changes.
o ST elevation doesn’t always mean an MI , the ECG can suggest other diagnoses as
well.
 MI.
• Inferior: AVF, II, III
• Anteroseptal: V1 – V4
• Lateral: I, AVL, V4 – V6
 Pericarditis.
• In uncoupled leads.
 Prinzmetal’s angina.
• Leads of affected coronary artery.
• Due to arterial spasm.
 Aortic dissection.
• If coronary artery disrupted.
 Left ventricular aneurysm.
• Persistant changes following infarct.
o ECG changes associated with PE.
 Sinus tachycardia.
 Atrial arrythmias.
 Right heart strain.
  Right bundle branch block.
 Right axis deviation.
 S1Q2T3.
• Deep S waves in I, deep Q waves in II and inverted T waves in III.

• Chest X – ray.
o This is good for demonstrating.
 Pneumothorax.
 Consolidation
 Widened mediastinum
• Aortic dissection.
 Pulmonary oedema.
• Myocardia ischaemia/ infarction.
• Heart failure.
 Fractured ribs.

• Arterial blood gases.

o Useful in determining the severity of.
 Pneumonia.
 PE
 Pulmonary oedema
 Obstructive lung disease.
o In hyperventilation due to anxiety, PaO2 may be slightly elevated, along with a
respiratory acidosis.

• Echocardiogram.
o Accurate in demonstrating.
 Cardiac dysfunction.
 Valvular pathology
 Pericardial effusions.
 Aortic dissection.
• Particularly transoesophogeal echo.
• CT is an alternative.

• Percutaneous coronary intervention.

o Angioplasty and coronary artery stenting can be used to reopen occluded arteries.
 Alternative to thrombolysis.
o Angiography allows direct visualisation of coronary artery anatomy.
 Used in angina to determine whether angioplasty or CABG would be of
benefit.

• V/Q scan.
o Used to diagnose PE.
o Sometimes interpretation may be difficult, so pulmonary angiography should be
used.
 Existing obstructive airway disease.
o CT pulmonary angiogram is the gold standard.

• Exercise test.
o Diagnostic for stable angina.
o Mainly used in risk stratification post – MI or in outpatients when investigating chest
pain.
o Absolute contraindication in acute coronary syndrome.
 • Upper GI endoscopy.
o Diagnostic test for oesophagitis.
o Also will identify Peptic ulcer disease.
o Should be used when cause of chest pain is unclear.

Ischaemic Heart Disease.

• IHD is a result of poor oxygenation of the heart muscle.
• The term covers a spectrum of diseases.
o Stable angina pectoris.
o Unstable angina
o Myocardial infarction.
• Commonest underlying pathology is atherosclerosis of the coronary arteries, which reduces
perfusion.
• More rarely, IHD can result from.
o Coronary artery spasm.
o Aortic stenosis
o Emboli
o Coronary osteial stenosis
o Hypertrophic obstructive cardiomyopathy
o Arrythmias causing decreased coronary perfusion pressure.
o Anaemia.
o Syndrome X
 Coronary arteries are normal.
 Thought to be due to abnormalities of the small coronary vessels.

• Incidence.
o Large geographical variation.
o About 100 in 100 000 mortality rate in Japan.
o About 600 in 100 000 mortality rate in Finland.
o In Western Europe, the incidence is declining.
o In England and Wales.
 1 in 6 men will have evidence of IHD by the age of 45
 1 in 3 men will have evidence of IHD by the age of 60.

• Risk factors.
o Although it tends to be old, fat, male smokers who get IHD, this may be due to
underlying factors.
o Increased incidence with obesity.
 May be due to association with raised cholesterol, hypertension and reduced
glucose tolerance.
o Sharp rise with increasing age.
 May be due to cumulative effects of raised cholesterol, hypertension,
cigarette smoking and other factors over time.
o Gender.
 Rate in young men is 6 times that of young women.
 Pre – menopausal women thought to be oprotected by their hormones.
 Sex difference decreases with age, and there is no difference by the age of
70.
o Family history.
 This seems to be independent of other major factors.
 • If 1st degree relatives under the age of 50 are affected.
 Although high cholesterol levels may cluster in families, only a small
proportion of these are associated with familial hypercholesterolaemia.
o Cigarette smoking.
 Risk of IHD raises proportionally with number of cigarettes smoked.
 Rate of IHD in current smokers is about 3 times that of lifelong non –
smokers.
 Giving up smoking leads to a rapid risk reducetion, followed by a more
gradual decline.
 By 10 years of having stopped, risk of IHD is nearly the same as a lifelong
non – smoker.

o Blood lipids.
 Risk of IHD increases as total cholesterol and LDL cholesterol increases.
 HDL cholesterol is protective against IHD, and risk decreases as HDL
increases.
 High triglycerides are also linked to higher rates of IHD, but when you take
into account the other lipids that also tend to be elevated when triglycerides
are up, there is not a huge effect due to the triglycerides.
o Hypertension.
 Both elevated systolic and diastolic blood pressures are linked to IHD.
 They are also linked to.
• Hypertensive disease.
• Stroke
• Renal failure.
 Treatment of hypertension with drugs reduces rates of IHD by 16%.
• Even greater benefit in the elderly.

o Diabetes Mellitus.
 In countries where IHD is common, Diabetes Mellitus is associated with a
two fold increase in rates of IHD.
o Race.
 Even taking into account increases in HDL, glucose intolerance and DM;
levels are taken into account, rate of IHD in British Asians is significantly
higher than those living in the Indian subcontinent.
o Weight.
 Obesity doubles the rate of IHD.
 This is probably mediated through increased
• Blood pressure.
• Cholesterol
• Insulin resistance
 Also mediated though decreased.
• HDL cholesterol
• Physical activity.
o Obstructive sleep apnoea
 There seems to be an association between sleep anpnoea and IHD,
independent of the association between sleep apnoea and obesity and
hypertension.
o Novel risk factors.
 Recently other risk factors have been identified, but they may be markers of
underlying inflammation.
• Hyperfibrinogenaemia.
• Hyperhomocysteinaemia.
 o Psychosocial factors.
 Although stress and strong emotional can precipitate an acute cardiac event,
it is yet to be shown that emotion is a risk factor for development of IHD.

o By considering all risk factors present will give a more accurate estimate than
looking at any single issue.
 Several different models for doing this, the most common one is the
Sheffield model which is found at the back of the BNF.

Pathology.
• Atherosclerosis is a slowly progressive, focal proliferation of connective tissue within the
arterial intima.
• It begins early in life, but obviously increases as you age.
• LDL is the main atherogenic lipid.
• Principle constituent of atherosclerotic plaques is collogen synthesised by smooth muscle
cells.

• Initial process consists of endothelial dysfunction in association with:

o High levels of circulating cholesterol.
o Inflammation of arterial wall
o Shear forces.
• Next, macrophages enter the arterial wall between endothelial cells to take up lipids to form
“foam cells.
• The accumulation of foam cells in the subendothelial zone leads to the formation of “fatty
streaks”.
• The accumulation of foam cells causes the release of toxic products, which causes:
o Aggregation of platelets.
o Proliferation of smooth muscle cells.
o Formation of thrombus.
• The lesion then becomes organised into an atherosclerotic plaque, surrounded by a fibrotic
cap.
• Progressive enlargement of the lesions causes narrowing of the arterial lumen.
o Reduces ability to increase perfusion and oxygenation when needed, leading to stable
angina.
• Atherosclerotic plaques are liable to rupture, leading to release of thrombosis producing
factors.
o Causes sudden thrombosis, resulting in acute coronary syndromes.
• Factors associated with plaque rupture, and consequent thrombosis, include.
o Large lipid core.
o High monocyte density.
o Low smooth muscle density.
• The association of raised CRP and other inflammatory markers with IHD has led to the
suggestion that atherosclerosis is an inflammatory process.
o Various pathogens have been suggested, including H. Pylori and Chlamydia
pneumoniae.
o This remains speculative.

Investigations.
• Electrocardiogram.
o A normal ECG doesn’t exclude a diagnosis of angina.
o During attacks there may be.
 ST depression.
 Symetrical T wave inversion.
o T wave inversion in V1 – 3 often suggests left coronary artery stenosis.
o The ECG may be complicated by evidence of an old MI or Left ventricular
hypertrophy.

• Exercise ECG.
o Absolute contraindication in:
 Acute coronary syndromes.
 Severe aortic stenosis.
 Severe pulmonary hypertension.
 Significant rhythm disturbances.
o In IHD, exercise ECG is:
 An indicator of exercise performance
 An independent indicator of prognosis.
o Test is usually regarded as positive if there is more than 1 mm of downsloping ST
depression after the J point.
 Junction of the ST segment with the T wave.
o If pre – test probability of angina is high, number of false positives is low.
o Causes of false positives include:
 Hyperventilation.
 Digoxin
 Hypokalaemia
 Hypertension
 Valvular heart disease
 Left ventricular hypertrophy
 Pre – excitation syndromes.

o Test should be terminated if there is:

 more than 3 mm of ST depression.
 Fall in blood pressure.
 Ventricular tachycardia
 Pallor
• Indicates circulatory collapse.
 If the end point is reached.

• Echocardiogram.
o Can be used to
 Assess ventricular function.
 Localise areas of ventricular wall involvement.
o In patients with angina, but no evidence of infarction, echo may be normal.
o With diffuse ischaemic changes, left ventricular function may be globally impaired.
 o Exercise/ pharmacological stress echocardiogram may be used to dewtect areas of
“hibernating myocardium”
 Areas that show reduced function with stress
• Due to decreased blood flow secondary to decreased coronary flow
reserve.
 Show normal function at rest.
 These may be areas which may improve with revascularisation procedures.

• Nuclear imaging.
o May be used to assess myocardial structure and function.
o Radioisotope (eg thallium) injected during exercise and a CT image taken soon
afterwards.
 If exercise not feasible, pharmacological stressing with adenosine is an
alternative.
o Isotope taken up by healthy myocardium, but poorly perfused areas show up as “cold
spots”.
o Test is repeated at rest to get a baseline for comparison.
 Disappearance of cold spots implies ischemia provoked by exertion, and
relieved by rest.
 Persistent cold spots implies infarction.
o Useful test when
 Exercise test is equivocal or contraindicated
 Indicates clinical significance of stenoses which are equivocal on
angiography.
• Coronary angiography.
o Technique for
 Visualising coronary arteries radiographically.
 Measuring intracardiac pressures
 Measuring blood oxygen in different chambers
 Measuring cardiac output.
o Test usually used to determine exact coronary anatomy and used to informa further
management, eg. chosing between
 Medical therapy
 Coronary angioplasty
 CABG surgery
o In stable angina, normally reserved for patients with:
 Angina resistant to optima medical treatment.
 Strongly positive exercise tolerance tests, indicating a poor prognosis.
 Evidence of reversible ischaemia on stress testing, with reduced left
ventricular function.
 After troponin confirmed acute coronary events, especially if pain
continues.
o More rarely used as a diagnostic test when less invasive tests have not been helpful
and symptoms persist.

o Mortality from procedure is 1 in 1000, complications include.

 Haemorrhage and haematoma at site of arterial puncture.
 Emboli into arteries, resulting in coronary or peripheral ischaemia.
 Stroke
 Arrythmias
 Coronary artery dissection.

Treatment of IHD.
• Chronic, stable angina is cause of considerable morbidity for patients and workload for health
services.
• As with all chronic diseases, management comprises.
o Patietn education.
 o Lifestyle changes
o Medication
• Non – coronary causes for angina should be sought and treated.
o Valvular heart disease.
o Anaemia.

• General measures
o Reduce risk factors.
 Stop smoking.
 Lose weight
 Increase exercise.
 Eat healthy diet.
o Avoid factors that precipitate patient’s angina.
 Cold weather.
 Extremes of emotion.
o Sublingal nitrate.
 Either tablets or spray.
o For relief of acute attacks and prophylactic use before exercise

• Drugs
o Antiplatelet drugs.
 All patients should have Aspirin 75 mg OD.
• Lowers incidence of MI and death.
 Risk of GI bleeding, so patients should be advised:
• Take tablets with food.
• Be vigilant for malaena
 If history of previous bleeding, add a proton pump inhibitor.
 If aspirin contraindicated, give clopidogrel.
• Anti – platelet aggregation.
• Evidence base is in NSTEMI and post – angioplasty.

o β – blockers.
 Act by reducing sympathetic tone, causing reduced:
• Myocardial contractility (negative inotropy)
• Heart rate (negative chronotrophy).
 These effects reduce oxygen demand.
 In addition to these effects, reduced heart rate lengthens diastolic time, so
allowing more time for coronary perfusion.
 Typical β – blockers include.
• Atenolol
• Bisoprolol
• Metoprolol
 Relative contraindications include:
• Asthma.
• Peripheral vascular disease with skin ulceration
• Second degree heart block
• Third degree heart block.
  Most effective class of drug in improving survival after myocardial
infarction.
• Should be first line.
• Formerly were contraindicated in heart failure.
• Probably a bad idea in acute or overt heart failure.
• Proven benefits in chronic heart failure.

o Nitrates.
 Cause peripheral vasodilatation, especially in veins.
• Reduces venous return.
• Ventricular preload is reduced.
 Reduction in distension of the heart wall reduces oxygen demand of the
heart.
• Reduces symptoms of angina.
 Mechanism.
• Converted to nitric oxide, which causes increase in intracellular
cyclic GMP in smooth muscle.
• cGMP stimulates calcium binding, which moips up free calcium.
• Reduces calcium available for muscle contraction.
 Short acting nitrates are mainstay of therapy for relieving acute angina.
• Can eliminate pain within minutes when combined with rest.
• If pain doesn’t decrease rapidly, this is a warning sign for the
patient.
 Longer – acting nitrates are more stable.
• Can be effective for several hours.
• Isosorbide dinitrate (ISDN) is rapidly metabolised in the liver to
main active metabolite, isosorbide mononitrate (ISMN).
• Giving ISMN may reduce the variable absorption and
unpredictable first – pass metabolism of the dinitrate.

 Adverse effects are normally due to arterial action and dilatation.

• Headache.
• Flushing
• Hypotension
• Fainting.
o Rare side effect.
• “Nitrate holidays” are the traditional way of minimising the
problem.
o Newer daily preparations reduce this effect.
• Due to the side effects, nitrates are not given overnight.

o Calcium channel blockers.

 Not to be called calcium channel antagonists.
• Don’t antagonise the channel, do block it.
 Inhibit influx of calcium into myocyte during action potential.
 Cause relaxation of peripheral vascular smooth muscle.
 Reduce angina by combination of:
• Reduced afterload.
o Hence myocardial oxygen demand.
• Reduced heart rate
• Increased coronary vasodilatation.
 Especially useful if there is a degree of coronary artery spasm
 Dihydropyridines, eg. nifedipine, can cause reflex tachycardia secondary to
peripheral vasodilatation.
• May be combined with β – blockers to treat this side effect.
  Diltiazem has a slightly negative inotropic and chronotropic effect.
• Patient should be carefully monitored if also on β – blocker therapy
due to risk of bradycardia.
 Verapramil is drug of choice for supraventricular tachycardia if β – blockers
are contraindicated.
 All calcium channel blockers are negatively inotropic to some degree, and
should be used very carefully in patients with impaired left ventricular
function.
• Amlodopine has been demonstrated to be safe in heart failure, but
still be careful.
 Side effects include:
• Headache.
• Flushing.
• Dizziness
• Constipation
• Gravitational oedema.

o Potassium channel activators.

 New class of drugs.
 Both arterial and venous vasodilating properties.
 May be useful in patients refractory to treatment with other antianginal
agents.
 Nicorandil is currently only licensed drug from this class.
o Statins.
 Also known as HMG CoA reductase inhibitors.
 Mainstay of lipid lowering therapy.
 Current maxim for cholesterol is “lower is better”
 Statins may also be helpful in
• Stabalising atherosclerotic plaques.
• Reducing frequency of acute cardiac events.
 Therefore, most IHD patients should be on a statin, even if their cholesterol
is normal.

o Angioplasty and stenting.

 Coronary artery stenoses can be dilated using a balloon after atherosclerotic
plaque visualisation on angiography.
• Improves blood flow.
 Best results in terms of patency and flow are achieved with stent insertion.
• Very safe procedure.
• Prefered to surgery in most cases.
• Subsequent treatment with clopidogrel and IIb/IIIa receptor
antagonists reduces stent restenosis.
o Drug eluting stents (eg. with sirolimus) may further
enhance this.
• Patients only require one night in hospital, and return to normal
activity faster than with surgery.

o Surgical management.
 CABG surgery should be considered in patients who’s angina is:
• Resistant to optimal medical therapy.
• Not suitable for surgery.
• Have failed angioplasty.
 Low mortality (2%) in otherwise well patients.
 Bypass using an internal mammary artery is better than the traditional vein
graft.
 • Better patency, flow and graft survival.
 Certain patient groups do better with surgery than with stents.
• Left main stem stenosis.
• Triple vessel coronary artery disease.
• Two vessel disease with proximal LAD disease.
• Left ventricular impairment.
 Post – operatively, number and dose of antiangina drugs can be reduced.

Acute coronary syndromes.

• Terminology to classify acute ischemic events has changed in the last few years.
o NSTEMI used to be known as
 Subendocardial MI
 Non – Q wave MI
• It is important to know if a MI is a STEMI or a NSTEMI as the management is different.

• NSTEMI.
o Clinical picture:
 Patient may have characteristic central crushing chest pain, or more non –
specific symptoms.
 Patients with existing stable angina may have
• Pain that isn’t resolved by their normal GTN.
• More intense symptoms than normal.
• Symptoms occurring at rest.
 All these symptoms refer urgent assessment.
o Approximately a third of general medical referrals are for chest pain.
 Many UK hospitals now have specialist chest pain assessment units.
• Allows more rapid and effective assessment, monitoring and
discharge.

o Diagnosis.
 As well as symptoms, the other important assessment is ECG, which may
show:
• ST depression
• T wave flattening.
• Biphasic changes
• T wave inversion.
 The deeper the changes on ECG, the more worrying.
 The initial ECG may be normal, so serial ones are needed.
• Preferably when pain occurs.
• Allows demonstration of dynamic ischemia.
o Management.
 Emergency.
• Adequate analgesia and oxygen are vital.
o Alleviate patient’s distress and reduces stress on the heart.
• Nitrates can be given sublingually or as an infusion.
o Relieve pain
o Offload heart
• Should be started unless hypotension prevents it.
 • Opiates may be needed if nitrates nor fully effective.

 Drugs.
• Anti – thrombosis drugs.
o Aimed at moderating thrombosis and preventing occlusion
of the artery.
o Very effective.
o Associated with an increased risk of bleeding.

o Aspirin.
 300 mg should be given straight away.
 Should be continued at 75 mg orally every day.
o Clopidogrel.
 Novel antiplatelet drug that has evidence base
supporting it’s use in NSTEMI.
 Should be used if aspirin contraindicated.
 First dose is 300 mg, and 75 mg daily following
this.
o Heparin.
 Give until pain free for 48 hours.
 Can be used as:
• Continuous IV infusion of
unfractionated heparin.
• Twice daily low molecular weight for
easier administration.
 Most hospitals use enoxaparin as it may be
beneficial over conventional heparin.
• Still a subject for debate.

• β – blockers.
o Unless contraindicated, β – blockers should be started.
 Contraindicated in:
• Overt heart failure
• Known Left ventricular dysfunction
o Effects:
 Immediate antianginal effect.
 Reduces progression to acute STEMI.
 Reduce arrythmias
 Improve survival
o Examples:
 Metoprolol
 Atenolol
 Carvedilol
• Diltiazem.
o Antianginal drug with a negatrive chronotropic effect.
o Used if β – blockers are contraindicated.
• Statins.
o Should be started on admission, regardless of cholesterol
levels.
o May improve outcome by anti – inflammatory stabalising
of atherosclerotic plaques.

• ACE inhibitors.
o Should start early in patients with NSTEMI.
o Reasonable to start at a low dose, and then review in 12
hours when acute event has settled.
 Risk of hypotension if high doses started before
this.

• Glycoprotein IIb/IIIa receptor antagonists.

o Potent antiplatelet agents.
o Block binding of fibrinogen at IIb/IIIa receptor on platelet
surface.
o Started if pain continues or ECG changes progress.
o May settle the acute event on their own.
 Usually part of a strategy including cardiac
catheterisation
o Most common drugs are:
 Tirofiban
 Eptifibatide.
o There is a significant risk of bleeding, which should be
assessed before starting the drug.

• Combinations of the above treatments will result in more than 90%

of NSTEMI patients becoming pain free and respond well.
o If complications develop, patient should be transferred to
centre which can offer interventional cardiac support.
 Continuing pain.
 Cardiogenic shock
 Progressing ECG changes.

• Place of thrombolysis or angioplasty.

o Thrombolysis only shown to have benefit in:
 STEMI
 New Left bundle branch block.
o Angiography and angioplasty is the best option in ongoing
NSTEMI who have responded well to therapy.
o The place of early or conservative interventional strategies
is controversial.

• Troponin.
o Measurement of Troponin I or T at 8 – 12 hours following
the onset of pain is crucial.
o Troponin levels are:
 Highly specific marker of myocardial damage.
  A marker of prognosis.
o Therefore, patients with the follow characteristics can be
safely discharged to outpatients, for exercise test and risk
factor stratification.
 Pain free.
 Non – evolving ECG.
 Negative troponin.
o Patinets with positive troponin NSTEMI are high risk for
further events.
 Should be evaluated for revasculation procedures
as an inpatient.

• Prevention.
o In patients with proven NSTEMI, mortality is 20% at 1
year.
o All patients should have their risk stratified.
o Unless contraindicated, patients should be started on:
 Long term antiplatelets.
 Statin
 Beta – blocker
 ACE inhibitor.
o The need for angioplasty or CABG should be considered.
 Stress testing.
 Angiography.

Acute MI.

• Affects 5 in 1000 of UK population every year.

• Most common cause of mortality in Western world.
• 90% of transmural MIs are caused by a thrombus occludsing a coronary artery, following
atherosclerotic plaque rupture.
• Underlying most cases is dynamic interaction between.
o Severe coronary atherosclerosis.
o Acute atheromatous plaque change
o Superimposed thrombosis
o Platelet aggregation
o Vasospasm
 • Microscopically, acute MI follows a predictable sequence.

Time after onset of symptoms Macroscopic changes Microscopic changes

Up to 18 hours None None
24 – 48 hours Pale oedematous muscle Oedema, acute inflammatory
cell infiltration, necrosis of
myocytes
3 – 4 days Yellow, rubbery centre with Obvious necrosis and
haemorrhagic border inflammation, early
granulomatous tissue
3 – 6 weeks Silvery scar, becoming rough Dense fibrosis
and white

• Overall mortality from acute MI has improved markedly in the last 20 years.
o Better medical care.
o Development of coronary care units
o Recognition of importance of early reperfusion in reducing infarct size.
 So important that “door to needle time” is one of the standards against
which acute cardiac care is judged.

• Adverse factors in patients admitted with acute MI include.

o Older age.
o Previous cardiovascular disease.
 Old MI
 Diabetes
o Indicators of a large infarct.
 Site of infarction.
• Anterior worse than inferior
o Low initial blood pressure.
o Presence of pulmonary congestion.
o Extent of ischemia.
 Expressed by ST elevation on ECG.

Diagnosis
• Based on two out of three from.
o History.
o ECG changes.
o Enzyme changes.

• Cardiac enzymes.
o Intracellular enzymes which leak from infarcted myocardium into the bloodstream.

CK
LDH
AST
Troponin
 0 1 2 3 4 5
Days

o Creatinine Kinase (CK)

 Peaks within 24 hours.
 Also produced by skeletal muscle and brain.
 In case of doubt, myocardial – bound isoenzyme (CKMB) can be requested.
 Site of infarct affects serum level of the enzyme.
o Aspartate aminotransferase and lactate dehydrogenase were formerly used to assess
MI.
 Remain elevated for several days after CK has settled.
 Now largely obsolete.
o Troponin I and T are highly sensitive and specific for myocardial damage.
 Not enzymes, but proteins involved in myocyte contration.
 Most reliable 8 – 12 hours post MI
 Remain elevated for several weeks.
• Therefore, CK still used to assess patients with a possible new MI
when previous MI has been recent enough for troponin to still be
elevated.

o Electrocardiogram.
 Earliest ECG changes (hyperacute changes) are.
• Tall, pointed T waves
• Elevation of ST segment.
 This is followed by:
• T wave inversion
• Decreased R wave voltage
• Development of Q waves.
 After a few weeks – months, the T waves may become upright again, but Q
waves will remain.

 Site of MI can be deduced from affected leads on the ECG.

Site Inferior Anterior Anterioseptal Lateral Posterior
Leads II, III, aVF Precordial V1 – 3 V4 – 6, I and V1 – 2
leads aVL Tall R wave,
V1 – 6 ST depression
and upright T
waves.

 There will also be reciprocal ST depression in opposite leads.

 The development of new left bundle branch block is an indicator of acute
MI.
• If coupled with pain is an indication for thrombolysis.
• However, LBBB is common and so old ECGs are needed to check
if it new onset or not.
 o Other investigations which may help with management by picking up underlying
problems include.
 FBC.
• Anaemia
 U&Es.
• Renal and electrolyte abnormalities
 CXR.
• Aortic dissection
• Signs of heart failure
• Assessment for cardiomegaly.
 Blood glucose.

Management.
• Emergency care.
o Main aims are to prevent or treat cardiac arrest and to relieve pain.
o Patient should ideally be managed:
 On a coronary care unit
 With continuous cardiac monitoring
 With good intravenous access.
o Pain relief given by a combination of:
 Opiates + antiemetics.
 Sublingual nitrates
 IV nitrates
o Relief of pain is important not only for humane reasons, but also to reduce
sympathetic activation due to pain, which would cause vasoconstriction and
increased work for the heart.
o Side effects of this management include:
 Nausea nd vomiting.
 Hypotension with bradycardia
 Respiratory depression
o If respiratory depression occurs, opiates should be antagonised with nalaxone.
o High flow oxygen should be given via facemask or nasal prongs, particularly to those
who are:
 Breathless.
 Showing signs of heart failure.
 Showing signs of shock.
o Anxiety is a natural response to the pain and circumstances surrounding a heart
attack.
 Make an effort to reassure and calm the patient and those closely associated
with them.

• Early care.
o Aims are to:
 Initiate reperfusion.
 Limit infarct size
 Prevent infarct extension
 Treat life threatening arrhythmias.

o Thrombolytic treatment.
  Patients with ST elevation or new LBBB should be thrombolysed within 12
hours of onset of pain.
• Prevents and reduces death.
• The earlier it is given, the better the prognosis.
 Administration within 30 minutes of arrival should be possible for most
patients attending hospital with a clear MI.
 Co – current aspirin should be given.
• Effects are additive, so more lives are saved with double therapy
than with either single therapy alone.
 Largest benefit seen in those at highest risk, which includes:
• Elderly
• Patients with hypotension of < 100 mmHg systolic
• Anterior infarction
 Large benefit also occurs with rapid treatment.
 Contraindications to thrombolysis include:
• Relative.
o TIA in preceding 6 months.
o Warfarin therapy.
o Pregnancy
o Non – compressible punctures.
o Traumatic resuscitation
o Refractory hypertension (Systolic > 180 mmHg)
o Recent retinal laser treatment.
• Absolute.
o Stroke.
o Major surgery, trauma or head injury within last 3 weeks.
o GI bleed within the last week
o Known bleeding disorder
o Dissecting aneurysm.
 Major bleeding complications are seen in approximately 1 – 3% of patients.
 The two main thrombolytics are:
• Streptokinase.
o Induces antibody response.
 Reduces effectiveness of repeat dose.
 Risk of anaphylactic reaction.
 Should not be readministered in the period
between 5 days – 2 years following first
treatment.
o Cheapest thrombolytic.
o Often first line in inferior MI
o Can result in hypotension
• Recombinant tissue polasminogen activator (tPA)/ Alteplase
o Most benefit in patients with anterior MI or hypotension
o Used when streptokinase contraindicated.
o Requires heparin infusion for 48 hours post
administration.
• Tenecteplase is also used.
o Given as bolus injection, so can reduce “door to needle”
time.

• Primary angioplasty
o If rapid assessment is possible, rapid angioplasty and stenting leads to better
outcomes in acute STEMI than thrombolysis.
 Not possible in most UK centres due to lack of facilites for rapid
assessment.
 Also appropriate if thrombolysis contraindicated.
• Other acute therapies.
o Aspirin.
 300 mg should be given early.
• 30% reduction in mortality
• This is 24 lives saved per 1000
 If aspirin not appropriate, clopidogrel is an alternative.
o Beta blockers.
 IV β – blockers in the acute phase may
• Limit infarction size.
• Reduces risk of fatal arrythmias
• Relieves pain.
 15% reduction in mortality at 1 week.
 Particularly appropriate in:.
• Tacchycardia in absence of heart failure.
• .Relative hypotension
• Pain unresponsive to opioids
 If IV formulation not available, start oral therapy.
o ACE inhibitors.
 All patients should have ACE inhibitors if tolerated.
• Improved survival.
 Most value in patients with:
• Signs or symptoms of heart failure.
• Impaired left ventricular function on echocardiogram.
 Opinions differ on best time to start treatment.
• Acutely
• After a few days.
 Benefits appear to be a class effect.
 Doses should be titrated to the target dose.
o Statins.
 Statin therapy should be started immediately, as with NSTEMI.
o Heparin.
 Forms part of most thrombolysis regimens.
 Once these are completed, give heparin prophylaxis until mobile.
o Control of blood glucose.
 Tight control of blood glucose improves outcome post – MI.
 Use insulin sliding scale.
 Commenced even if patient is not known diabetic.
• BM raised by variety of physical stresses.
 • Complications of MI
Complication Interval Mechanism
Sudden death Usually within hours Often ventricular fibrillation
Arrythmias First few days –
Persistant pain 12 hours to a few days Progressive myocardial necrosis
(extension of MI)
Angina Immediate or delayed (weeks) Ischemia of non – infracted
muscle
Cardiac failure Variable Ventricular dysfunction
following muscle necrosis.
Arrythmias
Mitral incompetence First few days Papillary muscle dysfunction,
necrosis or rupture.
Pericarditis 2 – 4 days Transmural infarct with
inflammation of the pericardium
Cardiac rupture and ventricular 3 – 5 days Weakening of wall following
septal defects muscle necrosis and acute
inflammation.
Mural thrombus One week or more Abnormal endothelial surfaces
following infarction
Pulmonary emboli One week or more DVT in lower limbs
Ventricular aneurysm Four weeks or more Stretching of newly formed
collagenous scar tissue.
Dressler’s syndrome Weeks to months Autoimmune
Late ventricular arrythmias – –

• Cardiac failure and shock.

o Left ventricular failure during acute phase is linked to poor prognosis.
o In all patients, closely monitor heart and lungs for signs of heart failure.
 Killip classification
Class Features
I No crepetations or 3rd heart sound.
II Crepetations over < 50% of lung fields or 3rd heart
sound.
III Crepetations over > 50% of lung fields.
IV Shock

o Chest X – ray and echocardiogram may be useful in assessment of:

 Ventricular function.
 Mitral regurgitation
 Ventricular septal defects.
o Management of heart failure will be described later.
o Cardiogenic shock is said to have developed when a patient has all the following:
 Systolic < 90 mmHg
 Peripheral vasoconstriction
 Low urine output
• < 0.5 ml/kg/hour
 Mental confusion.
o Other causes of hypotension should be excluded.
 Hypovolaemia
 Vasovagal reactions
 Electrolyte disturbances
  Drugs
 Arrythmias
o Ventricular and valvular function should be assessed with echocardiogram.
o Pulmonary artery catheter may be used.
 Value is much debated in critical care.
o Inotropic agents are of value.
 Doputamin ( 5 – 20 μg/kg/min) is first line.
o Correction of acidosis is important for myocardial function.
 Usually improves if cardiac output improves.
 Usually a lactic acidosis.
o Emergency angiography and angioplasty or surgery should be considered.

• Cardiac rupture and mitral regurgitation.

o Free wall rupture, if acute, is usually fatal within minutes.
 If subacute:
• Haemodynamic deterioration
• Hypotension
• Signs of cardiac tamponade
• Immediate surgery is needed.
o Ventricular Septal defects (VSD) occurs in 1% of all infarctions.
 Appears early after MI
 Without surgery, mortality is
• 50% within 1 week.
• 90% within 1 year.
 Should be suspected if there is:
• Clinical deterioration
• Loud pansystolic murmur at left sternal edge.
 Treatment is by:
• Surgical closure of defect.
• Bypass grafts as necessary.
o Mitral regurgitation.
 Moderately severe or severe mitral regurgitation has a:
• Incidence of approximately 4%.
• Mortality of about 20%.
 Valve replacement is procedure of choice in papillary muscle dysfunction
and rupture.
o Arrythmias and conduction disturbances.
 Extremely common in the early period post – MI
 Often arrythmias themselves are not hazardous themselves, but are markers
of underlying disorder.
• Ongoing ischemia
• Vagal overactivity
• Electrolyte disturbances

 Ventricular arrythmias.
• May present as:
o Ventricular ectopics
 Almost universal on first day.
 Require no treatment if patient asymptomatic.
o Ventricular tachycardia
 Short episodes are well tolerated, and require no
treatment.
 More prolonged episodes may cause:
• Hypotension
• Heart failure
  Amiodorone or lidocaine are drugs of choice.
 Direct current (DC) cardioversion may be
required if haemodynamically significant VT
persists.
o Ventricullar fibrillation
 Immediate defibrillation should be performed.

• Supraventricular arrythmias.
o Atrial fibrillation complicates 15 – 20% of MI.
 Associated with:
• Left ventricular damage
• Heart failure
 Usually self limiting
 If heart rate is fast.
• Digoxin is effective in slowing rate.
• Amiodarone may be more effective in
terminating the arrhythmia.
o Other supraventricular rhythms are rare.
 Usually self limiting.
 May respond to:
• Carotid sinus massage
• β – blockers
• DC shock

• Sinus bradycardia and heart block.

o Sinus bradycardia common early on.
 Especially in inferior MI
 Responds rapidly to atropine in boluses titrated
against response.
 Administration of unnecessarily large doses of
atropine should be avoided.
o AV block is common in inferior MI.
 Right coronary artery also supplies AV node
 May also respond to atropine.
• Many patients will need permanent
pacemakers.
• May take up to 2 weeks for normal
conduction to be restored.
o Heart block with anterior MI is ominous.
 Indicates a large infarct.
o Development of left bundle branch block or bifasicular
block may presage complete heart block.
 Indication for temporary pacemaker insertion.
 If complete block does occur, and persists,
permanent pacemaker will be needed.
• Subsequent inpatient management.
o General.
 Bed rest for the first 24 hours.
 If uncomplicated, patient can gradually be rehabilitated over next few days.
o DVT and PE.
 May be prevented by SC heparin when on bed rest.
 If they do occur.
• Initially treat with heparin.
• Follow up with oral anticoagulation
 Patients should be started on SC heparin, or LWMH on admission to
coronary care.
o Intraventricular thrombus and systemic emboli.
 Confirmed by echocardiogram.
 Treated with IV heparin, followed by oral anticoagulants.
o Pericarditis.
 Caused by CARDIAC RIND.
• Collagen vascular disease
• Aortic aneurysm
• Radiation
• Drugs
• Infections
• Acute renal failure
• Cardiac infarction
• Rheumatic fever
• Injury
• Neoplasms
• Dressler’s syndrome
 Can occur within first few days post – MI
 Causes pain that is:
• Sharp in nature.
• Varies with posture and respiration.
 Diagnosis confirmed by presence of pericardial rub.
 If troublesome, may be treated with:
• High dose aspirin
• NSAIDS
• Steroids
 Dressler’s syndrome:
• Clinical picture
o Fever
o Leucocytosis
o Pericarditis
o Serositis
• Occurs up to 3 months post MI.
 • Due to autoimmune reaction to damaged myocardium
• Treatment is as for pericarditis.
o Late ventricular arrythmias.
 Arrythmias occurring late after an MI are:
• Likely to recur.
• Associated with high risk of death.
 If likely that arrhythmia associated with ischemia.
• Consider revasculation.
 If unlikely that arrhythmia associated with ischemia.
• Β – blockers
• Amiodarone
• Electrophysiology – guided treatments.
• Implantable defibrillator insertion should be considered.

Rehabilitation.
• Aimed at restoring patient to as near to full function as possible.
• Must take into account various factors.
o Physical
o Physiological
o Socio – economic.
• Process should start as soon as possible after admission.
• Should be continued in the succeeding weeks and months.
• Depression and denial are common.
• Lifestyle advice should be individualised and include advice on:
o Smoking cessation
 Mortality in ex – smokers is less than half of that in continuing smokers.
 Potentially most effective secondary prevention strategy.
 Nicotine replacement therapy may be appropriate.
o Diet
 Encourage weight loss if overweight.
 Eating oily fish, rich in Omega – 3 fatty acids at least twice a week may
reduce the risk of reinfarction and death.
o Exercise

Secondary prevention.
• Hypertension.
o Blood pressure should be controlled to 130/80 mmHg if possible
• Fasting glucose & lipids.
o Assessment for diabetes before discharge is vital.
 New development worsens prognosis.
o Lipid levels immediately post – MI are unreliable.
o All patients should be put on statin therapy.
o Fasting lipid levels should be part of routine follow up in clinic over subsequent
years.
 Clear benefits with treatment with statins.
 Risk of subsequent major coronary heart disease events is lowered.
 All subgroups of patients appear to benefit from treatment.
• All patients should be discharged on “the big four” drugs unless contraindicated.
o All show benefits in secondary prevention.

• Risk stratification
o All post – MI patients should undergo echocardiography to assess valve and systolic
function.
o Most patients can undergo limited exercise testing when pain free for 5 – 7 days.
 o If exercise test normal.
 Follow up in clinic.
 No further testing needed.
o Risk factors for further events and death include:
 Continuing angina
 Heart failure
 Positive exercise, or pharmacological stressing, test.
o High risk patients should have angiography prior to discharge.

• Antiplatelet therapy.
o Aspirin 75 mg daily reduces risk of reinfarction and death by 25%.
o No clear benefit of oral anticoagulation over antiplatelt therapy.
 May be considered for patients with:
• Left ventricular aneurysm
• Atrial fibrillation
• Left ventricular thrombus on echocardiogram.

• β – blockers
o Reduce risk of mortality and reinfarction by 20 – 25%.
o Approximately 25% of patients have relative contraindications to β – blockers.
 Uncontrolled heart failure
 Respiratory disease
 Others
o Calcium channel blockers may be used if β – blockers are contraindicated.
 Verapamil
 Diltiazem
• ACE inhibitors.
o ACE inhibitors benefit all patients post – MI, unless contraindicated.
o Patients at low risk gain only marginal benefits.
o Often reserved for patients with:
 Clinical signs of heart failure.
 Low ejection fraction on echocardiogram
 Anterior MI.
Heart failure.
• Occurs when heart unable to maintain sufficient cardiac output to meet demands placed on it
by the body.
o Normally due to failure of the myocardium
o Can also be due to:
 Excessive pre – or afterload
 Rhythm disturbances
 Increased demand by the body.
o Incidence rises with age.
 Almost 1 million UK adults have heart failure.
o Classified based on severity.
New York Heart Association classification.
Class Features
I No limitation of physical activity
II Slight limitation of physical activity.
– Breathlessness after 2 flights of stairs.
III Marked limitation of physical activity.
– Breathlessness after 100m on the flat..
IV Inability to carry out any physical activity without
discomfort.
 o Mortality of severe heart failure is 40% at 1 year.
o Therapy of systolic heart failure has changed dramatically over past 20 years.
 Prognosis is improving.

************************Figure 27.20 Page 175 ****************************************

Causes of heart failure.

• High output failure.
o Normal heart that is unable to maintain an increased output in presence of grossly
elevated requirement.
o Caused by things such as:
 Thyrotoxicosis
 Anaemia
 AV shunts
 Beri beri
 Fever
 Paget’s disease
 Pregnancy.
o Such conditions may also cause previously silent cardiac conditions to manifest.
• Cardiogenic heart failure.
o Due to abnormality of heart.
o Can be unmasked when heart with reduced reserve unable to cope with minor
stresses.
o May manifest at rest, but normally on exertion.
o Causes include:
 IHD.
• 65% of new UK cases per year.
 Hypertension
 Valvular heart disease
 Infections.
• Viruses
• Chagas disease
 Toxins.
• Alcohol
• Chemotherapy
 Nutritional deficiencies
• Beri Beri
 Post partum
o Tachycardia induced.
 Atrial fibrillation
 Atrial flutter
o Genetic
 Hypertrophic obstructive cardiomyopathy
 Duchenner muscular dystrophy.
Clinical features.
• Left heart failure.
o In systolic heart failure, inadequate cardiac output leads to elevated atrial pressures.
o These combine to give the majority of the clinical features.
 Symptoms include:
• Exertional dyspnoea.
o Most common
• Orthopnoea
• Paroxysmal nocturnal dyspnoea
• Fatigue
• Wheeze.
 o “cardiac asthma”
• Cough
• Haemoptysis.
o Rare
 Signs include:
• Tachypnoea
• Tachycardia
• Pulsus alternans.
o Alternating large and small volume pulses
• Peripheral cyanosis and low pulse volume.
• Cardiomegaly
• Third heart sound.
o “S3 gallop”
• Functional mitral regurgitation.
o Secondary to mitral valve annulus
• Basal crepitations, including pulmonary oedema
• Plural effusions.

• Right heart failure.

o May occur secondary to:
 Chronic lung disease.
 Multriple pulmonary emboli
 Primary pulmonary hypertension
 Right heart valve disease
 Left – to – right shunt
 Isolated right ventricular cardiomegaly
o Commonly associated with LVF.
 Known as Congestive Cardiac Failure (CCF)
o Elevated right atrial pressures lead to peripheral fluid retention.
o Symptoms include
 Fatigue
 Nausea
 Wasting
 Swollen ankles
 Abdominal discomfort
 Anorexia
 Breathlessness
o Signs include:
 Raised JVP
 Smooth hepatomegaly
 Liver tenderness
 Pitting oedema
 Ascites
 Functional tricuspid regurgitation
 Tachycardia
 Right ventricular third heart sounds

Investigations.
• The cause of the heart failure must be sought, because heart failure is a symptom rather than a
diagnosis.
• After history and examination, investigations include:
o FBC
 Anaemia
o U&Es
 Renal dysfunction
  Electorlyte abnormalities
o LFTs
 Liver congestion
o Cardiac enzymes/ troponin.
 If acute onset
 Exclude acute coronary syndromes
o Thyroid function tests
o ECG.
 IHD
 Arrythmias
 Left ventricular hypertrophy
 A normal ECG has a very strong negative predictive value for it actually
being heart failure.
o CXR.
 Cardiomegaly
 Alveolar oedema
 “Bat wing” shadowing
 Prominent upper lobe vessels
 Kerley B lines
 Pleural effusions
o Echocardiography.
 Remains gold standard for assessing ventricular and valvular function.

• Other investigations to consider are:

o Exercise testing.
 Functional severity
 Prognosis
o Cardiac catheterisation.
 Assess and treat ischemia/ valve lesions.
 Rarely biopsy is taken of myocardium with cardiomyopathy.
o Nuclear techniques.
 Ejection fraction
 Cardiac function
 Reversible ischemia
o Brain (B – type) Natriuretic peptide.
 Marker of ventricular dysfunction
 May help in assessment of suspected cardiac failure.
 Low plasma level makes the diagnosis of heart failure unlikely.
 In future, may reduce need for echocardiogram.

Management
• There are two parts to heart failure management.
o Managemnt of chronic heart failure.
 Rapidly growing area as population ages and management of acute coronary
syndromes improve.
 Drug treatments have evolved rapidly with a large evidence base and
improved prognosis fro patients.
o Management of acute heart failure.
 Common scenario for all general medical doctors.

Chronic cardiac failure.

• General
o Cause should be sought and treated appropriately.
o Exacerbating factors should be treated.
 Hypertension
 Anaemia
 o Check patient’s drugs, as some may cause fluid retention.
 Eg. NSAIDS
o Patients should be advised:
 Optimise weight
 Avoid excessive salt intake.
 Avoid excessive alcohol intake.
 Stop smoking.
o Standard cardiac risks should be treated.
o Most patients should be taking:
 Antiplatelet drugs.
 Statins

• Drug treatment.
o Divided into:
 Drugs which improve symptoms of heart failure.
• Diuretics
• Digoxin
 Drugs which improve prognosis.
• ACE inhibitors
• β – blockers
• Spironolactone
o Prognosis improving drugs reduce risk of MI and increase survival.
o Treatment is best planned as a stepped care plan in outpatients when stable.

o ACE inhibitors.
 Renin – angiotensin – aldosterone system is activated in heart failure.
 ACE inhibitors reduce angiotensin mediated vasoconstriction.
• Reduces afterload.
• Decreases aldosterone – mediated salt and water retention.
• Improves function of damaged heart.
 There have been many studies of various ACE inhibitors at all stages of
heart failure.
• Have class effect.
 Have revolutionised systolic heat failure treatment.
• Reduce symptoms, admission and mortality.
• Should be started early in most patients with heart failure.
 Contraindications.
• Known or suspected bilateral renal stenosis
• Aortic stenosis
• Outflow tract obstruction#Pregnancy
• Porphyria
 Side effects.
• First dose hypotension
• Hyperkalaemia
• Worsening renal function
 Due to side effects, should be commenced at low dose and gradulally
increased.
• Monitor with regular electrolyte checking.
 Commonly used ACE inhibitors.
• Ramipril
• Captopril
• Perindopril
• Lisinopril.

o β – blockers
  β – blockers used to be contraindicated in heart failure.
• Sympathetic tone compensates in a failing heart.
 This is true with acute heart failure, as the negative inotropic and
chronotropic effect can be harmful.
 However, high levels of chatecholamines cause progressive myocardial
damage, and β – blockers will reduce these levels.
 The β – blockers that have shown improved function and survival in
moderate to severe heart failure are:
• Carvediolol
• Bisprolol
• Metoprolol
 Their action is by interfering with the renin – angiotensin – aldesterone axis.
• From opposite end to ACE inhibitors and spironolactone.
 Should be only started in stable paitents by experienced clinicians.
• Progress should be carefully monitored.
• Dose should be increased slowly.

o Spironolactone.
 Aldesterone antagonist.
• Also used in higher doses in acities as a diuretic.
 May act as a deleterious growth factor on myoctyes.
• Also causes retention of sodium and water.
 In a study using low (non – diuretic) doses, it improves mortality and
mobidity.
 Side effects include hyperkalaemia.
• As usually given with ACE inhibitors, electrolytes need careful
monitoring.

o Angiotensin II blockers.
 Similar to ACE inhibitors.
 Interfere with renin – angiotensin – aldersterone axis.
 Newer than ACE inhibitors, and place in therapy is still uncertain.
• Likely that they will have similar effects to ACE inhibitors.
 Usually used in patients that don’t tolerate ACE inhibitors.
• Eg. due to the side effect of coughing
 May have a role in addition to ACE inhibitors, as totally block angiotensin II
production.

o Loop diuretics.
 Commonly used drugs.
• Frusemide.
• Bumetanide.
 Very effective at reducing symptoms of heart failure.
• Both in acute and chronic presentations.
 Help manage fluid balance of the patient.
 Side effects include:
• Hypovolaemia.
• Renal impairment if diuresis is excessive.
• Rarely, ototoxicity
 Renal function should be monitored regularly
 No trial has demonstrated an improvement in survival.

o Thiazide diuretics.
 Rarely used alone in cardiac failure.
 Metolazone reserved for very severe symptomatic failure.
 • Causes profound diuresis if combined with loop diuretic.

o Digoxin.
 As well as effective rate control in AF, digoxin has a mild positive inotropic
effect.
• Increases intracellular calcium.
 May have benefit in cardiac failure, even in patients in sinus rhythm.
 Does not improve survival.
 Reduces symptoms and hospital admissions.
 Side effects may include:
• Rhythm disturbances.
• Nausea
• Visual disturbances.
 Therapeutic drug monitoring allows effective dosing to minimise
complications.
 Digoxin should only be added to patients in sinus rhythm with heart failure
not responding to accepted best practice..
 Remains more commonly used in the USA than the UK.

o Hydralazine and nitrates.

 Powerful vasodilating drugs.
 Can improve the symptoms of heart failure.
 May improve prognosis.
 Only use currently is in patients who are unable to take ACE inhibitors.
 May be more effective in black patients than standard therapy.

o IV therapy.
 Little role for IV inotropes in chronic heart failure.
• Are used as bridge to transplantation in end – stage disease.
 Inotropes used include:
• Milrinone
• Phosphodiesterase inhibitors.
• Dobutamine.
o A β – agonists
 Levosimendan produces positive inotropic effects for several months.
• Novel calcium – sensitising drug.
• Role in chroninc heart failure not known.

o Warfarin.
 Patients with severe heart failure and cardiomyopathy are at risk of:
• Thrombus formation
• Systemic emobolisation
 Warfarin should be considered in patients with poor systolic function,
regardless of AF.

• Non – drug therapy.

o Cardiac rehabilitation.
 Encourages activity and independence by:
• Graded exercise programs.
• Patient education.
 Long term effects unknown.

o Transplantation.
 Very good prognosis.
 1 year survival of > 80%
  Main problems are:
• Extreme shortage of donor organs.
• Co – morbidities.

o Biventicular pacemaker.
 Lack of donor hearts has lead to research into improving end – stage heart
function.
 It was noted that patients with intraventricular conduction delay.have poorly
coordinated ventricular contration.
• Poor conduction shown by wide QRS complex.
• Poor contration further reduces ejection fraction.
 Resynchronising can be done through coronary sinus with:
• Standard right and left ventricular pacemaker.
• Left ventricular pacing wire
 Improves cardiac output in some patients.
 If coupled with first degree heart block, improvement is even better.
 Long term benefits are uncertain.

o Arrythmias.
 Patients with cardiomyopathy often have abnormal conduction systems.
• Increased risk of dysrhythmias.
• Particularly ventricular fibrillation and ventricular tachycardia.
 One therapy is long term amiodarone.
• Effectiveness is doubted.
 If risk is significant, an implantable defibrillator is preferred option.

o Artificial heart.
 In spite of press reports, the widespread clinical use of mechanical heart or
ventricular assist device on a long term basis is a long way off.

Acute heart failure.

• Emergency characterised by:
o Acute breathlessness.
o Orthopnoea
o Wheezing
o Anxiety
o Sweating
• There may be
o Pink frothy sputum
o Ischemic chest pain
o Pulmonary oedema
• The order of priorities is:
o Relieve symptoms and stabilise patient.
o Support other organs with adequate perfusion
o Try and treat the cause.
• If severe, management should begin before investigations are completed.
o Sit patient upright
o Give high flow oxygen
o Support respiration with PEEP.
o If management failing, involve anaesthetist early.
• Additional therapy involves:
o Diamorphine.
 Reduces anxiety and venous capacitance
• Reduces preload.
 2.5 – 5 mg IV
  Slowly.
 Add antiemetic
o Frusemide.
 If renal function normal.
 40 – 80 mg IV.
 May work initially by vasodilatation.
o Glyceryl Trinitrate.
 Give IV.
 If systolic BP is > 100 mmHg.
 Reduces preload.
• Patient can enter cardiogenic shock due to poor fluid distribution rather than absolute
overload.
o Due to failing haemodynamics of the heart.
o First line therapy should be with sublingual nitrates.
 Next line is frusemide.
• Other conditions which may compromise cardiac function should be treated.
o Fast AF.
 Digoxin: Orally or IV
o Treat other arrhythmias appropriate.y.
 DC cardioversion may be required.

• If the above management is inadequate, transfer the patient to CCU/HDU/ITU.

o IV inotropic agents may be useful in hypotension.
 If pulmonary congestion is dominant.
• Dobutamine is preferred at 5 μg/kg/min
• Increase gradually to 20 μg/kg/min if needed.
• Dobutamine is a vasodilator, so may cause paradoxical
hypotension.
• Can be combined with low dose noradrenailne.
o If pulmonary oedema is not improving.
 Acute haemofiltration can rapidly remove fluid.
 Reduces need for intubation.
o Intra – aortic ballon counterpulsation in primary cardiac failure may be used as
support while therapy is planned.