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.
Transcript
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 FBCo U&Eo 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.
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 anginao 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 stenosiso Embolio Coronary osteial stenosiso Hypertrophic obstructive cardiomyopathyo 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
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 wallo 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 changeso Medication
Non – coronary causes for angina should be sought and treated.o Valvular heart disease.o Anaemia.
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:
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 paino 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.
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 changeo Superimposed thrombosiso Platelet aggregationo Vasospasm
Microscopically, acute MI follows a predictable sequence.
Time after onset of symptoms Macroscopic changes Microscopic changesUp to 18 hours None None24 – 48 hours Pale oedematous muscle Oedema, acute inflammatory
cell infiltration, necrosis of myocytes
3 – 4 days Yellow, rubbery centre with haemorrhagic border
Obvious necrosis and inflammation, early granulomatous tissue
3 – 6 weeks Silvery scar, becoming rough and white
Dense fibrosis
Overall mortality from acute MI has improved markedly in the last 20 years.o Better medical care.o Development of coronary care unitso 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 inferioro 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.
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
0 1 2 3 4 5
CKLDH
AST
Troponin
Days
Leads II, III, aVF Precordial leadsV1 – 6
V1 – 3 V4 – 6, I and aVL
V1 – 2Tall R wave, 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.
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 Pregnancyo Non – compressible punctures.o Traumatic resuscitationo 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 weeko Known bleeding disordero 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 MIo Can result in hypotension
Recombinant tissue polasminogen activator (tPA)/ Alteplaseo Most benefit in patients with anterior MI or hypotensiono 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 angioplastyo 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 MIComplication Interval MechanismSudden death Usually within hours Often ventricular fibrillationArrythmias 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
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 classificationClass FeaturesI 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:
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.
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 Fevero Leucocytosiso Pericarditiso 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 Physicalo Physiologicalo 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 stratificationo 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 – blockerso Reduce risk of mortality and reinfarction by 20 – 25%.o Approximately 25% of patients have relative contraindications to β – blockers.
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 myocardiumo 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 FeaturesI No limitation of physical activityII 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.
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 partumo 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
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:
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 Orthopnoeao Wheezingo Anxietyo Sweating
There may beo Pink frothy sputumo Ischemic chest paino Pulmonary oedema
The order of priorities is:o Relieve symptoms and stabilise patient.o Support other organs with adequate perfusiono Try and treat the cause.
If severe, management should begin before investigations are completed.o Sit patient uprighto Give high flow oxygeno 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.
