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CASE 1
Case 1
A 40-year-old male, teacher, arrives to the ED where you are an intern for intermittent episodes of chest pain that started 12 hours ago. For the last 3 hours the pain has been constant and this time radiates to the back and shoulder for which decided to present to the ED. The pain is very severe 8/10 and he looks pale and very uncomfortable.
Case 1
Your tasks are:
Take a focused history (you have 3 minutes for this).
Ask examiner for examination findings.
Arrange appropriate investigations
Discuss the most likely and differential diagnoses with the examiner.
Explain the management to the patient.
Case 1
HOPC:
• Onset and duration: pain started this morning gradually, for the last 3 hours stronger and constant.
• Location: Left chest.
• Character: Sharp.
• Aggravating factors: Movement, deep inspiration.
• Associated factors: SOB, diaphoresis.
• Radiation: Back and left shoulder.
Case 1
History:
• Diagnosed of hypertension 2 months ago.
• Non-smoker.
• No previous operations.
• No allergies.
• Alcohol socially, no IV drug use.
• Family history: Mother DVT, otherwise all well.
Case 1
Physical examination:
GA: Uncomfortable, pale.
BP: 145/90 HR 95 RR20 SO2: 99% RA Temperature: 36.
JVP: 8cm
Regular heart sounds, nil murmurs, nil friction rub.
Normal breath sounds, no added sounds.
Abdomen normal.
Extremities: Nil pitting edema, nil calf tenderness.
Case 1
Investigations:
• ECG
Case 1
Investigations:
• CXR: Looking for cardiomegaly, pericardial effusion.
• FBE, UEC, CRP, Cardiac biomarkers.
• ECHO: to demonstrate pericardial effusion.
Case 1
Differential diagnosis of pleuritic chest pain:
• Pericarditis.
• Myocarditis.
• PE
• Aortic dissection.
• Pneumothorax.
• Consolidation.
• Pleurisy.
Case 1
Differential diagnosis of STE on ECG:
• STEMI
• Prinzmetal angina.
• Pericarditis and myocarditis.
• LVH.
• Early repolarization.
• LBBB.
• Ventricular aneurysm, Brugada syndrome.
PERICARDITIS
Inflammation of the pericardium. Most cases are viral or idiopathic.
Severe secondary complications may arise, such as the development of a large pericardial effusion that may lead to cardiac tamponade, or the condition may become chronic, leading to chronic constrictive pericarditis.
PERICARDITIS
CAUSES:
Viral: Most common cause.
Bacterial.
Malignancy.
Auto-immune.
Radiation therapy.
Trauma.
Drug induced.
PERICARDITIS
CLINICAL FEATURES:
Chest pain: Pleuritic in nature, typically worse lying supine better by leaning forward.
Dyspnea is not a feature unless there are complications.
Caution if the patient is on anticoagulants.
Low grade fever.
Pericardial friction rub.
PERICARDITIS
INVESTIGATIONS:
FBE.
UEC.
CRP.
Cardiac enzymes.
ECG
CXR
PERICARDITIS
Classical teaching:
• Diffuse STE on ECG.
• STE is concave upwards.
• PR segment depression.
• PR segment elevation in AVR.
PERICARDITIS
In reality:
• Pericarditis may be localized instead of diffuse.
• NO reciprocal changes (except AVR and V1).
• AMI may have similar STE morphology (concave upwards). If STE is concave upwards or horizontal strongly favors STEMI.
• STE II > STE III favors pericarditis.
PERICARDITIS
• PR depressions: Only in viral pericarditis and it is transient.
• Friction rub is transient. Difficult in assessment.
• NO Q waves in pericarditis.
• T waves do not invert in pericarditis until the resolution of STE.
PERICARDITIS
Echocardiography may show supportive evidence (but not specifically diagnostic) of pericardial effusion or thickening of the pericardium.
It is useful for helping to rule out alternative diagnoses, or secondary complications, (such as cardiac tamponade).
PERICARDITIS
MANAGEMENT:
Pain control.
NSAIDs.
Colchicine.
Steroids: Connective tissue disorders.
Admission if presence of complications.
CASE 2
Case 2
A 70-year-old male presents to your rural ED 1 where you are the HMO for 4 episodes of epigastric pain and indigestion in the last 24 hours; the last one started 2 hours ago and did not resolve until the time of presentation. On examination his HR 90 regular, RR 20, BP 140/80 and SO2 99% RA, he looks uncomfortable. Aspirin and morphine were given in the ambulance. The nearest tertiary hospital is 2 hours away.
Case 2
Your tasks are:
Take a focused history from the patient.
Ask examiner for examination findings.
Arrange appropriate investigations.
Explain diagnosis and management to the patient.
Case 2
HOPC:
Onset: started last night during intercourse last night.
Location: left-sided.
Duration: Initially resolving with pain, constant for the last 2 hours.
Characteristic: Dull, like indigestion.
Aggravating factors: exercise.
Alleviating factors: Rest.
Associated symptoms: Nausea, 1 vomit, diaphoresis.
Radiation: Jaw
Case 2
Past medical history: Healthy. Walks every morning. High cholesterol: on diet control. Non smoker Father AMI at age 45. No alcohol Not on any medications.
Case 2
Physical examination:
GA: Looks well T 36 HR 90 BP 140/70 RR 20 SO2 99% ra
CV: normal breath sounds, no added sounds, regular heart sounds, nil murmurs. JVP not increased.
Abdomen: soft non tender, nil organomegaly.
Extremities: No edema, no calf tenderness.
Case 2
Management:
Transfer to resuscitation area.
Cardiac monitoring.
GTN sublingual.
Gets pain free after sublingual GTN with resolution of STE.
Discussion with cardiology, transfer, start on heparin.
Prinzmetal’s angina
Temporary increase in coronary vascular tone (vasospasm) causing a marked, but transient reduction in luminal diameter.
It can occur in either a normal or diseased vessel.
Medical therapy classically employs vasodilator drugs, which include nitrates and calcium channel blockers.
If associated with coronary atherosclerosis, the prognosis is determined by the severity of the underlying disease.
CASE 3
Case 3
You are an intern in a rural hospital emergency department when a 73 year-old lady is brought by ambulance for acute onset of sob, weakness and diaphoresis.
• Your tasks are: • Take a concise, relevant and focused history.
• Ask examiner for findings on physical examination.
• Tell the examiner your working diagnosis and the reason for this.
• Interpret ECG and explain the patient your management.
Case 3
HOPC:
• Onset: 2 hours ago.
• Feels very weak everywhere.
• Associated moderate SOB.
• Associated symptoms: Nausea, diaphoresis.
Case 3
History:
• Hypertension.
• Hyperlipidemia.
• DMT2.
• Chronic kidney disase.
• Laminectomy for spinal canal stenosis 2006.
• Medications: Ramipril, Metformin, atorvastatin.
Case 3
Physical examination:
GA: Overweight lady, looks uncomfortable, diaphoretic.
HR: 100 regular, BP160/80 RR26 SO2 93%RA
JVP increased, regular heart sounds nil murmurs, bibasal crackles on lung auscultation.
Soft abdomen, non tender.
Bilateral ankle pitting edema.
Case 3
Initial management:
• Resuscitation bed, cardiac monitoring.
• Oxygen, Aspirin 300 mg, LMWH.
• IV line, send blood for cardiac biomarkers, coagulation profile, FBE, UEC.
• Urgent consultation with cardiology team.
ACS ACS
NSTEACS
NSTEMI
UA
STEMI
ACS
PATHOPHYSIOLOGY:
Atherosclerosis.
Usually precipitated by acute thrombosis induced by a ruptured or eroded atherosclerotic coronary plaque.
With or without concomitant vasoconstriction.
Sudden and critical reduction in blood flow to the heart.
ACS
PATHOPHYSIOLOGY: Other causes
Arteritis/vasculitis.
Trauma
Dissection.
Cocaine abuse.
ACS
PREDISPOSING FACTORS:
Known ischemic heart disease.
Diabetes.
Cigarette smoking.
Hypertension.
Strong family history of ischemic heart disease.
Hyperlipidemia.
Increasing age, Lupus in young women.
ACS
CLINICAL PRESENTATION: Chest pain
Retrosternal, gradual onset, > 20 min.
Radiation to left shoulder, left arm.
Radiation to both shoulders.
Radiation to neck, jaw.
Described as heavy, dull, pressure.
Associated with nausea, diaphoresis, SOB.
ACS
The most frequent anginal equivalents reported were:
SOB: 58% Weakness: 55% Unusual fatigue: 43% Cold sweats: 39% Dizziness 39%
STEMI
STEMI is defined as presentation with clinical symptoms consistent with an acute coronary syndrome with ECG features including any of:
Persistent ST-segment elevation of ≥ 1mm in two contiguous limb leads.
ST-segment elevation of ≥ 2mm in two contiguous chest leads.
New LBBB pattern.
STEMI
First step in management:
ECG: is it STEMI?
Differential diagnosis of ST elevation in ECG.
STEMI
The area of the heart involved can be determined from the 12 lead ECG using the following:
II, III, AVF Inferior V1 – V4 Antero-septal
V5 – V6 Lateral
DI – AVL Upper lateral
ST depression V1 – V3 Posterior
The ECG can be normal initially. If this is the case, repeat the ECG after 15 minutes to check progressive changes.
ANTERIOR STEMI
Anterior STEMI results from occlusion of the left anterior descending artery (LAD).
Anterior myocardial infarction carries the worst prognosis of all infarct locations, mostly due to larger infarct size.
Reciprocal ST depression in the inferior leads (mainly III and aVF).
INFERIOR STEMI
Occlusion RCA, LCx.
Inferior MIs account for 40-50% of all myocardial infarctions.
Presents with symptoms of indigestion or epigastric pain.
Reciprocal change shows first (DI, AVL), ST elevation in inferior leads shows later.
Always suspect Right ventricle infarction (40%).
RIGHT STEMI
Right ventricular infarction complicates 40% of inferior STEMIs.
V1 ST elevation and V2 ST depression.
Do not give Nitrates as right ventricle needs blood from pre-load.
Nitrates: severe hypotension, instead give IV fluids!
RIGHT STEMI
POSTERIOR STEMI
Usually associated with inferior STEMI due to RCA or circumflex occlusion.
4% of STEMIs are isolated posterior STEMI.
Mirror image of anteroseptal leads V1-V3.
POSTERIOR STEMI
POSTERIOR STEMI
ACS
INITIAL MANAGEMENT:
Oxygen: Only indicated in patients with hypoxia (SaO2 < 95%), breathlessness or acute heart failure. (Class I)
Pain relief: Titrated IV opioids are indicated to relieve the pain. (Class I)
Aspirin: loading dose 300 mg. Reduces the incidence of recurrent MI or death.
Nitrates: Venodilator, reduces preload for which decreases myocardial oxygen consumption. Dilation of coronary arteries increasing coronary flow.
STEMI
MANAGEMENT:
Reperfusion therapy: Primary PCI. Fibrinolysis. Coronary bypass surgery and multi-vessel coronary
revascularization.
STEMI
PCI:
Perform within 60 minutes if patient’s presents within 1 hour of onset of symptoms.
Perform within 90 minutes (6-12 hours of onset of symptoms.
STEMI
PCI:
Reduces mortality and stroke compared with thrombolytic therapy.
Indications for referral from rural hospital: Contraindications for thrombolysis. Cardiogenic shock. Patients who have failed to reperfuse with
thrombolysis. High-risk NSTEMI
STEMI
THROMBOLYSIS:
Must be given as early as possible ideally within 1 hour of the onset of chest pain and preferably within the first 4 hours.
This is the option if there is going to be any delay for PCI. (rural setting).
STEMI
THROMBOLYSIS: Indications.
Ischemic chest pain ONGOING of > 30 minutes. ECG changes : New ST elevation of at least 1 mm in two
consecutive chest leads or two consecutive limb leads. New left bundle branch block.
STEMI
Fibrinolysis: Contraindications.
Hemorrhagic stroke ever. Thromboembolic stroke within the last 6 months. Active GI bleeding in the last month. Major trauma or surgery in the last 2 weeks. Relative: Pregnancy, proliferative diabetic retinopathy.
STEMI
FIBRINOLYSIS: 4 agents currently available:
Tenecteplase (TNK t-PA) Reteplase (r-PA) Alteplase (t-PA) Streptokinase
The choice depends on local availability.
STEMI
ADJUNCTIVE THERAPY:
Heparin: After fibrinolysis commence IV heparin immediately with a bolus of 5000 units and an infusion of 15000 units over 12 hours. (APTT 1.5 times normal).
IV β-blocker: Decreases mortality by limiting infarct size and reducing tachyarrhythmias.
ACE inhibitors.
NSTEACS
NSTEACS refers to any acute coronary syndrome which does not show S-T segment elevation.
The ECG may show S-T segment depression or transient S-T segment elevation, but often will be normal.
NSTEACS
NSTEMI:
By definition this will be shown by an elevation of serum troponin and CK levels in the absence of S-T segment elevation.
ECG must be done within 10 min or patient arrival: ST depression. T-wave inversion or flattening. Non-specific or transient changes. Normal.
NSTEACS
UNSTABLE ANGINA:
Unstable angina is ischemic chest pain over and above the patient’s usual pattern and where the ECG remains normal, (apart from transient changes which then return to normal) and cardiac markers (CK and troponin) are not elevated. It is diagnosed therefore on clinical on grounds.
NSTEACS
History:
After an initial history and examination, an estimate of the patient’s risk profile should be made.
High risk. Intermediate risk. Low risk.
NSTACS
High risk patients: clinical symptoms plus: ECG changes: S-T segment depression, new T wave
inversion, transient S-T segment elevation in more than 2 contiguous leads.
Hemodynamic compromise. Ongoing pain, or recurrent episodes (> 10 minutes),
whilst in the ED. Arrhythmias requiring treatment or ventricular
tachycardia. Elevated serum troponin. High risk co-morbidities.
NSTACS
Intermediate risk patients: Symptoms plus:
Chest pain that occurred within the last 48 hours. Known history of CAD. CV risk factors Previous or current aspirin use.
NSTEACS
Low risk patients are defined as those presenting with clinical symptoms consistent with ACS, but without any intermediate or high risk features.
This will include:
Onset of angina symptoms within the last month. Worsening in severity or frequency of angina or lowering
of anginal threshold.
NSTEACS
Cardiac markers: Troponin I or T CK-MB, CK.
They will be released from dead myocardial tissue.
An initial troponin level should be done on all cases of suspected ACS with a second level done at 8-12 hours from the onset of the chest pain.
NSTEACS
TROPONIN I or T:
Advantages: Highly specific and sensitive for myocardial necrosis. Troponin will be elevated with smaller amounts of necrosis
(micro-infarction) from prolonged ischemia where CK-MB will not rise.
NSTEACS
TROPONIN I or T:
Disadvantages: Do not become elevated until 4-6 hours after the onset of
myocardial necrosis. Remain elevated for prolonged period: Limited ability to
detect late re-infarction. Troponin may be elevated in uremia and diseased muscle
states (polymyositis, muscular dystrophy).
NSTEACS
CK-MB:
Advantages: Does not remain elevated for as long as Troponin so may be
useful In detecting late re-infarction.
Disadvantages: Lower specificity for myocardial necrosis. Low sensitivity during early phase of myocardial infarction.
NSTEACS
High dose oxygen.
Aspirin 300 mg unless contraindicated.
If aspirin contraindicated clopidogrel 300 mg.
Pain relief: GTN 150-300 µg sublingually. Morphine 2.5-5 mg IV with antiemetic.
NSTEACS
Heparin:
LMW heparin such as enoxaparin 1mg/kg
or UF heparin 5000 units IV as a bolus followed by an
infusion of 1000 units/h.
Beta blocker: No need in the first 8 hours.
Referral for angiography if high risk.
CASE 4
Case 4
A 33-year old female presents for 2-day history of right sided chest pain, severe, associated with SOB. For the last few hours finds it difficult to even go to the toilet. Called LMO who advised to present immediately to ED.
Your tasks are to:
Take focused history from the patient.
Ask examiner for examination findings.
Discuss differential diagnosis and perform investigations accordingly.
Discuss management with the patient.
Case 4
HOPC:
Onset: gradual, 2 days ago.
Location: right sided.
Duration: Constant for the last 2 days.
Character: Sharp.
Associated symptoms: SOB.
Pain worse on deep inspiration.
Radiation to the back.
Case 4
Past Medical History:
LMP 6 weeks ago.
Arrived from South America 2 weeks ago.
Mother AMI at age of 60
Non smoker
Denies alcohol consumption.
Case 4
Physical examination:
GA: pale, uncomfortable as per degree of pain.
BP 145/85, RR 24 HR 100 SO2 93% RA T 37.9
Not increased JVP, normal breath sounds, no added sounds, regular heart sounds, nil murmurs.
Soft abdomen non tender, nil organomegaly.
Extremities: no edema, no calf tenderness.
Case 4
Investigations and management:
V/Q scan: Preferred in young females as less radiation to breasts.
No need of d-dimer as high risk pre-test probability (2 risk factors, pleuritic chest pain, tachycardia, tachypnea).
If positive for PE anticoagulation.
PULMONARY EMBOLISM (PE)
Predisposing factors: Past history of DVT/PE (strongest). Decreased mobility: Plane flights. Recent limb trauma. Recent operation especially pelvic. Pregnancy, recent delivery. Oral contraceptive. Smoking. Obesity. Malignancy, procoagulation syndromes.
PE
Clinical features: Symptoms
Sudden onset of dyspnoea (commonest). Chest pain (usually pleuritic). Cough. Hemoptysis. Syncope.
PE
Clinical features: Signs
Tachypnea (commonest). Tachycardia. Low grade fever. Sweating. Large: Hypoxia, hypotension, elevated JVP. Signs of DVT in legs.
Clinical symptoms of PE?
YES 3
PE is the most likely diagnosis or equally likely
YES 3
HR > 100 YES 1.5
Immobilization at least 3 days or surgery in previous 4 weeks
YES 1.5
Previous PE or DVT
YES 1.5
Hemoptysis YES 1
Malignancy with treatment within 6 months or palliative care
YES 1
SCORE
PE
RISK SCORE (PROBABILITY OF PE):
> 6: High.
2-6: Moderate.
< 2: Low.
PE
Investigations:
CXR: To rule out other pathology, may be normal. D-dimer: Low pre-test probability. ECG Troponin: May be elevated in large PE’s, not diagnostic for
PE. Procoagulation screen. ABGs.
Pulmonary Embolism and ECG
Simultaneous T wave inversions in the inferior (II, III, aVF) and right precordial leads (V1-4) is the most specific finding in favour of PE, with reported specificities of up to 99% in one study.
Sinus tachycardia.
S1Q3T3
RAD
PE
Investigations:
CTPA: Best V/Q scan: Preferred in pregnancy 3rd trimester, renal
failure. Pulmonary angiogram: Gold standard however it is
invasive and carries risks. Rarely done.
PE
Management:
Oxygen. Morphine 5 mg IV if severe pain. Heparin: LMW 1mg/kg s.c 12 hourly or UH 5000 units IV
bolus followed by 1000 units/h infusion. Give initial dose of warfarin 5 mg. Subsequent dosing is given according INR.
PE
Management:
PE with shock: Thrombolysis Reteplase: 10 U bolus IV followed by 10 U bolus IV in
30 minutes. Heparin: 5000 U IV bolus followed by infusion.
CASE 5
Case 5
A 73-year-old male presents to the ED of a suburban hospital where you are the HMO. He has had severe chest pain for the last 40 minutes and also complains of pin and needles in his left leg. Since the onset of pain he has had nausea and vomited twice.
Your tasks are to:
Take focused history and perform physical examination.
Discuss differential diagnosis and perform investigations accordingly.
Discuss management with the patient.
Aortic dissection
Aortic dissection
Incidence: 3 per 100,000.
20% die without ever making it to hospital.
80% of dissections occur in non-aneurysmal vessels, so the term ‘dissecting aortic aneurysm’ is probably best avoided.
AORTIC DISSECTION
PREDISPOSED BY:
Hypertension.
Family history.
Age: Peak incidence 50-70 years.
Marfan syndrome.
Bicuspid aortic valve.
Coarctation or iatrogenic trauma.
AORTIC DISSECTION
Stanford classification:
Type A: Proximal dissections, where there is involvement of the ascending aorta, regardless of the site of entry.
Type B: Distal dissections, all dissections not involving the ascending aorta, therefore arch and descending.
AORTIC DISSECTION
CLINICAL FEATURES: Symptoms:
Abrupt onset with sudden pain.
Sharp or tearing pain.
Retrosternal, interscapular or lower in the back, migratory, severe, resistant to opiates.
PAIN GETS BETTER is the nature of dissection as pain is cataclysmic at onset. On the other hand chest pain with STEMI is crescendo.
AORTIC DISSECTION
CLINICAL FEATURES: Signs:
Unequal or absent pulses.
Difference of blood pressure in the arms.
Diastolic murmur if Aortic regurgitation occurred.
AORTIC DISSECTION
A small number of dissections occur with relatively little or no pain. These may present as:
Sudden death Neurological deficits. On investigation for aortic incompetence. Recognition of a wide mediastinum on CXR.
The combination of chest pain and neurological symptoms is suggestive of aortic dissection.
AORTIC DISSECTION
Investigations: FBE UEC Coagulation profile. Troponin. ECG.
AORTIC DISSECTION
CXR:
Widened mediastinum (56-63%). Abnormal aortic contour (48%). Aortic knuckle double calcium sign >5mm (14%). Pleural effusion (L>R), tracheal shift, left apical cap,
deviated NGT. Normal’ in 11-16%.
AORTIC DISSECTION
Imaging:
CT angiogram. MRI TOE
AORTIC DISSECTION
AORTIC DISSECTION
COMPLICATIONS:
Myocardial Infarction.
Acute aortic incompetence (regurgitation).
Pericardial effusion / cardiac tamponade.
Pleural effusion.
Intestinal ischaemia.
Oliguria and haematuria.
AORTIC DISSECTION
Management: ABCD Analgesia. B-Blockers:
as soon the diagnosis in made. These are used to reduce the shear stress on the
aortic wall, to prevent further dissection (Esmolol, metoprolol).
Vasodilators: If BP is not controlled. Surgery: All proximal.
