Case Protocol 9 Flashcards
A 58 y/o man presented to his local GP with a two hour hx of severe chest pain. The pain had commened while running, and was initially associated with nausea, vomiting and agitation. The patient had experience similar, less severe chest pain while running over the previous three weeks. He had a 27 year history of T1DM.
On examination the main was distressed, diaphoretic and mildly obese. Blood pressure was 165/105mmHg, pulse rate was 114/min with frequent ventricular ectopic beats (VEBs) and there was an S4 heard on auscultation of the praecordium. Respiratory rate was 22, temperature 36.5. Basal crepitations were audible over both lungs.
What is your provisional diagnosis?
Acute myocardial infarction
What cardiovascular risk factors are present and what additional risk factors should be assessed?
Risk factors in this man include DM and obesity. HTN is possible, although elevated BP in the setting of chest pain does not necessarily reflect sustained systemic HTN.
Other non-modifiable risk factors: family hx of CAD, past hx of CAD, hyperlipidaemia
Other modifiable risk factors: smoking
Outline the investigations you would perform, the costs and the results that you would expect.
The diagnosis of myocardial infarction rests on the findings on history and examination, in conjunction with:
Serial ECGs (x3): evolution of changes (ST segment elevation over areas of transmural ischaemia, followed by development of Q waves)
$23.30 each
Serial cardiac proteins/enzymes: evolution of changes (cardiac troponin [TnI and TnT] rise within 2 hours is indicative of myocardial necrosis, remain elevated for 10-14 days); sensitivity of troponins is greater than CK-MB isomer of creatinine kinase (rises with 2 hours, maximal 10-12 hours, return to normal within 24 hours)
$9.55
Echocardiogram: useful to show segmental wall motion abnormalities of the left ventricle, and a measure of overall left ventricular function
$93.25
UEC: maintenance of a normal to high serum potassium is important to prevent arrhythmias
$19.80
FBC: exclude anaemia as an exacerbating factor
$17.20
CXR: assess cardiac size and look for evidence of pulmonary oedema
$48.80
BSL, fasting lipids/HbA1c, CXR (assess cardiac size, pulmonary oedema as cause of basal creps)
Thalium scan to assess areas of myocardial hypoperfusion can be relevant to some cases - $385.45
The ECG was consistent with an acute myocardial infarction.
What abnormalities would have been present on the ECG, and what is the pathological basis of these changes? What is the significance of the biochemical abnormalities shown opposite?
Na 137 (135-145); K 4.3 (3.5-5.0); Cl 101 (95-107); HCO3 28 (24-32); urea 8.9 (3-8); creatinine 140 (60-110); BSL 12.9 (3-6); CK-MB 120 (
ECG changes: the initial area of tall peaked T waves is said to represent areas of epicardial injury (localised hyperkalaemia); hyperacute phase of myocardial infarction is characterised by the appearance of ST segment elevation (concave down), representing a zone of myocardial injury; Q waves represent a total loss of electrical activity in the wall of the left ventricle in an area of transmural infarction
Hyperglycaemia is consistent with the history of DM.
Raised urea, creatinine: long-standing DM –> CKD
Raised CK-MB and troponin: consistent with myocardial necrosis
Outline the likely sequence of events leading to this man’s clinical presentation.
Most likely secondary to the thrombotic occlusion of an atherosclerotic coronary artery.
Atherosclerotic plaque –> rupture or fissure –> exposure of thrombogenic subendothelial surface –> clot formation –> critical stenosis –> myocardial ischaemia –> myocardial infarction (when ischaemia lasts 20-40mins)
What are the important principles in the ED of this mans evolving myocardial infarction? What are the mechanisms of action of the drugs that would be administered?
In the ED, the goals for management of patients with suspected STEMI include the control of cardiac pain, rapid identification of candidates for urgent reperfusion therapy, triage of lower-risk patients, avoidance of inappropriate discharge of patients with STEMI.
ABC’s, GCS
Aspirin: effective across the entire spectrum of acute coronary syndromes; rapid inhibition of COX in platelets followed by a reduction of thromboxane A2 levels; 300mg tablet followed by daily oral 150mg
Supplemental oxygen: particularly if hypoxaemia is present, nasal prongs or face mask (2-4L/min) for the first 6-12h after infarction
Active chest pain:
Nitroglycerin, sublingual: 3x0.4mg/5min; decreases myocardial oxygen demand (lowering preload) + increases myocardial oxygen supply (dilating infarct-related coronary vessels or collateral vessels); nitric oxide –> smooth muscle relaxation –> vasodilation
Nitroglycerin, IV: if return of chest pain after favourable response to sublingual and other evidence of ischaemia (ST segment of T wave shifts); avoided in systemic BP venous pooling –> reduced cardiac output + arterial pressure (prompt elevation of legs); risk of bradycardia + advanced degrees of heart block (posteroinferior infarction) responds to atropine (0.5mg IV)
Beta Blockers, IV: diminish myocardial oxygen demand + ischaemia; may reduce in-hospital mortality (particularly in high-risk patients); metoprolol 5mg 2-5min (x3) if HR >60bpm, systolic BP >100, PR interval 0.24s; then oral 50mg every 6h for 48h, then 100mg every 12h; not if hypotensive, bradycardia or asthma
Heparin:
12-lead ECG: assess candidates for reperfusion therapy (if ST elevated at least 2mm in two contiguous precordial leafs and 1mm in limb leads)
Reperfusion therapy: if PCI (percutaneous coronary intervention) not available, then fibrinolytic therapy; if continued chest pain or failure to resolve ST elevation by 90 minutes then need rescue PCI; reteplase of tenectaplase; contraindications - active bleeding, bleeding diasthesis, significant head/facial trauma last 3 months, hx of intracranial bleed
Limitation of Infarction Size: central zone of necrotic tissue irreversibly lost, fate of surrounding ischaemic myocardium helped by timely restoration of coronary perfusion (fibrinolysis or PCI); PCI better when diagnosis in doubt, cardiogenic shock is present, bleeding risk is increased, or symptoms have been present for at least 2-3h when the clot is mature and less easily lysed by fibrinolytic drugs
Avoid: glucocorticoids and NSAIDs (except aspirin) as they can impair infarct healing and increase the risk of myocardial rupture (may lead to larger infarct scar), can increase vascular resistance
NSTEMI: aspirin + clopidogrel, don’t thrombolyse, re-stratify them (lower, intermediate, high) –> how much tissue will infarct without intervention (stress test, 2x serial negative troponins over 12 hrs, no changes in ECG; high risk –> cath lab); if undergoing PCI then give abciximab (GP2b3a inhibitor - stop platelet adherence to endothelium)
What complications might develop in the first 48 hours after admission?
Arrhythmias - ventricular fibrillation is the most common lethal arrhythmia
Extension of the area of the myocardial infarction
Cardiogenic shock
Left ventricular failure
On the 4th day of hospital, the patient developed severe chest pain lasting 60 minutes, requiring morphine for relief.
What is the most likely cause of this chest pain?
Ischaemic chest pain: due to further acute myocardial infarction
Pulmonary embolus and infarction
Pericarditis
Anxiety
What arteries, and areas of these, are likely to be diseased? Describe the sequential changes that occur in the myocardium following infarction.
Thrombotic occlusion is most likely to occur in the proximal 2cm of the left main trunk, left anterior descending or right coronary arteries.
Left anterior descending (50%); atherosclerosis site first 2cm; site of infarct - anterior and apical left ventricular infarct, anterior 2/3 of septum
Right coronary artery (30%); atherosclerosis site anywhere along course (proximal/distal 1/3); site of infarct - infero-posterior wall of left ventricle, posterior portion of the septum, inferoposterior wall of the right ventricle
Left circumflex coronary artery (20%); atherosclerosis site first 2cm; site of infarct - lateral left ventricular wall, excluding the apex
Macroscopic changes:
First 24hr - myocardium ceases to function, then begins to bulge during systole, myocardium becomes pale and swollen but not circumscribed; 1-3 days - infarct is clearly defined, dark mottling = reddish-blue discolouration caused by trapping of stagnant blood; 4-7 days - area of infarction becomes yellow and opaque in centre (yellow-tan central zone), with a zone of haemorrhage around the infarct and early granulation tissue formation (hyperaemic border); days 7-14 - sharp delineation by hyperaemic border, increasing development of granulation tissue (grey-white scarring); 2-8 weeks - granulation tissue becomes less pink, thinning of infarct with central depression obvious by 3 weeks, scarring visible by 6-8 weeks (mature grey-white scar); 3 months - white firm scar maximal by 2 months
Microscopic changes:
First 24 hr - oedema and haemorrhage (early features of coagulative necrosis and inflammation), change in permeability of membrane, metabolism of glycogen, structural change on EM, organelles swell and become vacuolated, hydropic change; 1-3 days - inflammatory change develops alongside necrosis (coagulative necrosis, pyknosis, myofibril changes, intense eosinophilia); 4-7 days - late acute inflammation (macrophage infiltrate - phagocytosis of necrosed cells), clear differentiation between viable and necrotic tissue, leucocyte infiltration; 7-14 days - phagocytosis, ingrowth of granulation tissue (little collagen, many fibroblasts, angiogenesis); 2-8 weeks - granulation tissue formation complete in five weeks (scar tissue - dense collagen, few fibroblasts, scar contraction); 3 months - decreased vascularity, dense connective tissue
The patient’s pain persisted and examination revealed pallor and diaphoresis, blood pressure 80/40mmHg, HR 110bpm with frequent ventricular ectopic beats (VEBs), S3 and S4 gallop rhythm and oliguria.
What is the most likely diagnosis? Explain the pathophysiological basis of this condition.
Cardiogenic shock
This is caused primarily by loss of functioning myocardium (>40%). It usually occurs in patients who have had one or more previous myocardial infarcts, but can also occur due to rupture of a papillary muslce (rare). It is characterised by a decreased cardiac output leading to under-perfusion of vital organs, and is usually associated with pulmonary oedema because of increased LV end-diastolic pressure.
Despite appropriate treatment, the patient died on the fifth hospital day.
What is the likely cause of death? Does this man require an autopsy under the Coroner’s Act? Outline the pathological findings expected at autopsy.
Likely cause of death = cardiogenic shock (arrhythmias); ventricular fibrillation, pulmonary embolus, embolic stroke, myocardial rupture and tamponade.
The Coroner’s Act does not require an autopsy in this case, because the patient died of a known illness and was not admitted to hospital or administered an anaesthetic in the last 24 hrs of life.
Findings at autopsy might include:
Heart - myocardial infarct, coronary atheroma and thrombosis, mural thrombus, pericarditis, LV dilation
Lung - pulmonary oedema (heavy), pulmonary embolus + infarct
Brain - cerebral atherosclerosis, cerebral infarction (embolic or “watershed” variety)
Kidneys - ATN, diabetic nephropathy
Arteries - atherosclerosis and complications; possible hypertensive changes
Peripheral veins - DVT
Pancreas - fibrosis and atrophy
