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18 Cards in this Set
- Front
- Back
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On admission, with the symptoms of a heart attack, such as chest pain, pale, sweating. What are the first tests that you would perform?
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ECG - check for cardiac abnormalities
X-ray to check for heart failure Troponin I and T |
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In an acute situation, what are the first treatments that you would give?
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Oxygen if saturation was below 94%
Morphine for pain 10mg IV, can cause nausea and hypotension Anti-emetic to combat nauseousness from presentation (or due to presentation): Metoclopramide or ondansetron 4mg Aspirin - 300mg orally antiplatelet treatment Clopidogrel - 300mg potent antiplatelet prevent re-infarction. Bleeding risk (given once diagnosis of ACS is made) |
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What are the two types of reperfusion therapy for a STEMI? What are the risks involved and contraindications?
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Primary percutaneous coronary intervention:
Invasive procedure to open the blocked artery and treat the underlying atheromatous plaque by baloon angiplasty and stent placement. Can restore coronary blood supply and minimise cardiac damage and improve outcome. Superior to thrombolysis. Risks:Vascular damage, stroke Contraindications: Can only be performed in specialist centres and is only the treatment of choice if it can be given within 90 minutes, (>40 min journey time) Thrombolytic therapy Tenecteplase (tissue plasminogen activator) 8000units (100u/kg) in 8ml as IV bolus in over 10s Breaks up the thrombus Risks: Haemorrhagic stroke Contraindicated: Recent surgery, previous stroke, GI bleeding, bleeding disorders Alteratiev to PCI Streptokinase no longer used due to systemic effect Heparin 5000u IV bolus. Followed by infusion of 1000u/h, subsequent dose guided by aPTT - anticoagulation to prevent further risk of thrombosis, Risk: bleeding |
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In the event of acute complete heart bloock, what options are there?
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atropine 600ug IV bolus
If this doesn't work temporary trancutaneous or transvenous pacemaker would be considered. |
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After acute situation is handled and PCI is considered, what other tests would you want to carry out?
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Troponin I and T, can confirm the diagnosis of ACS/MI and give an indication of how serious the MI was (normal = 0.04ug/l)
Blood glucose test Cholesterol test <5mmol/l Chest x - ray - check for heart size, lung fields clear, evidence of heart failure Echocardiogram - looking for LV function and severity of damage as this is a major prognostic factor |
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What are the complications of an acute MI?
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Arrhythmia - Ventricular (cardiac arrest due to MI, many die before they reach hospital
bradycardia, heart block due to vagal overactivity or damage to conducting system, atrial arrhythmia, commonest is atrial fibrillation which is transient Heart Failure - infarction can cause severe left ventricular dysfunction and heart failure. Can occur acutely with the development with pulmonary oedema. May resolve with treatments, mortality is directly rated to the extent of LV damage. Cardiogenic shock - severe LV damage results in shock, hypotension, heart failure and poor cardiac output. Very poor prognosis. Revascularisation by urgent angioplasty has been shown to improve outcome but mortality remains high. Myocardial Rupture - depends on site Free ventricular wall - usually fatal Septal - VSD, outcome depends on size of the defect, may be operable Papillary muscle - can cause mitral regurgitation Pericarditis causes chest pain and was usually self limiting after several days. It is uncommon in this era of early reperfusion Mural thrombus - may embolise to the brain and cause a stroke |
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Secondary Prevention
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(blood pressure and diabetes should obviously be controlled too)
Clopidogrel - 75mg Aspirin - 75mg Beta Blocker - Bisoprolol - β1-selective (heart specific) receptor antagonist. Shown to reduce mortality post MI 2.5mg titrated to 10mg if tolerated ACE inhibitor - Ramipril 2.5mg initially and titrated up to 5mg bd. Shown to reduce mortality post-mi (benefit is greatest in patients with left ventricular dysfunction and heart failure) Statin - Simvastatin 40mg - cholesterol lowering drug (an HMG-CoA reductase inhibitor has been shown to reduce mortality post-MI REGARDLESS OF CHOLESTEROL LEVEL |
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Lifestyle issues to be discussed after myocardial infarction
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The diagnosis of myocardial infarction "heart attack" - major life event for patient and diagnosis, risk factors and implications must be discussed
Secondary prevention drug therapy, patient should know what the drugs are and what they do Smoke cessation, importance of stopping smoking, NRT Exercise, advised about gradual increase in exercise post-MI. Exercise classes offered to help with this. Strenuous exertion should be avoided for the first weeks after MI, gradually building up the level of exertion over months Diet, improve diet, reduce their cholesterol and eat a health diet, reduce animal fats, increase fruit and vegetables Sexual activity - Return to normal life, if recovery is uncomplicated and patient able to briskly climb two flights of stairs without any chest pain or feeling breathless, they can usually safely have sex about two to three weeks after a heart attack Driving ACS/MI treated by angioplasty with good LV function, the patient should not drive for 1 week, if LV dysfunction should not drive for 4 weeks Returning to work, work may depend on the patients occupation and exercise tolerance, but the aim is for them to be back at work by 1-2 months post MI Rehabilitation classes, rehabilitation classes for education and support, and exercise classes to encourage graded increase in exercise have been shown to provide benefit. They usually start 4-6 weeks after discharge from hospital. |
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What are non-modifiable risk factors for CHD/CVD?
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Age, male sex, ethnicity, family history, social class?
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What are modifiable risk factors for CHD/CVD?
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Cholesterol, hypertension, diabetes, smoking, sedentary lifestyle/obesity
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What reduction in ST-elevation is deemed as a successful thromolysis treatment?
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At least 50% reduction.
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Define Glagov's original atherosclerosis hypothesis
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The new model of atherosclerosis was based on histological analysis of coronary artery sections reported by Glagov et al in 1987.1 The work they described showed that the early stages of disease were marked by plaque accumulation in the vessel wall, with subsequent enlargement of the EEM but no change in lumen size. In Glagov’s original hypothesis, plaque development is extraluminal until the lesion occupies ≥40% of the area within the EEM. Only then does the lumen begin to shrink.
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What is the diagnostic criteria for acute myocardial infarction?
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Any elevation in troponin accompanied by evidence of myocardial ischaemia:
Symptoms New ECG changes Imaging evidence of infarction CMR; SPECT; echo |
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What is the difference between STEMI, NSTEMI and unstable angina?
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ST elevation myocardial infarction. Usually caused by thrombotic occlusion of a coronary artery and thus will result in a transluminal infarction. Unless the artery is reopened (thrombolysis or primary angioplasty). The ECG shows ST elevation (a requirement before giving thrombolytic therapy_ and the troponin will be elevated.
NSTEMI- Non-st elevation myocardial infarction. Usually cause by an intracoronary thrombus, but without total occlusion of the artery. ECG may show st DEPRESSION. Troponin is positive (establishing the diagnosis of acute MI). Despite the presence of thrombus, it has been shown that thrombolytic therapy is not a benefit to NSTEMI. However, these patients are at risk of complications including death, and should be thoroughly investigated and treated Unstable angina - Patient with a history of acute coronary syndrome (e.g rest pain) but with no detectable troponin rise are considered to have unstable angina, and should be investigated with exercise testing and coronary angiplasty. |
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What do the results of ECG, troponin and imaging tell you after reperfusion from an STEMI
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Well, if there is pathological Q waves represented by a negative Q wave, then there is transmural MI which means that the reperfusion wasn't effective enough to stop ischaemic damage to the entire thickness of the myocardium. The lower the troponin result is the less severe the MI was, and correlates with outcome (the higher the troponin the greater the mortality)
Echocardiograph will show the extent of myocardial damage which should be performed in all patients with MI. |
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Absolute contraindications to thrombolytic therapy?
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History of intracranial bleed or neoplasma or recent head trauma (<4 weeks)
Recent (3 weeks) surgery (including dental surgery) and major trauma Ischemic stroke <6 months Active internal bleeding (< 1 month) Suspected aortic dissection Acute pancreatitis Bleeding disorder (menorrhagia, normal menstruation is not a bar to fibrinolysis Refractory hypertension (SBP > 160mmHg or DBP > 100mmHg), not responsive to anti-hypertensive therapy. |
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Relative contra-indications/cautions
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Transient ischemic attack (<6 months)
Pregnancy, or within 1 week of dlievery Active peptic ulceration Known bleeding diathesis or current use of anticoagulants Malignant disease Advanced Age (depending on general physical condition) Recent prolonged/traumatic resuscitation (sufficient to fracture rib) Known intra-cardiac or intravascular thrombus Oral anticoagulant therapy Non-compressible tissue/vascular punctures Advanced liver disease Infective endocarditis Diabetic retinopathy |
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Advantage of PPCI vs thrombolytics
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Cant think but
Tenectaplase can be administered as a single bolus |
