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Transcript
Electrolyte inbalance Calcium Hypercalcaemia and hypocalcaemia predominantly alter the action potential (AP) duration. An increased extracellular Ca concentration shortens the ventricular AP duration. In contrast, hypocalcaemia prolongs the ventricular AP duration. These cellular chancges correlate with abbreviation and prolongation of the QT interval (ST segment portion)) with hypercalcaemia and hypocalcaemia, respectively. Potassium Hyperkalaemia is associated with a distinctive sequence of electrocardiographic changes. The earliest effect is usually the narrowing and peaking (tenting) of the T wave. The QT interval is shortened by this stage, associated with decreased AP duration. The QRS begins to widen and P wave amplitude decreases. PR interval prolongation can occur followed by second/third degree AV block. Complete loss of P waves can occur too. Moderate to severe hyperkalaemia occasionally induces ST elevations in the righ precordial leads (V1 & V2). Severe hyperkalaemia can also present with atypical finds. Very marked hyperkalaemia leads to eventual asystole. The triad of (1) peaked T waves (from hyperkalaemia), (2) QT prolongation (from hypocalcaemia) and (3) LVH (from hypertension) is strongly suggestive of chronic renal failure. Hypokalaemia, in contrast, include hyperpolarisation of myocardial cell membranes and increased AP duration. The major manifestations are ST depression with flattened T waves and increased I wave prominence. Hypokalaemia also predisposes to tachyarrythymias. Magnesium Specific ECG findings of mild/moderate magnesium abnormalities are not well characterised. Severe hypermagnesaemia can cause AV and intraventricular conduction disturbances that may culminate in complete heart block and cardiac arrest. Hypomagnesaemia can pontentiatre certain digitalis toxic arrythymias. Sodium and other Hypo/hypernatraemia does not produce consistent effects on ECG. Systemic hypothermia may be associated with an appearance of a distinctive convex elevation of (J point) of ST segment and QRS complex (J wave or Osborne wave). Basics of ECG pattern Rate Rhythym Big square is 0.2s small square is 0.04s. To calculate rate, divide 300 divided by number of big squares Use the ‘card method’ to confirm whether regular/irregular Axis The mean frontal axis is the sum of all ventricular forces during ventricular depolarisation. The axis lies 90 degrees to the isoelectric complex. Generally if the complexes in leads I and II are both positive the axis is normal. P wave Absent P wave: AF, sinoatrial block. Dissociation between P and QRS indicates complete heart block. Bifid P wave indicates left atrial hypertrophy. Peaked P (P pulmonale) wave indicates right atrial hypertrophy. PR interval Range is 0.12-0.2s. Prolonged PR interval indicates delayed Av conduction (1st degree heart block). A short PR interval indicates unusual fast AV conduction down an accessory pathway e.g. WPW syndrome. QRS complex Normal duration <0.12s. If prolonged suggests ventricular conduction defect eg Bundle branch block. Large QRS complexes suggest ventricular hypertrophy. Normal Q waves (0.04s wide and <2mm deep) are often seen in leads V5 V6 aVL and I, and reflex normal septal depolarisation. Pathological Q waves may occur within a few hours of a MI. QT interval Varies with rate, normal is 0.38-.042s. The corrected QT interval equals the measured QT interval divided by the square root of the cycle length. ST segment Usually isoelectric. Planar elevation (<1mm) or depression (<0.5mm) usually implies infarction or ischaemia, respectively. T wave Normally inverted in aVR, V1 and occasionally V2. Abnormal if inverted in I, II, and V4-V6. Peaked in hyperkalaemia and flattened in hypokalaemia. J wave Seen in hypothermia, subarachnoid haemorrhage and hypercalcaemaia. Cardiac arrest Causes – two ways to remember H’s & T’s Hypovolaemia Hypoxia Hydrogen ions (acidosis) Hyper/hypokalaemia Hypothermia Hyper/hypoglycaemia Tablets/toxins Tamponade (cardiac) Tension pneumothorax Thrombosis (MI) Thromboembolism Trauma COLD PATCH C Cold (hypothermia) O Oxygen deficit L ‘Lytes’ (potassium) D Drugs P Pulmonary Embolus A Acidosis T Tension Pneumothorax C Cardiac Tamponade H Hypovolemia. Pathophysiology In VT/VF, acute myocardial ischaemia results in changes in the concentration of many components of the intracellular and extracellular milieu (e.g., pH, electrolytes, and ATP). In turn, these changes form the basis for pathogenic impulse formation and propagation of arrhythmia. In patients with areas of myocardial scarring, the mechanism for arrhythmia is likely to be a re-entrant circuit generated by surviving myofibrils within areas of fibrosis. Studies of non-ischaemic dilated cardiomyopathy have shown that the mechanism of arrhythmia is not re-entry, but more likely the initiation of VT/VF from early or late afterdepolarisations in the setting of a prolonged action potential duration, which in turn is due to the altered function of various ion channels. Despite widespread and long-standing use, no drug has definitively been shown to increase survival to hospital discharge in patients with cardiac arrest. In a patient with a peripheral IV line, drug administration is followed by a fluid bolus. Epinephrine is the main drug used in cardiac arrest although its benefit is increasingly challenged. It is given 3 to 5 min. Epinephrine has combined α- and β-adrenergic effects. The α-adrenergic effects may augment coronary diastolic pressure, thereby increasing subendocardial perfusion during chest compressions. Epinephrine also increases the likelihood of successful defibrillation. However, β-adrenergic effects may be detrimental because they increase O2 requirements (especially of the heart) and cause vasodilation. Intracardiac injection of epinephrine is not recommended because pneumothorax, coronary artery laceration, and cardiac tamponade may occur. Atropine sulfate is a parasympatholytic drug that increases heart rate and conduction through the atrioventricular node. It is given for asystole (except in children), bradyarrhythmias, and high-degree atrioventricular nodal block, although no survival benefit has been demonstrated. Amiodarone can be given once if defibrillation is unsuccessful following epinephrine Mg sulfate has not been shown to improve outcome in randomized clinical studies. However, it may be helpful in patients with torsades de pointes or known or suspected Mg deficiency (ie, alcoholics, protracted diarrhea). Prevention of cardiac arrest Early recognition of symptom and quick action – follow early warning scores Treat risk factors for cardiac arrest in community In hospital – recognition of at risk patients e.g. critically ill Improve education of cardiac arrest prevention Pulmonary embolism Risk factors Symptoms Signs Investigations Treatment Surgery Pregnancy Reduced mobility IV drug use Dyspneoa Pleuritic chest pain Haemoptysis Collapse Tachycardia Tachypnoeic Pleural rub Raised JVP In major PE signs of shock Baseline investigation for ill patient CXR Echo Pulmonary angiogram ECG D-Dimer Oxygen Morphine Heparin Aortic dissection Aortic dissection starts with a tear in the intima of the aortic lining. The tear allows a column of blood under pressure to enter the aortic wall forming a haematoma which separates the intima from the adventitia and creates a false lumen. The false lumen extends for a variable distance in either direction. Most common site is within 2-3cm of aortic valve. Risk factors include hypertension, smoking, cholesterol, etc. 90% of all patients with aortic dissection, present with a sudden severe pain of the chest or back, classically described as "ripping/sharp". In aortic dissection, pain is abrupt in onset and maximal at the time of onset. In contrast, the pain associated with acute myocardial infarction starts slowly and gains in intensity with time. It is usually more oppressive and dull. pain migrates as the dissection progresses. Investigations – ECG, CXR, CT/MRI Management – Morphine, manage hypertension, then placing of stents or grafts to the aorta. MI Risk factors Symptoms Signs Investigations Treatment Gender Smoking Diabetes Family history Hypertension Obesity Dull chest pain Dyspnoea Sweating, vomiting, nausea Low grade fever Pale clammy skin Pericardial rub Baseline investigation for ill patient ECG Cardiac enxymes (troponin) CXR Echo MONA – acute care Morphine Oxygen Nitro-glycerine Aspirin Reperfusion Fibrinolytic drugs (streptokinase/alteplase) Percutaneous coronary intervention CABG Aortic stenosis Senile calcification commonest cause Classic triad is angine, syncope and heart failure. Signs include slow rising pulse, aortic thrill, ejection systolic murmur which radiates to carotids. In severa AS second heart sound be inaudible. ECG and echo are used to diagnose AS. Treatment is valve replacement. Cardiomyopathy Is disease of the cardiac muscle. According to WHO 5 main Groups. Dilated cardiomyopathy: commonest form. The left or both ventricles are dilated with impaired contraction. Causes include: ischaemia, alcoholic, toxic, thyroid disorders, valvular, familial/genetic and idiopathic. Hypertrophic obstructive cardiomyopathy: 2nd commonest; left and/or right ventricular hypertrophy. Usually familial (autosomal dominant). Restrictive cardiomyopathy: rare; with restrictive filling and reduced diastolic filling of one/both ventricles and normal or near normal systolic function. Causes include: amyloidosis, endomyocardial fibrosis, and idiopathic. Arrhythmogenic right ventricular cardiomyopathy: with fibro-fatty replacement of right ventricular myocardium. Cause is unknown; familial form is usually autosomal dominant with incomplete penetrance but may be recessive. Unclassified: with no typical features of the above. Causes include: fibroelastosis, non-compacted myocardium, systolic dysfunction with minimal dilatation, mitochondrial diseases. Investigations – typical cardiac investigation i.e. bloods, ECG, echo, etc. Management – symptomatic and mainly directed towards heart failure treatments Ventricular tachycardia >120 BPM. Monophormic (regular) or polymorphic (irregular). Risk factors – coronary heart disease, electrolyte deficiencies, use of sympathomimetic agents e.g. caffeine/cocaine Presentation – symptoms of ischaemic heart disease/failure ECG Rate greater than 100 bpm (usually 150-200). Wide QRS complexes (>120 ms). Presence of atrioventricular (AV) dissociation. Fusion beats. Other investigations – U/E’s, CXR, levels of therapeutic drugs Management – see advanced life support protocol. Digoxin toxicity The therapeutic level for digoxin is 0.8-2.0 ng/mL. Hypokalaemia and renal failure increases the risk of digoxin toxicity and cardiac dysrhythmias. Symptoms Hyper salivation nausea/vomiting diarrhoea heart arrhythmia (classically paroxysmal atrial tachycardia with block) Digoxin should not be given if heart rate less than 60 BPM Treatment - Digoxin Immune Fab