ICP Panel Prep Flashcards
Adenosine Pharmacology
AV Node anti arrhythmic (produces transient atrioventricular nodal block)
Binds to a1 receptors in AV node, forces potassium out of the cell (hyperpolerises cell) + slows calcium flow in (slows conduction velocity through AV node).
Indications Adenosine
Regular SVT (Narror complex tachycardia)
Regular SVT with aberrancy of conduction (SVT-A)
Contraindications adenosine
Hx of second or third degree heart block or sick sinus syndrome (except for pt with functioning pacemaker)
Sinus node disease
Chronic obstructive lung disease (eg asthma)
Known Hypersensitivity
Precautions Adenosine
Current dipyramole therapy (Asantin, Persantin) - increases plasma levels / effects of adenosine
Pts on carbamazepine - increases level of AV block
Amiodorone Pharmacology
A class 3 anti arrhythmic agent
Blocks potassium channels that cause repolarisation at phase three of the cardiac action potential, which extends the duration of the action potential and the refractory period. This prolongation of the refractory period helps prevent reentrant arrhythmias.
Also has sodium and calcium channel blocking and beta adrenocepter blocking effects
Amiodorone indications
VF/ VT refractory to cardioversion
Sustained or recurrent VT
Amiodorone contraindications
VT with inadequate perfusion or in pregnancy
Known hypersensitivity to Amiodorone or Iodine
TCA overdose
Precautions Amiodorone
Nil of significance
Side effects Amiodorone
Hypotension (arterial vasodilation and negative inotropy effects) and bradycardia (from sodium, potassium, and calcium channels, as well as beta-adrenergic receptor blockade).
Atropine Pharmacology
Anticholinergic agent. Inhibits actions of acytocholyne on post gangleonic cholinergic nerves
Vagal blocker - allows sympathetic effect to increase SA node firing rate and increase conduction velocity through the AV node
Atropine Indications
Bradycardia with less than adequate perfusion
Organophosphate poisoning with excessive cholinergic effects
Nerve agent poisoning
Contraindications atropine
Nil
Precautions atropine
Atrial flutter
Atrial fib (increases SA node firing rate - atria already firing at high rate)
Do not increase hr over 100 (except in kids under 6)
Glaucoma
Side effects atropine
Tachycardia
Absolute contraindications to thrombolisis
Active bleeding or bleeding disorders
Severe uncontrolled BP > 180/110
Surgery or major trauma in past 6 week
GI/GU Bleeding in past 2-4 weeks
TIA/CVA in past 12 months
Prior intercranial haemorrhage
Suspected aortic dissection
Known malignant intracranial neoplasm
Relative Contraindications to Thrombolysis
Current anti coags
Traumatic or prolonged CPR >10 mins
Hx of chronic severe or uncontrolled hypertension
Advanced liver disease
Advanced metastatic cancer
Non compressible vascular puncture (eg fistula or central venous access)
Pregnancy or 1 week post partum
Magnesium Pharmacology
Magnesium acts as a smooth muscle relaxant by blocking calcium channel mediated contraction and decreasing acytocholine release (also through calcium channel blocking effects).
Asthma – Inhibits the release of acetylcholine at the neuromuscular junction and interferes with calcium influx into smooth muscle cells which leads to bronchodilation.
Torsade de point – Calcium channel blockage which prevents the prolongation of the QT interval. Suppresses early afterdepolarisations that lead to torsardes.
Eclampsia – Inhibits excitatory NMDA receptors, blocks calcium flow and neuroexcitation. Also causes cerebral vasodilatation (Cerebral vasoconstriction thought to play a role in eclamptic seizures).
Magnesium Indications
Torsardes de pointe
Eclampsia
Severe Preeclampsia
Pts with severe asthma unresponsive to salbutamol/ ipratroprium
Contraindications Magnesium
Known heart blocks
Known hypersensitivity
Impaired renal / hepatic function
Addison’s disease
Side effects magesium
Hypotension
Circulatory collapse
CNS and resp depression
Cardiac arrhythmias
Loss of deep tendon reflexes
Clopidogrel Pharmacology
Antiplatelet medication that inhibits platelet aggregation by irreversibly binding to the P2Y12 receptor on platelets, thereby preventing activation of the ADP mediated glycoprotein GP IIb/IIIa complex, which is necessary for platelet aggregation.
Enoxaparan Pharmacology
Low molecular weight heparin. Anticoagulant medication. Binds to and activates antithrombin III, a naturally occurring inhibitor of several clotting factors in the blood. primarily inhibits Factor Xa, a crucial enzyme in the coagulation cascade that converts prothrombin (Factor II) to thrombin (Factor IIa). Thrombin is responsible for converting fibrinogen into fibrin, the protein that forms the structural basis of a blood clot.
It is similar in structure and action to heparin. However, enoxaparin generally provides a greater safety profile and more predictable response when compared to heparin.
Heparin Pharmacology
Anticoagulant medication . Combines with antithrombin III (heparin co-factor), thrombosis is blocked through inactivation of activated factor X and inhibition of prothrombin’s conversion to thrombin. This also prevents fibrin formation from fibrinogen during active thrombosis. Heparin can prevent the formation of a stable fibrin clot by inhibiting the activation of the fibrin stabilising factor.
Tenectaplase Pharmacology
Tenecteplase is a tissue plasminogen activator that works by binding to the fibrin matrix of a thrombus and converting plasminogen to plasmin. This degrades the fibrin matrix of the thrombus and helps to restore perfusion to the affected vessel.
Thrombolysis Treatment <75 No Renal Failure
Clopidogrel 300mg OR
Enoxaparan 30mg IV
Tenectaplase weight based IV
15 mins later
Enxoparan 0.1mg/kg SC (max dose 100mg)
Thrombolysis Treatment >75 No Renal Failure
Clopidogrel 300mg OR
Enoxaparan .75mg/kg SC (Max dose 75mg)
Tenecteplase half of weight based dose IV
Thrombolysis Treatment any age Renal Failure
Clopidogrel 300mg OR
Heparin 5000IU OR
Tenectaplase weight based dosage IV (half dose for >75)
15 mins later
Heparin 1000IU infusion per hour
How to prepare heparin infusion
5000 IU (1mL) into 50mL saline to make 100 IU per mL
Commence at 10 mL per hour to achieve 1000 IU per hour
Bradycardia less than adequate perfusion treatment
Atropine IV 600mcg repeat 600mcg @ 3-5 mins if required
Adrenaline infusion 5mcg per min, increase by 5mcg/min at 2 min intervals to max of 20 per min (draw up 3mg of adrenaline into 47 ml D5W)
Bolus adrenaline 5mcg intervals as required
Transcutaneous Pacing
SVT Treatment
Modified valsalva x 2
Adenosine 6mg, repeat 12 mg at 2 mins, repeat 12mg at 2 mins if required.
Sedate and cardioversion
Sedate 2mg Midaz IV, repeat 1mg IV at 2 min intervals to max of 5mg
Sync cardiovert 100j, repeat 200j
Adenosine Special considerations
Caffeine, aminophylline and theophylline block the adenosine receptors and the full incremental dosage may be required.
Carbamazepine (‘Tegretol’) can increase the level of atrioventricular block. Reduced dosage by half should be considered.
Dipyramole (a platelet aggregation inhibitor) increases the plasma levels and cardiovascular effects of Adenosine. Reducing dose by half should be considered.
Heart Transplant recipients should receive half doses.
Torsardes Treatment
Magnesium Infusion 2G over 10 mins
Repeat once at 10 mins if nil or no response
Stable VT Treatment
Amiodorone infusion
5mg/kg IV (Max 300mg) over 20 mins once only (diluted with D5W to make 50ml)
Unstable VT treatment
If sedation required 2mg Midazolam IV, repeat 1mg at 2 min intervals max 5mg.
Sync cardiovert 100j then repeat 200j if required
If reversion amidorone infusion as stable VT
Hypothermic arrest alterations
Hypothermic Cardiac Arrest <30°C
If VF/VT is present, then Defibrillate 200j.
If after 3 defibrillation attempts VF/VT persist, then delay further defibrillation attempts until the patient’s temperature is >30°C.
Withhold adrenaline and amiodarone until the patient’s temperature is >30°C.
Hypothermic Cardiac Arrest >30°C
If VF/VT is present, then Defibrillate 200j every 2 minutes.
Administer Adrenaline and Amiodarone as indicated. The standard interval between drug administration should be doubled.
Inadequate perfusion treatment cardiogenic cause
If chest clear 250ml bolus up to 20ml/kg
Adrenaline infusion 3mg to make up 50ml D5W. Start at 5mcg / min, increased by 5mcg/min 2 minutely to max of 20mcg
Adrenaline bolus upto 100mcg as required
Why give heparin and not enoxaparan in renal failure patients
Heparin is a large, negatively charged molecule that does not undergo renal elimination to a significant extent. Instead, it is mainly metabolized in the liver and reticuloendothelial system.
Since heparin is not primarily excreted by the kidneys, it does not accumulate in patients with renal failure, and its anticoagulant effect is not significantly altered in this population.
Enoxaparin is a low molecular weight heparin (LMWH) that is partially eliminated by the kidneys. It undergoes both renal and hepatic metabolism.
In patients with renal failure, the clearance of enoxaparin is reduced, leading to its accumulation in the body.
Inadequate perfusion associated with hypovolaemia treatment
If BP <100 or HR >100 20 ml/kg normal saline
If BP still <100 or HR >100 20ml/kg normal saline
After 40ml/kg consult for further 20ml/kg if required
