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
Modifying factors for fluid administration
Pt with isolated neurogenic shock can be given up to 500ml Normal Saline bolus to correct hypotension. No further fluid should be given if SCI is the sole injury.
Penetrating Trunk Injury, suspected aortic aneurysm or uncontrolled haemorrhage - Accept palpable carotid pulse with adequate conscious state and transport immediately
Treatment crush injury
Prior to removing force:
Supplemental oxygen
500ml bolus normal saline
If hyperkalemia suspected 50ml sodium bicarb IV
Ventilation rates asthma for infant, small child and large child
Infant 15-20 ventilations / min
Small child 10-15 ventilations / min
Large child 8-12 ventilations / min
Sedation to maintain intubation dosages peadiatrics
Infusion:
Morphine/Midaz: 0.1-0.2mg/kg/hour OR
Fentanyl/Midaz: 1-2mcg/kg/hr + 0.1-0.2mg/kg/hour
Bolus:
Morphine/midaz: 0.1mg/0.1mg/kg
Fent/Midaz: 0.1mg/1mcg/kg as required
Bradycardia Treatment Paediatric
Correct Hypoxia
Chest compressions if <60 in infants or <40 in children
Adrenaline 10mcg/kg IV repeat 3 minutely as required
Normal saline 20ml/kg
Consult for pacing if required
Treatment SVT Paediatrics
Valsalva
Adenosine 100mcg/kg IV
After 2 mins Adenosine 200mcg/kg IV
If unresponsive consider cardioversion
If sedation required 50mcg midazolam / kg IV repeat at 2 min intervals (Max 200mcg/kg)
Sync cardiovert at 1 j / kg
Paediatric Pain Relief dosages
Paracetamol 15mg/kg
Ibuprofen 10mg/kg
Fentanyl IN Small child (10-24kg) 25mcg repeat 3 times
Fentanyl IN Large child (>25kg) 50mcg repeat 3 times
Methoxyflurane 3ml repeat once
Morphine IM 0.1mg/kg (max 5mg) consult for further dosages
Morphine IV 0.05mg/kg repeat 5 mins. Consult after 0.2mg/kg
Fentanyl IV 0.5mcg /kg repeat 5 mins. Consult after 2mcg/kg
Medical consult for ketamine 0.5mg/kg
Treatment Croup
5mg/5ml Nebulised Adrenaline
600mcg/kg IV/IM/Oral Dexamethasone
Treatment Asthma Paediatric
Salbulatoml pDMI (Repeat 20 mins)
1-5 years 6 puffs
>6 years 12 puffs
Ipratropium PDMI (Repeat 20 mins max 3 times)
1-5 years 4 puffs
>6 years 8 puffs
Salbulatmol IB neb
1-5 years 2.5mg Salbutamol + 250mcg IB
>6 years 5mg Salbutamol + 500mcg
Adrenaline IM 10 mcg per kg max 500mcg repeat 5 mins
Normal Saline up to 20ml/kg
Dexamethasone 600mcg/kg (max 8mg) IM /IV /ORAL
Adrenaline infusion 0.1mcg/kg/min titrated to response or adverse effects
Magnesium 50mg/kg (max 2G) Infusion over 20 mins
Treatment nausea and vomiting paediatrics
Ondansatron 0.1 mg/kg IV or IM (max 4mg) only in patients over 2
Treatment hypoglycaemia paediatrics
Glucagon IM
<25kg 0.5 IU
>25kg 1 IU
Glucose IV
10% 500mg/kg or 5ml/kg with 10ml saline flush
Repeat same at 5 min intervals as required
Treatment hyperglycaemia paediatrics
10ml kg normal saline IV
Treatment continuous seizures paediatric
Midazolam 0.15mg/kg IV / IM (max 10mg)
Repeat IV at 5 mins OR IM at 10 mins
Consider intubation
Anaphylaxis Treatment paediatric
10mcg / kg IM Adrenaline (max 500mg) repeat at 5 min intervals
(Salbutamol / IB / adrenaline Neb as per relevant guidelines)
Adrenaline infusion commencing at 0.1mcg/kg/min tirated to response max starting rate 10mcg per minutes
Saline 20ml/ kg, repeat same then consult
Paediatric organophosphate treament
Atropine 20 mcg/kg IV
Repeat same at 5 mins
Treatment for overdose paediatrics
Narcotics:
Naloxon 10mcg / kg IM/IV Repeat same IV at 5 mins
(Max 400mcg per bolus total max 2mg)
TCA overdose:
Hyperventilate to aims for CO2 of 25-30
Sodium Bicarbonate 2ml/kg IV over 2 minutes
Repeat after 10 mins if symptoms persist
WHO Paediatric Shock Criteria for Emergency Triage Assessment and Treatment (ETAT)
Patients must meet ALL 4 criterion to satisfy the criteria.
Capillary Refill >3 seconds
Cold Extremities
Fast pulse
Weak Pulse: For children under one year old, assess the brachial pulse. For all other children assess the radial pulse.
Sepsis treament paediatric
Normal Saline 10ml/kg IV Repeated once after 15 mins
Ceftriaxone 50mg / kg if over 1 hour from hospital on consult
Adrenaline infusion starting at 0.1mcg/min on consult
Ketamine Pharmacology
Ketamine is an intravenous anesthetic agent (NMDA receptor antagonist). By blocking NMDA receptors, ketamine inhibits the excitatory effects of glutamate, leading to decreased neuronal excitability. This contributes to its analgesic and anesthetic effects.
Secondarily also interacts with: Opioid Receptors: Ketamine has some affinity for opioid receptors (may contribute to its analgesic properties), Monoaminergic Receptors (affecting the reuptake of neurotransmitters serotonin, norepinephrine, and dopamine), Cholinergic Receptors (inhibits nicotinic acetylcholine receptors)
At lower doses it is a significant analgesic whilst preserving airway reflexes and respiratory drive.
There is minimal haemodymanic compromise as Ketamine acts as a sympathomimetic which may lead to transient tachycardia and hypertension.
Ketamine produces a dissociative state that in a small number of patients may potentially cause them to have issues with perception resulting in disinhibition or emergence phenomenon.
Contraindications Ketamine
Known hypersensitivity
Age <1 year
Traumatic Head Injury
Hypertension BP > 180mm Hg sys, 100mm Hg Dia
Suspected Acute Coronary Syndrome
Suspected Heart Failure
Known Hydrocephalus or raised intraoccular pressure
Precautions Ketamine
Age > 60yrs
Prior administration of midazolam or other CNS depressant drugs
Significant hypovolaemia
Globe injury
Complex facial injuries and factures
Impaired respiratory function
Symptoms of psychosis
Side effects Ketamine
Dissociation and trance like state
Potential transient hypertonicity and nystagmus
Disinhibition – disturbed perception
Emergence
Hypertension, Tachycardia
CNS and rarely respiratory depression
Hypersalivation
Vomiting
Laryngospasm
How to prepare GTN for infusion for APO
Draw up 1ml (5mg) of GTN with 49ml D5W (makes solution of 5mg in 50ml)
GTN infusion dosage for APO
Start 10 mcg/min / 6ml/hour in conjunction with CPAP. Increase in 10 mcg intervals every 3-5 minutes. Consider decreasing if BP drops below 120systolic.
Frusemide dosage APO
20 - 40mg IV (if evidence of fluid overload)
Sodium bicarbonate pharmacology
A hypertonic crystalloid solution which contains sodium and bicarbonate ions in a solution of high pH
This raises Raises pH by increasing plasma bicarbonate levels, which are known to buffer excess hydrogen ion concentration
Indications Sodium Bicarbonate
Symptomatic Tricyclic Antidepressant (TCA) overdose or hyperkalaemia
Crush Syndrome with evidence of hyperkalaemia
Cardiac arrest with suspected hyperkalaemia or TCA overdose
Sodium Bicarbonate dosage for TCA overdose
100ml Sodium bic given over 3 minutes
Consider consult for further dosages
Lignocaine preperation for concious IO Paed / Adult
Both 0.5mg / kg
Max dose paed 20mg
Max dose adult 40 mg
Frusemide Pharmacology
Furosemide is a potent loop diuretic that acts on the kidneys to ultimately increase water loss from the body. Causes venous dilatation and reduces venous return
Contraindications Frusemide
Nil of significance
Precautions Frusemide
Hypotension
Side effects frusemide
Hypotension
Dysrhythmia due to electrolyte imbalance
Lignocaine Pharmacology
A local anaesthetic agent. Prevents initiation and transmission of nerve impulses causing local anaesthesia (1% solution). Specifically targets voltage-gated sodium channels located on the membranes of nerve cells and inhibits sodium influx. This inhibition of sodium ion movement effectively stops the depolarization of the neuron, preventing the initiation and propagation of the action potential.
Also is class 1B antiarrhythmic: works by blocking fast voltage-gated sodium channels (reduces the rate of depolarization/phase 0 during the action potential). Decreases the automaticity of these abnormal pacemaker cells
Lignocaine Contraindications
Known hypersensitivity
Bradycardia with inadequate perfusion
Evidence of 2° or 3° heart block
Precautions Lignocaine
When using Lignocaine 1% as diluent for IM Ceftriaxone it is important to rule out inadvertent IV administration due to potential CNS complications
CPAP Contras
Asthma
Pts <16
Pts with inadequate respiratory effort
Heart failure with hypotension
GCS <13
Pneumothorax
Facial injury or facial deformity
Epistaxis
Post Partum Haemorrage Treatment
600ml blood loss first 24 hours or excessive haemorrage 1-6 weeks post partum
High flow oxygen 10-15L
Fundal massage / void bladder / infant suckle
Oxytocin 10 IM repeat 10 IM at 5 minutes
Oxytocin 20 units in 20ml NS infusion at 10 units per hour
TXA 1G over 10 minutes
External aortic compression
Bimanual aortic compression
Ergometron Pharmacologuy
Causes contraction of the uteration and vascular smooth muscle
General Vasocontriction
Ergometron Contraindications
Known allergy
Past history of pre-eclampsia
Hypertension
For an adrenaline infusion (3mg in 1000ml) how many mcg per mil and what infusion rate does 1mcg/min equal
Adrenaline infusion
3mg of 1:1000 Adrenaline added to 47ml D5W = 60mcg/ml
Infusion rate 1mls/hr = 1mcg/min titrated up or down according to response
How to prepare infusion of adrenaline where infusion pump unavailable in anaphylaxis
Adrenaline Infusion pump unavailable
Mix 500mcg (0.5ml) of 1:1000 Adrenaline with 500ml Normal Saline = 1mcg/1ml
Start Adrenaline infusion at 10ml/min (10mcg/min - 200 drops per minute) titrating up or down according to response.
Indications for SVT adenosine
Symptomatic signs and symptoms:
Rate related severe or persistent chest pain
Shortness of breath with crackles
Unstable signs and symptoms for cardioversion for VT
Unstable signs and symptoms:
Congestive cardiac failure
Systolic BP < 80mmhg
GCS < 13
Rapidly deteriorating
VT ECG Criteria
HR >100
Sustained >30 seconds
QRS>0.12secs
Mostly regular
AV dissociation / absence of p waves
Signs TCA OD toxicity
Less than adequate perfusion
Positive R wave >3mil in AVR
Progressively widening QRS >0.12
QT prolongation > 1/2 R-R interval
QTc >500msec
Adrenaline Pharmacology / Actions
Pharmacology: A naturally occurring Alpha and Beta-adrenergic stimulant, primarily acts on adrenergic receptors, which are divided into two main types: alpha (α) receptors and beta (β) receptors.
Beta 1: Increases pulse rate by increasing S.A. Node firing rate, Increases conduction velocity through the A.V. Node, Increases myocardial contractility, Increases the irritability of the ventricles
Beta 2: Causes bronchodilatation, Causes Glycogenolysis and Lipolysis
Alpha: Causes peripheral vasoconstriction and subsequent Increased Peripheral Resistance.
Droperidol Pharmacology
Droperidol exerts its effects primarily by antagonizing dopamine receptors in the brain. By blocking dopamine receptors, droperidol reduces the activity of dopamine, which can help alleviate symptoms of agitation, psychosis, and hyperactivity. This leads to a calming effect on the patient, contributing to sedation.
Highly effective in preventing and treating nausea and vomiting (antagonist of dopamine D2 receptors. These receptors are found in high concentrations in the chemoreceptor trigger zone (CTZ) of the brain, which is an area that detects toxins in the blood and triggers the vomiting reflex.)
CPAP Mechanism
Maintains a constant positive pressure throughout the respiratory cycle which keeps the alveoli splinted open assisting gas exchange by increasing the surface available for gas exchange reducing VQ mismatch. Increasing intrathoracic pressure may also reduce preload (elevated pressure in thoracic cavity compresses large veins reducing return to the heart).
GTN Mechanism
Principally, a vascular smooth muscle relaxant: Venous dilatation promotes venous pooling and reduces venous return to the heart (reduces preload) and Arterial dilatation reduces systemic vascular resistance and arterial pressure (reduces after load).
GTN is metabolized primarily in vascular smooth muscle cells to produce nitric oxide. NO activates guanylate cyclase in the vascular smooth muscle, increasing the production of cyclic guanosine monophosphate (cGMP). Elevated cGMP levels lead to the dephosphorylation of myosin light chains, resulting in relaxation of smooth muscle cells and vasodilation.
The effects of reducing preload and afterload: reduce myocardial oxygen demand, reduce systolic, diastolic and mean arterial blood pressure, whilst usually maintaining coronary perfusion pressure, Mild collateral coronary arterial dilatation may improve blood supply to ischemic areas of myocardium, Mild tachycardia secondary to slight fall in blood pressure.
Anatomical Difference Paediatrics
Smaller Airway
Relatively larger tongue and smaller oral cavity
Infants have a relatively larger occiput
Infants are nose breathers first 4-6 months of age
Trachea is more cartilaginous and soft -
The narrowest part of a paediatric airway is the cricoid cartilage (compared with the vocal cords in adults). This is located just below the vocal cords.
Cause of Bronchoconstriction Anaphylaxis
Histamine binds to H1 receptors in the smooth muscle lining the bronchi, causing bronchoconstriction.
Leukotrienes are much more potent than histamine in causing bronchoconstriction. Increase smooth muscle contraction, mucus production, and vascular permeability.
Prostaglandin D2 is a potent mediator that can exacerbate hypotension and bronchoconstriction.
Cause of Hypotension Anaphylaxis
Histamine is a potent vasodilator
Leukatrines increased vascular permeability
Prostaglandin D2 is a potent mediator that can exacerbate hypotension and bronchoconstriction
Why no dexamethasone anaphylaxis
Acute stage of treatment high focus on timely adrenaline administration and supportive measures. Typically used in the post-acute phase to prevent a recurrence of symptoms and manage lingering inflammation. Any benefits are unproven
Pacing Mechanism of action
The electrical impulse delivered by the pacing device depolarizes the heart muscle cells, causing them to contract. This depolarization essentially forces the heart to beat at the desired rate set on the pacing device.
Trigger for decompression:
Suspected pnueomothorax with decreasing conscious state AND/OR reduction of perfusion.
Reversible causes of Traumatic Cardiac Arrest – HOTT
Hypovolaemia, Oxygenation, Tension Pneumothorax, Tamponade
Midazolm Mechanism
Midazolam binds to specific sites on the GABAa receptor, a ligand-gated chloride channel. When midazolam binds to the GABAa receptor, it increases the receptor’s affinity for GABA. This potentiation enhances the inhibitory effects of GABA. The enhanced GABA binding leads to increased opening of the chloride channels, allowing more chloride ions to enter the neuron. The influx of chloride ions into the neuron causes hyperpolarization of the neuronal membrane. Hyperpolarization makes it more difficult for the neuron to reach the threshold potential needed to fire an action potential. This hyperpolarization effectively reduces neuronal excitability, thereby dampening abnormal electrical activity that characterizes seizures.
Hyperkalameia ECG Changes
Peaked T waves
P wave widening/flattening, PR prolongation
Bradyarrhythmias:sinus bradycardia, high-grade AV block with slow junctional and ventricular escape rhythms, slow AF
Conduction blocks (bundle branch block, fascicular blocks)
QRS widening with bizarre QRS morphology
