Special Circumstances Cardiac Arrest - not hypothermia Flashcards
Hypothermic patient without cardiac instability - action?
Rewarmed externally with minimally invasive techniques
Hypothermic patient with cardiac instability - action?
Transferred directly to ECLS (extracorporeal life support) centre
When is ECLS indicated in rewarming avalanche burial victims?
- Duration of burial >60 minutes.
- Core temperature at extrication is <30 degrees.
- Serum potassium at hospital admission is < or equal to 8.
First line for acute asthma
inhaled beta 2 agonists eg salbutamol. Only IV if cannot inhale
Most common non-cardiac cause of cardiac arrest?
Asphyxia - ultimately hyperaemia causes arrest before hypercarbia.
At what oxygen saturations is consciousness lost at?
60% (arterial)
Common rhythms in asphyxia?
PEA/Asystole (VF very rare)
Most common electrolyte imbalance causing life-threatening arrhythmias?
Potassium disorders- hyperkalaemia is most common.
Who is at risk of electrolyte disturbances?
Renal failure, severe burns, cardiac failure and diabetes.
Normal extracellular potassium concentration?
3.5-5.0mmol/l
What happens to serum potassium when serum pH decreases?
In acidaemia - serum potassium increases -> from cellular to vascular space.
Causes of hyperkalaemia?
- Impaired kidney excretion: AKI/CKD
(CKD and diet) - Drugs: ACE-I, ARB, k-sparing diuretics, NSAIDs, beta blockers, trimethoprim
- Increased K release from cells: tissue breakdown; rhabdomyolysis, tumour lusis, homeless
- Metabolic acidosis - renal failure, DKA
Also - Pseudo-hyperkalaemia describes the finding of a raised serum (clotted blood) K+ value concurrently with a normal plasma (non-clotted blood) potassium value. The clotting process releases K+ from cells and platelets, which increases the serum K+ concentration by an average of 0.4 mmol/L. The most common cause of pseudo-hyperkalaemia is a prolonged transit time to the laboratory or poor storage conditions
By how much does the incidence of hyperkalaemia increases as GFR drops from 60ml/min to 20 ml/min?
2 -> 42%
Hyperkalaemia defintion
Above 5.5mmol/l
Severe: above 6.5mmol/l
Symptoms of hyperkalaemia?
Weakness -> flaccid paralysis.
Paresthesia.
Depressed deep tendon reflexes.
ECG changes in hyperkalaemia?
First degree heart block. (PR >0.2) Flattened/absent P waves. Tall, tented T waves (larger than R in more than one lead) ST depression S and T wave merging (sine wave pattern) Wide QRS (>0.12) VT Bradycardia Arrest
What are 5 key treatment strategies for hyperkalaemia?
- Cardiac protection.
- Shifting K into cells.
- Removing K from body.
- Monitoring K/glucose.
- Preventing recurrence
Mild hyperkalaemia treatment?
Consider cause/prevent recurrence.
Consider calcium resonium to remove from body (15g x4/day oral or 30g x2/day PR)
Monitor K/glucose
Moderate/severe hyperkalaemia with ECG changes treatment?
(Severe - get expert help as well)
- IV calcium - 10 ml 10% calcium chloride IV or 30 ml 10% calcium gluconate IV
- Insulin-glucose IV infusion (25g glucose with 10 units insulin over 15 mins)
- 10-20mg salbutamol nebulised
- ? dialysis/monitor glucose/K
- Cause/prevent recurrence
Risk associated with treatment of hyperkalaemia?
- Hypoglycaemia due to gluc/insulin infusion(1-3 hours of treatment)
- Tissue necrosis (2nd to extravasation of Iv calcium salts)
- Intestinal necrosis/obstruction 2nd to potassium exchange resins. Avoid prolonged and give laxative.
- Rebound hyperkalaemia after drugs worn off.
Moderate hyperkalaemia without ECG changes - treatment?
Glucose/insulin
Dialysis?
Severe hyperkalaemia without ECG changes - treatment?
Expert help
Glucose/insulin
Salbutamol
Dialysis?
Indications for dialysis?
Severe/life-threatening with or without ECG changes/arrythymias. Resistance to medical tx End stage renal disease Oliguric AKI (<400ml/day urine output) Marked tissue breakdown
Define hypokalaemia and severe.
Serum potassium <3.5,
severe if <2.5
Most common electrolyte disturbance seen in clinical practice?
Hypokalaemia (20% of hospital patients)
Causes of hypokalaemia?
GI loss - diarrhoea
Drugs - diuretics, laxatives, steroids.
Renal loss - renal tubular disorders, diabetes insipidus, dialysis.
Endocrine disorders - Cushing’s, hyperaldosteronism
Metabolic alkalosis
Magnesium depletion
Poor diet
Symptoms of hypokalaemia?
Muscle weakness Leg cramps Constipation Fatigue Severe - rhabdomylosis, ascending paralysis and respiratory difficulties
ECG features of hypokalaemia
U waves T wave flattening ST segment changes Arrhythmias (esp if digoxin) Arrest
Max recommended IV dose of potassium
20 mmol/hour
Can do more rapid if unstable arrhythmias.
Potassium deficiency often co-exists with?
Magnesium deficiency - important for K uptake/maintenance of intracellular K values.
Define accidental hypothermia
Temp drop below 35 degrees
How does hypercalcaemia present?
Confusion, weakness, abdominal pain, hypotension, arrhythmias and cardiac arrest
How does hypocalcaemia present?
Paresthesia, seizures, tetany, av-block and cardiac arrest
Normal values for calcium?
2.1-2.6 mmol/l
ECG changes for hypocalcaemia?
Prolonged QT, T wave inversion, heart block and arrest
ECG changes for hypercalcaemia?
Short QT interval, prolonged QRS, Flat T waves, AV block and rest
Causes of hypercalcaemia?
Primary/tertiary hyperparthyroidism, malignancy, sarcoidosis, drugs
Causes of hypocalcaemia?
Chronic renal failure, acute pancreatitis, CCB overdose, toxic shock syndrome, rhabdomyolysis, tumour lysis syndrome.
Normal magnesium levels?
0.6-1.1mmol/l
Symptoms of hypermagnesaemia?
Confusion, weakness, resp depression, AV block, arrest
ECG changes - hypermagnesaemia?
Prolonged PR and QT intervals, T wave peaking, AV block and arrest
Symptoms of hypomagnesaemia?
Tremor, ataxia, nystagmus, seizures, arthymias - torsades des pointes
ECG changes with hypomagnesaemia?
Prolonged PR/QT intervals, ST depression,, T wave inversion, flattened P waves, increased QRS inversion
Treatment of hypercalcaemia?
IV fluid replace Furosemide 1 mg/kg IV Hydrocortisone 200-300mg IV Pamidronate 30-90 mg IV Underlying cause
Treatment of hypocalcaemia?
Calcium chloride 10% 10-40ml
Magnesium sulphate if necessary
At what levels (biochem) would you consider treating hypermagnesaemia?
> 1.75 mmol/litre
Treatment of hypermagnesaemia?
Calcium chloride 10% if necessary
Saline diuresis - saline with furosemide.
Haemodialysis.
Treatment of severe/symptomatic hypomagnasaemia?
2g 50% magnesium sulphate IV over 5 minutes
Treatment of hypomagnasaemia with torsades des pointes?
2g 50% magnesium sulphate IV over 1-2 minutes
Treatment of hypomagnasaemia with seizure?
2g 50% magnesium sulphate IV over 10 minutes
Progression of heat-related conditions?
heat stress -> heat stroke -> MODS -> arrest
What drugs can precipitate malignant hyperthermia?
Halogenated anaesthetics.
Depolarizing muscle relaxants
What differentiates heat exhaustion from heat stroke?
No change in mental status, core temp still below 40 degrees.
Definition of heat stroke?
Hyperthermia accompanied by SIRS with a core temperature above 40 degrees, accompanied by mental state change and varying levels of organ dysfunction.
Average fluid replacement in heat exhaustion?
1-2l crystalloid at 500ml/hour
What are the two forms of heat exhaustion?
Classic Heat Stroke (non-exertional) e.g. elderly in heat waves
Exertional Heat Stroke - strenuous physical exercise in high ttemps/humidity (healthy young adults)
Aim when cooling?
Rapidly to 39 degrees.
Increased core temp - causes?
Drug withdrawal, drug toxicity, heat stroke, sepsis, neuroleptic malignant syndrome, thyroid storm, pheochromocytoma, CNS infection etc.
Seizing due to heat stroke?
Diazepam may be useful
What drug can be of use if malignant hyperthermia is caused by amphetamines?
Dantrolene.
Anaphylaxis - why do people arrest?
Relative hypovolaemia
Define anaphylaxis.
Severe, life-threatening, generalised/systemic hypersensitivity reaction
Anaphylaxis criteria:
Any 1 of these 3:
1. Acute onset with skin/mucosal tissue involvement and at least one of:
- Resp compromise
- Reduced BP/symptoms of end-organ dysfunction
2. Two or more of following:
- Skin/mucosal tissue
- Resp compromise
- Reduced BP/associated symptoms
- Persistent GI symptoms
3. Reduced BP after exposure to known allergen
(Infants/kids cutoff vs adults?)
For last anaphylaxis criteria, what is low systolic BP?
1 month - 1 year: <70mmHg
1 - 10 years: <70mmHg + (2x age)
11 years and above: <90mmHg or 30% decrease from their baseline.
Anaphylaxis treatment - adrenaline dose?
Adult/child over 12 years: 500 mcg IM (0.5 mL of 1:1000)
Child 6-12: 300mcg
Child less than 6 years: 150 mcg
Anaphylaxis treatment - chloramphenamine dose?
Adult/child over 12 years: 10mg
Child 6-12: 5mg
Child 6 months-6 years: 2.5mg
Child less than 6 years: 250 mcg/kg
Anaphylaxis treatment - hydrocortisone dose?
Adult/child over 12 years: 200mg
Child 6-12: 100mg
Child 6 months-6 years: 50mg
Child less than 6 years: 25mg
IV fluid challenge in anaphylaxis?
Adult: 500-1000mL
Child: 20mL/kg
NB; stop colloid, use crystalloid
How does adrenaline help in anaphylaxis?
Alpha receptor agonist - reverses peripheral vasodilation and reduces oedema.
Beta receptor - reverses bronchospasm, increases myocardial contraction and suppresses histamine/leukotriene release - - on mast cells there are beta 2 adrenergic receptors. When activated inhibits their activation.
Why IM adrenaline?
Greater safety margin, no IV access, easier to learn and easier to self-administer.
Best site for Im injection?
Anterolateral aspect of middle third of thigh.
What kind of anti-histamine?
H1 antihistamines - chloramphenamine (counter cutaneous symptoms, vasodilation and bronchospasm)
Role of glucocorticoids in anaphylaxis?
More to prevent refractory/prolonged episodes. 2nd prevention.
Other drugs for anaphylaxis?
?treat bronchospasm with salbutamol/ipatropium etc. If bet-blocker reaction ? glucagon
What test confirms an anaphylaxis diagnosis?
Mast cell tryptase (from degranulation) - typically at least 30 mins or after
TCA - survival factors?
PEARL, organised ECG and resp activity.
Also age, VF (v rare)
TCA - withholding resus?
• no signs of life within the preceeding 15 min;
• massive trauma incompatible with survival (e.g. decapitation,
penetrating heart injury, loss of brain tissue).
We suggest termination of resuscitative efforts should be con- sidered if there is:
• no ROSC after reversible causes have been addressed; • no detectable ultrasonographic cardiac activity.
In TCA, what happens simultaneously to starting ALS?
Address reversible causes (hypoxia, tension pneumothorax, tamponade and hypovolaemia):
- Control external catastrophic bleed
- Airway and maximise oxygenation.
- Bilateral chest decompression.
- Cardiac tamponade
- Surgery for haemorrhage control/aortic compression
- Transfusion/fluids.
Damage control resuscitation principles?
Hypotensive resuscitation (permissive - maintain radial pulse until surgery/around 80-90mmHg for 1 hr) -> haemostatic resuscitation (early blood products: 1:1:1 - packed RBC: FFP: Platelets and TXA etc) -> damage control surgery
Why can positive pressure ventilation be a problem in hypovolaemic patients?
Impedes venous return to the heart -> worsening hypotension. As a result - low tidal volumes and slow resp rates are better.
Criteria for proceeding with resuscitative thoracotomy after hospital arrival?
Blunt trauma with less than 10 mins of prehsop CPR
Penetrating trauma with less than 15 mins prehosp CPS
Successful RT: 4 Es rule?
Expertise, Equipment, Environment, Elapsed time (no longer than 10 mins)
Why is needle aspiration of tamponade unreliable?
Pericardium often full of clotted blood.
Signs of PE on ECG?
Right or left ventricular strain:
Inversion of T waves in leads V1-V4, QR pattern in V1, S1 Q3 T3, incomplete or complete RBBB.
Most common rhythm in PE cause of cardiac arrest?
PEA
Most likely underlying cause of arrest if patient is in VF?
Occluded coronary artery - MI
Dermal decontamination?
Remove clothes, water irrigation (reactive alkali metals that can ignite).
GI decontamination
Activated charcoal - if airway intact or protected. Most effective within 1 hr.
What does activated charcoal not bind to?
Lithium, heavy metals and toxic alcohols
Patient presents more than 2 hours after ingestion?
Whole bowel irrigation
Enhances elimination techniques?
Multiple-dose activated charcoal, urinary alkalinisation and extracorporeal elimination.
Dose of activated charcoal if doing MDAC?
50-100g in adults, 25-50g in children.
How to do urinary alkalinisation? When is most useful?
IV sodium bicarbonate.
For salicylate intoxication (before dialysis levels), phenobarbitol/herbicide poisoning.
Most common complication of urinary alkalinisation?
Hypokalaemia
Benzodiazepine OD - presentation and treatment with mechanism.
LOC, resp depression, hypotension. Flumazenil - competitive anatgonist (only if no history of seizing)
Opioid OD - presentation and treatment?
Pinpoint pupils, Reduced GCS and resp depression.
Naloxone - rapid reversal.
Opioid acute withdrawal - presentation?
Sympathetic excess state - pulmonary oedema, ventricular arrhythmias and severe agitation.
Naloxone dosing?
0.4-2mg - repeat every 2-3 mins.
Intranasal: 2mg.
Large overdose may require up to 10mg in total
What do before naloxone administered?
Airway opening, oxygenation/ventilation.
What arrthymia is common in TCA overdose and why?
VT - wide complex tachycardia due to anticholinergic and sodium channel blocking effects.
TCA overdose - presentation?
Seizures, hypotension (exacerbated by alpha-1 receptor blockade), coma, arrthymias
Anticholinergic effects?
Mydriasis, fever, dry skin, delirium, tachycardia and urinary retention.
How to treat TCA-induced VT?
Sodium bicarbonate 1-2mmol/kg
Cocaine overdose -what drugs are useful?
In patients with severe cardiovascular toxicity:
- alpha blockers (phentolamine),
- benzodiazepines (lorazepam, diazepam)
- calcium channel blockers (verapamil)
Also - morphine and sub- lingual nitroglycerine may be used as needed to control hypertension, tachycardia, myocardial ischaemia and agitation.
Additional treatment for local anaesthetic systemic toxicity?
IV 20% lipid emulsion
(Give an initial intravenous bolus injection of 20% lipid emulsion 1.5 mL kg−1 over 1 min followed by an infusion at 15 mL kg−1 h−1 . Give up to a max- imum of two repeat boluses at 5-min intervals and continue until the patient is stable or has received up to a maximum cumulative dose of 12 mL kg−1 of lipid emulsion.)
Beta-blocker toxicity treatment?
Glucagon (50-150mcg/kg) high dose insulin/glucose Lipid emulsions Phosphodiesterase inhibitors Calcium salts
CCB OD tx?
Calcium chloride 10% (20ml) every 2-5 minutes in severe bradycardia/hypotension. This is not enough for stability.
High dose insulin and glucose etc.
Digoxin OD tx?
(NB mortality high)
digoxin-Fab; specific antibody fragments: if haem unstable.
Give 2 bolus of 2 vials (38 mg/vial)
What drugs can also push digoxin into lethal levels?
CCBs
Amiodarone
Digoxin effect on heart?
Atrioventricular conduction abnormalities and ven- tricular hyperexcitability -> severe arrhthymias and arrest.
Mechanism of cyanide toxicity?
Inactivation of cytochrome oxidase (at cytochrome a3) -> uncoupling mitochondrial phosphorylation and inhibiting cellular respiration.
Options for cyanide scavenger therapy?
Hydroxocobalamin 100mg/kg IV
Nitrite -
Either of those followed by IV sodium thiosulfate.
