PARA210 Week 7 CAL Questions - ALOC PDF

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PARA210 – LECTURE 7 REVIEW QUESTIONS 1. What do our brains need in order to function properly and what can go wrong with each.  

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Strong walls – to protect from trauma, toxins and diseases  Disease infiltration (herpes simplex, encephalitis, meningococcal meningitis, other virus and bacteria Space to stretch out – so you’re not cramped  Swelling due to TBI  Intraparenchymal intrusion e.g. space occupying lesion or haemorrhage - Coning (Cushings reflex/triad) Systolic hypertension / diastolic hypotension (widening pulse pressure) Bradycardia Cheyne-Stokes respirations Food – lots of good food, no toxins or poisons, a way to eliminate waste  To maintain supply of nutrients  Electrolytes (sodium, potassium, chloride, magnesium)  Affected by - Increased urination, defecation, dehydration - Malnutrition, GI absorption diseases (IBS, etc) - Alcoholism - Abnormal metabolic states (cancer, endocrine disease, etc)  Liver and/or kidney failure causes toxins to be retained Fresh air – oxygen in, carbon dioxide out  Oxygen in: hypoxia or hypoperfusion  investigate cardiac function  Carbon dioxide out: hypoperfusion/hypoventilation  hypercarbia (high CO2) acts like a narcotic in the CNS Plumbing – no blocked or burst pipes, sufficient pressure, water in and wastes out  Cerebrovascular accident (CVA)  blocked or burst pipes  Dilated blood vessels  insufficient pressure for perfusion  Sufficient perfusion pressure  adequate blood pressure (good MAP, no shock – PP = MAP – ICP)  syncope Wiring – no short circuits, internet  Brain needs organised electrical activity to function properly  disorganised, chaotic activity leads to ALOAs and seizure activity Thermostat – not too hot, not too cold  No hyperthermia  endogenous increase in temp i.e. heat exhaustion  No hyperpyrexia  exogenous increase and temp i.e. infection  No hypothermia  Something nice to look at – nothing too shocking, horrifying or terribly upsetting  Psychogenic syncope – ALOC in response to horrible imagery e.g. blood

2. What’s the difference between neurogenic and spinal shock?  Neurogenic shock: generalised low perfusion due to CNS pathology  Spinal shock: localised trauma to the CNS which usually does not have profound systemic effects 3. Fill in the correct temperature for each of the following findings: a) Normal temperature

37

°C

b) Early hypothermia

< 35

°C

c) Loss of shivering

< 32

°C

d) Deep hypothermia

< 30

°C

e) Asystole

~ 15

°C

13

°C

f)

Coldest survived body temperature

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PARA210 – LECTURE 7 REVIEW QUESTIONS 4. The ‘8 S’ differential diagnosis of altered mental status was presented in the unit. Explain what is meant by each of the following components. a) Smashed b) Sugar

c) Salt

d) Substances

e) Stroke

f)

Trauma e.g. haemorrhage and CNS injury Hyperglycaemia e.g. BGL > 10mmol/L DKA or HHS Hypoglycaemia e.g. BGL < 4.0mmol/L – always check in ALOC patients ↑ Sodium (hypernatremia)  Dehydration: lack of intake, sweating, vomiting, diarrhoea, urination, hyperventilation  SIADH (Syndrome of inappropriate anti-diuretic hormone secretion): possibly due to pneumonia, brain diseases, cancer, thyroid problems, and some medications. ↓ Sodium (hyponatremia)  Usually due to haemodilution due to excessive water intake (> 1 litre/hour) ↓ Potassium (hypokalaemia)  Usually lost from GI tract or kidneys (vomiting, diarrhoea, ileostomy, laxatives, HCTZ, Furosemide, Prednisone, hypokalaemic periodic paralysis  Presents as muscle weakness, muscle aches, muscle cramps, and palpitations Drugs can affect haemodynamics, with some having a more profound effect than others.  Narcotic analgesics – Morphine, Fentanyl  Alcohol – Ethanol, Methanol  Anaesthetics – Nitrous Oxide, Ketamine  Anti-anxiety/sedative – Diazepam, Midazolam  Antipsychotics – Perphenazine, Olanzapine, Haloperidol, Clozapine, Risperidone Psychogenic syncope – psychologically shocking or overwhelming stimuli causes bradycardia and peripheral vasodilation  cerebral hypoperfusion Vasovagal syncope – PSNS stimulation (bradycardia & vasodilation) that originates in the baroreceptors of large arteries (vaso-) and produce reflex vagal effects (-vagal)  syncope (coughing, “necktie syndrome”, Valsalva manoeuvre) Gastrogenic syncope – Vagus nerve innervates the GI tract from mouth to anus – GI stimulation can therefore cause a vagal response. Can be due to gastric or colonic distension, gagging, diarrhoea, oesophageal obstruction, abdominal/genital trauma. Neuro-cardiogenic syncope – standing for prolonged periods of time promotes pooling of blood in the legs, which is opposed by sympathetic stimulation to constrict blood vessels and shunt blood to the heart. The sympathetic overload ↑ pressure in the LV which triggers a ‘slow-down reflex (the Bezold-Jarisch reflex) in the heart and lungs  ↓ output and cerebral hypoperfusion  syncope Induced vagal response – Carotid Sinus Massage, Valsalva manoeuvre, gagging, cold water facial immersion, rectal stimulation, direct ocular or sinus pressure.

Seizure

g) Spacious syncope

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PARA210 – LECTURE 7 REVIEW QUESTIONS 5. What six common factors can quickly lead to dehydration in a patient? 1) Lack of intake 2) Vomiting 3) Diarrhoea 4) Urination 5) Sweating 6) Hyperventilation 6. Describe SIADH and list some possible causes.  SIADH (Syndrome of inappropriate anti-diuretic hormone secretion): possibly due to pneumonia, brain diseases, cancer, thyroid problems, and some medications. 7. How much water does the average person have to drink to reach a lethal dose?  6 litres for a 75 kilogram person 8. Describe some possible causes of hypokalaemia, and how hypokalaemia could present in a patient.  Usually lost from GI tract or kidneys - Vomiting - Diarrhoea - Ileostomy - Laxatives - HCTZ - Furosemide - Prednisone - Hypokalaemic periodic paralysis  Presents as muscle weakness, muscle aches, muscle cramps, and palpitations 9. List some drugs (and their classes) that can have a specific effect on levels of awareness.     

Narcotic analgesics Alcohol Anaesthetics Anti-anxiety/Sedative Antipsychotics (EPS)

i.e. Morphine, Fentanyl i.e. Ethanol, Methanol i.e. Nitrous Oxide, Ketamine i.e. Diazepam, Midazolam i.e. Perphenazine, Olanzapine, Haloperidol, Clozapine, Risperidone

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PARA210 – LECTURE 7 REVIEW QUESTIONS 10. Differentiate between:  







Psychogenic syncope – psychologically shocking or overwhelming stimuli causes bradycardia and peripheral vasodilation  cerebral hypoperfusion Vasovagal syncope – PSNS stimulation (bradycardia & vasodilation) that originates in the baroreceptors of large arteries (vaso-) and produce reflex vagal effects (-vagal)  syncope (coughing, “necktie syndrome”, Valsalva manoeuvre) Gastrogenic syncope – Vagus nerve innervates the GI tract from mouth to anus – GI stimulation can therefore cause a vagal response. Can be due to gastric or colonic distension, gagging, diarrhoea, oesophageal obstruction, abdominal/genital trauma. Neuro-cardiogenic syncope – standing for prolonged periods of time promotes pooling of blood in the legs, which is opposed by sympathetic stimulation to constrict blood vessels and shunt blood to the heart. The sympathetic overload ↑ pressure in the LV which triggers a ‘slow-down reflex (the Bezold-Jarisch reflex) in the heart and lungs  ↓ output and cerebral hypoperfusion  syncope Induced vagal response – Carotid Sinus Massage, Valsalva manoeuvre, gagging, cold water facial immersion, rectal stimulation, direct ocular or sinus pressure.

11. Two other mnemonics are commonly used as an aid in the differential diagnosis of altered mental status. Can you recall them?

A

AEIOU TIPS Alcohol: ethanol, methanol Abuse of substances: drugs Acidosis: DKA, COPD Epilepsy: seizure activity

UNCONSCIOUS

U Units of insulin

E I Infection: sepsis, meningitis, encephalitis O Overdose Underdose

U Uraemia T I P S

N Narcotics C Convulsions O Oxygen N Non-organic

Trauma Tumour Insulin: high or low Psychogenic: Stroke: haemorrhagic Shock

S

Stroke

C Cocktail I ICP O Organism U Urea S Shock

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PARA210 – LECTURE 7 REVIEW QUESTIONS 12. Summarise the treatment approach of the following CPGs:

Agitated patient

Overdose

Hypoglycaemia

Hyperglycaemia

Hypothermia / Cold exposure

Environmental Hyperthermia / Heat stress

Electrolyte

        

Try to communicate with the patient and deescalate and calm them Attempt to gather a detailed patient history Assess VSS, RSA, PSA and SAT Score – attempt to determine underlying cause (BGL, infection, etc) Consider sedating the patient if agitation persists utilising the SAT score > 2 and QPS backup if required Provide supportive care to patient post-sedation and vigilant monitoring of VSS Pre-notify hospital Consider EEA Treat patient symptomatically and provide supportive care Attempt to determine: Substance ingested Route of administration Quantity taken Time since ingestion Any other substances taken Take any drug packaging to hospital  Consider: Oxygen  IPPB, IPPV Naloxone IV access IV fluid 12-lead ECG Sodium bicarbonate Droperidol Relevant resuscitation  Assess VSS, RSA, PSA  Attempt to gather a detailed patient history  Consider the possibility of accidental or intentional hypoglycaemic medication overdose  Consider most appropriate form of glucose to administer: oral or parenteral  Assess VSS, RSA, PSA  Attempt to gather a detailed patient history  For severe dehydration and/or altered perfusion status consider IV access and IV fluid, oxygen, 12-lead ECG  Be cautious of promoting cerebral oedema and/or APO if fluid resuscitation is too rapid  Do not initiate active warming in the field  It’s OK to protect the patient from further heat loss by drying the patient if wet and removing wet clothing, removing from contact with cold surfaces and windy environments and insulating the patient with linen and space blankets.  In hypothermic patients with no signs of life and no palpable output commence CPR  If the patient remains in VF or pulseless VT after a total of three defibrillations cease all further defibrillation and continue CPR  Do not administer any more than the first round of cardiac arrest medications and continue CPR  “They’re not dead until they’re warm and dead” (>35oC).  Pathophysiology of Hyperthermia Increased heat causes cell shrinkage, loss of sodium into the vascular volume, and therefore it heightens the threshold potential for depolarization (importantly, in nerve conduction and muscle contraction) causing diminished reflexes, altered mentation and weakness A greater increase in heat causes loss of intracellular water, distortion of the cell membrane (blebs), swelling of the mitochondria and collapse of the cytoskeleton Red blood cells deform from disks to spheres and diminish in their oxygen carrying capabilities. Hypoxia leads to agitation and eventually delirium Excessive heat can also precipitate a sickle cell crisis in susceptible patients.  Presentation is along a range from: → heat fatigue (weakness, lack of coordination) → heat exhaustion (as above, but ↓ LOAs, ↑ HR, ↑ RR, ≈ BP) → heat cramps (due to sodium imbalance) → heat stroke (frank confusion/delirium, hyperpyrexia) → Anhidrosis (loss of sweating) → Exertional rhabdomyolysis (“muscle melting”)  Core temperature above 42oC is incompatible with cell integrity (proteins denature).  The patient who is “hot to the touch” and not sweating is DYING … cooling must begin immediately (opposite of hypothermia)  Optimal treatment is evaporative cooling (mist, fan, no dripping), next best is ice packing (you can do both)  Strip  misting  fan  ice packs to axilla/groin/back of neck  Fluid replacement is essential, start with 10 mL/kg NSS.  Very difficult to correct prehospitally, although hyponatremia is amenable to treatment with saline

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PARA210 – LECTURE 7 REVIEW QUESTIONS imbalance

 Priority is recognition of the condition and notifying the receiving hospital  Full treatment is guided by electrolyte measurements in the ER  Correcting too much too fast can be worse than not correcting at all, so be careful!

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