Hypoglycemia, Nociception, and Antiemetics

Insulin: Lowers blood glucose by driving it into cells.

Glucagon: Raises blood glucose by triggering the liver to release stored glycogen.

The brain relies almost exclusively on glucose and has essentially no fuel reserve of its own.

Altered level of awareness (LOA)
Confusion
Seizure-like activity
Combativeness

Too much insulin/oral hypoglycemic relative to food intake
Missed meals
Alcohol use
Exercise
Sepsis

Dextrose and Glucagon. They work by directly or indirectly restoring blood glucose so the brain has fuel again.

The process where a noxious stimulus (mechanical, thermal, or chemical) is converted into an electrical signal by nociceptors (free nerve endings throughout the body)

The pathway where the electrical signal travels along peripheral nerves, up the spinal cord, and to the brain.

The step where the brain interprets the signal as pain.
Mood, prior experience, and anxiety all influence how severe the pain actually feels.

The process where the body's descending pathways and administered analgesics dampen the pain signal at multiple points along the pathway (with different drug classes acting at different steps).

Vomiting is coordinated by the vomiting center in the medulla, which receives input from several different sources.

The CTZ sits outside the blood-brain barrier, allowing it to directly sample circulating toxins, drugs, and metabolic byproducts in the blood as a major trigger pathway for nausea

The vestibular system (motion sickness)
The GI tract itself (irritation, distension)
Higher cortical centers (sight, smell, anxiety, pain)

Ondansetron and dimenhydrinate. They block different receptors along these pathways, which is why one may work when the other hasn't.

on everything that is chemically induced, like alchohol or chemo

anything to do with movement

The hypothalamic-pituitary-adrenal (HPA) axis is the body's central stress-response system.
Pathway: Hypothalamus: Receives a stress signal.
Pituitary Gland: Releases ACTH.
Adrenal Cortex: Stimulated by ACTH.
Cortisol: Released into the bloodstream

The surge of cortisol helps maintain blood pressure, blood glucose, and overall stress tolerance.

Definition: Primary adrenal failure where the patient cannot produce a cortisol surge on their own.
Effect of stress: Under physical stress (illness, injury, infection), they can rapidly decompensate into an adrenal crisis: hypotension, hypoglycemia, and shock.

Because you are replacing a hormone their body cannot produce in a crisis, rather than treating a new problem from scratch.

They are responsible for most of an opioid's analgesic effect and also for its most dangerous side effect: respiratory depression.

Excess mu-receptor stimulation blunts the brainstem's response to rising CO2, causing the patient to stop breathing adequately due to loss of respiratory drive (rather than the heart stopping first).

It acts as an antagonist that competitively displaces opioids from the mu receptor without activating it itself, rapidly reversing respiratory depression.

It binds mu receptors very tightly but only partially activates them—enough to relieve withdrawal symptoms without producing the same overdose risk as a full opioid agonist.

suspected hypoglycemia

>2years old
altered
hypoglycemia

altered
hypoglycemia

allergy or sensitivity

allergy or sensitivity
pheochromocytoma

If the patient responds to dextrose or glucagon, they may receive oral glucose or other simple carbohydrates.

The patient may receive oral glucose or other simple carbohydrates instead of dextrose or glucagon.

A final set of vital signs including blood glucometry must be attempted and documented.

itration goal: Titrate gradually toward a level of awareness where the patient can safely consume carbohydrates on their own.
Risks: Overcorrecting risks rebound hyperglycemia, and dextrose is genuinely irritating to peripheral veins.
Age requirement: IV dextrose requires age 2 years or older

Dose & Reassessment: 15 g and every 15 min
Indications: Appropriate alternative if the patient is alert with only mild symptoms, or responds to dextroselucagon.

It must trigger the liver to break down glycogen stores first.
Patients with depleted glycogen stores (e.g., chronic alcohol use, malnourishment) may not respond well

1-2 min (IV)

3-5min

variable - depnds on ongoing carbohydrate intake

Dextrose is glucose in an injectable form that is absorbed directly into the bloodstream and immediately available as fuel for glucose-dependent tissue, most critically the brain

10-20 min (IM/IV)

20-30 mins

60-90 mins

Glucagon is a naturally occurring pancreatic hormone that acts on liver cells to trigger glycogenolysis—the breakdown of stored glycogen into glucose, which is then released into the bloodstream.

Because it has to work through the liver rather than delivering glucose directly into the bloodstream.

suspected opiod toxcicity

≥ 24 hours
altered
< 10 breaths/min
inability to adequately ventilate OR persistent need to assist ventillations

≥ 16
unaltered
received naloxone for current opioid toxicity episode AND cows score ≥ 8

allergy or sensitivity

allergy or sensitivity to buprenorphine
taken mathadone in the past 72 hours

to try to blow off the large amounts of CO2 that they have so you dont send them into a hufe catecholamine release

2 min intervals IV
0.08
0.08
0.08
0.08
Calls for a nice smooth wake up they tend to be less angry and it gives you a lot more time to blow off the CO2

A patient who has taken methadone in the past 72 hours is contraindicated due to potential unpredictable interactions between methadone's long half-life and buprenorphine's strong receptor affinity.

2-5 min (IM/IN/SC)

5-10 min

30-90 mins shorter than the opiod itself

Binds to mu receptors with high affinity without activating them, physically displacing bound opioid molecules and rapidly reversing respiratory depression

Binds mu receptors with high affinity but only partially activates them—providing enough stimulation to relieve withdrawal symptoms without inducing severe respiratory depression or overdose risk.

15-30 mins

1-2 hrs

24 hours

a pateint with primary adrenal failure who is experiencing clinical signs of an adreanl crisis

Paramedics are presented with a vial of hydrocortisone for the identified
patient AND
Age - related hypoglycemia OR
GI symptoms (vomiting, diarrhea, abdominal pain) OR
Syncope OR
Temperature ≥38C or suspected/history of fever OR
Altered level of awareness OR
Age - related tachycardia OR
Age - related hypotension

The patient must have known primary adrenal failure (it is NOT for a general "looks like shock" presentation)

withun 1 hour

1-2 hours

8-12 hours

Mechanism: In primary adrenal failure, the adrenal cortex cannot mount a cortisol response to physical stress.
Action: Hydrocortisone directly replaces the missing cortisol hormone, restoring the physiological functions normally provided by cortisol:
- Maintaining vascular tone
- Maintaining blood pressure
- Maintaining blood glucose under stress

pain

≥ 12 years
unaltered

≥ 12 years
unaltered

≥ 12 years
unaltered

Acetaminophen use within previous 4 hours
Allergy or sensitivity to acetaminophen
Hx of liver disease
Active vomiting
Unable to tolerate oral medication
Suspected ischemic chest pain

"Always Avoid Harm: Assess Unfit Symptoms"

NSAID use within previous 6 hours
Allergy or sensitivity to ASA or NSAIDs
Patient on anticoagulation therapy
Current active bleeding
Hx of peptic ulcer disease or GI bleed
Pregnant
If asthmatic, no prior use of ASA or other NSAIDs
CVA or TBI in the previous 24 hours
Known renal impairment
Active vomiting
Unable to tolerate oral medication
Suspected ischemic chest pain

NSAID use within previous 6 hours
Allergy or sensitivity to ASA or NSAIDs
Patient on anticoagulation therapy
Current active bleeding
Hx of peptic ulcer disease or GI bleed
Pregnant
If asthmatic, no prior use of ASA or other NSAIDs
CVA or TBI in the previous 24 hours
Known renal impairment
Suspected ischemic chest pain

P.I.C.K. S.P.A.N. C.H.

Renal colic: Because it reduces intrarenal pressures.
Hip fracture: When the patient must remain supine and cannot tolerate PO medications due to being on their back.

30-60 min

1-2 hr

4-6 hr

30-60min

1-2 hr

4-6 hr

10-30 minsn

1-2 hr

4-6 hr

Nausea OR vomiting

> or = to 25 kg
unaltered

> or = to 25 kg
unaltered

Allergy to ondansetron
Prolonged QT syndrome (known
to patient)
Apomorphine use

Allergy or sensitivity to dimenhyDRINATE or other antihistamines
Overdose on antihistamines or anticholinergics or tricyclic antidepressants
Co - administration of diphenhydrAMINE

10-15 min IV

30-60 min

4-8hr

Mechanism: Selectively blocks serotonin (5-HT3) receptors.
Sites of Action:Peripherally: On vagal nerve terminals in the GI tract. Centrally: In the chemoreceptor trigger zone (CTZ).

1-2hr

20-30 min

3-6 hr

Mechanism: Blocks H1 histamine receptors both peripherally and centrally. Additional Properties: Exhibits anticholinergic and antivertigo properties.

Acts on the vestibular system and the chemoreceptor trigger zone (CTZ).
Particularly effective for nausea related to motion or vestibular causes, alongside its general antiemetic effect.

Acetaminophen and ibuprofen.

Considered for anti-inflammatory action and smooth muscle relaxation.

A hemorrhage that cannot be controlled

1500ml to 3000ml

Fast touch fibers stimulate inhibitory interneurons in the dorsal horn.

500-1500ml

300-500ml

250-350ml

Torn intraosseous and haversian vessels are held open by rigid, calcified bone architecture and cannot naturally constrict.

Pelvic Binder: Placed over greater trochanters to reduce pelvic volume and promote retroperitoneal tamponade.

Traction Splint: Re-aligns femur, decreases thigh volume, and limits hematoma expansion space.

Bones have a rich blood supply

Unyielding fascial envelopes trap bleeding, causing intramuscular pressure to rise sharply.

Antiplatelets: Stop platelets from sticking together to form a plug (works in fast-flowing blood like arteries).

Anticoagulants: Block clotting factors to stop a fibrin mesh from forming (works in slow-moving blood like veins or stasis).

ASA, plavix

Heprin, Warfrin

Mostly affects Type 1 diabetics. The body has zero insulin, so it starts burning fat for fuel, which creates toxic acids called ketones.

14mmol

Mostly affects Type 2 diabetics. The body has just enough insulin to stop ketones from forming, but not enough to control blood sugar, leading to extreme dehydration.

33mmol

Nausea/vomiting, fruity/sweet breath (from ketones), abdominal pain, and Kussmaul respirations (deep, fast breathing trying to blow off body acid).

Severe dehydration, extreme weakness, dry mouth, and confusion, lethargy, or coma due to thick, concentrated blood and very high sugar.

Rapid onset (minutes). The brain is starved of its primary fuel instantly, causing an acute medical emergency.

Gradual onset (hours to days or weeks). The body slowly builds up high sugar and dehydration over time.

Shaky/tremors, sweating (diaphoresis), tachycardia, anxiety, pale skin, and hunger. Confusion, bizarre or aggressive behavior, slurred speech, weakness, decreased level of alertness (LOA), seizures, or unresponsiveness.

Polyuria (excessive urination), Polydipsia (excessive thirst), and Polyphagia (excessive hunger). Extreme fatigue, dry skin and mucous membranes, blurry vision, and poor skin turgor from dehydration.

Brain cells cannot store their own sugar.
When blood sugar drops, brain cells instantly starve, leading to rapid neurological decline.

IV Dextrose: Puts pure glucose directly into the bloodstream for immediate brain recovery.

IM Glucagon: Forces the liver to break down its stored sugar reserves. (Does NOT work if liver glycogen is empty, e.g., malnutrition, alcoholism, chronic illness).

Insulin turns on the cell pumps that push sugar inside.

At the same time, it pushes potassium into the cells, lowering the level of potassium in the blood.

Giving insulin suddenly pushes all that potassium back into the cells.

Blood potassium levels plummet, which can cause lethal heart rhythms if not monitored and treated.

Breaking down stored glycogen into glucose (fast).

Making new glucose from non-carbohydrates like fat/protein (slow).

infection / sepsis:
Trauma, Surgery, or Severe Injury:
Abrupt Withdrawal of Systemic Corticosteroids:
Severe Dehydration / Vomiting / Emotional Stress.

Check CSM (Circulation, Sensation, Motor) before and after splinting.

Immobilize the joint above and below a fracture site.

If distal pulse is absent, attempt manual inline traction once to restore blood flow before splinting

Vasodilation: Increases local blood flow (redness, heat).
Vessel Permeability: Capillaries leak protein-rich fluid into tissues, causing swelling and pain.

Decreased LOA, pinpoint pupils, slow/shallow breathing.

Normal shape, but slow rate (bradypnea).

Hyperkalemia (lethal heart rhythms) and severe fluid overload (pulmonary edema).

Never take BP or start IVs on the fistula arm. Direct pressure if bleeding.

Severe abdominal pain and cloudy dialysate fluid.

Physical/chemical stimuli converted into electrical signals at nerve endings.

Signal travels along primary afferents, spinal cord, and brainstem to cortex.

Conscious recognition and emotional processing of pain in the brain.

Endogenous amplification or suppression of pain signals in the nervous system.

Lightly myelinated, fast-conducting; relay sharp, localized, acute "first" pain.

Unmyelinated, slow-conducting; relay dull, aching, burning, poorly localized "second" pain.

Inhibit COX enzymes to stop prostaglandin synthesis $\rightarrow$ blocks peripheral Transduction.