test 2 directives and patho

Antiplatelet/COX-1 inhibitor

permanently inhibits cox1 enzymes insdie platelets, blocking the synthesis of thromboxane A2 to prevent plateletes from sticking together to stop clot growth

venodilator/vascular smooth muscle relaxant

cconverts to nitric oxide in vascular smooth muscle, causing systemic venodilation to drop preload, reduce myocardial O2 demand, and unload the left ventricle

sympathomimetic/selective B2-adrenergic agonist

selectively binds to B-2 adrenergic receptors on airway smooth muscle cells, activating adenylylate cyclase to convert ATP to cAMP, decreasing intracellular calcium and caousing smooth muscle relaxation

non selective adrenergic agonist

stimulates a1 (vasoconstriction), B1 (positive inotropy and chronotropy) and B2 receptors (massive bronchodilation) simultaneously

first generation antihistamine

Benadryl (diphenhydramine) is a first-generation H 1 ​ -antihistamine. It treats allergies by blocking H 1 ​ receptors to stop histamine from causing itching, swelling, and mucus production. Because it easily crosses the blood-brain barrier, it also blocks central H 1 ​ and muscarinic receptors, causing marked drowsiness and anti-nausea effects.

IgE-mediated type 1 hypersensitvity triggers mast cell degranulation releasing histamine, luekotrienes and prostaglandins. Mediators bind H1 receptors on bronchial smooth muslce causing spasm, mucosal edema and hypersecreation of mucus

Viral invasion of upper airway epithelium causes diffuse edema.

systemic type 1 IgE-mediated hypersensitvity causing widespread degranulation of mast cells and basophils. relase of histamine, leukottriens and bradykinis leads to capillary leak, distributive shock, bronchospasm and laryngeal edema

LV dysfunction causes fluid accumulation backward into pulmonary veins/capillaries. When pulmonary capillary hydrostatic pressure exceeds plasma oncotic pressure (>25-30 mmHg), fluid transudates into alveoli, causing severe hypoxemia

imbalance between O2 supply and demand. switch to anaerobic glycolysis causes inadequate ATP and lactic acid build up (angina). NA+/K+ pump failre leads to cellular swelling and extracellular K+ accumulation, predisposing to arrhythmias

suspected cardiac ishemia

greater or = 18 years old, unaltered and able to chew and swallow

greater or = 18 years old, unaltered, 60-159 bpm, normotension, prior history of nitro use OR IV acess obtained

allegy or sensitivity to NSAIDS, if asthmatic no prior use of ASA, current active bleeding, CVA or TBI in the previous 24 hours

allergy or sensitvity to nitrates, PDE-5 inhibitors use within that previous 48 hours, SBP drops by 1/3 of its inital value after nitro is administered, 12 lead ECG complatible with RV MI

3

6

> or = to 100mmHg

you must have an IV in place before administration

Inferior STEMI, STE in lead III > lead II, strongly suggests right coronary artery (RCA) occlusion, increasing the likelihood of RV involvement.

V4R is placed in the 5th intercostal space at the right midclavicular line.

< 10 minuates

PADS!!!

has a wide therapeutic index so you can give ASA whether or not PT has already taken some

II, III, avF. RCA

I, avL, V5 and V6. LCX OR LAD

V1 & V2 LAD

V3 & V4 LAD

Respiratory distress AND suspected bronchoconstriction!

< 25 kg: 600 mcg MDI / 2.5 mg NEB q5–15 min PRN · max 3

≥ 25 kg: 800 mcg MDI / 5 mg NEB q5–15 min PRN · max 3

0.01 mg/kg IM (1 mg/mL) · max 0.5 mg · 1 dose

BVM ventilation required, Hx of asthma

Hx of asthma OR COPD OR 20 pack-year histroy of smoking

allergy or sensitivity to steroids, currently on PO or parenteral steriods

0.5 mg/kg PO/IM/IV · max 8 mg · 1 dose

Ventilate slowly at 6–8 breaths/min using small breaths and a long 1:4 or 1:5 exhalation time (permissive hypercapnia). attempt to maintain EtCO2 between 50 and 60 mmHg to prevent further respiratory compromise due to hypercapnia and to avoid worsening acidosis

the rate of administration should be 100 mcg approximately every 4 breaths

exposure to a probable allergen AND signs and/or symptoms of a moderate to severe allergic reaction (including anaphylaxis)

For anaphylaxis

> or = 25kg

dose: 0.01mg/kg
max dose: 0.5mg
interval: minium 5 minuates
IM

mainfests in multiple body systems
integumentary: Hives, ithcing, flushing, swelling, angioedema
Cardiovascular: increased HR, decreased BP, syncope, decreased LOC, hypoxia
RESP: SOB, wheeze, cough, stridor
gastro: cramping, nausea, vomiting, diarrhea

an initial reaction that meets criteria for anaphylaxis, followed by an asymptomatic period, and then a subsequent return of symotoms meeting the creteria for anaphylaxis without further exposure to the antigen

Weight (kg) = (Age x 2) + 8

Diphenhydramine is WITHHELD under standard PCP/ACP directives because the calculated volume is under 0.5\ mL (hard to measure accurately in a standard syringe, raising the risk of dosing errors).

Current history of URTI;
AND
Barking cough or recent history of a barking cough.

Age ≥ 6 months to < 8 years
HR <200 bpm
Other Stridor at rest

< 10 kg 2.5 mg
≥ 10 kg 5 mg · 1 dose

0.5 mg/kg PO · max 8 mg · 1 dose

Steroids received within the last 48 hours

Mild Croup: Stridor only when agitated. Give Dexamethasone only.

Moderate/Severe Croup: Stridor at rest + retractions. Give Nebulized Epinephrine + Dexamethasone

Epinephrine wears off in 1–2 hours, leading to a severe rebound effect (recurrent airway swelling).

Dexamethasone takes 1–4 hours to work, leaving a dangerous gap where Epinephrine wears off before steroids kick in.

Small pediatric airways can occlude rapidly if swelling returns.

high fever + severe stridor suggests bacterial tracheitis or epiglottitis rather than simple viral croup.
Bacterial upper airway infections respond poorly to nebulized Epinephrine.
Fever increases agitation and tachycardia, worsening airway distress—prioritize keeping the child calm and giving Dexamethasone.

Moderate to severe respiratory distress;
AND
Suspected acute cardiogenic pulmonary edema.

nitro:
Age ≥ 18 years
HR 60-159 bpm
SBP Normotension

nope!

The fluid bolus is permitted despite the presence of crackles on auscultation in cases where the administration of nitro results in hypotension

follow the cardiac ischemia medical directive as it pertains to nitroglycerin administrartion and dose schedulng

Cardiogenic (ACPE): Driven by high hydrostatic pressure from LV failure. Patient is hypertensive with JVD/edema. Treat with Nitroglycerin + CPAP.

Non-Cardiogenic (ARDS/Injury): Driven by leaky capillaries (damage). Patient is normotensive/hypotensive with no JVD. Treat with CPAP/Oxygen (NO Nitroglycerin).

Severe respiratory distress;
AND
Signs and /or symptoms of acute pulmonary edema or COPD.

Age ≥ 18 years
RR Tachypnea
SBP Normotension
Other SpO2 <90% or accessory
muscle use

Asthma exacerbation
Suspected pneumothorax
Unprotected or unstable airway
Major trauma or burns to the head
or torso
Tracheostomy
Inability to sit upright
Unable to cooperate

Initial Setting 5 cm H2O
Titration increment 2.5 cm H2O
Titration interval 5 min
Max. setting 15 cm H2O

should be considered as additive therapy to the bronchoconstriction or ACPE not a replacement

alpha1 (vasoconstriction): Increases blood pressue, reverses shock, and reduces upper airway mucosal edema (stridor).

alpha2 brain and presynaptic modulates sympathetic release and contributes to peripheral vasoconstriction.

beta1 (Cardiac Stimulation): Increases HR (chronotropy) and contractility (inotropy), boosting cardiac output.

beta 2 (Bronchodilation): Relaxes bronchial smooth muscle, reversing severe lower airway bronchospasm and stabilizing mast cells.

1:1,000 = IM (1 mg/1 mL); 1:10,000 = IV (1 mg/10 mL)

dose:0.01mg/kg
max dose: 0.5mg
max doses 2
route IM

onset: IV: rapid · IM: 3–10 minutes
peak: IV: < 5 minutes IM: 20 minutes
duration: IV: 5–10 minutes · IM: 20–30minutes

creates a significant, potentially dangerous drug-drug interaction that can cause severe high blood pressure or reduce the effectiveness of emergency allergy treatment

glucagon

Inhaled air that undergoes no gas exchange

Fluid backs up into pulmonary circulation.
Signs: Crackles, orthopnea, PND, pink frothy sputum, SpO2 drop.
Mnemonic: Left = Lungs.

Right Heart Failure (Body):Fluid backs up into systemic circulation.
Signs: JVD, peripheral pitting edema, ascites, hepatomegaly, weight gain.
Mnemonic: Right = Rest of Body.

Phase 0 (Upstroke): Na+ Influx (Rapid depolarization).
phase 1 (Early Repol): Brief K + Efflux.
Phase 2 (Plateau): Ca2+ Influx balances K+ Efflux (Triggers contraction)
Phase 3 Massive K+ Efflux (Resets membrane voltage).
Phase 4 (Resting): Na+/K+ Pump restores resting ion concentration 3Na+out / 2\ K+.

Blocks Angiotensin II & Aldosterone.
Decreases Afterload (dilates arteries) & Preload (reduces fluid retention).
Stops structural ventricular remodeling.

Blocks beta receptors against sympathetic overdrive.
Decreases HR and myocardial O₂ demand increases diastolic filling time.
Protects against fatal arrhythmias and reverses structural remodeling.

B1 primary -80%
increased chronotrophy (HR)
increased Inotropy (Contractility)
increased Dromotropy (AV Conduction Speed)
increased Lusitropy (Relaxation Rate)

Fixed plaque. Predictable pain with exertion, < 15mins, relieved by rest/Nitro. Troponin (-).

Plaque rupture with partial clot. Pain at rest, > 20 mins, unresponsive to Nitro. Troponin (-).

Partial occlusion causing subendocardial necrosis. ST-depression / T-wave inversion. Troponin (+).

100% total occlusion causing transmural necrosis. ST-elevation in2 contiguous leads. Troponin (+). Emergency PCI/Fibrinolysis.

Lethal Arrhythmias: V-Fib or pVT caused by acute ischemic instability.

Pump Failure: Cardiogenic shock from massive LV necrosis (≥40% tissue loss).

Mechanical Rupture: Free wall rupture (causing acute tamponade) or papillary muscle rupture (causing acute massive mitral valve failure and ACPE).

Age ≥ 18 years
LOA Unaltered
HR ≥ 150 bpm
SBP Normotension
Other Narrow complex and regular rhythm

Sinus tachycardia or atrial fibrillation or atrial flutter

Perform a maximum of 2 attempts lasting 10 to 20 seconds duration each.

The patient must meet all of the following criteria:
• the patient is ≥ 18 AND < 65 years old;
• patient must have a prior history of SVT;
• the patient presented with narrow complex and regular rhythm Supraventricular
Tachycardia (SVT);
• the patient must have only had a single SVT episode in the past 24 hours
• the patient has returned to normal sinus rhythm (NSR) either spontaneously or
with a valsalva maneuver and is now asymptomatic;
• the patient has returned to their normal level of consciousness;
• a complete set of vital signs are within expected normal ranges with a HR
<100bpm and the patient remains in NSR for at least 15 minutes post conversion;
AND
• the patient is not pregnant;
• the SVT must not be related to alcohol or substance abuse or withdrawal, and;
• the patient has no fever or preceding illness.
In addition to the above criteria, if all of the following requirements have been met, the
patient can be discharged by paramedics:
• a responsible adult agrees to remain with the patient for the next 4 hours;
• all of the patient or substitute decision makers questions were answered and a
care plan was developed;
• the patient or substitute decision maker has been advised to follow up with their
primary health care team or provider;
• clear instructions to call 911 were provided should symptoms redevelop;
• patient or substitute decision maker has the ability to access 911 should
symptoms redevelop, and;
• patient or substitute decision maker consents to the discharg

to start an intravenous on the pateint due to thr small rish that the pateint may become hypotensive during the procedure

STEMI-positive 12-lead ECG;
AND
Cardiogenic shock

Age ≥ 18 years
SBP Hypotension
Other Chest auscultation is clear

Infusion 10 ml/kg
Infusion interval N/A
Reassess every 250 ml
Max. volume 1,000 ml

Suspected hemorrhage due to trauma
AND
Hemodynamic instability

Age ≥ 16 years
Other HR ≥ 110 BPM or hypotension

Allergy or sensitivity to TXA
Greater than 3 hours from the time of injury to
drug administration OR unknown time of
injury
Isolated head injury

Route IV
Initial dose 1000 mg
Max. single dose 1000 mg
Dosing interval N/A
Max. # of doses 1

Route IM
Initial dose 1000 mg
Max. single dose 1000 mg
Dosing interval N/A
Max. # of doses 1

center the device directly over the patient's greater trochanters (the bony outer hip prominences) rather than the higher iliac crests to ensure proper circumferential compression

chewing increases surface area and speeds absorption.

Concomitant phosphodiesterase type 5 (PDE5) inhibitor use can cause severe hypotension

Airway obstructed by a foreign object
Known esophageal disease (varices)
Trauma to the oropharynx
Caustic ingestion

2

Method Method
ETCO2 (Waveform capnography)

Primary Secondary
ETCO2 (Non-waveform device)
Auscultation
Chest rise

Trach Suctioning Pressure: Adults 100–150mmHg; Peds 100–120mmHg; Infants 60–100mmHg:
Limits: Max 10 seconds per pass; max 2 passes. Pre-oxygenate with 100% O2

Trach Reinsertion: Technique: Use Obturator + water-soluble lube = insert curved "In and Down". Critical Step: REMOVE OBTURATOR IMMEDIATELY after seating (obturator = zero airflow).
Max Attempts: 2 attempts. If failed cover stoma and BVM from above OR bag directly over stoma with pediatric mask.

Zero-Tolerance Protocol: Mandatory 2-person independent double-check (or deliberate verbalized self-check if solo) before drug administration.

• Verify "7 Rights": Right Patient, Drug, Dose, Route, Time, Expiry/Integrity, Contraindications/Allergies.

• Stop the Line: Either provider must pause administration if any discrepancy or ambiguity exists.

Medication Bag Rules (50 mL IV):

• Labeling: Mandatory bedside label (Drug, Dose, Date/Time, Paramedic Name/Initials).

• Single-Drug Limit: Strictly 1 medication per bag; no mixing.

• Volume & Flush: Does not count toward fluid resuscitation totals; line must be flushed with 10 mL NS/D5W post-infusion to clear tubing dead space.

Kinetics: Onset 2–5 min| Peak 30–60min| Duration 2–6hr.
Side Effects: Tachycardia, muscle tremors, anxiety, hypokalemia, throat irritation.

Kinetics: IV: Onset 5–10 min peak 15–30min | Duration 4–6 hr. IM/PO: Onset 15–30min| Peak 1–4 hr | Duration 4–8 hr
Side Effects: Sedation/drowsiness, anticholinergic dryness (dry mouthrinary retention), mild hypotension.

onset: PO: 30 minutes. peak PO: 1–2 hours
onset: IV: rapid peak

the volume of inhaled air that stays in the conducting airways and does not take part in gas exchange
Roughly 150 mL in an average adult, which is about 30% of a normal 500 mL tidal volume.

the total volume of air inhaled or exhaled from the lungs in one minute
Approximately 5 to 8 liters per minute

unloads O2 easier Increased CO₂, decreased pH (acidosis/Bohr effect), increased temperature, or higher 2,3-BPG (2,3-diphosphoglycerate).

Hemoglobin lets go of oxygen more readily

Decreased CO₂, increased pH (alkalosis), decreased temperature, lower 2,3-BPG, or fetal hemoglobin (HbF).

Hemoglobin holds onto oxygen more tightly and releases it less easily

a condition where deoxygenated blood passes from the right side of the heart to the left side without getting oxygen in the lungs

Chemoreceptors regulate breathing by sensing changes in blood and brain chemistry (CO₂, O₂, and pH) and sending signals to the brainstem to adjust the rate and depth of ventilation

Bronchospasm + inflammation = Wheezing, prolonged expiration.

Fixed airflow obstruction (Chronic Bronchitis + Emphysema).

Alveolar infection = Fever, crackles, focal hypoxia.

Thrombus blocks pulmonary flow = Unexplained tachypnea, clear lungs, pleuritic pain.

Air in pleural space = Absent breath sounds, sudden pain (Tension = tracheal deviation, hypotension).

Distress: higher Work of breathing, tachycardic, anxious, retractions.

failure Exhaustion, bradycardia (ominous), altered/lethargic, cyanotic

the abnormal retention of air inside the lungs because it cannot be fully exhaled
"Shark Fin" waveform

Severe respiratory distress
AND
Signs and /or symptoms of acute pulmonary edema or COPD.

Age ≥ 18 years
RR Tachypnea
SBP Normotension
Other SpO 2 <90% or accessory muscle use

A – Asthma exacerbation

S – Suspected pneumothorax

T – Tracheostomy

H – Head or torso major trauma / burns

M – Mask resistance (Unable to cooperate)

A – Airway unprotected / unstable

U – Upright positioning impossible (Inability to sit upright)

Initial Setting 5 cm H 2O

Titration increment 2.5 cm H 2O

Titration interval 5 min

Max. setting 15 cm H 2O

ACPE Directive:
First-line treatment.
Physiology: Recruits alveoli (pushes fluid back into vasculature) & decreases cardiac preload/afterload.
Concurrent Therapy: Co-administered with Nitroglycerin.

COPD (Bronchoconstriction):
Indicated.
Physiology: Overcomes intrinsic PEEP (air trapping) and keeps collapsing airways open.
Concurrent Therapy: Administered with inline Salbutamol

CPE (Acute Cardiogenic Pulmonary Edema): Crackles, orthopnea, pink frothy sputum, high BP.

Severe COPD Exacerbation: Wheezing, air trapping, history of COPD.