Medical Cardiac Arrest Directive

Non-Traumatic Cardiac Arrest

≥ 24 hours
altered
VF OR pulseless VT

≥ 24 hours
altered
Defibrillation indicated

EPINEPHrine
Age ≥ 24 hours
LOA Altered
Anaphylaxis suspected as causative event

≥ 16 years
Altered
Arrest not witnessed by
paramedic
AND
No ROSC after 20 minutes of
resuscitation
AND
No defibrillation delivered

Pregnancy presumed to be ≥ 20 weeks gestation
Suspected hypothermia
Airway obstruction
Non - opioid drug overdose/toxicology

Cardiac arrest secondary to severe blunt or penetrating trauma.

≥ 16 years
Altered
HR 0
RR 0

Other No palpable pulses AND
No defibrillation delivered AND
Rhythm Asystole AND
No signs of life at any time since fully extricated OR
Signs of life when fully extricated with the closest ED ≥30 min
transport time away OR
Rhythm PEA with the closest ED ≥30 min transport time away

Age <16 years
Defibrillation delivered
Signs of life at any time since fully
extricated.
Rhythm PEA and closest ED <30 min
transport time away
Patients with penetrating trauma to the
torso or head/neck and Lead Trauma
Hospital < 30 min transport time away

rhythms other than VF or pulseless VT

Non -shockable rhythm

Newborn Patient

< 24 hours
< 100 bpm

< 24 hours
< 60 bpm
After 30 seconds of PPV using room air

Obviously dead as per BLS PCS
Presumed gestational age less than 20 weeks

Obviously dead as per BLS PCS
Presumed gestational age less than 20 weeks

Patient with return of spontaneous circulation (ROSC) after the resuscitation was
initiated.

≥ 2 years
SBP Hypotension
Other Chest auscultation is clear

IV
10ml/kg
immediate
100ml
1000ml

IV
10ml/kg
immediate
250ml
1000ml

Rapid depolarization caused by the influx of sodium ions hrough fast voltage-gated sodium channels.

Influx of calcium through L-type calcium channels balanced by outward potassium efflux, triggering contraction via calcium-induced calcium release.

Maintained around -90mV by the NA/K ATPase pump.

Depletion of cellular ATP, leading to failure of the NA/K ATPase pump and intracellular sodium and calcium accumulation.

Re-entrant loops created by desynchronized repolarization and localized conduction blocks across partially depolarized ischemic myocardial tissue.

CPP = Diastolic Aortic Pressure - Right Atrial Diastolic Pressure

A minimum CPP of 15mmHg is required to restore cellular ATP production and allow successful defibrillation.

The first 0 to 4 minutes of arrest where high ATP levels remain and immediate defibrillation has the highest success rate.

The phase occurring after 10 minutes characterized by severe global ischemia, cellular necrosis, and heavy reliance on post-resuscitation care.

To provide high-energy electrical depolarization that simultaneously resets all chaotic re-entrant myocytes into Phase 4, allowing the SA node to re-establish control.

Rhythm interpretation and analysis must be performed at strict 2-minute intervals.

10 breaths per minute (1 breath every 6 seconds) delivered asynchronously with continuous chest compressions.

Increases intrathoracic pressure, decreases venous return (preload) to the right atrium, and severely reduces Coronary Perfusion Pressure.

Acts as an alpha-1 receptor agonist causing peripheral vasoconstriction, increasing systemic vascular resistance and raising aortic diastolic pressure to augment CPP.

Hypoxic or respiratory arrest rather than primary cardiac ischemia.

Severe bronchoconstriction and dynamic hyperinflation (auto-PEEP) create high intrathoracic pressure that impedes venous return, leading to PEA or asystole.

Charge the manual defibrillator during ongoing chest compressions to minimize the pause before shock delivery.

There is no organized or chaotic electrical activity present to depolarize or reset; the myocardium is electrically silent.

Class III (Amiodarone) and Class I (Lidocaine) antiarrhythmics that stabilize cell membrane potentials and suppress recurrent VF/VT.

Administer a single dose of IM Epinephrine (1:1,000) immediately without delaying standard cardiac arrest interventions and defibrillation.

Rapid repolarization caused by the closure of L-type calcium channels and opening of delayed rectifier potassium k channels, restoring the negative interior.

Maintain the resting membrane potential near-90mV alongside the Na/K ATPase Pump

The window between 4 and 10 minutes post-collapse where ATP is depleted and high-quality CPR is required to build Coronary Perfusion Pressure prior to defibrillation.

Epinephrine increases systemic vascular resistance via $\alpha_1$ vasoconstriction, which elevates aortic diastolic pressure while right atrial pressure remains relatively stable, raising CPP.

30 compressions to 2 ventilations.

Elevates intrathoracic pressure, decreases right atrial preload, reduces cardiac output, and destroys Coronary Perfusion Pressure.

Refractory VF or pulseless VT after initial defibrillation attempts and epinephrine administration.

Allow passive exhalation and relieve dynamic hyperinflation (brief BVM disconnection if needed) to restore venous return to the heart.

Simultaneous depolarization of all myocardial cells to terminate chaotic re-entry circuits and allow a higher pacemaker (SA Node) to resume control.

Intracellular and sarcoplasmic reticulum calcium overload causes spontaneous diastolic calcium $ release, triggering inward sodium-calcium exchange currents that generate ectopic action potentials.

Lactic acid accumulation and severe intracellular acidosis pH 7.0 which impairs contractile proteins and desensitizes myofilaments to calcium.

Acidosis blunts and adrenergic receptor responsiveness, diminishing the vascular and inotropic efficiency of administered Epinephrine.

Intact electrical depolarization (Phase 0–3) occurring without mechanical contraction, driven by profound ATP depletion, severe hypovolemia, hypoxia, or mechanical obstruction.

Immediately attempt to clear the obstruction; if cleared and patient is pulseless, transition directly to standard medical cardiac arrest protocols.

They prolong the effective refractory period and depress Phase 0 conduction velocity in ischemic tissue, preventing re-entry circuits from re-establishing VF/VT.

Safely pull over the vehicle, stop transport, perform 1 immediate rhythm analysis, deliver treatment as indicated, and resume transport.

Reduces the cerebral metabolic rate of oxygen, suppresses free radical production, and limits cellular apoptosis and reperfusion injury.

Paramedics do not count pre-arrival interventions into patient care time. Paramedics should complete a full 20 minutes of resuscitation on scene before considering a medical TOR patch.

Compressions should be continued during the charger cycle of the manual defibrillator.

The ambulance must be stopped to minimize artifact and the risk of an inaccurate rhythm analysis.

Paramedics can decide whether to stay and perform three full analyses before proceeding/patching, or to provide one analysis and go.

Continuous chest compressions with asynchronous ventilations at 10 breaths/minute (1 every 6 seconds) for adults, and 20 breaths/minute (1 every 3 seconds) for children and infants.

IV, IO, and CVAD routes are preferred. ETT may only be utilized if preferred routes are delayed by more than 5 minutes.

Proceed with administration, ensuring a saline flush is provided between the two medications

1. Pull over;
2. Initiate one immediate rhythm interpretation;
3. Treat rhythm appropriately;
4. Continue transportation with no further stops.

Simple electrocution is treated as a medical cardiac arrest (responds well to defib); electrocution associated with significant trauma must be treated as a trauma cardiac arrest.

Subsequent pulse checks are indicated only when a rhythm analysis reveals a non-shockable rhythm (PEA/Asystole) or there are signs of life present.

loss of o2 leads to ATP collapse

PEA/Asystole

High-efficiency oxygenation/ventilation

loss of preload / intravascular volume

narrow complex PEA

Fluid bolus (ACP scope)

Inactivates $Na channels

Wide QRS PEA / Sine wave

Identify history (dialysisenal failure)

PEA

VF/ pulseless VT

needle decompression

Defibrillation, CPR, Epinephrine

Mechanical IVC obstruction

Ischemic re-entry loops

Establishing adequate lung inflation and ventilation after birth to facilitate transition from intra-uterine to extra-uterine life.

Applies only to patients $24 ohours of age.

Cardiac monitoring (ECG). If delayed, clinical assessment can be completed by auscultation, palpation of the brachial pulse, or SpO2 probe on the right hand.

Paramedics cannot titrate oxygen flow; PPV is provided using either 100% oxygen (if SpO2 is below range) or room air (if SpO2 is above range).

Routine suctioning is not required if the newborn is breathing effectively, even if meconium is present.

Indicated if meconium is present AND the newborn has poor muscle tone or is not breathing/crying (relying on obligate nose-breather physiology).

Mask seal (Adjust mask/size)
Reposition airway ("sniffing" position)
Suction mouth and nose
Open mouth (manual maneuvers)
Pressure increase (achieve chest rise)
Alternate Airway (SGA / ETT)

ONLY the 1:10,000 (0.1 mg/mL) solution is used, regardless of the route of administration.

The ETT dose of Epinephrine is 10 times the IV/IO dose.

Target 94% to 98% (avoiding 100%) to ensure adequate oxygenation while minimizing vasoconstriction and oxygen free radical damage.

Oxygen administration should be continued if the patient remains clinically unstable.

There is insufficient evidence to support the routine use of antiarrhythmics post-ROSC.

A fluid bolus precedes Dopamine administration; time must be allowed to evaluate fluid response prior to starting Dopamine.

IV, IO, and CVAD are appropriate routes for fluid administration.

Adults: 10 breaths/min (1 breath every 6 seconds)

Children & Infants: 20 breaths/min (1 breath every 3 seconds)

30 to 40 mmHg.

Avoid hyperventilation, but do not hypoventilate to artificially raise a low ETCO2 as low readings may reflect underlying metabolic acidosis

10 mL/kg fluid bolus (up to a maximum of 1,000 mL) if chest auscultation is clear, targeting a SBP ≥ 90 mmHg

Medical arrest is primarily an electrical or pump problem (treated with CPR and defibrillation), while traumatic arrest is a plumbing and volume problem (hypovolemia from hemorrhage or obstructive tension pneumothorax).

Compressions on an empty, obstructed heart cannot generate effective cardiac output until the reversible cause is corrected; CPR only buys time.

Asystole with no signs of life after trauma behaves physiologically different from a medical arrest that has simply not converted yet.

Pulmonary vascular resistance drops dramatically, shifting circulation from placental to pulmonary oxygenation.

Most newborns needing help simply require their transitional state supported (establishing lung inflation), as primary arrest is usually respiratory rather than cardiac.

Reperfusion after global ischemia can stun the myocardium and drop systemic pressure right when the brain is most vulnerable and requires perfusion.

Optimize oxygenation, support blood pressure with fluid boluses, and obtain a 12-lead ECG to protect and manage the fragile reperfused heart.

Perform three analyses in the initial pad orientation, followed by one further shock in the second orientation or with a second set of pads (four shocks total) before resuming transport.

On-scene management allows six shocks total (three plus three), whereas en-route management limits attempts to four shocks total to trade defibrillation attempts for reaching definitive care sooner.

Stop attempting further shocks and initiate transport immediately.

Unless a patient arrests or re-arrests for the very first time, paramedics do not pull over the ambulance while en-route to the receiving facility.

Allows up to 20 minutes of on-scene resuscitation with a minimum of four analyses for patients who do not meet Termination of Resuscitation (TOR) criteria.

younger age, arrest witnessed by paramedics, availability of ACP-level care, or non-agonal PEA rhythm.

Patch to the BHP to assist with the decision, and document the clinical rationale for scene resuscitation versus early transport either way.

A single dose of IM Epinephrine 1:1,000 (1 mg/mL) administered immediately. It does not alter the timing of IV Epinephrine doses and must not delay defibrillation.

Treat them as medical cardiac arrests (simple electrocution responds well to defibrillation); switch to the Trauma directive only if significant trauma is also present.

Stimulates alpha-1, beta-1, and beta-2 adrenergic receptors, causing peripheral vasoconstriction that raises coronary and cerebral perfusion pressure, while increasing heart rate and contractility.

Indicated only when anaphylaxis is suspected as the cause of the arrest; it is not given empirically for every arrest rhythm at the PCP scope.

Onset: 3 to 10 minutes; Peak Effect: 20 minutes.

20 to 30 minutes.

2 J/kg, followed by 4 J/kg for subsequent shocks.

As per RBHP

Every 2 minutes with no maximum dose limit.

Paramedic reads the rhythm and decides to shock, eliminating automated analysis time, shortening the peri-shock pause, and allowing the unit to charge while compressions continue.

Shocking artifact/organized rhythm due to misreading, missing fine VF mistaken for asystole, and skin burns or arcing from poor pad contact or overlapping pads.

PCPs may only use manual mode if certified and authorized by their service and base hospital; if unable to confidently read the rhythm, use SAED.

Ventricular Fibrillation (VF) and pulseless Ventricular Tachycardia (VT).

Confirm pulselessness, because a wide, fast rhythm with a pulse is not a cardiac arrest and falls outside this directive.

Monomorphic VT repeats one QRS shape while polymorphic VT changes shape beat-to-beat (torsades is a form of it); both are shocked when pulseless, and either can degenerate into VF between analyses.

VF is completely chaotic with no identifiable QRS complexes. Because fine VF can mimic asystole, paramedics must check leads, gain, and view a second lead before calling it non-shockable.

Zoll: 120 to 150 to 200 J;
LIFEPAK 15: 200 to 300 to 360 J.

Count fire's shocks toward escalation; if fire delivered two shocks, your first manual shock is the third overall, so set maximum energy (Zoll 200 J, LP15 360 J).

pick the closest available joule setting on the monitor, as SWORBHP no longer directs rounding up.

Overcomes refractory rhythms by changing or adding a new electrical vector (via anterior-posterior pad placement or a second set of pads) to depolarize more myocardial mass than a single, unchanged vector can reach.

VCD shifts pad placement to an alternative vector (e.g., anterior-posterior)

Utilize Vector Change Defibrillation (VCD); the lack of a second unit is not a reason to skip further defibrillation.

CPR runs in strict two-minute intervals, but the algorithm branches immediately based on rhythm

no palpable pulses AND
No defibrillation delivered AND
Rhythm is asystole AND
Either no signs of life since full extrication OR a prolonged transport time (all elements must be present).

Control external hemorrhage, splint the pelvis to manage hypovolemia, and prioritize basic airway/ventilation to correct hypoxia (advanced airway used only as needed).

IV fluid boluses may be considered only where they do not delay transport and are not prioritized over managing other reversible pathology, representing a more restricted fluid philosophy than medical arrest.

Patch to the BHP for authorization to apply the Trauma TOR; if the patch fails or TOR criteria do not apply, transport to the closest appropriate receiving facility following the first analysis or defibrillation.

Term gestation?
Good muscle tone?
Breathing or crying?(A 'yes' to all three means routine supportive care, not resuscitation).

Every step runs in fixed 30-second blocks, with heart rate reassessed at the end of each block.

Cardiac monitoring (ECG); fall back to auscultation, a brachial pulse, or an SpO2 probe on the right hand only if monitoring is delayed.

Targeted preductal SpO2 (right hand) rises gradually over 10 minutes; chasing high saturation too quickly leads to unnecessary oxygen administration and hyperoxia.

Compressions are added only if the heart rate remains $<60\text{ bpm}$ after 30 seconds of effective PPV with room air; once compressions start, PPV switches to 100% oxygen.

Initiate resuscitation and transport rather than withholding care; resuscitation is considered futile only below 20 weeks gestation (and even then, warmth and a patch to the BHP are appropriate).

660 nm (Red light — absorbed more by oxyhemoglobin) and 940 nm (Infrared light — absorbed more by deoxyhemoglobin).

LEDs shine light through a pulsing tissue bed to a photodetector; the monitor isolates the pulsatile arterial blood signal from the static background of bone, tissue, and venous blood.

By measuring the ratio of red to infrared light absorption and referencing a calibration curve built from healthy volunteers deliberately desaturated to about 70%.

Total hemoglobin concentration, presence of carbon monoxide (CO) or methemoglobin, cardiac output, actual tissue oxygen utilization, or ventilation

High CO2, Acidosis (low pH), High Temperature, High 2,3-DPG, and Exercise. Hemoglobin releases O2 more easily to tissues.

Low CO2 / Alkalosis, Hypothermia, Carbon Monoxide, Methemoglobin, and Fetal Hb. Hemoglobin holds O2 tighter, so SPO2 looks fine while tissues starve.

Large drops in PaO2 barely change SPO2; it is a late warning of hypoxemia and cannot detect hyperoxia.