ACLS

Leads II, III, and avF

Leads I, avL, V5, and V6

Leads avR, V1, and V2

Leads V1 - V4

PRIMARY ASSESSMENT (ABCDE)
- Airway: patent? (head tilt-chin lift; OPA or NPA necessary?) indication for advanced airway?
- Breathing: ventilation and oxygenation adequate? SpO2 WNL? monitor quantitative waveform capnography and oxyhgb sat?
- Circulation: effective chest compressions (ETCO2 <10 mm Hg = improve CC)? cardiac rhythm - is defib or cardioversion indicated? IV/IO established? ROSC? Pulse or pulseless? Meds for rhythm or BP indicated? Check BG and temp
- Disability: neurofunction, GCS, AVPU
- Exposure: remove clothing for physical assessment, look for obvious signs of trauma, bleeding, burns, unusual markings, or medical alert bracelets

SECONDARY ASSESSMENT (SAMPLE)
- S/S (dyspnea, tachypnea, tachycardia, fever, HA, abd pain, bleeding)
- Allergies (meds, foods, latex; associated reactions)
- Medications (and last dose taken; OTC, vitamins, INH, herbal supplements; meds found in pt's home/ belongings)
- PMH (esp r/t current illness; previous hospitalizations; family hx esp in ACS or stroke; immunization status)
- Last meal consumed (time and nature of last food or fluid intake)
- Events (leading up to illness/injury, sudden or gradual onset, type of injury, attempted tx, estimated time of onset)

- Hs and Ts are potential reversible causes of cardiac arrest and emergency cardiopulmonary conditions
- Hs: hypovolemia, hypoxia, hydrogen ion (acidosis), hypo-/hyperkalemia, hypothermia
- Ts: tension pneumothorax, tamponade (cardiac), toxins, thrombosis (pulmonary OR coronary)
--> hypovolemia and hypoxia are the 2 most common underlying and potentially reversible causes of PEA

- airway compromise
- RR <6 or >30
- HR <40 or >140
- SBP <90
- sympomatic HTN
- unexpected decrease in LOC
- unexplained agitation
- seizure
- significant decrease in urine output
- subjective concern about the pt

Recent GI bleeding, true ASA allergy
--> use ASA PR for pts with N/V, active PUD, or other disorders of the upper GI tract

- give 1 SL NTG tablet/dose q3-5min for ongoing symptoms up to a total of 3 doses
- administer only if pt hemodynamically stable (SBP >90 mm Hg or no lower than 30 mm Hg below baselin and HR 50-100 bpm)

- pts presenting >24hr after symptom onset
- pts with ST-segment depression, unless true posterior MI suspected
- active bleeding (excluding menses)
- significant head injury or facial trauma within 3 months
- recent Intracranial or spinal surgery
- severe uncontrolled hypertension (alternates from absolute to relative contraindication when SBP >180 or DBP >110)

Diabetes, HTN, arrhythmias (specifically, AFib), high cholesterol, smoking

Within 3 hr after symptom onset (4.5 hr for select pts) and within 45 min after hospital arrival

Recognized as MAXIMUM times
- immediate general assessment <10 min
- immediate neuro assessment <20 min
- acquisition of CT/MRI of the head <20 min
- interpretation of CT/MRI scan <45 min
- admin of fibrinolytic therapy <60 min
- interfacility transfers for EVT (endovascular therapy) <1 hr

- Last known well/normal (symptom onset) AND time of symptom discovery
- N/V
- Change in vision? Unilateral or bilateral?
- BG if indicated
- NIH Stroke Scale

- sudden weakness or numbness of the face, arm or leg, especially on one side of the body
- trouble speaking or understanding ("say 'you can't teach an old dog new tricks'")
- sudden trouble seeing in one or both eyes
- sudden trouble walking
- dizziness or loss of balance or coordination
- sudden severe HA with no known cause
- sudden confusion

- 1 small square = 0.04 sec
- 5 small squares/1 large square = 0.2 sec

Beginning of the P-wave to beginning of the QRS complex, respresents the time from beginning of atrial contraction to beginning of ventricular contraction
WNL = 0.12 - 0.20 sec (3-5 small squares)

End of QRS interval to beginning of T-wave

WNL = 0.06 - 0.12 sec (should be <3 small squares)

- 1st Degree AV block
- 2nd degree AV block T1 (Wnckebach): successive PRi prolongation, until QRS dropped; often repeats
- 2nd degree AV block T2: constant but prolonged PRi, dropped QRS ocassionaly
- 3rd degree AV block

- FIRST, 1mg of atropine, repeat every 3-5 min, up to maximum TOTAL of 3 mg
- If atropine ineffective, transcutaneous pacing and/or dopamine or epinephrine infusion
--> Do not rely on atropine in Mobitz type II 2nd degree or 3rd degree AV block or in pts with 3rd degree AV block with a new wide QRS complex, as these are likely to not respond to atropine

Pts with ACS should be paced at the lowest HR that allows clinical stability; higher HR can worsen ischemia bc HR is a major determinant of myocardial O2 demand. Ischemia, in turn, can precipitate arrhythmias.

The HR takes on clinical significance around 150 bpm and higher because at this point it is more likely attributable to an arrhythmia

- pathophys: heard is either beating too fast resulting in reduced CO (leading to pulm edema, coronary ischemia, and hypotension with reduce end-organ perfusion) and/or beating ineffectively so that coordination between atria and ventricles or the ventricles themselves reduce CO
- S/S: hypotension, altered mental status, S/S shock, ischemic chest discomfort, acute HF
- tx: UNLESS sinus tachy, consider cardioversion with sedation and, if regular narrow complex, consider adenosine

SYNCHRONIZED (lower energy, synchronized to peak of QRS)
- unstable SVT, afib, aflutter, or regular monomorphic tachycardia with pulses
UNSYNCHRONIZED (higher energry, defib "doses"):
- pulseless pt (VF/pVT)
- clinical deterioriation (prearrest), e.g. severe shock or polymorphic VT, when delay in converting rhythm may result in cardiac arrest
- unstable/deteriorating pt when synchronization cannot be immediately accomplished
- when unsure whether monomorphic or polymorphic VT is present in unstable pt

--> if the shock causes VS (theoretical risk), immediately attempt defibrillation

If additional synchronized shock indicated, activate sync mode after delivery of each synchronized shock; most defibrillators default back to unsynchronized mode after each shock to allow for immediate shock if cardioversion produces VF

- O2 saturation monitor
- suction device
- IV line
- intubation equipment

- if monomorphic wide-complex rhythm AND pt unstable, consider adenosine, antiarrhythmic infusion, and expert consultation
- polymorphic wide-complex tachycardia tx with immediate unsynchronized shock
- if narrow QRS (<0.12 sec): unstable pt (hypotension, acute HF, chest discomfort, altered mental status): cardioversion; currently stable: Vagal, then adenosine, then beta blocker or CCB

Avoid AV nodal blocking agents (e.g., adenosine, CCBs, digoxin, and possibly beta blockers) in pts with pre-excitation afib because these drugs may cause a paradoxical increase in the ventricular response

- generally don't give adenosine to pts with astham or COPD, particularly if pts are actively bronchospastic; adenosine may cause bronchospasm

RESPIRATORY DISTRESS
- tachypnea
- increased resp effort (nasal flaring, retraction) or inadequate resp effort (hypoventilation, bradypnea)
- abnormal airway sounds (stridor, wheezing, grunting)
- tachycardia
- pale, cool skin (however, some causes of resp distress, like sepsis, may cause warm, red, and diaphoretic skin)
- changes in LOC/agitation
- use of abd muscles to help breathe
RESPIRATORY FAILURE
- marked tachypnea; bradypnea; apnea
- no resp effort
- poor to abset distal air movement
- tachycardia (early); bradycardia (late)
- cyanosis
- stupor, coma (late)

- typically 6-8 mL/kg maintains normal oxygenation and elimination of CO2
- for adult in resp arrest, provide tidal volume of approx 500-600 mL (6-7 mL/kg) or enough to produce chest rise
--> pts with airway obstruction or poor lung compliance may need higher pressures to produce visible chest rise (may need to bypass bag's pressure-relief valve)

Excessive ventilation can
- increase intrathoracic pressure
- decrease venous return to the heart
- diminsh cardiac output and survival
- may cause cerebral vasoconstriction, reducing blood flow to the brain

- 1 breath q6sec (or 10 breath/min) delivered over 1 sec; typically 500-600 mL or until chest rise
- check pulse about every 2 min, taking between 5-10 sec to check; if no pulse, start CPR

adjust supplemental O2 to maintain
- at least 95% SpO2 in resp distress
- at least 90% for ACS
- 92-98% for post-cardiac arrest care
- 95-98% for stroke pts

- ONLY for use on the unconscious pt; may cause gagging and vomiting in the semiconscious pt; NPAs may be used in the conscious or semiconscious pt
- sizing: place OPA against the side of the face, correct size OPA will align with flange of OPA at the corner of the mouth and tip at the angle of the mandible
- insert with OPA upside down or at 90 degree then rotate to correct position after passing through the oral cavity and approaching the posterior wall of the pharynx (the goal of this is to curve the device around the tongue so that you don't inadvertently push the tongue back into the pharynx rather than pull it forward)

Ideally, CCF (chest comrpession fraction), or the proportion of time during cardiac arrest resuscitation when the rescuer is performing chest compressions, should be greater than 80%
- to calculate: CCF = actual chest compression time divided by total code time

Epinephrine hydrochloride is used in resuscitation primarily for its alpha-adrenergic effets (i.e., vasoconstriction). Vasoconstriction increases cerebral and coronary blood flow during CPR by increasing MAP and aortic diastolic pressure.

- amiodarone or lidocaine is used for pts in VF/pVT that is unresponsive to defibrillation (may be particularly useful for pts with witnessed arrest, for whome time to drug administration may be shorter)
--> amiodarone 300 mg bolus IV/IO then consider 1 additional 150 mg
--> lidocaine 1-1.5 mg/kg first dose, the 0.5-0.75 mg/kg at 5-10 min intervals to a max dose of 3 mg/kg
- Mg sulfate for torsades de pointes; 1-2 g IV/IO diluted in 10 mL (e.g., D5W, NS); typically given over 20 min