Case 84 - CPR Flashcards
What are components of high quality chest compressions?
- “push hard and push fast”
- adeqate rate: > 100 compressions per min
- adequate depth: > 2 inches
- full chest recoil
- minimize interrupations in chest compresions
- avoid excess ventilation
How can you determine that you have adequate chest compressions?
- EtCO2 > 10 mm Hg
- diastolic blood pressure > 20 mm Hg (via A line)
why should excess ventilation be avoided during CPR?
- decrease CBF secondary to resp alkalosis
- increase intrathoracic pressure impedes venous return –> decrease CO during chest compression
- increased gastric inflation –> regurg and aspiration
How do chest compressions produce a CO?
thoacic pump theory:
- forward blood flow is achieved by phasic changes in intrathoracic pressure produced by chest compression
-
downward phase of chest compression:
- Positive intrathorac pressure created –> proples blood out of chest into aorta and extrathoracic vessels
-
upward phase of chest compression
- negative intrathoracic pressure –> inc venous return
You are called for a code, at bedside you have grade 2 view and intubate the patient. However, you do not see ETCO2. What are reasons for this, and how can you confirm tube position?
Reasons for no ETCO2 with proper ETT placement
-
ETCO2 can be associated with low blood flow states, decreased gas exchage at pulmonary alevoli to capillary surface :
- inadequate chest compression
- PE
- severe airway obstruction (status asthmaticus)
- pulmonary edema
Confirm tube positoin - visualize ETT through cords
How does epinephrine work in CPR?
- Epi = alpha adrenergic effects –> increase arterial presure and improves myocardial and cerebral perfusion pressure
What is the indication for vasopressin in CPR?
Vasopressin
- aka ADH
- potent vasoconstrictor
- vasoconstrictive effect increases blood flow to brain and heart during CPR
- mediated by V1 receptors
- use vasopressin 40 U in replacement of 1st or 2nd dose of EPI during CPR
what are the detremential effects of sodium bicarb admin during CPR? When should you give sodium bicarb during CPR?
Detrimental effects:
1) intracellular acidosis
- HCO3 + H -> h2Co3 -> Co2 + H2O
- bicarb will produce increase Co2 in blood, which will freely diffuse into intracellular space –> intracellular acidosis
2) O2-Hgb curve to left
* extracellular alkalosis will shift O2-hgb dissociation curve to the left –> reduce O2 unloading to tissues
reasons to give NaCo3
- severe hyperkalemia
- pre-existing metabolic acidosis
when should calcium be given during CPR?
- hyperkalemia
- document hypocalcemia
- CCB overdose
how is vfib/pulseless VT managed?
Call for help
initiate ACLS protocol
Get the debrillator
perform CPR in the meantime
- defib pads placeed, shock biphasic 120-200J (1st shock)
- resume CPR
- look for IV/IO access
- asses rhythm, shock as indicated (2nd shock)
- continue CPR
- admin 1 mg of Epi or 40 U of vasopressin
- epi q 3-5 min
- 40 U vasopressin replace 1st or 2nd dose of EPI
- asses rhythm, shock as indicated (3rd shock)
- continue CPR
- admin amio 300 mg
- 2nd dose of amio is 150 mg
- if hypomagnesia or torsades –> MgSo4 2mg IV
- 5 H’s & 5 T’s
How is symptomatic bardycardia managed?
- bradycardia is HR < 60 BPM
- most comon cause of bradycardia is hypoxia
Management
-
Evaluate respiratory system:
- patency of airway, signs of increased work of breathing, SaO2
- supplemental oxygen
- EKG
- IV
-
HD stable or unstable
- unstable = hypotension, AMS, heart faiulre, shock, angina
-
Atropine
- 0.5 mg IV up to 3 mg
- ineffective for heart tx patients (denervation)
- use cautiously in ACS or MI pts (will increase O2 consumption and exacerbate injury)
-
transcutaenous pacing
- 80 bpm
-
B-adrengic therapy
- Dopamine - 2 to 20 mcg/kg/min
- Epi - 2-10 mcg/min
Patient has unstable SVT, how will you manage them?
- tachycardia = HR > 100bpm
SVT
- HR > 150
- p buried within qrs complexes
- reguar R-R interval
Unstable SVT
-
signs of unstability:
- hypotension, acute AMS, shock, angina, CHF
-
Goal - immediate synchronized electrical cardioversion (biphasic doses)
- narrow complex & regular: 50 - 100 J
- narrow complex & irregul: 120 - 200 J
- Wide complex & regular: 100 J
- wide complex & irregular: Unsynchronized 120 - 200 J
How do you tx stable SVT with narrow QRS?
- asses QRS width; narrow = < 0.12 sec QRS
narrow Regular
-
First: valva manuevers or Adenosine
- 6 mg rapid bolus, wait 2 min, give 12 mg
- use adenosine cautiously in asthmatics and WPW
-
second: pharmacologic agents
-
BB - esmolol
- 0.5 mg/IV bolues + infusion 50 mcg/kg/min
-
BB - metoprolol -
- 1 - 2.5mg IV bolus initially, repeat dose or double dose, max 15 mg
-
CCB - diltiazem -
- 5-10mg IV over 2 min
-
antiarrhythmic - Amiodarone
- 150mg bolus over 10 min + infusion of 1 mg/min for 6 hours
-
BB - esmolol
how do you tx stable SVT with narrow complex & irregular rhythm (ex A fib)?
- stable or unstable
- if unstable, sync cardiovert 120 - 200 J biphasic
- unstable = hypotension, AMS, angina, CHF, shock
- QRS < 0.12 sec, regular or irregular rhythm
regular complex and irregular rhythm (afib):
- goals - control rate, rhythm, and provide a/c
- electrical cardioversion
- onset of afib ( less or greather than 48 hrs)
- > 48 hrs - use TEE to assess for thrombi in LA
- if thrombi present - control rate, A/C for 3 weeks, electrical cardiovert afte
Pharmacologic therapy
BB - esmolol
- 0.5 mg/IV bolues + infusion 50 mcg/kg/min
BB - metoprolol -
- 1 - 2.5mg IV bolus initially, repeat dose or double dose, max 15 mg
CCB - diltiazem -
- 5-10mg IV over 2 min
DIgoxin (if EF < 35%)
antiarrhythmic - Amiodarone
- 150mg bolus over 10 min + infusion of 1 mg/min for 6 hours
patient has wide complex & regular rhythm, how would you tx that. Suppose he has wide complex and irregular rhythm (polymoprhic VT), how would you tx that?
Wide complex + regular rhythm (monomorphic)
- Adenosine 6 mg IV push, wait 2 min, 12 mg IV push if necessary
- amiodarone bolus + infusion
wide complex + irregular rhythm (polymorphic)
- immediate UNSYNC DEFIB 120 - 200 J
