ECPR til refraktært hjertestop

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scanFOAM

Thomas Birkelund at circulation session of #cphcc2018. Rest of talks: https://scanfoam.org/cphcc18/ http://cphcc.dk/

Health & Medicine

ECPR til refraktært hjertestop
Thomas Birkelund
Intensiv &
Præhospitalet
AUH No COI

ALS?
Hjerte
stop
Refraktært
Hjertestop
Død
ROSC Center

ECPR
Hjerte
stop
Refraktært
Hjertestop
Død
ROSC Center
Center/ECPR

ABCDE
A = Anamnese
B = Basic Stuff
C = Clever stuff
D = Diesel
E = ECPR

Stay and play!
Årsag ?
Anamnese
“Objektiv US”
H & T
Ultralyd?

Tænk efter 10 min!
Klinisk meningsfulde
interventioner!
Hjertestop er IKKE en
diagnose
ECPR mulighed (6%)
Resuscitation. 2015 Jun;91:131-6

Scoop and run play!
Optimer:
Intuber
Mekanisk CPR
DC – stød
Medicin

Respirator
Manuel ventilation
Volumenkontrol
CPAP
Pressure support
Passiv oxygenering
Circulation. 2002;106:373-378
Resuscitation and Emergency Medicine (2016) 24:67

Adrenalin
J Am Coll Cardiol 2014;64:2360–7
Frankrig: Max 5 mg.

På vej til center:
Arterietryk
Kapnografi
Kontakt til ECPR-team

Komplikationer under ECPR
Neth Heart J (2018) 26:58-66

ECPR outcome 2015-17
30 måneder (79 ptt):
22 overlever i 6 måneder (27%)
20 CPC 1+2
2 CPC 3
15 mulige incarcerede
5 donationer

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The use of adrenaline in cardiac arrest resuscitation has been advocated since the 1960s. Laboratory studies and anecdotal experience showed improved rates of return of spontaneous circulation (ROSC) with the use of adrenaline at a dosage of approximately 0.01 mg/kg. This led to the widespread adoption of adrenaline administration during cardiac arrest into every resuscitation guideline for decades to come. Extensive laboratory studies characterized the beneficial physiological effects of adrenaline during cardiac arrest and closed-chest cardiopulmonary resuscitation (CC-CPR). Adrenaline administered during CC-CPR results in peripheral arterial vasoconstriction that raises the aortic pressure, particularly during the relaxation phase of CC-CPR. This increase in aortic pressure results in an increased aortic to right atrial pressure gradient that drives blood flow to the myocardium during CC-CPR. This pressure gradient is known as the coronary perfusion pressure (CPP) and has been shown to correlate with ROSC in both laboratory investigations and clinical studies. During the 1990s, the use of “high-dose” adrenaline showed increased rates of ROSC compared to “standard-dose” adrenaline. However, it was subsequently recognized that larger doses of adrenaline did not result in improved survival. Furthermore, questions have been raised as to whether or not “standard-dose” adrenaline improves survival from cardiac arrest. Recent meta-analyses have raised serious questions about the value of adrenaline, showing a benefit for achieving ROSC but no clear evidence of improved long-term survival. Controlled clinical trials to address this question are now underway. However, there is another important issue that needs to be addressed: the “route” of administration. With the growing interest in endovascular resuscitation, the use of intra-aortic adrenaline titration offers a means of rapidly and effectively delivering adrenaline to peripheral arterial effector sites while providing arterial pressure and CPP monitoring to guide titration of adrenaline doses to achieve an optimal hemodynamic effects while avoiding excessive adrenaline doses. To enable screen reader support, press shortcut Ctrl+Alt+Z. To learn about keyboard shortcuts, press shortcut Ctrl+slash.

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Dr. Faiza delivers an insightful lecture on the distinguishing characteristics of skeletal, smooth, and cardiac muscles, offering a comprehensive understanding of their histology, physiological anatomy, electrophysiological properties, and contractile mechanisms. Through meticulous tabulation and comparison, she aims to equip learners with a detailed comprehension of the unique features and functionalities of each muscle type. Beginning with a detailed exploration of histological differences, Dr. Faiza outlines key distinctions such as multinucleation in skeletal muscle, mononucleation in smooth and cardiac muscles, and the presence of striations in skeletal and cardiac muscles. She meticulously elucidates the structural arrangement of each muscle type, highlighting their cellular morphology and organization within tissues. Transitioning to physiological anatomy, Dr. Faiza navigates through various aspects including innervation, level of control, initiation of contraction, and modification by hormones. By delineating the role of the somatic nervous system in skeletal muscle control, and contrasting it with the autonomic nervous system's influence on smooth and cardiac muscles, she offers a nuanced understanding of neural regulation in muscle physiology. Furthermore, Dr. Faiza delves into electrophysiological properties, elucidating the mechanisms underlying action potential generation, duration, and ionic basis in each muscle type. Through insightful analysis, she reveals how differences in action potential characteristics contribute to variations in muscle contraction speed, duration, and resistance to fatigue. Finally, Dr. Faiza meticulously examines the contractile mechanisms of skeletal, smooth, and cardiac muscles, shedding light on the sliding filament theory, mechanisms of calcium action, and speed of contraction. By comprehensively comparing these mechanisms, she provides learners with a deep understanding of the intricate processes governing muscle contraction and function. Through engaging presentation and meticulous analysis, Dr. Faiza's lecture serves as a valuable resource for students seeking a thorough understanding of the fundamental differences between skeletal, smooth, and cardiac muscles.

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