Download Free Medical CBP-Cardiac Arrest PowerPoint Presentation

CBP-Cardiac Arrest PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical PowerPoint presentation titled "CBP: Cardiac Arrest".

This medical PowerPoint presentation is a case presentation on Cardiac arrest during cardiopulmonary bypass CPB.

Cardiopulmonary bypass (CPB) is a technique used in cardiac surgery to temporarily replace the function of the heart and lungs during the surgery. It involves diverting the patients blood through a machine that oxygenates it and removes carbon dioxide, before returning it to the patients body.

Cardiac arrest can occur during CPB due to various reasons such as air embolism, hypothermia, electrolyte imbalances, and technical errors. If cardiac arrest occurs during CPB, the surgical team must act quickly to restore circulation and prevent permanent brain damage or death.

The first step is to stop the CPB machine and identify the cause of the cardiac arrest. The surgical team will then perform cardiopulmonary resuscitation (CPR) and may administer medications such as epinephrine to help restore the patients heartbeat. If necessary, the surgeon may open the chest to access the heart and perform internal cardiac massage.

It is important to note that while CPB can be a life-saving technique in cardiac surgery, it also carries risks, including the risk of cardiac arrest. The surgical team takes extensive precautions to minimize these risks, but complications can still occur. Patients should discuss the potential risks and benefits of CPB with their healthcare provider before undergoing cardiac surgery.

Tags : Cardiac arrest, cardiopulmonary bypass, CPB, cardiac surgery, cardiology

Published on : Mar 17, 2023 | Views : 846 | Downloads : 0

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

CBP: Cardiac Arrest
Slide 2-

Case Presentation A 55 year old business man collapses at work. This is witnessed by his colleagues who find him pulseless. They initiate CPR and call 911. EMS arrive 5 minutes later. They confirm the pulseless state and place the patient on a monitor; he is in V. Fib. Standard ACLS protocols are initiated; the patient is intubated and transported to the closest ED. The patient arrives at the ED 7 minutes later. He has received 2 doses of Epinephrine and one dose of Atropine. He has received 2 shocks and is currently in PEA arrest.
Slide 3-

In the ERP confirms ETT placement, the rhythm of PEA, and performs a quick bedside ECHO, all the while continuing with CPR. The ECHO shows cardiac motion. The patient is given another dose of Epinephrine and Atropine. By 6 minutes of his arrival, he is noted to have Return of Spontaneous Circulation and to have reverted to NSR. ICU is consulted
Slide 4-

Vital signs: HR – 112, RR – 6/poor effort, BP 65/40 (MAP 48), 36.5 Rectal Temp, Glucose 17.8, Sat’n 100%. Quick exam reveals: A: ETT in place. B: GBS x2. +ve ETCO2 Capnography. C: As above. N HS. D: GCS of 3T, absent gag/corneal/papillary response. E: Nothing obvious. And no calf edema. Past medical history reveals a 30 pack-year smoking history. He is on no meds and has no known drug allergies. He is known to travel abroad frequently with his work.
Slide 5-

Question 1 Please define Post-Cardiac Arrest Syndrome and its 4 pathophysiologic components. (Erik)
Slide 6-

Definition Post-cardiac arrest syndrome is a unique and complex combination of pathophysiological processes, which include post-cardiac arrest brain injury, post-cardiac arrest myocardial dysfunction, and systemic ischemia/reperfusion response. This state is often complicated by a fourth component: 4. the unresolved pathological process that caused the cardiac arrest.
Slide 7-

Phases – for Therapy & for Science The immediate post-arrest phase could be defined as the first 20 minutes after ROSC. The early post-arrest phase could be defined as the period between 20 minutes and 6 to 12 hours after ROSC, when early interventions might be most effective. An intermediate phase might be between 6 to 12 hours and 72 hours, when injury pathways are still active and aggressive treatment is typically instituted. Finally, a period beyond 3 days could be considered the recovery phase, when prognostication becomes more reliable and ultimate outcomes are more predictable.
Slide 8-

Pathophysiology The 4 key components of post-cardiac arrest syndrome are: post-cardiac arrest brain injury, post-cardiac arrest myocardial dysfunction, systemic ischemia/reperfusion response, and persistent precipitating pathology.
Slide 9-

Pathophysiology The unique features of post-cardiac arrest pathophysiology are often superimposed on the disease or injury that caused the cardiac arrest, as well as underlying comorbidities. Therapies that focus on individual organs may compromise other injured organ systems. The severity of these disorders after ROSC is not uniform and will vary in individual patients based on the severity of the ischemic insult, the cause of cardiac arrest, and the patient’s pre-arrest state of health.
Slide 10-

ppt slide no 10 content not found
Slide 11-

Foundation on which to grow… In a study of dogs with induced cardiac arrest… In a single observational human study… Biochemical and neurohormonal models suggest… A growing body of evidence… These findings suggest, in theory, that… These findings do not rule out the potential effect of… Limited evidence is available to guide…
Slide 12-

Forrest through the trees
Slide 13-

Fundamentals Who remembers 5:1, 15:2, 30:2, 10:1, vs continuous? (AHA, ACC, ILCOR) ETT vs supraglottic device? (AHA, ACC, ILCOR) BLS plus AED vs ACLS (OPALS, PAD) Push hard, push fast, push often! (ROC-BC)
Slide 14-

Question 2 How do you treat Post-Cardiac Arrest Syndrome. (Federico)
Slide 15-

Early HD optimization No evidence based guidelines Suggestion is to have a similar approach as EGDT for Sepsis MAP goals undefined Loss of Cerebral Autoregulation CPP dependent on MAP ICP generally not elevated
Slide 16-

MAP Goals >65, <90 Mixed venous gases Venous Hyperoxia Falsely elevated levels due to poor tissue extraction related to epi use and mitochondrial failure Follow urine output (careful in hypothermia) Follow lactates (need to follow trends)
Slide 17-

Avoid hyperoxia Ptl for increased free radical production PaO2 goals of 92 – 96% Aim for normocarbia Volume resuscitate Consider intropes/vasopressors
Slide 18-

Treat for ACS Noemie Hypothermia Ibrahim Treat seizures Increase cerebral metabolism No Evidence for prophylaxis Myoclonus Clonazepam
Slide 19-

Treat hyperglycemia No evidence for Neuroprotective medications Adrenal dysfunction Renal failure Infection More prone to aspiration pneumonia
Slide 20-

Question 3 Should we cool this patient? Who do we cool, what parameters do we use, what are the complications of hypothermia therapy? What if the original documented rhythm was PEA? (Ibrahim)
Slide 21-

Who should be cooled? Out-of-hospital VF/PVT Arrest RCTs:HACA and Bernard et al (NEJM, 2002): significant survival to d/c and neuro recovery (NNT 6 in a meta-analysis) In-hospital VF Arrests Small subset within HACA: favorable survival Out-of-hospital all-rhythms, or non-VF 4 retrospective studies for all (Oddo 2006, Scott 2006, Arrich 2007, Hay 2008), one retrospective and 2 observational for non-VF: possible benefit Pyrexia within 72 Hr (>37C--> poor neuro outcomes), all patients
Slide 22-

Bernard, 2002, NEJM
Slide 23-

HACA, 2002, NEJM
Slide 24-

What are the parameters of cooling protocol? Target core temp: 33C, or 32-34C Onset: variable, ASAP (2-8 Hr, up to 24Hr) Duration: 12-24 Hr Further data required NRCPR, HACA-R
Slide 25-

Complications of TH Technical: Shivering, use of ongoing sedation and NMB, to prevent shivering (with 30% dec clearance with T=34C), fluctuations of temp HD: inc SVR, dec COP, arrhythmias (esp brady) Diuresis, hypovolemia, dec K, Ca, Mg, PO4 --> arrhythmia MgSO4: NMDA blocker, so dec shivering, vasodilator, so facilitate cooling induction, antiarrhythmic, and ? additive Neuroprotective (animal data)
Slide 26-

Impaired glucose tolerance (dec insulin level and sensitivity) Coagulopathy Lower immunity--> infections Higher pneumonias in TH group in HACA, but NS
Slide 27-

Should we cool this patient? Yes! Out-of-hospital VF arrest
Slide 28-

Question 4 His wife has just arrived with his 3 kids (16, 15, and 9 years old). They want to know what his prognosis is. What do you tell them and how do you prognosticate patients post arrest? Please discuss clinical and lab findings and imaging modalities. Would things be looked at differently if he was cooled? (Neil)
Slide 29-

. What do you tell them and how do you prognosticate patients post arrest? Timing What is a “poor outcome”? Prognostication Clinical EEG Biomarkers Imaging
Slide 30-

Timing Very difficult to prognosticate in the first 24 hours Most evidence is derived on testing at 72 hours Therapeutic hypothermia changes the timeline
Slide 31-

What is a poor outcome?
Slide 32-

What is a poor outcome? Poor outcome is defined as death, unconsciousness after one month, or unconsciousness or severe disability after six months.
Slide 33-

Clinical signs Absence of pupillary light reflexes 100% specificity in meta analysis LR+ 10.5 (CI 2.1-52.4) Absence of motor response to pain 100% specificity in meta analysis LR+ 16.8 (CI 3.4 – 84.1) Myoclonic status epilepticus Can be predictive early Much worse than SE
Slide 34-

Clinical Signs Which are not good prognositcators Age Sex Cause of arrest Type of arrhythmia Total arrest time Duration of CPR
Slide 35-

ppt slide no 35 content not found
Slide 36-

EEG Overall prognostication ability is not strong Variety of studies have looked into it Lack of a standardized classification system Concerning features Burst suppression Nonreactive alpha and theta patterns Generalized periodic complexes
Slide 37-

SSEP’s Tests integrity of the neuronal pathways from peripheral nerve, spinal cord, brainstem, and cerebral cortex
Slide 38-

N20 Best studied waveform Robust as it is not strongly influence by meds and metabolic derangements LR+ 12 (CI 5.3-27.6)
Slide 39-

ppt slide no 39 content not found
Slide 40-

Biomarkers Dead brain releases biomarkers 3 have been “well” studied Neuron specific enolase (NSE) S-100 Creatinine kinase BB isoenzyme (CK-BB)
Slide 41-

ppt slide no 41 content not found
Slide 42-

Imaging Although not strong enough to prognosticate reliably, a bad scan is a bad scan Problem lies in that a good scan may not be a good scan
Slide 43-

ppt slide no 43 content not found
Slide 44-

ppt slide no 44 content not found
Slide 45-

Question 5 His EKG shows normal sinus rhythm with non-specific changes. Should he go to the cath lab? If so, what are the recommendations for cath post cardiac arrest? If he arrested again, would you thrombolyse him? What is the etiology of the vast majority of cardiac arrests? (Noamie)
Slide 46-

Questions His EKG shows normal sinus rhythm with non-specific changes. Should he go to the cath lab? If so, what are the recommendations for cath post cardiac arrest? If he arrested again, would you thrombolyse him? What is the etiology of the vast majority of cardiac arrests?
Slide 47-

Etiology of cardiac arrests
Slide 48-

65-70 % 10% 5-10% 15 to 35%
Slide 49-

Etiology of Sudden Cardiac Death Age < 20: Myocarditis (22%), HCM (22%) and conduction system abnormalities (13%) Age 20-29: CAD (24%), myocarditis (22%) and HCM (13%). Age 29-39: CAD (58%), myocarditis (11%). Am J Cardiol 1991;689(13):1388-1392
Slide 50-

Should he go to the cath lab? Yes Even if no evidence of an ACS, need to exclude stable/chronic CAD Sudden cardiac arrest may be first indication of CAD But, does he need it right now?
Slide 51-

1994-1998 Pt post cardiac arrest btw 30-75 Immediate cath if no obvious non-cardiac cause 1st rhythm recorded: 93% VF/VT 84% had 0 or 1 cardiac RF 71% had clinically significant CAD NEJM 1997;336:1629-1633
Slide 52-

poor predictive value of CP and ECG changes for coronary-artery occlusion.
Slide 53-

Recommendations for cath post cardiac arrest
Slide 54-

Recommendations Recommendations for Coronary Angiography in Patients With Known or Suspected CAD Who Are Currently Asymptomatic or Have Stable Angina. Class I: Patients who have been successfully resuscitated from sudden cardiac death or have sustained (>30 s) monomorphic ventricular tachycardia or nonsustained (<30 s) polymorphic ventricular tachycardia. (Level of Evidence: B)
Slide 55-

If he arrested again, would you thrombolyse him?
Slide 56-

ppt slide no 56 content not found
Slide 57-

TROICA (NEJM 2008) Tenecteplase vs placebo Stopped early for futility Lancet 2001 rt-PA vs placebo Improved ROSC but no difference in 24HR survival or survival to discharge AJC 2006 No statistically significant benefit
Slide 58-

Treatment recommendation: “Fibrinolysis should be considered in adult patients with cardiac arrest with proven or suspected pulmonary embolism. There are insufficient data to support or refute the routine use of fibrinolysis in cardiac arrest from other causes.”
Slide 59-

Question 6 Patient arrests again and family wants EVERYTHING done. His wife is a cardiac nurse and asks if ECMO is an option. What do you tell her?
Slide 60-

ECMO in cardiac arrest = Extracorporeal Life Support (ECLS) Few small, observational and retrospective studies (5 studies: 3 adult, 2 pediatric) All in hospital arrests
Slide 61-

2005 ACLS guidelines, consider in: In hospital patient Brief pulseless period (rapid ECLS response teams) Reversible causes (OD’s, revascularization/heart transplant) Realistically, not feasible for every patient Modality of choice for severe hypothermia in cardiopulmonary arrest
Slide 62-

Question 7 Assuming he survives to discharge, should he get an ICD implanted? (Marios)
Slide 63-

Question 8 Patient does well and eventually gets discharged to a ward bed. However, he has another cardiac arrest. Are there any differences between in-hospital and out-of-hospital cardiac arrest? What can be done to improve the outcome of in hospital cardiac arrest? (Marios)
Slide 64-

Question 7: Indications for ICD implantation post-arrest
Slide 65-

Indications for ICD 2008 ACC/AHA/HRS guidelines state that most survivors of VT/VF arrest that are not due to reversible causes should be offered an ICD. Reversible causes: Polymorphic VT/VF clearly due to ischemia that is amenable to revascularization. Polymorphic VT in the setting of reversible QT prolongation Exceptions: Wolff-Parkinson-White syndrome – tx is ablation Fulminant myocarditis in which LVAD will be used as a bridge to recovery Drug-induced arrhythmias Electrolyte abnormalities (rarely an isolated cause however) Epstein, AE, DiMarco, JP, Ellenbogen, KA, et al. ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines Circulation 2008; 117:e350.
Slide 66-

Question 8a: Are there any differences between in-hospital and out-of-hospital cardiac arrest? VS
Slide 67-

Differences between in-hospital and out-of-hospital cardiac arrests Initial rhythm VT/VF is the first monitored rhythm in only 15-23% of in-hospital cardiac arrests (IHCAs) In out-of-hospital arrests (OHCAs) VF/VT occur in 45% of cases IHCAs more likely to be due to hypoxemia and hypotension  more likely to cause PEA or asystole OHCAs more often precipitated by ischemia which more commonly leads to VT/VF Sandroni C, et al. In-hospital cardiac arrest: incidence, prognosis and possible measures to improve survival. Intensive Care Medicine (2007) 33:237-245 Dichtwald S, et al. Improving the outcome of in-hospital cardiac arrest: the importance of being earnest. Seminars in Cardiothoracic and Vascular Anesthesia (2009) 13(1):19-30
Slide 68-

Question 8b: What can be done to improve the outcome of in hospital cardiac arrest?
Slide 69-

“Survival” post in-hospital cardiac arrests Between 25% and 67% of successfully resuscitated patients die within 24h of ROSC Survival to discharge ranges from 0% to 28%%, with major studies reporting ~ 20% survival to discharge rate. 14% to 47% of patients discharged die within one year In other words, IHCA is a bad prognostic sign. Sandroni C, et al. In-hospital cardiac arrest: incidence, prognosis and possible measures to improve survival. Intensive Care Medicine (2007) 33:237-245
Slide 70-

Strategies to improve outcomes MET teams: Initially showed positive effects in reducing both cardiac arrests and in-hospital mortality Many of these studies were of low quality A recent meta-analysis showed no effect on mortality despite a reduction in cardiac arrests (? ICU arrests vs more patients being made DNR by MET team) Sandroni C, et al. In-hospital cardiac arrest: incidence, prognosis and possible measures to improve survival. Intensive Care Medicine (2007) 33:237-245
Slide 71-

Strategies to improve outcomes DNR status: By addressing level of care, CPR may be targeted to those who are more likely to benefit from it. This would be expected to improve survival rates of in hospital arrests. No studies have looked at this. Sandroni C, et al. In-hospital cardiac arrest: incidence, prognosis and possible measures to improve survival. Intensive Care Medicine (2007) 33:237-245
Slide 72-

Strategies to improve outcomes ACLS training Chest compression rate and depth inadequate in a third of codes Lower immediate survival rate in patients receiving compression rates < 80/min Immediate survival rate nearly 4 times higher when resuscitated by ALS-trained vs non-ALS-trained nurse. Immediate survival better in hospitals after completion of a resuscitation training program. Sandroni C, et al. In-hospital cardiac arrest: incidence, prognosis and possible measures to improve survival. Intensive Care Medicine (2007) 33:237-245
Slide 73-

Strategies to improve outcomes CPR Adjuncts: Active Compression Decompression CPR Impedance Threshold Valve Though promising animal and physiologic date, conclusive outcome data is still pending. Dichtwald S, et al. Improving the outcome of in-hospital cardiac arrest: the importance of being earnest. Seminars in Cardiothoracic and Vascular Anesthesia (2009) 13(1):19-30
Slide 74-

Active Compression/Decompression CPR Frascone RJ, et al. Combination of active compression decompression cardiopulmonary resuscitation and the inspiratory impedance threshold device: state of the art. Curr Opin Crit Care.(2004): 10:193–201
Slide 75-

Impedance threshold valve Lurie K, Zielinski T, McKnite S, et al. Improving the efficiency of cardiopul- monary resuscitation with an inspiratory impedance threshold valve. Crit Care Med 2000; 28:N207–N209.
Slide 76-

Hemodynamic effects of devices Lurie K, Zielinski T, McKnite S, et al. Improving the efficiency of cardiopul- monary resuscitation with an inspiratory impedance threshold valve. Crit Care Med 2000; 28:N207–N209.
Slide 77-

Strategies to improve outcomes Early defibrillation Response time of code teams may be unacceptably long in remote areas of hospitals (up to 6 minutes in larger hospitals) One before-after study showed an improved survival from VT/VF arrest from 2.2% to 15.6% after implementation of an AED program Randomized controlled trials are needed Sandroni C, et al. In-hospital cardiac arrest: incidence, prognosis and possible measures to improve survival. Intensive Care Medicine (2007) 33:237-245
Slide 78-

Strategies to improve outcomes Post-resuscitation care Therapeutic hypothermia As opposed to out-of-hospital arrests, in-hospital cardiac arrests are more often non-VT/VF. Neurological injury less often a cause of death in IHCA patients Impact of therapeutic hypothermia may therefore be reduced for in-hospital cardiac arrests Sandroni C, et al. In-hospital cardiac arrest: incidence, prognosis and possible measures to improve survival. Intensive Care Medicine (2007) 33:237-245
Slide 79-

The End