Physiology Directed CPR
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Physiology Directed CPR
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Physiology Directed CPR
- 1. Physiology directed CPR Dr Kerry Gomes 16/8/2018
- 3. Cardiac Arrest is NOT a diagnosis It’s the final pathway for all pathologies leading to death Important to consider underlying pathologies - ?reversible causes Presumed cardiac Structural – CAD, cardiomyopathies, WPW, genetic Electrical – long QT, Brugada Informed suspicion Electrolyte, toxic, metabolic, hypo/hyperthermia Mechanical interference – PE, tamponade Aortic dissection Respiratory arrest
- 4. Physiology of circulation during closed chest compressions CCC and recoil of chest generate a proportion of cardiac output by two means – Cardiac pump model Thoracic pump model Cardiac output Severely depressed during CPR (10-33% prearrest values in exp. animals) Majority directed to organs above the diaphragm brain blood flow 50-90% Cardiac blood flow 20-50% Lower extremeties and abdominal visera <5% Flow to brain and heart improved by vasopressors
- 5. Assessing circulation adequacy during CPR Coronary Perfusion Occurs primarily during diastolic phase Myocardial blood flow is optimum during CCC when aortic diastolic pressure >40mmHg Vascular pressures below critical levels associated with poor outcomes Exhaled CO2 Excellent non-invasive indicator of effective resus After intubation CO2 levels are primarily dependant on blood flow During CPR if blood flow starts to increase, more alveoli are perfused and etCO2 levels rise Spontaneous circulation etCO2 value < 40mmHg etCO2 corresponds with coronary perfusion pressure, cardiac output and survival
- 7. Studies Patient-centric blood pressure-targeted cardiopulmonary resuscitation improves survival from cardiac arrest. Sutton et al. Am J Respir Crit Care Med. 2014 Dec 1;190(11):1255-62 20 female 3-month-old swine After 7 minutes of asphyxia (ETT clamped), VF was induced randomly received 10 minutes period of CPR before defibrillation blood pressure-targeted care consisting of titration of compression depth to a systolic blood pressure of 100 mm Hg and vasopressors to a coronary perfusion pressure greater than 20 mm Hg (BP care) American Heart Association Guideline care consisting of depth of 51 mm with standard advanced cardiac life support epinephrine dosing (Guideline care). The 24-hour survival was higher in the BP care group (8 of 10) compared with Guideline care (0 of 10); P = 0.001. Coronary perfusion pressure was higher in the BP care group (+8.5 mm Hg; vs 3.9-13.0 mm Hg; P < 0.01) Blood pressure-targeted CPR improves 24-hour survival compared with optimal American Heart Association care in a porcine model of asphyxia-associated VF cardiac arrest.
- 8. Studies A quantitative comparison of physiologic indicators of cardiopulmonary resuscitation quality: Diastolic blood pressure versus end-tidal carbon dioxide R.W. Morgan et al. Resuscitation 104 (2016) 6–11 Two models of cardiac arrest (primary ventricular fibrillation [VF] and asphyxia-associated VF) 3-month old swine received either standard AHA guideline-based CPR or patient-centric, BP-guided CPR. Mean values of DBP and ETCO2 in the final 2 min before the first defibrillation attempt were compared 60 animals, 37 (61.7%) survived to 45 min. DBP was higher in survivors than in non-survivors (40.6 ± 1.8 mmHg vs. 25.9 ± 2.4 mmHg; p < 0.001) ETCO2 was not different (30.0 ± 1.5 mmHg vs. 32.5 ± 1.8 mmHg; p = 0.30 In both primary and asphyxia-associated VF porcine models of cardiac arrest, DBP discriminates survivors from non-survivors better than ETCO2. Failure to attain a DBP >34 mmHg during CPR is highly predictive of non-survival.
- 9. ABP and CVP Supine CVP similar to pressures in femoral artery In supine patient arterial BP ≡ CVP Femoral artery cannulation Continuous pressure monitoring Access to ABGs Direct feedback from the intraarterial pressure waveform Improved CCC technique
- 10. Assess HD goals CVP <10mmHG Rapid fluid bolus thinking is that CVP <10 = volume down, so giving volume improves venous return Interpediance threshold device / pulmonary vasodilator Study by fire department – gave 2L crystalloid to arrest pt = florid pulm oedema CVP >20mmHG Consider echo to evaluate possible cause PE -> tPA PTx/effusion -> drain it Sepsis -> inotropes
- 11. Assess HD goals Diastolic BP <35-40mmHg Consider more frequent adrenaline or adrenaline infusion Consider vasopressin Systolic BP <100mmHg Optimise hand position - by improving impulse -> get better sBP on ejection Use echo to check Change depth and rate increased depth leads to increased ejection and higher sBP Increased rate to 130, but may inversely decrease depth
- 12. “next cycle” Assess vent and O2 (if HD goals met) ABGs If pH <7.2, paO2 < 70 - > increase vent rate 50% (8 -> 16/18) Does VBG represent venous pooling Focusing on oxygenation Current trail doing ABG and VBG – ABG better thus far NIRS – near infrared spectroscopy (pulse Ox) If >50% and paO2 >200 -> decrease FiO2 50%
Editor's Notes
- In a recent emcrit podcast Scott had discussion with Dr Sutton (a paediatric intensivist and researcher), about physiology directed CPR. So today we will refresh ourselves with the physiology of CPR and then look at the suggestions made in the podcast and whether we can incorporate them into our CPR efforts.
- Current algorithm is “one fits all” and is very much resuscitator orientated. Current training focuses on a uniformed approach to resus care that doesn’t incorporate an individualised response to resus efforts. It assumes all cardiac arrest victims can be treated with a uniform chest compression depth and standardised interval administration of vasopressor drugs. This design is important for easy of training especially for all the out of hospital arrests, but can skilled in-hospital teams be trained to tailor resus. efforts to the individual patients physiology.
- We already tailor some aspects of the resus in so much as to seek and treat any reversible causes. The loved T’s and H’s. Most common cause is coronary atherosclerosis *Cardiomyopaties – dilated, hyperthrophic* *Genetic- valve, congenital, ion-channel abnormality* *Resp – asthma, drowning*
- While T’s and H’s are important the main focus today is on what’s actually happening during CPR. What is the physiology of the circulation. We need to consider the cardiac and thoracic pumps – can someone tell me… Cardiac – direct compression b/w sternum and vertebral bodies squeezes blood out of heart. Fresh blood in during recoil. Thoracic – thoracic pressure changes themselves responsible for blood flow being generated during CCC. *flow to rest of body below diaphragm unchanged or decreased*
- For successful resus you need a myocardial blood flow of 15-30ml/min/100g body mass. To achieve this, CCC need to generate adequate cardiac output and CPP. Myocardial blood flow is optimum during CCC when aortic diastolic pressure >40mmHg and myocardial perfusion pressures >20-25mmHg. Below this outcomes are poor. *CPP = aortic end diastolic pressure – right atrial diastolic pressure* Decreased pulm blood flow during CPR causes lack of perfusion of many alveoli. Therefore alveolar content – no CO2. Therefore mixed alveolar etCO2 will be low and correlate poorly with arterial CO2. However during CPR if…… If CPR successful, CO2 values correlate with success of CPR
- Busy slide form Emcrit podcast as discussed with Dr Robert Sutton. In USA approx. 200000 patients each year have an in hospital arrest with professional CPR. Most occurring in ICU perhaps due to the successful implementation of early warning signs and MET teams. So can we tailor CPR to the patient The CPR algorithm needs to be straight forward for teams to follow, but as emergency/icu physicians, can we direct CPR to individual patients and hopefully positively affect outcomes.
- 1. CVP in femoral vessels??? - looking at pressure difference in supine patient – really not that different. - And what are we really looking for in resus?? We are looking for trends and responses So not 100% perfect in groin but enough to give us a trend and implement change. 2. Arterial vs vein – there is no colour or pressure difference in CPR between artery and vein, but in age of ultrasound this is unlikely to be issue. We have ‘real time’ -
- No real data to support these guidelines yet. CVP <10 Rapid fluid bolus - thinking is that CVP <10 = volume down, so giving volume improves venous return ITD –pulmonary vasodilator again improves venous return. FD study – not enough to just give fluids. CVP >20 – what could be causing raised pressures that can essentially be reversed -> echo box CVP 10-20 – no change to algorithm
- Targeting BP better than just standard care for everyone. Better to use coronary perfusion pressures if you could, but difficult to get. dBP is there -> ‘look up at the monitor’ …… needs study Bolus adrenaline q1min > infusion anyway (1mcg/kg/min) just basal amount in background. No survival benefit shown Vaspressin – already had some β on board from adrenaline so try vasopressin instead of noradrenaline. Increase rate may inversely decrease depth. Need to check with echo and be ready to have more hands for CCC, or mechanical compression device.
- If HD goals met then assume some pulm blood flow. Increasing rr will have HD consequence (why HD goals need to be met) but heart not happy in acidic environment – wont beat If hurts HD’s can back off. But if you can blow off some CO2 then can possibly improve patients chances. Pulse ox and waveform – picks up pulsitility – don’t know what average BP is when it starts to pick up. Is rate its getting picked up under our CPR rate ??? Is it first sign there's a rhythm there.