There is increasing recognition that systematic post–cardiac arrest care after return of spontaneous circulation (ROSC) can improve the likelihood of patient survival with good quality of life. This is based in part on the publication of results of randomized controlled clinical trials as well as a description of the post–cardiac arrest syndrome. 1–3 Post–cardiac arrest care has significant potential to reduce early mortality caused by hemodynamic instability and later morbidity and mortality from multiorgan failure and brain injury. 3,4 This section summarizes our evolving understanding of the hemodynamic, neurological, and metabolic abnormalities encountered in patients who are initially resuscitated from cardiac arrest. The initial objectives of post–cardiac arrest care are to ● Optimize cardiopulmonary function and vital organ perfusion. ● After out-of-hospital cardiac arrest, transport patient to an appropriate hospital with a comprehensive post–cardiac arrest treatment system of care that includes acute coronary interventions, neurological care, goal-directed critical care, and hypothermia. ● Transport the in-hospital post–cardiac arrest patient to an appropriate critical-care unit capable of providing comprehensive post–cardiac arrest care. ● Try to identify and treat the precipitating causes of the arrest and prevent recurrent arrest.

http://www.kardio.hu/feltoltott/dokumentumok/fajl_201148104747Cardiopulm_resuscit_Pt9_Post_cardiac.pdf

Part 9: Post-Cardiac Arrest Care: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care

https://genoplivning.dk/wp-content/uploads/2013/07/european-resuscitation-council-guidelines-for-resuscitation-2010-section-4-adult-advanced-life-support.pdf

European Resuscitation Council Guidelines for Resuscitation 2010 Section 4 Adult advanced life support

Introduction: Ventilator-induced Lung Injury: Not Only Air Leaks Ventilation-induced Pulmonary Edema and Related Findings: A Historical Perspective Ventilation-induced Pulmonary Edema: Hydrostatic or Permeability Edema? Experimental Evidence for Increased Vascular Transmural Pressure Evidence for Alterations in Alveolar–Capillary Permeability Contributions of the Static and Dynamic Lung Volume Components to Ventilator-induced Edema High-volume Lung Edema Low Lung Volume Injury Effects of High-volume Ventilation on Abnormal Lungs Effects of High-volume Ventilation on Injured Lungs Interaction between Severe Alveolar Flooding and Mechanical Ventilation Effects of Resting the Lung on Ventilator-induced Lung Injury Possible Mechanisms of Ventilation-induced Lung Injury Mechanisms of Increased Vascular Transmural Pressure Mechanisms of Altered Permeability Clinical Relevance

Ventilator-induced lung injury: lessons from experimental studies.

In contrast to adults, cardiac arrest in infants and children does not usually result from a primary cardiac cause. More often it is the terminal result of progressive respiratory failure or shock, also called an asphyxial arrest. Asphyxia begins with a variable period of systemic hypoxemia, hypercapnea, and acidosis, progresses to bradycardia and hypotension, and culminates with cardiac arrest.1

Another mechanism of cardiac arrest, ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT), is the initial cardiac rhythm in approximately 5% to 15% of pediatric in-hospital and out-of-hospital cardiac arrests;2,–,9 it is reported in up to 27% of pediatric in-hospital arrests at some point during the resuscitation.6 The incidence of VF/pulseless VT cardiac arrest rises with age.2,4 Increasing evidence suggests that sudden unexpected death in young people can be associated with genetic abnormalities in myocyte ion channels resulting in abnormalities in ion flow (see “Sudden Unexplained Deaths,” below).

Since 2010 marks the 50th anniversary of the introduction of cardiopulmonary resuscitation (CPR),10 it seems appropriate to review the progressive improvement in outcome of pediatric resuscitation from cardiac arrest. Survival from in-hospital cardiac arrest in infants and children in the 1980s was around 9%.11,12 Approximately 20 years later, that figure had increased to 17%,13,14 and by 2006, to 27%.15,–,17 In contrast to those favorable results from in-hospital cardiac arrest, overall survival to discharge from out-of-hospital cardiac arrest in infants and children has not changed substantially in 20 years and remains at about 6% (3% for infants and 9% for children and adolescents).7,9

It is unclear why the improvement in outcome from in-hospital cardiac arrest has occurred, although earlier recognition and management of at-risk patients on general inpatient units …

https://www.ahajournals.org/doi/pdf/10.1161/CIRCULATIONAHA.110.971101

Part 14: Pediatric Advanced Life Support 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care

https://nrr.org/wp-content/uploads/0000/10/02_ERC_Guidelines_2005_Section2.pdf

European Resuscitation Council Guidelines for Resuscitation 2010 Section 2. Adult basic life support and use of automated external defibrillators.

Background Water is an indispensable nutrient because of its physicochemical properties. People seem to consume more water than before although the scientific basis for this has not been firmly established. Material and methods We present a short overview of data retrieved from the databases PubMed and Ovid, with particular emphasis on the regulation of water intake and water excretion in adults. Results Water excretion is mainly regulated through the production of urine. Anti-diuretic hormone plays a key role. The intake of water is mainly governed via the poorly defined sense of thirst. Circumstantial evidence supports an increased intake of water to prevent certain cancers and cardiovascular diseases. Interpretation Both excessive hydration and dehydration can cause serious illness, in particular in the elderly. There is a lack of firm scientific support for the beneficial health effects of increased water intake.

[Water--for life]

We have followed the time course of the effect of the carbonic anhydrase inhibitor acetazolamide injected i.v. in unanesthetized healthy human beings. The dose administered was 500 mg as a bolus. Cerebral blood flow (CBF) was measured continuously before, during and after the injection, using a pulsed ultrasound doppler system, which measured the instantaneous mean velocity across the lumen of the internal carotid artery, just below its entrance into the skull. Ventilation, heart-rate, end-expiratory PC02, arterial PC02, pH and systemic blood pressure was also measured. We found that acetazolamide caused a rise in CBF which could be detected as early as 2 min after the injection. A maximal average response of 75 % increase in CBF was seen after 25 min. The half-time of the declining phase of the response was 95 min. There were no systematic differences in the COz reactivities, given as ACBF/APAC02 in % of CBF at normocapnia, before and after acetazolamide injection, regardless of the absolute PAC02 level. The present dose of the drug caused no change in ventilation, alveolar and arterial PC02 or in arterial blood pH indicating that the carbonic anhydrase was not fully inhibited. Our observations show that acetazolamide nevertheless caused a rapid vasodilation in the brain and over a wide range of PC02’s. We suggest that this agent has a local vasodilator effect on the cerebral arterioles, unrelated to its specific effects as a carbonic anhydrase inhibitor.

Acute effects of acetazolamide on cerebral blood flow in man.

The effect of moderate hypoxia on cerebral blood flow (CBF) in man has not been well described, and little is known about the interaction of changes in arterial PO2 and PCO2 as regards CBF. Using a non-invasive doppler ultrasound method we have measured the instantaneous mean blood velocity (which is proportional to CBF as long as the cross-section of the vessel is constant) in the carotid artery in four healthy unanaesthetized subjects. We found in all subjects that a reduction in alveolar PO2 from about 13 to about 8.7 kPa with maintained constant alveolar PCO2 (PA, CO2) caused CBF to increase gradually over 10 min (half-time about 4 min) to about 125% of control. The CBF decreased quickly (half-time about 45 s) towards control when alveolar PO2 was reset to 13 kPa. As measured 5 min after a step-change in PA, O2, the change in CBF was independent of PA, CO2 within the range 3.3-6.7 kPa. An increase in PA, O2 to about 33 kPa reduced CBF only if PA, CO2 was in the hypercapnic range. Unexpectedly we found that the CBF response showed 'adaptation' during both maintained increase and decrease in PA, CO2. The CBF started to return towards control level within 10 min after induction of hypo- or hypercapnia. We conclude that also moderate hypoxia causes increased CBF in unanaesthetized man within a wide range of PA, CO2.

Changes in human cerebral blood flow due to step changes in PAO2 and PACO2.

Distribution of pulmonary blood flow has traditionally been regarded as determined by gravity. This view has been challenged recently by reports describing marked gravity-independent distribution of flow. These reports were based on experiments in which local blood flow was measured by methods that have not been thoroughly evaluated. In the present study, we showed that in the goat lung regional trapping of i.v. infused microspheres (O = 15 microns) correlated to endothelial uptake of a simultaneously i.v. infused diamine (r = 0.99, region size approximately 1.5 cm3, dry weight approximately 40 mg). This indicates that the deposition of microspheres reflects true regional pulmonary blood flow. Using the microsphere method, we found a marked gravity-independent heterogeneity in blood flow (coefficient of variation approximately 40%) in the awake goat. We could find no pattern related to anatomy that could account for this variability. We re-examined the influence of gravity by analysing the distribution of pulmonary blood flow in anaesthetized goats both in prone and supine positions. The dorsal to sternal distribution of flow appeared to be inverted when the animals were turned from prone to supine recumbency, indicating that gravity influenced the distribution of pulmonary blood flow along this axis. However, along the gravitational axis, distribution of blood flow varied considerably from lung to lung. It appears that in awake goats the distribution of pulmonary blood flow is the result of several different determinants.

Both gravity and non‐gravity dependent factors determine regional blood flow within the goat lung

In 1985 both Pendergast et al. and Piiper et al. described a major regional heterogeneity in blood flow within single skeletal muscles both at rest and during exercise. Based on the microsphere method they described large variations in blood flow between muscle samples as large as 1 g each.



The aims of the present study were:



1
 To test this notion of regional heterogeneity in microsphere deposition within single skeletal muscles both at rest and during exercise.

2
 To compare the distribution of microspheres with other blood flow tracers.

3
 To test whether or not any heterogeneity was due to vasomotion in small arteries or arterioles.





Microspheres were infused into anaesthetized rabbits over either 10, 30 or 120 s, or 10 min. Exercise was mimicked by tetanic contractions obtained by electrical stimulation of the motor nerves. Three hindleg muscles were divided into samples of 0.25 g each. Regional heterogeneity was expressed as the coefficient of variation corrected for statistical distribution of microspheres (CVc). The CVc at rest was about 0.34. The CVc was unaffected by the various infusion periods and did not change during exercise. Simultaneous infusions of microspheres and 86Rb+ or antipyrine gave high correlations between the two blood flow tracers, with all r values exceeding 0.83 (n= 18).



We conclude that the microsphere method provides reliable estimates for regional blood flow within single skeletal muscles. The distribution of blood flow was markedly heterogeneous both at rest and during exercise. The heterogeneity in blood flow was apparently not a result of vasomotion.

Gunnar Nicolaysen

Papers

[Water--for life]

Acute effects of acetazolamide on cerebral blood flow in man.

Changes in human cerebral blood flow due to step changes in PAO2 and PACO2.

Both gravity and non‐gravity dependent factors determine regional blood flow within the goat lung

Marked regional heterogeneity in blood flow within a single skeletal muscle at rest and during exercise hyperaemia in the rabbit