Loose cuff hypertension.

In this study, an analysis of the effects of cuff looseness on mean blood pressure readings was performed. Using a standard adult blood pressure cuff, pressure readings were taken on each arm at a cuff looseness of 0, 2, 4, and 6 cm beyond patient arm circumference. The cuff was then switched to the opposite arm and the procedure repeated. Blood pressure readings taken from the left arm with the cuff at an appropriately snug fit served as the reference. Increasing cuff looseness simulates the possibly incorrect blood pressure cuff placement by health care workers in the clinical setting. Data from 24 subjects support the claims that mean blood pressure increases with respect to increasing cuff looseness. It was shown that measurements taken on left and right arms will result in significantly different blood pressure readings (p < 0.001). It is therefore crucial to properly place the cuff at a snug fit on the patient's arm for each measurement procedure, to prevent false readings. Lack of consistent cuff size and snugness procedures can lead to misdiagnosis of hypertension, acute patient discomfort, and inconvenient costs to the patient and health care provider.

Structures and heats of formation of the neutral and ionic PNO, NOP, and NPO systems from electronic structure calculations.

High level ab initio electronic structure calculations using the coupled cluster CCSD(T) method with augmented correlation-consistent basis sets extrapolated to the complete basis set limit have been performed on the PNO, NOP, and NPO isomers and their corresponding anions and cations. Geometries for all species were optimized up through the aug-cc-pV(Q+d)Z level and vibrational frequencies were calculated with the aug-cc-pV(T+d)Z basis set. The most stable of the three isomers is NPO and it is predicted to have a heat of formation of 23.3 kcal/mol. PNO is predicted to be only 1.7 kcal/mol higher in energy. The calculated adiabatic ionization potential of NPO is 12.07 eV and the calculated adiabatic electron affinity is 2.34 eV. The calculated adiabatic ionization potential of PNO is 10.27 eV and the calculated adiabatic electron affinity is only 0.24 eV. NOP is predicted to be much higher in energy by 29.9 kcal/mol. The calculated rotational constants for PNO and NPO should allow for these species to be spectroscopically distinguished. The adiabatic bond dissociation energies for the P[Single Bond]N, P[Single Bond]O, and N[Single Bond]O bonds in NPO and PNO are the same within approximately 10 kcal/mol and fall in the range of 72-83 kcal/mol.

A new paradigm for human resuscitation research using intelligent devices.

OBJECTIVES: To develop new methods for studying correlations between the performance and outcome of resuscitation efforts in real-world clinical settings using data recorded by automatic devices, such as automatic external defibrillators (AEDs), and to explore effects of shock timing and chest compression depth in the field. METHODS: In 695 records of AED use in the pre-hospital setting, continuous compression data were recorded using AEDs capable of measuring sternal motion during compressions, together with timing of delivered shocks and the electrocardiogram. In patients who received at least one shock, putative return of spontaneous circulation (P-ROSC) was defined as a regular, narrow complex electrical rhythm > 40 beats/min with no evidence of chest compressions at the end of the recorded data stream. Transient return of spontaneous circulation (t-ROSC) was defined as the presence of a post-shock organized rhythm > 40 beats/min within 60s, and sustained > or = 30 s. 2x2 contingency tables were constructed to examine the association between these outcomes and dichotomized time of shock delivery or chest compression depth, using the Mood median test for statistical significance. RESULTS: The probability of P-ROSC for first shocks delivered < 50 s (the median time) after the start of resuscitation was 23%, versus 11% for first shocks > 50 s (p=0.028, one tailed). Similarly, the probability of t-ROSC for shorter times to shock was 29%, compared to the 15% for delayed first shocks (p=0.016). For shocks occurring > 3 min after initiation of rescue attempts, the probability of t-ROSC with pre-shock average compression depth > 5 cm was more than double that with compression depth < 5 cm (17.7% vs. 8.3%, p=0.028). For shocks > 5 min, the effect of deeper compressions increased (23.4% versus 8.2%, p=0.008). CONCLUSIONS: Much can be learned from analysis of performance data automatically recorded by modern resuscitation devices. Use of the Mood median test of association proved to be sensitive, valid, distribution independent, noise-resistant and also resistant to biases introduced by the inclusion of hopeless cases. Efforts to shorten the time to delivery of the first shock and to encourage deeper chest compressions after the first shock are likely to improve resuscitation success. Such refinements can be effective even after an unknown period of preceding downtime.

A new cardiopulmonary resuscitation method using only rhythmic abdominal compression: a preliminary report.

This article introduces 2 new cardiopulmonary resuscitation (CPR) concepts: (1) the use of only rhythmic abdominal compression (OAC) to produce blood flow during CPR with ventricular fibrillation and (2) a new way of describing coronary perfusion effectiveness, namely, the area between the aortic and right atrial pressure curves, summed over 1 minute, the units being millimeters of mercury per second. We call this unit the coronary perfusion index (CPI). True mean coronary perfusion pressure is CPI/60. We also relate CPI during CPR with ventricular fibrillation to the CPI for the normally beating heart in the same animal, obtained before each experiment. This 11-pig (25-35 kg) study compares the CPI for standard chest-compression CPR and that obtained with OAC-CPR. The coronary perfusion ratio for OAC-CPR compared with standard chest-compression CPR was 1.6 +/- 0.73 (P = .024). In other words, OAC-CPR produced 60% more coronary perfusion than standard chest-compression CPR, with no damage to visceral organs.

Sustained abdominal compression during CPR raises coronary perfusion pressures as much as vasopressor drugs.

OBJECTIVES: This study investigated sustained abdominal compression as a means to improve coronary perfusion pressure (CPP) during cardiopulmonary resuscitation (CPR) and compared the resulting CPP augmentation with that achieved using vasopressor drugs. METHOD: During electrically induced ventricular fibrillation in anesthetized, 30kg juvenile pigs, Thumper CPR was supplemented at intervals either by constant abdominal compression at 100-500mmHg using an inflated contoured cuff or by the administration of vasopressor drugs (epinephrine, vasopressin, or glibenclamide). CPP before and after cuff inflation or drug administration was the end point. RESULTS: Sustained abdominal compression at >200mmHg increases CPP during VF and otherwise standard CPR by 8-18mmHg. The effect persists over practical ranges of chest compression force and duty cycle and is similar to that achieved with vasopressor drugs. Constant abdominal compression also augments CPP after prior administration of epinephrine or vasopressin. CONCLUSIONS: During CPR noninvasive abdominal compression with the inflatable contoured cuff rapidly elevates the CPP, sustains the elevated CPP as long as the device is inflated, and is immediately and controllably reversible upon device deflation. Physical control of peripheral vascular resistance during CPR by abdominal compression has some advantages over pharmacological manipulation and deserves serious reconsideration, now that the limitations of pressor drugs during CPR have become better understood, including post-resuscitation myocardial depression and the need for intravenous access.

The natural biochemical changes during ventricular fibrillation with cardiopulmonary resuscitation and the onset of postdefibrillation pulseless electrical activity.

OBJECTIVE: The objective of this study was to document the biochemical changes during ventricular fibrillation (VF) with cardiopulmonary resuscitation (CPR), and to identify factors associated with postdefibrillation pulseless electrical activity (PD-PEA). BACKGROUND: It has been reliably estimated that as much as 60% of out-of-hospital sudden cardiac death can be attributed to the onset of PD-PEA (Niemann JT, Cruz B, Garner D et al. Immediate countershock versus CPR before countershock in a 5-minute swine model of ventricular fibrillation arrest. Ann Emerg Med 2000;36:543-6). Previous attempts to treat reversible causes of pulseless electrical activity have not been successful clinically (Niemann JT, Stratton SJ, Cruz B, Lewis RJ. Outcome of out-of-hospital postcountershock asystole and pulseless electrical activity versus primary asystole and pulseless electrical activity. Crit Care Med 2001;29:2366-70). METHODS: This investigation used 22 studies on 14 anesthetized pigs breathing 100% oxygen. Ventricular fibrillation was induced with a right ventricular catheter electrode, and the chest was compressed with a pneumatically driven Chest Thumper (Michigan Instruments) (80-100 lb at 60/min). The electrocardiogram and aortic pressure were recorded continuously. Arterial pH, P(O2), P(CO2), Na+, K+, Ca2+, Cl-, SaO2, glucose, hematocrit, and hemoglobin level were measured at selected times. Ventricular defibrillation was achieved with transchest electrodes. RESULTS: Typically, during VF with CPR, mean aortic pressure was 20 to 25 mm Hg. In all cases aortic P(O2) decreased to about 20% of the initial value in 10 minutes, and aortic blood K+ increased by 50% in 6 minutes. By 5 to 8 minutes, the incidence of PD-PEA was 50%. CONCLUSION: Ventricular fibrillation duration, arterial K+, and arterial P(CO2) were statistically correlated with the onset of PD-PEA in this study. In addition, trends suggest an association of mean arterial blood pressure and arterial P(O2) with the onset of PD-PEA.

Heel calf capillary-support pressure in lithotomy positions.

A three-part analysis was undertaken to increase understanding of the occurrence of pressure ulcers in lithotomy positions. An innovative measuring device was used to determine capillary pressure. Ankle blood pressure was measured compared to ankle height in 11 participants. Ankle systolic and diastolic pressure decreased approximately 20 mmHg per foot of elevation. Calf and heel capillary-support pressures were measured in 15 participants in the standard lithotomy position. Capillary-support pressure for the calf was substantially less than for the heel. Heel capillary-support pressures were measured in 16 participants in the high lithotomy position. As heel height increased, capillary-support pressure also increased.

The duration of ventricular fibrillation required to produce pulseless electrical activity.

The duration of untreated (no cardiopulmonary resuscitation) ventricular fibrillation (VF) needed to produce postdefibrillation pulseless electrical activity (PEA) was determined in 9 anesthetized swine ranging in weight from 20 to 30 kg. VF was induced electrically by a right ventricular catheter electrode, while arterial pressure and the electrocardiogram were recorded. VF was confirmed by the presence of VF waves in the electrocardiogram and a loss of pulsatile arterial pressure. VF was allowed to persist for 15-second increments (eg, 15, 30, 45, etc), after which defibrillation was achieved with transchest electrodes and the presence or absence of PEA was noted. If PEA was present, rhythmic chest compressions were applied to rescue the animal. Just after initiation of VF and just before defibrillation, VF wave frequency was measured. PEA was encountered in 100% of the trials after 180 seconds of VF. The threshold duration for PEA was 60 seconds. VF wave frequency decreased with the passage of time. At VF initiation, VF wave frequency (f0) ranged from 6 to 15 per second, with a mean of 10.1+/-2.1 per second. At 180 seconds (f180), the mean frequency was 4.0+/-0 per second. It was only possible to eliminate PEA and restore pumping in 1 animal when untreated VF lasted more than 180 seconds. There was no clear transition in the frequency of the VF waves with the passage of time that could predict the possibility of postdefibrillation PEA. Moreover, because of the different initial VF wave frequencies and the different rates of decrease with time, a measurement of VF wave frequency is unlikely to be informative on how long VF had been present. A consistent finding in this swine study of prolonged untreated VF was a rise in blood K+ which increased from a normal prefibrillation value of about 4 mEq/L to 8 to 12 mEq/L at 180 seconds. The longer the duration of VF, the higher the K+.