Analysis of 23 364 patient-generated, physician-reviewed malpractice claims from a non-tort, blame-free, national patient insurance system: lessons learned from Sweden.

CONTEXT: In Sweden, patient malpractice claims are handled administratively and compensated if an independent physician review confirms patient injury resulting from medical error. Full access to all malpractice claims and hospital discharge data for the country provided a unique opportunity to assess the validity of patient claims as indicators of medical error and patient injury. OBJECTIVE: To determine: (1) the percentage of patient malpractice claims validated by independent physician review, (2) actual malpractice claims rates (claims frequency / clinical volume) and (3) differences between Swedish and other national malpractice claims rates. DESIGN, SETTING AND MATERIAL: Swedish national malpractice claims and hospital discharge data were combined, and malpractice claims rates were determined by county, hospital, hospital department, surgical procedure, patient age and sex and compared with published studies on medical error and malpractice. RESULTS: From 1997 to 2004, there were 23 364 inpatient malpractice claims filed by Swedish patients treated at hospitals reporting 11 514 798 discharges. The overall claims rate, 0.20%, was stable over the period of study and was similar to that found in other tort and administrative compensation systems. Over this 8-year period, 49.5% (range 47.0-52.6%) of filed claims were judged valid and eligible for compensation. Claims rates varied significantly across hospitals; surgical specialties accounted for 46% of discharges, but 88% of claims. There were also large differences in claims rates for procedures. CONCLUSIONS: Patient-generated malpractice claims, as collected in the Swedish malpractice insurance system and adjusted for clinical volumes, have a high validity, as assessed by standardised physician review, and provide unique new information on malpractice risks, preventable medical errors and patient injuries. Systematic collection and analysis of patient-generated quality of care complaints should be encouraged, regardless of the malpractice compensation system in use.

Analysis of 23 364 patient-generated, physician-reviewed malpractice claims from a non-tort, blame-free, national patient insurance system: lessons learned from Sweden.

CONTEXT: In Sweden, patient malpractice claims are handled administratively and compensated if an independent physician review confirms patient injury resulting from medical error. Full access to all malpractice claims and hospital discharge data for the country provided a unique opportunity to assess the validity of patient claims as indicators of medical error and patient injury. OBJECTIVE: To determine: (1) the percentage of patient malpractice claims validated by independent physician review, (2) actual malpractice claims rates (claims frequency / clinical volume) and (3) differences between Swedish and other national malpractice claims rates. Design, setting and material: Swedish national malpractice claims and hospital discharge data were combined, and malpractice claims rates were determined by county, hospital, hospital department, surgical procedure, patient age and sex and compared with published studies on medical error and malpractice. RESULTS: From 1997 to 2004, there were 23 364 inpatient malpractice claims filed by Swedish patients treated at hospitals reporting 11 514 798 discharges. The overall claims rate, 0.20%, was stable over the period of study and was similar to that found in other tort and administrative compensation systems. Over this 8-year period, 49.5% (range 47.0-52.6%) of filed claims were judged valid and eligible for compensation. Claims rates varied significantly across hospitals; surgical specialties accounted for 46% of discharges, but 88% of claims. There were also large differences in claims rates for procedures. CONCLUSIONS: Patient-generated malpractice claims, as collected in the Swedish malpractice insurance system and adjusted for clinical volumes, have a high validity, as assessed by standardised physician review, and provide unique new information on malpractice risks, preventable medical errors and patient injuries. Systematic collection and analysis of patient-generated quality of care complaints should be encouraged, regardless of the malpractice compensation system in use.

Angiotensin II type 2 receptor is essential for left ventricular hypertrophy and cardiac fibrosis in chronic angiotensin II-induced hypertension.

BACKGROUND: The roles of angiotensin II (Ang II) in the regulation of heart function under normal and pathological conditions have been well documented. Although 2 types of Ang II receptor (AT(1) and AT(2)) are found in various proportions, most studies have focused on AT(1)-coupled events. In the present study, we examined the hypothesis that signaling by AT(2) is important to the development of left ventricular hypertrophy and cardiac fibrosis by Ang II infusion in mice lacking the AT(2) gene (Agtr2-/Y). METHODS AND RESULTS: Male Agtr2-/Y and age-matched wild-type (WT) mice were treated long-term with Ang II, infused at a rate of 4.2 ng. kg(-1). min(-1) for 3 weeks. Ang II elevated systolic blood pressure to comparable levels in Agtr2-/Y and WT mice. WT mice developed prominent concentric cardiac hypertrophy, prominent fibrosis, and impaired diastolic relaxation after Ang II infusion. In contrast, there was no cardiac hypertrophy in Agtr2-/Y mice. Agtr2-/Y mice, however, did not show signs of heart failure or impairment of ventricular relaxation and only negligible fibrosis after Ang II infusion. The absence of fibrosis may be a clue to the absence of impairment in ventricular relaxation and account for the normal left ventricular systolic and diastolic performances in Agtr2-/Y mice. CONCLUSIONS: Chronic loss of AT(2) by gene targeting abolished left ventricular hypertrophy and cardiac fibrosis in mice with Ang II-induced hypertension.

Effects of spaceflight on human calf hemodynamics.

Chronic microgravity may modify adaptations of the leg circulation to gravitational pressures. We measured resting calf compliance and blood flow with venous occlusion plethysmography, and arterial blood pressure with sphygmomanometry, in seven subjects before, during, and after spaceflight. Calf vascular resistance equaled mean arterial pressure divided by calf flow. Compliance equaled the slope of the calf volume change and venous occlusion pressure relationship for thigh cuff pressures of 20, 40, 60, and 80 mmHg held for 1, 2, 3, and 4 min, respectively, with 1-min breaks between occlusions. Calf blood flow decreased 41% in microgravity (to 1.15 +/- 0.16 ml x 100 ml(-1) x min(-1)) relative to 1-G supine conditions (1.94 +/- 0.19 ml x 100 ml(-1) x min(-1), P = 0.01), and arterial pressure tended to increase (P = 0.05), such that calf vascular resistance doubled in microgravity (preflight: 43 +/- 4 units; in-flight: 83 +/- 13 units; P < 0.001) yet returned to preflight levels after flight. Calf compliance remained unchanged in microgravity but tended to increase during the first week postflight (P > 0.2). Calf vasoconstriction in microgravity qualitatively agrees with the "upright set-point" hypothesis: the circulation seeks conditions approximating upright posture on Earth. No calf hemodynamic result exhibited obvious mechanistic implications for postflight orthostatic intolerance.

Evidence for angiotensin II type 2 receptor-mediated cardiac myocyte enlargement during in vivo pressure overload.

The pathophysiological roles of the angiotensin II type 2 receptor (AT(2)) in cardiac hypertrophy remain unclear. By the targeted deletion of mouse AT(2) we were able to prevent the left ventricular hypertrophy resulting from pressure overload, while cardiac contractile functions remained normal. This implies that AT(2) is a mediator of cardiac hypertrophy in response to increased blood pressure. The effects of AT(2) deletion were independent of activation of embryonic genes for cardiac hypertrophy. However, p70(S6k), one of the key factors in cardiac hypertrophy, was markedly and specifically reduced in the ventricles of Agtr2(-)/Y mice. We propose that p70(S6k) plays a major role in AT(2)-mediated ventricular hypertrophy. This article may have been published online in advance of the print edition. The date of publication is available from the JCI website, http://www.jci.org.

Prehospital ECG monitoring of chest pain patients.

Prehospital electrocardiograms (ECGs) have been shown to decrease the time from onset of pain to onset of treatment. They are obtained prior to treatment while the patient is likely to have his/her most intense pain. With paramedics initiating care in the field, patient assessments may be clinically different by the time the patient reaches the hospital. Thus, obtaining an ECG as early as possible during treatment could aid in the access to treatment for the few patients whose ECGs improve with prehospital care. We present a case in which the prehospital presentation was indicative of an acute myocardial infarction (MI), whereas the presentation to the hospital was not as clear-cut. The patient was taken immediately to the catheterization laboratory based on the prehospital findings and was found to have an acute MI that was treated. Laboratory findings indicated that there was a significant improvement in patient outcome based on this early treatment. This case further illustrates the role of a prehospital ECG.

Alterations in the volume stimulus-renal response relationship during exposure to simulated microgravity.

We measured central venous pressure (CVP), plasma volume (PV), urine volume rate (UVR), and circulating hormones (renin activity (PRA), vasopressin (AVP), atrial natriuretic peptide (ANP), and cortisol) before and after acute volume infusion (Dextran-40) to test the hypotheses that head-down tilt bedrest (HDT) caused (1) a resetting of the CVP operating point and (2) attenuated urine excretion. Six rhesus monkeys underwent two experimental conditions (HDT and control, each of 48 hour duration) with each condition separated by nine days of ambulatory activities to produce a cross-over counterbalance design. One test condition was continuous exposure to 10 degrees HDT and the second test condition was a control, defined as approximately 12-14 hours per day of 80 degrees head-up tilt and 10-12 hours prone. Following 48 hours of exposure to either test condition, 20-minute continuous infusion of Dextran-40 was administered. CVP in HDT was lower than the control condition. Similar elevations in CVP occurred 30 min post-infusion in both test conditions, and returned to pre-infusion baseline levels between 22 and 46 h post-infusion in both treatments. The UVR response during infusion was attenuated by HDT despite similar elevation in CVP. Elevation in ANP and reduction in PRA at the end of infusion were greater in Control compared to HDT. No differences between control and HDT were detected for AVP and cortisol responses to infusion. Since CVP returned to its pre-infusion levels following volume loading in HDT and control conditions, it appeared that the lower CVP may reflect a new operating point about which vascular volume is regulated. Further, attenuated ANP and PRA responses during vascular volume loading may contribute to depressed UVR in low gravity exposure.

Measurement of net whole-body transcapillary fluid transport and effective vascular compliance in humans.

BACKGROUND: Net whole-body transcapillary fluid transport (TFT) between the circulation and the interstitial (extravascular) space may be calculated as: IV - deltaPV - UV - IL, where IV=infused or ingested volume (when applicable), deltaPV = change in plasma volume, UV=urine volume, and IL=insensible loss. RESULTS: Infusion of 30 mL/kg isotonic saline over 25 minutes increased supine TFT from a basal capillary reabsorption of -106+/-24 mL/h (mean+/-SE) to a net filtration of 1,229+/-124 mL/h. One hour after infusion, reabsorption of -236+/-102 mL/h was seen, and control reabsorption levels returned by 3 hours. Four hours of 30 mm Hg lower body negative pressure (LBNP) elicited no net TFT, probably because of upper body reabsorptive compensation for lower body capillary filtration. When ingestion of 1 L of isotonic saline accompanied LBNP, filtration of 145+/-10 mL/h occurred. Reabsorption of extravascular fluid into the circulation always followed LBNP. CONCLUSION: Application of this technique could aid understanding of physiologic conditions, experimental interventions, disease states, and therapies that cause or are influenced by fluid shifts between intravascular and interstitial compartments.

Evidence for increased cardiac compliance during exposure to simulated microgravity.

We measured hemodynamic responses during 4 days of head-down tilt (HDT) and during graded lower body negative pressure (LBNP) in invasively instrumented rhesus monkeys to test the hypotheses that exposure to simulated microgravity increases cardiac compliance and that decreased stroke volume, cardiac output, and orthostatic tolerance are associated with reduced left ventricular peak dP/dt. Six monkeys underwent two 4-day (96 h) experimental conditions separated by 9 days of ambulatory activities in a crossover counterbalance design: 1) continuous exposure to 10 degrees HDT and 2) approximately 12-14 h per day of 80 degrees head-up tilt and 10-12 h supine (control condition). Each animal underwent measurements of central venous pressure (CVP), left ventricular and aortic pressures, stroke volume, esophageal pressure (EsP), plasma volume, alpha1- and beta1-adrenergic responsiveness, and tolerance to LBNP. HDT induced a hypovolemic and hypoadrenergic state with reduced LBNP tolerance compared with the control condition. Decreased LBNP tolerance with HDT was associated with reduced stroke volume, cardiac output, and peak dP/dt. Compared with the control condition, a 34% reduction in CVP (P = 0.010) and no change in left ventricular end-diastolic area during HDT was associated with increased ventricular compliance (P = 0.0053). Increased cardiac compliance could not be explained by reduced intrathoracic pressure since EsP was unaltered by HDT. Our data provide the first direct evidence that increased cardiac compliance was associated with headward fluid shifts similar to those induced by exposure to spaceflight and that reduced orthostatic tolerance was associated with lower cardiac contractility.

Effect of microgravity on renal and femoral flows during LBNP & intravenous saline load.

NASA: Renal and femoral hemodynamics were studied in crew members at rest and during lower body negative pressure before and after the D-2 Spacelab mission and with intravenous saline loading. Specific measurements included renal vascular resistance, femoral arterial flow, and vascular resistance, along with other cardiovascular parameters. Cardiovascular adaptation to microgravity is discussed with a focus on changes observed in femoral and renal vascular resistance.^ieng

Maximal exercise performance after adaptation to microgravity.

The cardiovascular system appears to adapt well to microgravity but is compromised on reestablishment of gravitational forces leading to orthostatic intolerance and a reduction in work capacity. However, maximal systemic oxygen uptake (Vo2) and transport, which may be viewed as a measure of the functional integrity of the cardiovascular system and its regulatory mechanisms, has not been systematically measured in space or immediately after return to Earth after spaceflight. We studied six astronauts (4 men and 2 women, age 35-50 yr) before, during, and immediately after 9 or 14 days of microgravity on two Spacelab Life Sciences flights (SLS-1 and SLS-2). Peak Vo2 (Vo2peak) was measured with an incremental protocol on a cycle ergometer after prolonged submaximal exercise at 30 and 60% of Vo2peak. We measured gas fractions by mass spectrometer and ventilation via turbine flowmeter for the calculation of breath-by-breath Vo2, heart rate via electrocardiogram, and cardiac output (Qc) via carbon dioxide rebreathing. Peak power and Vo2 were well maintained during spaceflight and not significantly different compared with 2 wk preflight. Vo2peak was reduced by 22% immediately postflight (P < 0.05), entirely because of a decrease in peak stroke volume and Qc. Peak heart rate, blood pressure, and systemic arteriovenous oxygen difference were unchanged. We conclude that systemic Vo2peak is well maintained in the absence of gravity for 9-14 days but is significantly reduced immediately on return to Earth, most likely because of reduced intravascular blood volume, stroke volume, and Qc.

Central venous pressure in space.

Gravity affects cardiac filling pressure and intravascular fluid distribution significantly. A major central fluid shift occurs when all hydrostatic gradients are abolished on entry into microgravity (microG). Understanding the dynamics of this shift requires continuous monitoring of cardiac filling pressure; central venous pressure (CVP) measurement is the only feasible means of accomplishing this. We directly measured CVP in three subjects: one aboard the Spacelab Life Sciences-1 space shuttle flight and two aboard the Spacelab Life Sciences-2 space shuttle flight. Continuous CVP measurements, with a 4-Fr catheter, began 4 h before launch and continued into microG. Mean CVP was 8.4 cmH2O seated before flight, 15.0 cmH2O in the supine legs-elevated posture in the shuttle, and 2.5 cmH2O after 10 min in microG. Although CVP decreased, the left ventricular end-diastolic dimension measured by echocardiography increased from a mean of 4.60 cm supine preflight to 4.97 cm within 48 h in microG. These data are consistent with increased cardiac filling early in microG despite a fall in CVP, suggesting that the relationship between CVP and actual transmural left ventricular filling pressure is altered in microG.

Orthostatic intolerance after spaceflight.

Orthostatic intolerance occurs commonly after spaceflight, and important aspects of the underlying mechanisms remain unclear. We studied 14 individuals supine and standing before and after three space shuttle missions of 9-14 days. After spaceflight, 9 of the 14 (64%) crew members could not complete a 10-min stand test that all completed preflight. Pre- and postflight supine hemodynamics were similar in both groups except for slightly higher systolic and mean arterial pressures preflight in the finishers [15 +/- 3.7 and 8 +/- 1.2 (SE) mmHg, respectively; P < 0.05]. Postflight, finishers and nonfinishers had equally large postural reductions in stroke volume (-47 +/- 3.7 and -48 +/- 3.3 ml, respectively) and increases in heart rate (35 +/- 6.6 and 51 +/- 5.2 beats/min, respectively). Cardiac output during standing was also similar (3.6 +/- 0.4 and 4.1 +/- 0.3 l/min, respectively). However, the finishers had a greater postflight vasoconstrictor response with higher total peripheral resistance during standing (22.3 +/- 1.2 units preflight and 29.4 +/- 2.3 units postflight) than did the nonfinishers (20.1 +/- 1.1 units preflight and 19.9 +/- 1.4 units postflight). We conclude that 1) the primary systemic hemodynamic event, i.e., the postural decrease in stroke volume, was similar in finishers and nonfinishers and 2) the heart rate response and cardiac output during standing were not significantly different, but 3) the postural vasoconstrictor response was significantly greater among the finishers (P < 0.01).

Mechanisms of post-flight orthostatic intolerance.

Post-flight orthostatic intolerance is a dramatic physiological consequence of human adaptation to microgravity made inappropriate by a sudden return to 1-G. The immediate mechanism is almost always a failure to maintain adequate tissue perfusion, specifically perfusion of the central nervous system, but vestibular dysfunction may occasionally be the primary cause. Orthostatic intolerance is present in a wide range of clinical disorders of the nervous and cardiovascular systems. The intolerance that is produced by spaceflight and 1-G analogs (bed rest, head-down tilt at a moderate angle, water immersion) is different from its clinical counterparts by being only transiently present in subjects who otherwise have normal cardiovascular and regulatory systems. However, the same set of basic pathophysiological elements should be considered in the analysis of any form of orthostatic intolerance.

Central hemodynamics in a baboon model during microgravity induced by parabolic flight.

We developed a chronically instrumented nonhuman primate model (baboon) to evaluate the central cardiovascular responses to transient microgravity induced by parabolic flight. Instrumentation provided simultaneous recording of high fidelity (Ao) and pulmonary artery (PA) pressures, right and left ventricular and atrial pressures, Ao and PA blood flow velocities and vessel dimensions, ECG and pleural pressures. Four daily flights in 1991 and five in 1992 were flown with forty parabola per flight. Animals flown in 1991 were not controlled for volume status. Animals flown in 1992 were studied in one of three conditions: 1) volume depleted by furosemide (DH), 2) volume expanded by saline infusion (VE), and 3) euvolemic (EU, no intervention, used for echo only). Mean right atrial pressures (RAP) during 1991 flights had a variable early microgravity response: increases in n=3 and decrease in n=3 (supine) and increases in n=5, decreases in n=2 (upright). In 1992 flights, DH, upright and supine, changed -10 +/- 4.1 mmHg, -3.2 +/- 2.2 mmHg, respectively (p < .05) compared to the pull-up phase. In contrast, VE changed (from pull-up to microgravity) +13 +/- 1.5 mmHg and +4.25 +/- 2.9 mmHg (upright and supine, respectively, p < .05). EU increased with microgravity +6.9 +/- .9 mmHg (upright only). LAP responses were similar, but more variable. Finally, heart chamber areas paralleled pressure changes. Thus, right and left heart filling pressure changes with sudden entry into microgravity conditions were dependent on initial circulatory volume status and somewhat modified by position (supine vs upright).

Effects of orthostatic and anti-orthostatic stress on patent and stenotic coronary arteries in swine.

Head-up tilt (HUT) followed by head-down tilt (HDT) has been used to simulate the acute phase of adaptation to microgravity. This study evaluates the effects of HUT and HDT on the coronary circulation before and during coronary stenosis. Seven pigs were placed in the prone position and exposed to the following orientations for 20 min each: 1) 0 degrees horizontal (HZ); 2) +70 degrees HUT; and 3) -15 degrees HDT. The swine were then placed in the HZ position for 20 min while hemodynamics returned to baseline. The diameter of the left anterior descending (LAD) coronary artery was reduced to a point slightly less than that which produced a decrease in blood flow and the protocol was repeated. Heart rate (HR), contractility (dP/dt), mean arterial blood pressure (MABP), left ventricular pressure (LVP), coronary sinus pressure (CSP), left-ventricular end-diastolic pressure (LVEDP), coronary blood flow (CBF), coronary vascular resistance (CVR), myocardial oxygen consumption (MVO2) and coronary sinus lactate were determined after 20 min in each position. The transition from HUT to HDT elicited a significant (p < 0.05) increase in MABP, LVP, CSP, LVEDP, MVO2, and CBF and a significant decrease in CVR. During HDT, MVO2 increased 20 +/- 10% from Hz and 68 +/- 15% from HUT. There was a comparable increase in coronary artery flow. The hemodynamic responses were not significantly altered during pneumatic coronary occlusion. However, coronary sinus lactate was significantly elevated in the HDT positions. This study demonstrates a substantial increase in CBF during HUT to HDT with and without coronary stenosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Transesophageal echocardiographic evaluation of baboons during microgravity induced by parabolic flight.

The central cardiovascular responses to transient microgravity are not well understood. Theoretically, entrance into microgravity results in the loss of the hydrostatic pressure head and an increase in central venous pressure (CVP) as a consequence of augmented venous return. However, controversy exists regarding the time course and magnitude of cephalad blood volume shifts and its relationship to central atrial filling pressures. On the June 1991 STS 40 shuttle mission, pre-launch echocardiograms suggested changes in cardiac dimensions occurred while the astronauts were in the supine, feet-up position. Furthermore, a CVP line in an astronaut (n=1) demonstrated an unexpected abrupt decrease in CVP during orbital insertion. In April 1991, our laboratory performed Doppler echocardiography in 6 normal human volunteers during parabolic flight. Increases in right ventricular velocities reflecting a central shift of blood volume was demonstrated in subjects examined in the sitting position. However, test subjects examined in the horizontal positions had no significant rise in Doppler velocities. In addition, Latham et al noted variable central cardiovascular responses in chronically instrumented baboons during early microgravity. Transthoracic echocardiography (TTE) is a feasible method to noninvasively examine cardiac anatomy during parabolic flight. However, transducer placement on the chest wall is very difficult to maintain during transition to microgravity. In addition, TTE requires the use of low frequency transducers (2.5 MHz) which limits resolution. Transesophageal echocardiography (TEE) is an established imaging technique which obtains echocardiographic information from the esophagus. It is a safe procedure and provides higher quality images of cardiac structures than obtained with TTE. Since there are no interposed structures between the esophagus and the heart, higher frequency transducers can be used and resolution is enhanced. With TEE, a flexible transducer tip permits contact with the esophageal mucosa, allowing for consistent imaging. This study was designed to determine whether TEE was feasible to perform during parabolic flight and to determine whether acute central volume responses occur in acute transition to zero gravity (0G) by direct visualization of the cardiac chambers.

Head-down tilt bedrest. HDT'88--an international collaborative effort in integrated systems physiology.

An international collaborative project, initiated by the DLR-NASA Life Sciences Working Group, led to the performance of a head-down tilt bedrest (HDT) study at the DLR Institute for Aerospace Medicine. Scientific and operational questions were addressed in preparation for the D-2 Spacelab mission. Principal areas of interest were cardiovascular regulation and fluid/electrolyte metabolism. The results are detailed in a series of 13 reports to which the present paper serves as an introduction.