Drop In Stroke Volume Research Articles

Comparative study between effects of single and dual chamber pacemaker on stroke volume, cardiac output and strain using 3D echocardiography, pulsed Doppler method and global longitudinal strain (GLS)

Abstract Background Dual-chamber cardiac pacing is thought to deliver higher clinical benefits as compared with single-chamber ventricular pacing. During the last two decades, 3D-echocardiography developed from a sophisticated, time-consuming method preferably used as a scientific tool towards a routine clinical approach. At present, available evidence suggested that 3D echocardiography provided improved accuracy and reproducibility over 2D methods for LV volume and function calculation. It was also more useful for early detection of volumetric changes associated with changes in cardiac hemodynamics. Methods This was an observational study of fifty consecutive patients without structural heart disease and preserved ejection fraction (EF>50%) presented with high grade atrioventricular block for permanent pacemaker implantation. They were assigned to receive a single-chamber ventricular pacemaker (23patients) or a dual-chamber pacemaker (27 patients). Stroke volume and cardiac output was assessed by full volume 3D echo and pulsed wave Doppler before implantation, at one-week and 6-months after implantation. For the Doppler method, LVOT diameter was measured for each patient at baseline and same value was used at follow up to avoid any confounding factors. GLS was measured at all visits. Results At one-week post pacing, both groups showed a significant decrease in SV due to a drop in EDV while ESV did not change significantly. There was a significant increase in cardiac output (COP) more in dual-chamber pacing group than in the group with single-chamber pacing. However, there were no significant differences between both groups regarding stroke volume (SV), end-systolic volume (ESV), end-diastolic volume (EDV) or ejection fraction (EF) during all time intervals (pre-pacing, at one-week and 6-months post pacing). GLS showed equal decrease in both groups. At 6 months, SV continued to decrease, and COP showed significant decrease. This drop in SV and COP was due to a significant increase in ESV while EDV did not show significant change at 6-month follow up. There was no significant difference between full volume 3D and Doppler methods regarding SV and COP values at all time intervals in both groups. GLS showed additional equal decrease in both groups. Conclusion Dual chamber pacing provided higher COP than single chamber pacing. This is due to pacing at higher heart rates, not due to increase in SV by maintaining atrioventricular synchrony. It was shown in both experimental and clinical studies that RV pacing leads to ventricular dyssynchrony, similar to that of left bundle branch block with subsequent electrical, mechanical and anatomical changes leading to detrimental effects on left ventricular structure and function. Both groups showed significant drop in GLS plus SV, COP and EF at 6-months due to significant increase in ESV. 2D echocardiography and Doppler method were not inferior to 3D echocardiography regarding calculation of SV and COP. Haemodynamics of single & dual pacing Funding Acknowledgement Type of funding source: None

Untreated Stroke as Collateral Damage of COVID-19: "Time Is Brain" Versus "Stay at Home".

For decades, neurologists have been advocating that anyone with acute focal deficits report immediately to the closest hospital’s emergency room. Major advancements in the hyperacute diagnosis and treatment of stroke have justified our call-to-action slogan of “Time is Brain”—faster therapy leads to superior outcomes. However, this mantra has been recently usurped by the catchphrase “Stay at Home” during the coronavirus disease 2019 (COVID-19) pandemic. Fewer patients are presenting to hospitals with acute stroke; our census is down. Presumably the etiology of this phenomenon is either strict “social distancing” that some people may misperceive to exclude even emergent situations, or fears of contracting the virus while hospitalized. In this Short Report, we describe the year-over-year drop in stroke volume (ischemic and hemorrhagic both) coinciding with a paradoxical rise in acute reperfusion therapies at our university hospital. These data imply that stroke patients with mild/moderate symptoms are most likely staying home, and not receiving urgent therapies, and correspondingly, only the most severely disabled stroke patients are ultimately seeking and receiving help. We must remind our patients and the general public that our services are essential and available, as stroke still remains a medical emergency, and carries a likely higher overall mortality risk than COVID-19. As neurologists, we also must be vigilant for the atypical presentations and varied etiologies of stroke associated with COVID-19 as well.

Knee-high compression socks minimize head-up tilt-induced cerebral and cardiovascular responses following dynamic exercise.

In healthy individuals during a non-exercised state, knee-high compression socks (CS) may reduce the magnitude of lower limb venous pooling during orthostasis but are not effective at minimizing the incidence of pre-syncopal symptoms. However, exaggerated reductions in cerebral blood flow velocity (CBV) and cardiac stroke volume (SV) occur during passive head-up tilt (HUT) testing following dynamic exercise. It is unknown if CS can minimize post-exercise HUT-induced decrements in CBV and SV in this population. To test the hypothesis that CS will attenuate the reductions in SV and CBV during 60° HUT following 60minutes of moderate-intensity (60% VO2 peak) cycling exercise. Ten healthy volunteers (22.6±2.1years, 24.1±2.5kg/m2 ) completed pre- and post-exercise 15-minute HUT tests during randomized CS and Control (no CS) conditions. Changes in blood pressure (finger plethysmography), SV (Modelflow® method), and CBV (Transcranial Doppler) were measured during HUT and preceding supine rest periods. Pre-exercise HUT-induced similar (all, P>.47) reductions in SV (Control; -23.1±11.5%, CS; -20.5±10.9%) and CBV (Control; -18.1±6.3%, CS; -15.3±9.0%). However, larger post-exercise decreases in SV and CBV during HUT were observed in the Control versus CS condition. Specifically, CS attenuated the drop in SV (Control: -32.9±5.6%, CS: -24.3±11.6%; P=.01) and CBV (Control: -25.1±5.8%, CS: -17.6±7.8%; P=.02) during the post-exercise HUT test. These results indicate that CS attenuated HUT-induced reductions in SV and CBV following moderate-intensity cycling exercise and suggest that CS may be an effective countermeasure to reduce the incidence of post-exercise syncope in vulnerable populations.

Systolic and Diastolic Heart Failure Are Overlapping Phenotypes Within the Heart Failure Spectrum

Should chronic heart failure (HF) be subdivided into 2 distinct phenotypes? Current knowledge supports the view that the complexity of HF cannot be captured by answering this question with a yes or a no. Recent developments in the biosciences, particularly systems biology approaches and studies of phenotypic disease networks, have indicated that such questions are becoming obsolete, and perhaps even irrelevant. Response by Borlaug and Redfield on p 2005 Chronic HF is a complex, multifactorial syndrome consisting of many overlapping phenotypes. A unifying hypothesis to explain the development and progressive character of HF has not withstood the test of time (Figure 1). Despite improvements in clinical management, the incidence and mortality of chronic HF remain high. Attempts to further improve its prognosis have failed, and conceptual progress seems to stagnate. Figure 1. Evolving paradigms of heart failure progression. Each of the paradigms highlights a different aspect of the syndrome. In the vicious circle paradigm of heart failure ( left ), the pernicious, progressive, and irreversible character is emphasized as propelled by endothelial dysfunction and (mal)adaptive activation of neurohormones and cytokines. In the time progression paradigm ( middle ), the progressive nature of heart failure is equally emphasized, but focus is on the consecutive stages of failing cardiac performance: failure of the heart first as a muscular suction pump, then as a hemodynamic compression pump, and finally of the whole cardiovascular system, with drop in stroke volume (SV), cardiac index (CI), and eventually of arterial blood pressure (Part). The spectrum paradigm of heart failure ( right ) visualizes the manner in which each patient follows a unique disease trajectory during heart failure progression. The trajectories depend on the relative contribution of the patient's traits and comorbidities (coined disease modifiers ), are thus patient specific, and hence create a spectrum of phenotypes throughout the entire population of heart failure patients. CV …

Right Atrial Pacing Increases Maximal Heart Rate But Does Not Alter Vo2Max Or Maximal Exercise Performance In Healthy Humans

Aerobic power (VO2max) and exercise performance is limited by a restricted cardiac output during maximal exercise, but the mechanisms restricting cardiac output remain unknown. The attainment of maximal heart rate (HR) could be a factor limiting cardiac output, but the effect of increasing maximal HR has not been investigated in healthy humans. PURPOSE: To investigate the effect of HR pacing on cardiac output, VO2max and exercise performance during maximal cycling. METHODS: We measured systemic and peripheral hemodynamics during incremental (25, 40, 55, 70, 85, 100% of maximal workload (WLmax)) cycling to exhaustion with and without atrial pacing (control HR+ 15-20 beats/min) in 8 endurance trained cyclists (28±2 years, 181±2 cm, 72±2 kg, 66±1 mlO2/min/kg). Data were analyzed by repeated measures one-way ANOVA and Tukey's honestly significant difference (HSD) post hoc procedure. RESULTS: Atrial pacing increased HR by 17±1 beats/min during submaximal cycling and peak HR by 16±3 beats/min (184 ± 2 and 198 ± 4 beats/min in control and pace, respectively) (P<0.05). However, cardiac output and leg blood flow increased similarly in both trials and there was no difference in VO2max or exercise performance (time to exhaustion was 11:41±0.01 and 11:21±0.01 min in control and pace, respectively). In both trials, cardiac output increased linearly until 85% of WLmax but then plateaued in parallel to a drop in stroke volume and an increase in central venous, pulmonary arterial and mean arterial pressures (MAP)(P<0.05). CONCLUSION: The present results demonstrate for the first time that healthy humans can achieve a higher peak HR during atrial pacing and that increasing HR does not increase peak cardiac output, VO2max or maximal exercise performance Supported by Team Denmark

Effects of pericardial constraint and ventricular interaction on left ventricular hemodynamics in the unloaded heart

Pericardial constraint and ventricular interaction influence left ventricular (LV) performance when preload is high. However, it is unclear if these constraining forces modulate LV filling when the heart is unloaded, such as during upright posture, in humans. Fifty healthy individuals underwent right heart catheterization to measure pulmonary capillary wedge (PCWP) and right atrial pressure (RAP). To evaluate the effects of pericardial constraint on hemodynamics, transmural filling pressure (LVTMP) was defined as PCWP-RAP. Beat-to-beat blood pressure (BP) waveforms were recorded, and stroke volume (SV) was derived from the Modelflow method. After measurements at -30 mmHg lower body negative pressure (LBNP), which approximates the upright position, LBNP was released, and beat-to-beat measurements were performed for 15 heartbeats. At -30 mmHg LBNP, RAP and PCWP were significantly decreased. During the first six beats of LBNP release, heart rate (HR) was unchanged, while BP increased from the fourth beat. RAP increased faster than PCWP resulting in an acute decrease in LVTMP from the fourth beat. A corresponding drop in SV by 3% was observed with no change in pulse pressure. From the 7th to 15th beats, LVTMP and SV increased steadily, followed by a decreased HR due to the baroreflex. A decreased TMP, but not PCWP, caused a transient drop in SV with no changes in HR or pulse pressure during LBNP release. These results suggest that the pericardium constrains LV filling during LBNP release, enough to cause a small but significant drop of SV, even at low cardiac filling pressure in healthy humans.

Effect of repeated water immersions on orthostatic tolerance and cardiovascular regulation during 70° head‐up tilt testing

Water immersion (WI) reduces orthostatic tolerance (OT) and alters physiological responses to orthostatic stress, but the effect of repeated WI is unknown. Eight healthy men (35±2 yrs; mean±SEM) underwent 70° head‐up tilt (HUT) testing before and after 6‐hr O2‐breathing WI on 5 consecutive days (e.g. WI/1..WI/5). Heart rate (HR), blood pressure (BP: SBP, DBP, MAP), cardiac output (Q), limb blood flow (BF), stroke volume (SV), plasma volume (PV) and systemic vascular resistance (SVR) were measured during supine baseline (BL) and HUT. All data are compared to pre‐WI/1 BL values. Supine: HR and MAP were unchanged after repeated WI. Q, SV, and PV were reduced, and SVR increased after WI/1 (p&lt;0.001). The drop in SV (~15 ml) persisted despite a return of PV to BL before WI/4 and/5. HUT: After WI/1, HR increased more than pre‐WI/1 (+32±3 vs +23±3 bpm) to compensate for lower SV, but SBP was reduced (−10±4 mmHg) (p&lt;0.001). The tachycardic response to HUT was augmented over the week (+42±3 bpm, p&lt;0.001), and SBP was further reduced after WI/5 (p=0.03), even though SV, SVR, and limb BF at post‐WI/5 were comparable to post‐WI/1. OT (max ΔHR during HUT) declined after WI/1 (p&lt;0.001) and continued to diminish over repeated WI (p=0.02). We conclude that repeated WI exposures exacerbate immersion‐related reductions in OT. The responses suggest a shift in systemic and regional mechanisms to maintain BP and BF.Support: ONR N0001409WX20220

The role of muscle pump in the development of cardiovascular drift

This study examined the role of muscle pump in the development of cardiovascular drift (CVdrift) during cycling. Twelve healthy males (23.4 +/- 0.5 years, mean +/- SE) exercised for 90 min with 40 and 80 pedal revolutions per minute (rpm) at the same oxygen consumption, in two separate days. CVdrift was developed in both conditions as indicated by the drop in stroke volume (SV) and the rise in heart rate (HR) from the 20th min onwards (Delta SV = -16.2 +/- 2.0 and -17.1 +/- 1.0 ml beat(-1); Delta HR = 18.3 +/- 2.0 and 17.5 +/- 3.0 beats min(-1) for 40 and 80 rpm, respectively, P < 0.05) but without difference between conditions. Mean cardiac output (CO2 rebreathing) was 14.7 +/- 0.3 l min(-1) and 15.0 +/- 0.3 l min(-1), and mean arterial pressure was 100.0 +/- 1.0 mmHg and 96.7 +/- 0.8 mmHg for 40 and 80 rpm, respectively, without significant changes over time, and without difference between conditions. Electromyographic activity (iEMG) was lower throughout exercise with 80 rpm (35.6 +/- 1.2% and 11.0 +/- 1.0% for 40 and 80 rpm, respectively). Similarly, total hemoglobin, determined with near-infrared spectroscopy (NIRS) was 58.0 +/- 0.8 (AU) for 40 rpm and 53.0 +/- 1.4 (arbitrary units) for 80 rpm, from 30th min onwards (P < 0.05), an indication of lower leg blood volume during the faster pedal rate condition. Thermal status (rectal and mean skin temperature), blood and plasma volume changes, blood lactate concentration, muscle oxygenation (NIRS signal) and the rate of perceived exertion were similar in the two trials. It seems that muscle pump is not an important factor for the development of CVdrift during cycling, at least under the present experimental conditions.

Sublingual Nitroglycerin Used in Routine Tilt Testing Provokes a Cardiac Output-Mediated Vasovagal Response

We set out to determine the effect of sublingual nitroglycerin (NTG), as used during routine tilt testing in patients with unexplained syncope, on hemodynamic characteristics and baroreflex control of heart rate (HR) and systemic vascular resistance (SVR). Nitroglycerin is used in tilt testing to elicit a vasovagal response. It is known to induce venous dilation and enhance pooling. Also, NTG is lipophilic and readily passes cell membranes, and animal studies suggest a sympatho-inhibitory effect of NTG on circulatory control. Routine tilt testing was conducted in 39 patients with suspected vasovagal syncope (age 36 +/- 16 years, 18 females). Patients were otherwise healthy and free of medication. Before a loss of consciousness set in, oncoming syncope was cut short by tilt-back or counter-maneuvers. Finger arterial pressure was monitored continuously (Finapres). Left ventricular stroke volume (SV) was computed from the pressure pulsations (Modelflow). Spontaneous baroreflex control of HR was estimated in the time and frequency domains. During tilt testing, 22 patients developed presyncope. After NTG administration but before presyncope, SV and cardiac output (CO) decreased (p < 0.001), whereas SVR and HR increased (p < 0.001) in all patients. Arterial pressure was initially maintained. Baroreflex sensitivity decreased after NTG. On Cox regression analysis, the occurrence of a vasovagal response was related to a drop in SV after NTG (hazard ratio 0.86, p = 0.005). The cardiovascular response to NTG is similar in vasovagal and non-vasovagal patients, but more pronounced in those with tilt-positive results. The NTG-facilitated presyncope appears to be CO-mediated, and there is no evidence of NTG-induced sympathetic inhibition.

Endoscopic localization and assessment of coronary arteries by 13 MHz epicardial ultrasound

Background In totally endoscopic coronary artery bypass grafting the target coronary artery is difficult to locate and assess. We explored the capacity of a high-frequency epicardial ultrasound mini-transducer (Aloka, Tokyo, Japan) to endoscopically locate and assess the left anterior descending (LAD), third obtuse marginal (OM3), and right posterior descending (RDP) coronary arteries. Methods In eight pigs, the LAD, OM3, and RDP were endoscopically exposed. The mini-transducer was manipulated by the “da Vinci” telemanipulation system (Intuitive Surgical, Inc, Mountain View, CA) over the unstabilized and stabilized epicardium to identify the target artery, obtain a scout scan, and both transverse and longitudinal images. Results In both unstabilized and stabilized conditions, the LAD and RDP were identified within a median of 29 seconds. In stabilized conditions, assessment was complete in 112 seconds (92 to 205) (median with range) for the LAD and 140 seconds (54 to 197) for the RDP. Stabilization of the OM3 was required for identification (16 [5 to 60]) and assessment (111 [82 to 225]). Overall identification was correct in 23 of 24 arteries. The OM branches and RDP became fully exposed endoscopically with stroke volume (SV) and mean arterial pressure (MAP) remaining at 67% ± 11% (mean ± standard error of the mean) and 70% ± 5% of baseline values, respectively. Scanning itself did not augment the decrease in SV and MAP significantly. Conclusions After proper endoscopic exposure and stabilization, robot-assisted epicardial ultrasound scanning enabled endoscopic identification and assessment of major coronary arteries within a median of 169 seconds per artery. Exposure, stabilization, and scanning were accompanied by an acceptable drop in stroke volume and mean arterial pressure.

Influence of gravity on cardiac performance.

Results obtained by the investigators in ground-based experiments and in two parabolic flight series of tests aboard the NASA KC-135 aircraft with a hydraulic simulator of the human systemic circulation have confirmed that a simple lack of hydrostatic pressure within an artificial ventricle causes a decrease in stroke volume of 20%-50%. A corresponding drop in stroke volume (SV) and cardiac output (CO) was observed over a range of atrial pressures (AP), representing a rightward shift of the classic CO versus AP cardiac function curve. These results are in agreement with echocardiographic experiments performed on space shuttle flights, where an average decrease in SV of 15% was measured following a three-day period of adaptation to weightlessness. The similarity of behavior of the hydraulic model to the human system suggests that the simple physical effects of the lack of hydrostatic pressure may be an important mechanism for the observed changes in cardiac performance in astronauts during the weightlessness of space flight.

Hemodynamic changes during displacement of the beating heart by the Utrecht Octopus method

Coronary bypass grafting of posterior circumflex branches requires full displacement of the heart (apex pointing ventrally), which, in the beating heart, results in an arterial pressure drop. We analyzed its origin. To facilitate displacement, the Utrecht "Octopus" method was applied in 8 anesthetized beta-blocked pigs and the beating heart was fully retracted. Displacement decreased stroke volume from 75 +/- 17 mL (mean +/- standard deviation) to 43 +/- 13 mL (p < 0.001), a 44% +/- 3% decrease that resulted in a decrease in cardiac output by 32% +/- 5% (mean +/- standard error of the mean; p < 0.001), a decrease in mean arterial pressure by 26% +/- 5% (p < 0.01), and an increase in heart rate by 26% +/- 6% (p < 0.01). Right ventricular end-diastolic pressure increased from 5 +/- 1 to 8 +/- 1 mm Hg (p < 0.01). Twenty degrees head-down tilt normalized cardiac output and mean arterial pressure. Right ventricular end-diastolic pressure increased to 10 +/- 2 mm Hg (p < 0.001) and left ventricular end-diastolic pressure to 11 +/- 3 mm Hg (p < 0.01). Displacement of the beating heart in the pig induced a 44% drop in stroke volume, which is attributed to biventricular interference with pump function. The Trendelenburg maneuver reestablished the control circulatory status at the expense of augmented right and left ventricular preloads and an increased heart rate.

Hemodynamic adaptation to orthostatic stress after orthotopic heart transplantation

The purpose of this study was to compare the effects of orthostatic stress on cardiovascular stability in heart transplant recipients early and late after transplantation and in healthy controls. After transplantation, cardiac reinnervation is heterogeneous, with reports of sympathetic reinnervation after 5 months and parasympathetic reinnervation after 2 to 3 years. Sixteen heart transplant recipients early (less than 5 months) after transplantation, 17 recipients late (1 year or more) after transplantation, and 16 matched healthy controls were subjected to 45 minutes of passive upright tilt, with the following variables measured before, during, and after the procedure: cardiac output, heart rate, stroke volume, mean arterial pressure, systemic vascular resistance, and plasma norepinephrine. At rest, heart rate (p < 0.0005) and mean arterial pressure (p = 0.003) were higher, and stroke volume was lower (p < 0.0005), in transplant recipients than they were in controls. With orthostasis, heart rate increased by 30% in controls and by 23% in the late posttransplantation group compared with 13% in the early posttransplantation group (p = 0.028); drop in stroke volume was three times more among controls than among those in either transplantation group (p < 0.001); late transplant recipients had higher norepinephrine increases than did the other two groups (p = 0.012). With the exception of heart rate, patterns of hemodynamic response to orthostatic stress after transplantation remain consistent over time and differ from controls. Among transplant recipients, higher mean arterial pressure mitigates the force of gravity and prevents drops in stroke volume. Clinicians may anticipate that transplant recipients will tolerate postural maneuvers well. Later after transplantation, however, orthostatic tolerance is associated with increased norepinephrine release, consistent with enhanced sympathoactivation.

Cardioinhibitory effect of atrial peptide in conscious rats

The hemodynamic and renal excretory responses to 150-min atriopeptin II (AP II) infusion (330 ng X kg-1 X min-1) were assessed in five chronically instrumented rats with (FR protocol) and without (NR protocol) replaced urinary fluid losses. The observed changes were compared with those obtained by vehicle in the same rats. The hypotension seen with AP II infusion (120-min value: -27 +/- 2%, FR and NR responses combined) was due solely to a decreased cardiac output (CO; 120-min combined value: -34 +/- 3%). Total peripheral resistance remained unchanged or slightly elevated. A drop in stroke volume plus a later-developing (by 75-90 min) decrease in heart rate contributed to the CO decline. This latter bradycardic component, the opposite response to that typically produced reflexly by hypotension, was reversed by atropine sulfate treatment at 120 min and may thus be neural in origin. The finding of similar hemodynamic changes in the FR and NR rats and the lack of a significant effect of AP II on hematocrit suggest that volume depletion or a plasma extravasation were not contributors to the cardioinhibitory effect of the peptide.

The early circulatory and ventilatory response to voluntary and electrically induced exercise in man.

1. The ventilatory and circulatory responses to electrically induced leg exercise (EEL) were studied in seven normal subjects and compared with the responses to performing the same exercise voluntarily (EV). 2. EEL was produced by surface electrode stimulation of the quadriceps and hamstring muscle groups. This produced a push-relax pattern of exercise against a spring load and was free of any pain or discomfort. EV, at the same level, was achieved by subjects copying a display of timing and force information on a storage oscilloscope. 3. Cardiac output was estimated using validated Doppler ultrasound measurements of the velocity in the ascending aorta, combined with an estimate of aortic cross-sectional area using M-mode echocardiography. 4. Data from EV and EEL exercise runs were matched, within subjects, for the increase in oxygen consumption during the first 30 s of exercise; there were no significant differences between the resting states prior to either form of exercise. 5. The first ten beats of exercise were used to study the circulatory on-transient. The cardiac output responses to both EV and EEL were similar; however, in EV alone there was an initial significant drop in stroke volume and a slightly greater rise in heart rate. 6. The first five breaths of the response were used to study the ventilatory on-transient, and by measuring cardiac output, stroke volume and heart rate throughout each breath, the relationship between circulatory and ventilatory variables could be assessed. Ventilation showed a significantly greater rise at the onset of exercise during EV than during EEL; PET,CO2 (end-tidal CO2 pressure) showed small but significant falls for both EV and EEL. 7. The circulatory changes on a breath-by-breath basis are similar for EV and EEL although the ventilatory changes differ. In both EV and EEL the average increase in ventilation at the onset of exercise is proportionally greater than the average increases in cardiac output. Individual exercise runs show no particular relationship between circulatory and ventilatory change. 8. The results provide no support in man during mild leg exercise for a 'cardiodynamic' drive to breathing.

Extending the limits of hemodilution on cardiopulmonary bypass using stroma-free hemoglobin solution

Ten swine were subjected to exchange transfusion to a hematocrit level of 5% with either stroma-free hemoglobin solution (SFHS) or 7% albumin solution. Myocardial performance, oxygen kinetics, and myocardial metabolism were subsequently examined using a perfused, in situ, right heart bypass, swine heart model with control of preload, afterload, and heart rate. Animals were tested during a control period (hematocrit = 30%) and following exchange transfusion with either solution to a hematocrit level of 5%. We found that myocardial performance following albumin solution exchange could not be sustained on right heart bypass, and these animals had a stroke volume of zero at a left ventricular end-diastolic pressure of 14 torr. SFHS animals had a significant drop in stroke volume at 14 torr following exchange (20 +/- 3 versus 10 +/- 4, p < 0.025), but this 50% performance level could be sustained. Coronary blood flow rose and myocardial oxygen consumption fell in both groups, although the statistically nonsignificant mean differences were less with SFHS. Arterial-coronary sinus oxygen difference fell significantly (p < 0.05) with albumin solution (7.3 +/- 0.8 versus 2.2 +/- 0.2) and nonsignificantly with SFHS (5.6 +/- 0.4 versus 4.1 +/- 0.7). Lactate production occurred in both groups, but was greater with albumin (34% +/- 6%) than with SFHS (3% +/- 16%). No changes in myocardial tissue gasses were noted in either group. Although myocardial performance decreased and some lactate production occurred with SFHS, we believe these comparative results provide promise in the eventual utilization of an oxygen-carrying agent such as SFHS to extend the limits of hemodilution to a hematocrit value of 5% or less.

Mechanical performance of the left ventricle at early stages of experimental ischaemia. Mechanism of shortening of ejection period.

A marked decrease in the duration of left ventricular ejection time and a drop in stroke volume were observed in the dog during the first 30–60 sec of experimental occlusion of the left descending coronary artery. It has been found that these changes in ventricular performance result from additional displacement (shortening) of the non-ischaemic parts of the left ventricle leading to early dissipation of wall tension. This additional displacement is evoked by shortening of the time-to-peak tension and early relaxation of the ischaemic area. The mechanism described in this paper is proposed as a model of ventricular performance during coronary pain.