Karin Toska

Respiration-synchronous fluctuations in stroke volume, heart rate and arterial pressure in humans.

1. Simultaneous recordings of beat‐to‐beat left cardiac stroke volume (SV, pulsed ultrasound Doppler), mean arterial pressure (MAP) and heart rate (HR) were obtained in ten healthy young adults during spontaneous respiration at supine rest, before and after cholinergic blockade by atropine (0.035 mg kg‐1). 2. Respiration‐synchronous fluctuations in SV, HR, cardiac output (CO) and MAP were quantified by spectral analysis of the recordings of each of these variables. 3. Before atropine administration, respiration‐synchronous fluctuations in HR and SV were prominent. The changes in HR and SV were inversely related and variation in SV was the main source of respiratory variability in CO. Respiration‐synchronous fluctuations in MAP were mainly caused by variations in CO. 4. After cholinergic blockade, respiratory HR variations were eliminated, whereas the respiratory fluctuations in SV persisted. The fluctuations in CO and MAP increased. In this situation, mechanically induced variations in SV were not counteracted by inverse HR fluctuations and the influence on CO thus increased. 5. The main source of respiratory fluctuations in MAP in supine humans is thus variation in SV, while inverse, vagally mediated HR variations tend to reduce the fluctuations in CO and MAP.

Changes in blood pressure during healthy pregnancy: a longitudinal cohort study.

Objective: To study longitudinally changes in blood pressure (BP) and heart rate (HR) during healthy pregnancies and to evaluate the influence of parity, pregestational overweight, and excessive weight gain. Methods: A prospective longitudinal cohort study of 57 healthy white women with singleton pregnancies. BP and HR were measured repeatedly at gestational age 14–16 weeks, 22–24 weeks, 30–32 weeks, 36 weeks, and 6 months postpartum using both an oscillometric measurement device (Dinamap) and finger arterial pressure (Finometer PRO). Results: SBP, DBP, and mean arterial pressure (MAP) reached a statistically significant trough at gestational age 22–24 weeks using both measurement devices. When compared with the nonpregnant measurement, SBP at gestational age 22–24 weeks was 6.2 mmHg [95% confidence interval (95% CI) 1.3–11.2] lower measured by Finometer and 7.2 mmHg (95% CI 4.2–10.1) lower measured by Dinamap. DBP and MAP were 8.9 mmHg (95% CI 4.6–13.2) and 9.8 mmHg (95% CI 5.3–14.2) lower measured by Finometer. Measured by Dinamap, DBP and MAP were 4.5 mmHg (95% CI 1.7–7.3) and 5.4 mmHg (95% CI 2.8–7.9) lower at gestational age 22–24 weeks when compared with the nonpregnant state. SBP was significantly higher in women with pregestational BMI at least 25 kg/m2 with both measurement devices (both P < 0.05). There were no differences in SBP, DBP, or MAP depending on parity or excessive weight gain. Conclusion: BP measured repeatedly by two different noninvasive devices during pregnancy and postpartum showed a statistically significant drop in mid-pregnancy, followed by a progressive increase until term.

Respiratory sinus arrhythmia: opposite effects on systolic and mean arterial pressure in supine humans

1 Are arterial blood pressure fluctuations buffered or reinforced by respiratory sinus arrhythmia (RSA)? There is still considerable debate about this simple question. Different results have been obtained, triggering a discussion as to whether or not the baroreflexes are responsible for RSA. We suspected that the measurements of different aspects of arterial pressure (mean arterial pressure (MAP) and systolic pressure (SP)) can explain the conflicting results. 2 Simultaneous recordings of beat‐to‐beat MAP, SP, left cardiac stroke volume (SV, pulsed ultrasound Doppler), heart rate (HR) and respiration (RE) were obtained in 10 healthy young adults during spontaneous respiration. In order to eliminate HR variations at respiratory frequency we used propranolol and atropine administration in the supine and tilted positions. Respiration‐synchronous variation in the recorded variables was quantified by spectral analysis of the recordings of each of these variables, and the phase relations between them were determined by cross‐spectral analysis. 3 MAP fluctuations increased after removing heart rate variations in both supine and tilted position, whereas SP fluctuations decreased in the supine position and increased in the head‐up tilted position. 4 RSA buffers respiration‐synchronous fluctuations in MAP in both positions. However, fluctuations in SP were reinforced by RSA in the supine and buffered in the tilted position.

Stroke volume decreases during mild dynamic and static exercise in supine humans.

Aim:  The contributions of cardiac output (CO) and total peripheral resistance to changes in arterial blood pressure are debated and differ between dynamic and static exercise. We studied the role stroke volume (SV) has in mild supine exercise.

Changes in pulmonary function during pregnancy: a longitudinal cohort study

Please cite this paper as: Grindheim G, Toska K, Estensen M, Rosseland L. Changes in pulmonary function during pregnancy: a longitudinal cohort study. BJOG 2012;119:94–101.

Low-frequency fluctuations in heart rate, cardiac output and mean arterial pressure in humans: what are the physiological relationships?

Objective Cardiovascular variability is a complex physiological phenomenon associated with the outcome of cardiovascular diseases. Blood pressure oscillations may cause cardiovascular complications, which, however, are also claimed to have antihypertensive effects. The physiological understanding is limited. This study evaluates whether oscillations in heart rate (HR) and cardiac output (CO) buffer fluctuations at approximately 0.1 Hz in arterial blood pressure (Mayer waves). Method We recorded mean arterial pressure (MAP), left cardiac stroke volume (SV), and HR in 10 healthy humans during autonomic blockade in supine and tilted (30 degrees) position. Variability in the cardiovascular variables at 0.04–0.15 Hz and phase angles (time lags) between the variables were calculated by spectral analysis. Results Fluctuations in cardiovascular variables at 0.1 Hz decreased after removal of HR variability (HRV) by propranolol and atropine in the supine position. Tilting from supine did not change fluctuations in MAP or total peripheral resistance (TPR), whereas variations in CO decreased. Variations in CO remained decreased in tilt after atropine compared to supine control, whereas variations in MAP and in TPR were unchanged. HRV were in phase with oscillations in CO. Variations in CO were in inverse phase with variations in TPR. Conclusion TPR oscillations produce fluctuations in MAP at 0.1 Hz. HRV produces CO variations, but CO variations do not efficiently buffer MAP variations during supine rest and mild ortostasis. Both feedback and feedforward mechanisms are responsible for the interaction between HR and MAP.

Handgrip contraction induces a linear increase in arterial pressure by peripheral vasoconstriction, increased heart rate and a decrease in stroke volume.

Aim:  The hypothesis that isometric handgrip induces a progressive increase in arterial pressure and a linear increase in setpoint for arterial pressure control was tested.

Model simulations of cardiovascular changes at the onset of moderate exercise in humans.

We have tested whether the cardiovascular changes at the onset of exercise could be simulated only by an increase in the baroreflex set point and locally induced vasodilatation in the exercising muscles. The mathematical model consists of a heart, a linear elastic arterial reservoir and two parallel resistive vascular beds. The arterial baroreflex loop is modelled by three separate time domain processing objects, each with its own gain, time constant and delay. These are intended to simulate the action of a sympathetic signal to the peripheral vascular bed, a parasympathetic signal to the heart and a sympathetic signal to the heart. We used this model with previously published experimental data to estimate the unknown parameters in the reflex control loop. In all 10 subjects and in the global averaged response, the short‐term cardiovascular responses were adequately simulated by using individual sets of parameters in the model. An increase in the baroreflex set point and locally induced vasodilatation in the exercising muscles can explain almost all of the cardiovascular changes in the recorded variables (mean arterial pressure, RR interval and stroke volume) at the onset of exercise.

Lactate elimination and glycogen resynthesis after intense bicycling

Objective. Muscles break down glycogen to lactate during intense exercise, and in the recovery period, glycogen reappears while lactate disappears. The purpose of this study was to examine to what extent lactate is resynthesized to glycogen within the formerly active muscles themselves in man. Material and methods. Fifteen healthy young men cycled for 2 min to exhaustion. Muscle biopsies were taken from the knee extensor muscle before the exercise, just after the ride, and again after 45 min of recovery. In addition, blood samples were taken from the femoral artery and vein, and the leg blood flow was measured using the ultrasound Doppler technique. The muscle biopsies were analysed for glycogen, lactate and other metabolites, and the blood samples were analysed for lactate and glucose. The exchanges of lactate and glucose of the leg were assessed by multiplying the measured arterio–venous (a–v) differences by the blood flow. Results. During the exercise the muscles broke down 20±4 mmol glycogen kg−1 wet muscle mass and produced 26±1 mmol lactate kg−1. In the recovery period after 24±1 mmol lactate kg−1 had disappeared, of which 48 % was released to the blood, 52 % disappeared within the muscle. An R‐value of 0.62 across the leg suggests that none of the lactate was oxidized. Altogether, 10±3 mmol glycogen kg−1 reappeared during recovery. Glucose uptake accounted for 2 mmol kg−1 and glycolytic intermediates (G‐6‐P and free glucose) accounted for 4 mmol kg−1; 4 mmol glycogen kg−1 (42 %) reappeared from unknown sources. Conclusions. The present data are compatible with the idea that around half of the lactate produced during intense bicycling is resynthesized to glycogen within the working muscles themselves in the recovery period after the bicycling.

Beat-to-beat measurement of the finger arterial pressure pulse shape index at rest and during exercise

Arterial pressure waveform can be characterized by the pulse shape index kpulse determined as kpulse = (Pmean − Pdiast) / (Psyst − Pdiast). For brachial artery, the shape index value of 0·33 is usually applied to approximate Pmean from the measured Psyst and Pdiast. Our purpose was to test whether this value can validly be applied to finger vascular beds under different experimental conditions. By using Finapres®, we non‐invasively estimated the beat‐to‐beat values of kpulse in the fingers of young healthy persons in supine position at rest and during a 4‐min moderate exercise (rhythmical exercise with the quadricep muscles in combination with handgrip compression). To detect intensive peripheral vasoconstrictions, a laser‐Doppler probe was attached to the thumb pulp of the same hand. Periods of 30 s without intensive vasoconstriction for rest, different stages of exercise and recovery were involved in the analysis in every subject. The results demonstrated that the group‐averaged value of kpulse (median with a 95% confidence interval) in the fingers of 11 healthy volunteers aged from 20 to 24, equalled 0·33 (0·31– 0·34), 0·31 (0·28–0·34), 0·35 (0·33–0·39) and 0·38 (0·34–0·43) for rest, first and second stages of exercise and recovery, respectively. We conclude that in the fingers of young healthy persons in supine position formula Pmean = Pdiast + 1/3 (Psyst − Pdiast) gives an adequate approximation for rest and low intensity exercise (first stage), and slightly underestimates the actual finger mean blood pressure during moderate exercise (second stage) and recovery.