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Biomedical subjects

K Pavek

Publications and source records attributed to K Pavek.

18 recordsLinked to original sources
PubMed1990

Salt sensitivity of blood pressure in patients with primary hypertension.

Objective measures of blood pressure (BP) sensitivity to 72-h salt depletion were evaluated. Salt sensitivity is defined as a measurable decrease of diastolic BP (DBP) after depletion. Changes in office auscultatory and oscillometric DBP were compared with oscillometric ambulatory DBP. In 35 women and men with mild hypertension, 24-h ambulatory DBP; sodium, potassium, albumin, and creatinine in 24-h urine; serum-creatinine; and body weight were measured before and at the end of the salt-free period. The oscillometric method detected larger and more uniform decreases in DBP compared to the auscultatory method. The salt depletion-induced changes in auscultatory DBP but not in ambulatory DBP were positively related to its baseline level. The salt sensitivity was positively related to the age and negatively related to the number of hypertensive symptoms. It was not related to body mass index and body weight decrease after salt depletion. The changes in ambulatory DBP were correlated to changes in office DBP (r = 0.46 for the auscultatory method; r = 0.58 for the oscillometric method). In only half the cases, the direction and size of pressure changes were reflected similarly in all three methods. Although the correlation between the methods points to the biological soundness of the salt sensitivity concept, the individual classification is prone to variation.

Adult↗
PubMed1989

Change in posture during sleep causes errors in non-invasive automatic blood pressure recordings.

When measured with automatic non-invasive monitors blood pressure is seen to fluctuate during sleep. The recorded blood pressure is influenced by the vertical distance between the heart level (zero reference) and the level of the brachial artery at the point of compression by the inflated cuff. In 20 randomly selected men, blood pressure was measured every 20 min during the night. The difference between consecutive recordings was 7.6 mmHg +/- 5.7/5.0 (s.d.), range 0-23/0-20 mmHg. The maximum blood pressure difference was 19 +/- 6.8/15 +/- 6.0, range 7-32/6-26 mmHg. These results were compared with the difference in blood pressure recorded on the left arm in 20 volunteers changing posture between four standardized recumbent postures. The posture change caused an average blood pressure difference of 9 +/- 6.1/9 +/- 6.5 mmHg, range 0-28/0-30 mmHg. The maximum blood pressure difference was 15 +/- 5.1/12 +/- 5.5 mmHg, range 5-27/(-)2-23 mmHg recorded between lying supine and lying on the right side. The similarity between differences and the variation in blood pressure during the recumbent posture indicates that changes in posture cause most of the night-time blood pressure variation recorded with non-invasive devices.

Blood Pressure↗
PubMed1981

[Physiopathology of anaphylactic and anaphylactoid shock. A cooperative retrospective study].

The pathophysiology of anaphylactic and anaphylactoid shock states suggests that the rapidly initiated, intensive therapeutic measures to be taken must involve: breathing (ventilation) of (with) 100% oxygen, continuous or semi-continuous sympathicomimetic therapy (epinephrine, isoprenalin, orciprenalin) avoiding excessive single doses, rapid intensive volume substitution, control of metabolic acidosis, bronchospasmolytic therapy, in case of laryngospasm intubation, if not possible coniotomy or transtracheal punction. In case of circulatory arrest possibly also cardiac massage, defibrillation, lidocain, cardioversion. In a retrospective study 91 cases of anaphylactic and anaphylactoid shock were analyzed. Cutaneous vascular changes. Vasodilation was reported in 30 cases, vasoconstriction in 15 cases. Hypovolemia. CVP as measured in 23 cases was less than or equal to 2 cmH2O in 12 cases; in 4 of these cases the early finding and in 2 a rather low hematocrit are in favour of venous blood sequestration. In 2 cases the increase of the hematocrit suggests an extravasation of as much as 1,2 and 1,81 of plasma, respectively. Increase of pulmonary arterial pressure. CVP increased in 2 out of 9 cases suggesting a high pulmonary arterial pressure. Decreased cardiac output (CO). In 3 cases CO as determined in a late shock phase diminished by 37--55%. Blood gas changes. PaO2 was as low as 47--61 mmHg in 4 out of 8 cases, PaCO2 being 29--34 mmHg in 2 of them. It suggests an insufficient oxygen transport. Myocardial involvement. Arrhythmias (non sinus-) were found in 38 cases, of which 14 ventricular arrhythmia and 13 asystole. Serious wave deformation concerned QRS (3), AV-block (2), intraventricular blocks (4). 5 times the reaction resulted in myocardial infarction. A localized coronary spasm in anayphylactic shock was observed during a coronary angiography. Respiratory impairment. Severe respiratory impairment was associated with anaphylactic and anaphylactoid shock in 31 cases (26 bronchospasm, 4 apnea, 1 laryngospasm).

Adolescent↗
PubMed1980

Videodensitometry and thermodilution for measuring left ventricular function.

In animal experiments contrast medium and physiologic saline were found to be equivalent as indicator substances in thermodilution. The ejection fraction is determined with approximately the same accuracy with thermodilution as with videodensitometry. The cardiac output, on the other hand, is smaller when determined with videodensitometry than with thermodilution. The results indicate that thermodilution gives too high values.

Animals↗
PubMed1979

Anaphylatoxin-induced shock and two patterns of anaphylactic shock: hemodynamics and mediators.

In the dog, different cardiorespiratory reactions were identified in two types of anaphylactic shock and in C5a-AT (anaphylatoxin)-induced shock. All three types had in common a portal blood pooling with consequent decrease in the venous return, cardiac output, and arterial pressure. In anaphylaxis (a) of the first type, at a low titer of hemagglutinating antibodies, the latent period was 68 s and heart and lung function was unchanged. In the second type, at high titer, the latency was 19 s and pulmonary hypertension and decreased heart contractility occurred. After AT injection pulmonary hypertension appeared with tachypnea and unchanged heart function. Tachyphylaxis, but not cross-over tachyphylaxis against the anaphylactic agent and AT was observed in dogs and isolated guinea pig lungs. AT induced a transient release and a, a prolonged release of histamine, prostaglandins (PGs), and thromboxane A2 and endoperoxides from guinea pig lungs. SRS-A was released only in a. Indomethacin inhibited AT-induced release of PGs in guinea-pig lungs and AT-induced hypotension in the dog though it did not prevent the drop in cardiac output. These model studies suggest that different patterns of clinical a. can occur, depending on the type of antibodies and/or mediators involved.

Anaphylatoxins↗
PubMed1978

Shock of anaphylactoid type induced by protamine: a continuous cardiorespiratory record.

The intravenous administration of protamine to a patient after cardiac bypass caused a sudden increase in airway resistance and lung stiffness, and a severe drop in arterial blood pressure. The ventilatory obstruction reached its maximum after 30 s and had returned almost to normal in 3 min. Arterial hypotension with low pulse amplitude, decreased heart rate and ST depression in the ECG tracing developed 1.5 min after the respiratory symptoms. In spite of rapid blood transfusion, arterial pressure reached a low level after 5 min, but rose after isoprenaline administration. It is suggested that changes in the vascular and respiratory compartments occur in parallel with, but independently of, myocardial injury and depressed cardiac contractility.

Airway Resistance↗