Systole duration, heart rates

Low-level, chronic-duration exposure of rats to lead (30 ppm lead acetate in the drinking water) for 18 months resulted in a 10-15 mm Hg increase in both systolic and diastolic blood pressure without any change in heart rate or histopathological evidence of damage to the kidney, heart, brain, aorta, or liver... 

Ephedrine increases systolic and diastolic blood pressure heart rate is generally not increased. Contractile force of the heart and cardiac output are both increased. Ephedrine produces bronchial smooth muscle relaxation of prolonged duration when administered orally. Aside from pupillary dilation, ephedrine has little effect on the eye. 

In 1964, Calesnick and Calesnlck et al. 5 reported that, when I was injected intravenously into normal male and female volunteers at 15 mg/kg (three subjects), both systolic and diastolic blood pressures were Increased immediately after the end of the infusion (usual duration, 15 min). The hypertension lasted for 1.5-4 h and was accompanied by a slight increase In heart rate. The plasma concentra-... 

Q1 Coronary arteries are the first to branch off the aorta. The heart has a large blood flow (200 ml min-1) but also has great metabolic needs and so has a relatively poor oxygen supply, with little in reserve when oxygen demands increase. At each heart beat (systole), the coronary arteries are compressed by cardiac contraction and blood flow diminishes to a low level. This effect is very marked in the left ventricle, and over 80% of coronary flow to the left ventricle occurs in the periods between beats (diastole). When heart rate increases (tachycardia), the duration of diastole decreases much more than the duration of systole, and the period available for perfusion of cardiac muscle diminishes. 

Cardiac muscle has a large oxygen requirement, and extraction of oxygen from coronary blood is high. The coronary arteries are compressed in systole, particularly in the left ventricle. Sympathetic stimulation, which increases heart rate and force, reduces the duration of diastole and increases myocardial oxygen consumption. A slow heart rate improves coronary perfusion, reduces oxygen demand and is beneficial for coronary perfusion. 

Quinidine has anticholinergic properties that can result in the blockade of impulses from the vagus nerve to the heart. This would prevent the slowing of the heart rate that is ordinarily produced by normal vagal stimulation. The resulting increased heart rate counters the direct depressant effect on the pacemaker. This can understandably complicate therapy from the clinical standpoint. The effectiveness of quinidine and procainamide treatment can be traced on ECG by the increase in the Q-T interval, which can be attributed to the increased duration of systole, as well as decreased intraventricular conduction velocity. 

Coronary blood flow is enhanced by Epi or by cardiac sympathetic stimulation under physiological conditions. The increased flow, which occurs even with doses that do not increase the aortic blood pressure, is the result of two factors. The first is the increased relative duration of diastole at higher heart rates (see below) this is partially offset by decreased blood flow during systole because of more forceful contraction of the surrounding myocardium and an increase in mechanical compression of the coronary vessels. The increased flow during diastole is further enhanced if aortic blood pressure is elevated by Epi as a consequence, total coronary flow may be increased. The second factor is a metabolic dilator effect that results from the increased strength of contraction and myocardial consumption due to direct effects of Epi on cardiac myocytes. This vasodilation is mediated in part by adenosine released from cardiac myocytes, which tends to override a direct vasoconstrictor effect of Epi that results from activation of a receptors in coronary vessels. 

Carbimazole abolished the systolic blood pressure decrease seen in the first 3 hours with digoxin, and also reduced the duration of the digoxin-induced diastolic blood pressure fall from 12 to 6 hours. The changes in heart rates, cardiac output and stroke volumes were not statistically significant, but inter-individual differences were large. " ... 

The relationship between the duration of the activation function (in ms) and the heart rate can be deduced from the duration of the QS2 interval. As shown in Beyar and Sideman (1984b), the end of systole is close to the peak of the activation function. It is assumed here that the duration of the activation function T is twice the duration of the QS2 interval. 

Heart rate, systolic/diastolic tension and electrocardiographic parameters (P-wave duration and QTc duration) were not statishcally different before compared with after treatment. As far as it is known, there is no study researching the effect of 1ST on P and QT wave measurements, in the literature, and further studies with longer periods of follow-up are needed to understand the effect of 1ST on the cardiovascular system. 

By increasing the rates of ventricular contraction and relaxation, Epi preferentially shortens systole and usually does not reduce the duration of diastole. Epi speeds the heart by accelerating the slow depolarization of sinoatrial (SA) nodal cells that takes place during phase 4 of the action potential (see Chapter 34). The amplitude of the AP and the maximal rate of depolarization (phased) also are increased. A shift in the location of the pacemaker within the SA node often occurs, owing to activation of latent pacemaker cells. In Purkinje fibers, Epi accelerates diastolic depolarization and may activate latent pacemakers. If large doses of Epi are given, premature ventricular contractions occur and may herald more serious ventricular arrhythmias. Conduction through the Purkinje system depends on the level of membrane potential at the time of excitation. Epi often increases the membrane potential and improves conduction in Purkinje fibers that have been excessively depolarized. 

---