The cardiac output is the volume of blood pumped from the heart every minute. It is obtained by the volume pumped with each beat (stroke volume) multiplied by the heart rate. The cardiac output increases during exercise and falls in the common type of heart failure. The stroke volume depends in part on the amount of blood in the ventricule at the end of diastole. This determines the degree of stretch of the myocardial fibre. The greater the stretch (within limits) the stronger the force of contraction and the greater the stroke volume (Starlings law of the heart).Control of the heart rate depends on the ratio of the sympathetic (increases) and parasympathetic (decreases) impulses to the sino atrial node which is the cardiac pacemaker. Receptors sensitive to pressure are located in the carotid sinus and the wall of the arch of the aorta.When the carotid sinus detects a sudden rise in arterial pressure, impulses pass from the carotid baroreceptors to the cardiac control centre in the medulla and impulses sent through the parasympathetic system reduce the heart rate. Similar effects result from the aortic baroreceptors as well. If the blood pressure drops the heart rate is reflexly increased. Various other reflexes from anger, fear, pain,temperature, etc. also increase the heart rate.
Blood Pressure
An adequate level of pressure is needed in the arteries to keep the blood flowing through the cardiovascular system. The chief determinant of arterial pressure is the volume of blood in the arteries and the important determinants of this are the cardiac output and the peripheral vascular resistance. The resistance offered by the arterioles accounts for almost half the total resistance in the systemic circulation. The muscle in the arterial wall allows them to constrict or dilate. When they constrict, the resistance increases and the blood pressure increases. The vasomotor centre in the medulla when stimulated sends impulses via the sympathetic to the smooth muscle in the arteries, arterioles and veins which results in their constriction.
Determinants of Vascular Tone
The vascular tone increases as the arterial size decreases. The tone at any time reflects the effects of excitory and inhibitory pathways. Neurotransmitters, physical forces like shear stress,intravascular pressure, metabolites and milleu of the surrounding tissue can all affect the vascular tone. Arterial segments where the endothelium is absent can also respond to stretch-the so-called
intrinsic myogenic tone.
The endothelium is an important modulator of tone. It can produce, release, activate many vasoactive factors like NO (nitric oxide), prostacyclin and thromboxane. Cholinergic stimulation releases an Endothelium derived relaxation factor (EDRF) shown to be NO. Endothelial denudation abolishes the vasodilatory effect of acetylcholine.There are chemoreceptors in the aortic and carotid bodies which sense a rise in PCO 2 (hypercapnia) and fall in O 2 saturation (hypoxia) and changes in pH. Appropriate stimuli are sent to the medullary centers. Vasomotor control is also exercised by higher centres in the cerebral cortex and hypothalamus which send impulses to the medullary centres. Local tissue mechanisms also affect local vasoconstriction and vasodilatation.
Venous Return
Blood Pressure
An adequate level of pressure is needed in the arteries to keep the blood flowing through the cardiovascular system. The chief determinant of arterial pressure is the volume of blood in the arteries and the important determinants of this are the cardiac output and the peripheral vascular resistance. The resistance offered by the arterioles accounts for almost half the total resistance in the systemic circulation. The muscle in the arterial wall allows them to constrict or dilate. When they constrict, the resistance increases and the blood pressure increases. The vasomotor centre in the medulla when stimulated sends impulses via the sympathetic to the smooth muscle in the arteries, arterioles and veins which results in their constriction.
Determinants of Vascular Tone
The vascular tone increases as the arterial size decreases. The tone at any time reflects the effects of excitory and inhibitory pathways. Neurotransmitters, physical forces like shear stress,intravascular pressure, metabolites and milleu of the surrounding tissue can all affect the vascular tone. Arterial segments where the endothelium is absent can also respond to stretch-the so-called
intrinsic myogenic tone.
The endothelium is an important modulator of tone. It can produce, release, activate many vasoactive factors like NO (nitric oxide), prostacyclin and thromboxane. Cholinergic stimulation releases an Endothelium derived relaxation factor (EDRF) shown to be NO. Endothelial denudation abolishes the vasodilatory effect of acetylcholine.There are chemoreceptors in the aortic and carotid bodies which sense a rise in PCO 2 (hypercapnia) and fall in O 2 saturation (hypoxia) and changes in pH. Appropriate stimuli are sent to the medullary centers. Vasomotor control is also exercised by higher centres in the cerebral cortex and hypothalamus which send impulses to the medullary centres. Local tissue mechanisms also affect local vasoconstriction and vasodilatation.
Venous Return
This is the amount of blood that is returned to the heart by the veins. This is influenced by various factors. Inspiration decreases the pressure in the central veins and thus increases the pressure gradient between the peripheral and central veins thus augmenting venous return. Skeletal muscle contraction also milks the venous flow towards the heart and the valves in the veins prevent gravitational return backwards. Significant veno dilatation can occur with conditions like sepsis and the use of certain drugs like nitrates. This can result in a serious fall in venous return. This can result in marked deterioration in conditions like right ventricular infarction and pericardial tamponade.
Preload
If other factors are unchanged the force of contraction depends on the degree of stretch of the myocardial fibres. In effect the preload is the ventricular end diastolic volume. It is influenced by the venous return, the compliance or distensibility of the ventricle and the atrial kick or atrial component of ventricular filling. The atrial contribution is particularly important in hypertrophied non compliant ventricules.
Afterload
The afterload is the resistance imposed by the aortic valve, aorta and peipheral arterial resistance.The left ventricule has to develop sufficient tension to overcome the afterload. This becomes increasingly difficult with a failing heart. Afterload reduction is therefore one of the targets in heart failure therapy.
Preload
If other factors are unchanged the force of contraction depends on the degree of stretch of the myocardial fibres. In effect the preload is the ventricular end diastolic volume. It is influenced by the venous return, the compliance or distensibility of the ventricle and the atrial kick or atrial component of ventricular filling. The atrial contribution is particularly important in hypertrophied non compliant ventricules.
Afterload
The afterload is the resistance imposed by the aortic valve, aorta and peipheral arterial resistance.The left ventricule has to develop sufficient tension to overcome the afterload. This becomes increasingly difficult with a failing heart. Afterload reduction is therefore one of the targets in heart failure therapy.
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