Haemodynamics II PRESSURES IN THE CARDIOVASCULAR SYSTEM Dr. shafali singh

Contd.. Mean pressure in the aorta is very high, averaging 100 mm Hg. This high mean arterial pressure is a result of two factors: (a)the large volume of blood pumped from the left ventricle into the aorta (cardiac output) (b)and the low compliance of the arterial wall. The pressure remains high in the large arteries, which branch off the aorta, because of the high elastic recoil of the arterial walls. Thus, little energy is lost as blood flows from the aorta through the arterial tree

Beginning in the small arteries, arterial pressure decreases, with the most significant decrease occurring in the arterioles. At the end of the arterioles, mean pressure is approximately 30 mm Hg. This dramatic decrease in pressure occurs because the arterioles constitute a high resistance to flow. Since total blood flow is constant at all levels of the cardiovascular system, as resistance increases, downstream pressure must necessarily decrease (Q = ΔP/R )

Contd.. In the capillaries, pressure decreases further for two reasons:  frictional resistance to flow and  filtration of fluid out of the capillaries When blood reaches the venules and veins, pressure has decreased even further. Pressure in the vena cava is only 4 mm Hg and in the right atrium is even lower at 0 to 2 mm Hg.

DETERMINANTS OF ARTERIAL BLOOD PRESSURE

Static elastic characteristics (compliance)

Factors Affecting Systolic Pressure Systolic blood pressure is the highest pressure in the systemic arteries during the cardiac cycle(which is during the max ejection phase of systole). The main factor determining systolic blood pressure on a beat-to-beat basis is stroke volume. An increase in stroke volume increases systolic blood pressure and a decrease in stroke volume decreases systolic blood pressure.

Factors Affecting Diastolic Pressure Diastolic blood pressure is the minimum pressure reached in the systemic arteries during the diastole of the heart. The main factor determining diastolic blood pressure is peripheral resistance, which is determined by the resistance of the arterioles. Other factor is the elasticity of the aorta and large branches ( i.e recoil of the aorta)

Factors Affecting Mean Pressure Mean pressure = diastolic + 1/3 pulse pressure Mean arterial pressure (MAP) is the average of all the pressures measured during the cardiac cycle. determined by only two variables: cardiac output and TPR. CO can be considered circulating volume. The blood stored in the systemic veins and the pulmonary circuit would not be included in this volume. TPR is the resistance of all vessels in the systemic circuit. By far the largest component is the resistance in the arterioles.

Pulse pressure Is the difference between the systolic and diastolic pressures. Two major factors affect the pulse pressure: (1) the stroke volume output of the heart and (2) the compliance(total distensibility) of the arterial tree. A third, less important factor is the character of ejection from the heart during systole.

Pulse pressure Other factors remaining unchanged,the magnitude of pulse pressure indicates the stroke volume. As blood is ejected from the left ventricle into the arterial system, arterial pressure increases because of the relatively low compliance of the arteries. Because diastolic pressure remains unchanged during ventricular systole, the pulse pressure increases to the same extent as the systolic pressure.

Pulse Pressure Is Determined Largely by Stroke Volume and Arterial Compliance Arterial compliance is a nonlinear variable that depends on the volume of the aorta and major arteries. The volume of the aorta and major arteries is dependent on mean arterial pressure, meaning that pulse pressure is indirectly dependent on mean arterial pressure As mean arterial pressure increases, arterial compliance decreases. As arterial compliance decreases, a given stroke volume causes a larger pulse pressure

Q Pulse pressure is (A) the highest pressure measured in the arteries (B) the lowest pressure measured in the arteries (C) measured only during diastole (D) determined by stroke volume (E) decreased when the capacitance of the arteries decreases (F) the difference between mean arterial pressure and central venous pressure

IN THE CLINIC Patients who have severe congestive heart failure or who have suffered a severe hemorrhage –are likely to have a very small arterial pulse pressure because their stroke volumes are abnormally small. Individuals with aortic valve regurgitation have-large stroke volumes, as in, are likely to have an increased arterial pulse pressure. Well-trained athletes at rest – tend to have large stroke volumes because their heart rates are usually low. The prolonged ventricular filling times in these individuals induce the ventricles to pump a large stroke volume, and hence their pulse pressure is large.

What are the physiological variations in blood pressure? Age Sex Body build and obesity Diurnal variation; sleep Digestion Emotional stress Posture Muscular exercise

Effect of Gravity

Fluid standing in a container exerts pressure proportional to the height of the fluid above it. The pressure at a given depth depends only on the height of the fluid and its density and not on the shape of the container. This hydro-static pressure is caused by the force of gravity acting on the fluid.

Blood Pressure Measurement in Humans In hospital intensive care units, needles or catheters may be introduced into the peripheral arteries of patients to measure arterial blood pressure directly by means of strain gauges. Ordinarily, blood pressure is estimated indirectly by means of a sphygmomanometer

Regulation of Blood pressure  Rapid control a.Baroreceptor reflex b.chemoreceptor reflex c.Low pressure receptors- atrial &pulmonary artery & vein. d.CNS ischemic response- last ditch stand-cushings reaction  Intermediate control a.Stress relaxation mechanism b.Capillary fluid shift mechanism  Long term regulation a.Renin- Angiotensin mechanism

Reflexes- simple feedback loops That include sensors to monitor pressure and flow, an integrator to compare cur-rent with preset pressure values, and effector mechanisms that make any necessary adjustments

Sensors 1.High-pressure arterial baroreceptors located in the aortic arch and carotid sinus, 2.Low-pressure cardio-pulmonary receptors, 3.Chemoreceptor

Baroreceptor areas in the carotid sinus and aortic arch. X, sites where receptors are located. The carotid and aortic bodies, which contain chemorecept ors, are also shown.

V The main receptors of the system are located in the carotid sinus. Here the receptors monitor the stretch of the vessel wall as an index of arterial blood pressure. The afferents are always active, with impulses traveling centrally. This is necessary if both increases and decreases in blood pressure are to be detected.

V The medulla interprets only the afferent activity as an index of blood pressure. A rise in afferent activity signals of an increase in blood pressure, and a loss of afferent activity signals of a decrease in blood pressure. An increase in afferent activity stimulates parasympathetic centers and inhibits sympathetic centers in the medulla and vice versa

Cardiopulmonary receptors: A second set of baroreceptors is found in low- pressure regions of the cardiovascular system. They provide the CNS with information about the “fullness” of the vascular system, and their principal role is in modulating renal unction. However, because fullness correlates with ventricular preload, they also have a role in maintaining MAP.

Chemoreceptor reflex Carotid & aortic bodies Stimuli - ↓O 2, ↑CO 2 & ↑H + ion. Signals from chemoreceptor excite vasomotor center, which elevates BP More important in respiratory control

Baroreceptor Reflex (posture )

Chemoreceptor reflex BP < 60 mm Hypoxia hypercapnoea Chemoreceptor Respiratory centre NTS Vaso Motor Center Sympathetic Cardio inhibitory center Vagal tone tachycardia COBP

Cushing reflex mechanism: BP <40 mm of Hg Cerebral hypoxia,Hypercapnoea Vaso Motor Center Symp Nervous System vasoconstriction BP +

Integration with other central and peripheral pathways a. Brainstem: The brainstem also contains a respiratory cen- ter that controls breathing. The cardiovascular and respiratory centers work in close cooperation with each other to maintain optimal arterial PO2 and PCO2. b. Hypothalamus: Hypothalamic control centers help coordi- nate vascular responses to changes in external and internal body temperatures c. Cortex: Cortical control centers account for changes in cardiovascular performance induced by emotions (fainting or anticipatory changes associated with exercise, for example). d. Pain centers: Pain centers can precipitate profound changes in blood pressure by manipulating cardiovascular center output.

Renin-Angiotension-Aldosterone System When blood pressure and flow are reduced in renal artery, juxtaglomerular apparatus secretes renin. Renin converts angiotensinogen to angiotensin I. Angiotensin I is converted to angiotensin II by ACE. Angiotensin II: – Powerful vasoconstrictor. – Stimulates production of aldosterone. – Stimulates thirst.

Renin-Angiotension-Aldosterone System (continued)

Angiotensin II has four effects (1) It stimulates the synthesis and secretion of aldosterone by the adrenal cortex. ■ Aldosterone increases Na+ reabsorption by the renal distal tubule, thereby increasing extracellular fluid (ECF) volume, blood volume, and arterial pressure. ■ This action of aldosterone is slow because it requires new protein synthesis. (2) It increases Na+–H+ exchange in the proximal convoluted tubule. ■ This action of angiotensin II directly increases Na+ reabsorption, complementing the indirect stimulation of Na+ reabsorption via aldosterone. ■ This action of angiotensin II leads to contraction alkalosis. (3) It increases thirst. (4) It causes vasoconstriction of the arterioles, thereby increasing TPR and arterial pressure.