(5)Cardiac_out_put.pptx respiratory physiology

Cardic physiology

1. Regulation of arterial blood pressure(1) Cardiac out put

2. Objectives Describe how the pattern of contraction and relaxation in the heart results in a normal pattern of blood flow. Delineate the ways by which cardiac output can be up-regulated in the setting of specific physiologic demands for increased oxygen supply to the tissues, such as exercise . Describe how the pumping action of the heart can be compromised in the setting of specific disease states.

3. Introduction   Normal arterial blood pressure depends on: Cardiac output Peripheral resistance and Blood volume

4. Arterial blood pressure : Is the force that causes the blood flow in the vessels to maintain tissues perfusion . Pressure = Flow x Resistance. The blood flows to the tissues per unit of time is proportional with the cardiac output

5. Cardiac output Defined as the volume of blood pumped by each ventricle per minute. In healthy adults it is about 5L/min at rest. The COP depends on the heart rate and on the stroke volume. The COP =heart rate × stroke volume = 72/min × 70 ml = 5040 ml/l ≈ 5L/min

6. Control of cardiac output   The control of COP is essential for adjustment of the blood pressure and blood flow under different physiological and pathological conditions

7. Regulation of the heart rate It can be neural or humoral .  Neural regulation: Depends on the cardiac innervation. The sympathetic and the parasympathetic exert their effects on the SA node (the pace maker) and therefore modify the heart rate.

8. The vagus exerts a continuous flow of impulses (the vagal tone) which tends to slow the heart rate. Inhibition of vagal tone cause the heart to beat faster Inhibition of the sympathetic nerves cause a slight decrease in the heart rate but their stimulation results in a great increase in sinus rhythm.

9. The regulation of the heart rate by autonomic nerves is achieved by the cardiac centers which located mainly in the medulla oblongata. They include two main centers: The cardioinhibitory centre (depressor area) The vasomotor area (pressor area). These centers receive inputs from the baroreceptors and chemoreceptors.

10. Nervous Control of Cardiac Activity

11. The baroreceptors Are stretch receptors located in the arterial system mainly in the carotid and aortic sinuses. They are sensitive to the changes in the blood pressure within the physiological ranges.

12. Stimulation of the baroreceptors by a rise in the blood pressure produces reflex slowing of the heart by excitation of the cardioinhibitory centre and therefore decreasing the cardiac output

13. There is also a reflex inhibition of the vasomotor centre. This causes a decrease in the sympathetic vasoconstrictor tone to blood vessels leading to vasodilatation in the peripheral circulation and therefore a decrease in the peripheral resistance

14. The baroreceptors reflex decrease the blood pressure and bringing it back to normal. When the blood pressure falls, the baroreceptors impulses rapidly decrease in frequency leading to an increase in the heart rate, strength of myocardial contraction and peripheral vasoconstriction. All of these result in rapidly elevating the blood pressure to normal.

15. The chemoreceptors There are two types of chemoreceptors central and peripheral Are special cells situated in the carotid and aortic bodies. These receptors are sensitive to the changes in the po2, H + concentration and Pco 2 . They are stimulated by decrease in the po 2 (hypoxia) and a fall in the PH (acidosis). PCo2 is more effective on central chemoreceptors

16. When they are stimulated, the chemoreceptors send impulses to the cardiac centers which lead to an increase in the heart rate → cardiac output → blood pressure and improve the o2 delivery and co2 uptake by the circulation.

17. The Bainbridge reflex: Acts as a safeguard against accumulation of blood in the right side of the heart and venous system. The heart responds to an increase in the venous return by increasing the heart rate and possibly the stroke volume (i.e. COP).

18. Properioceptors in the joints and tendons detect the skeletal muscle movement and as a response they accelerate the heart rate. Emotional factors working through hearing, vision or even thought and dreams can accelerate the heart rate.

19. Regulation of stroke volume Volume of blood ejected by each ventricle with each beat   Depends on the venous return and myocardial contractility. Myocardial contractility : There are many factors that affect the myocardial contractility

20. The effect of Na + , K + and Ca ++ ions: Excess K + ( hyperkalaemia ) cause the cardiac muscle fibers to become weak Excess Ca ++ causes the myocardium to contract more strongly and the heart may go into spasm (Ca ++ rigor). Low Ca ++ causes relaxation of the cardiac muscle

21. Mechanical factors These are related to the state of stretch of the cardiac muscle at the beginning of contraction and this depend on the cardiac filling and therefore on the venous return(preloading of the cardiac muscle) and the resistance to myocardial muscle during contraction which proportional to the pressure in Aorta and pulmonary arteries ( afterloading of the cardiac muscle).

22. The length-tension relationship(preloading) According to the Starling's law , the stretch of the myocardium causes the muscle to contract more strongly. Thus the myocardial strength increases as the filling of the heart increases (i.e. as the venous return increases). This autoregulation mechanism safeguards against blood accumulation in the venous system or in the pulmonary circulation.

23. Aortic and pulmonary impedance ( afterloading ) High pressure in the aorta and pulmonary artery causes the contractile force to decrease because the ventricles have to contract against increased resistance and therefore the stroke volume decreased.

24. The heart rate As the heart rate increases, the duration of diastole becomes shorter and the EDV smaller (the filling of the heart decreases and the stroke volume decreases).

25. Effects of neural regulation Sympathetic stimulation increases the force of ventricular contraction. Parasympathetic stimulation has a little negative inotropic effect on the ventricles, while atrial contraction decreases.

26. The venous return Many factors affects return the blood through the venous system to the heart: Increase in blood volume (water & electrolytes). The venous pressure gradient The muscle pump. Respiratory pump. Gravity.

27. The muscle pump Many of the large veins in the extremities lie between skeletal muscles, so muscle contraction compresses the veins. This increases venous pressure, squeezing fluid in the veins forward toward the heart

28. Congestive Heart Failure Cardiac failure occurs when the cardiac output is insufficient to maintain the blood flow required by the body. This may be due to: Heart disease—resulting from myocardial infarction Congenital defects or to hypertension

29. Treatment of congestive heart failure is aimed at: Improving cardiac contractility Treating the symptoms Decreasing the load on the heart.

30. Shock is inadequate tissue perfusion Hypovolemic shock Distributive vasogenic or low resistance shock. C ardiogenic shock