-12. -Ensherah Mokheemer - ABDULLAH ZREQAT. -Faisal Mohammad. 1 P a g e

Transcription

1 -12 -Ensherah Mokheemer - ABDULLAH ZREQAT -Faisal Mohammad 1 P a g e

2 In the previous lecture we talked about: - cardiac index: we use the cardiac index to compare the cardiac output between different individuals, and we said that the cardiac index equals the cardiac output divided by body surface area, so cardiac index unit will be L/min/m 2. - You should know that there are differences in the basic cardiac output values between individuals, since it is affected by the size and weight so to solve this there is what we call the cardiac index - We also said that the cardiac output is proportional to oxygen consumption, the higher the oxygen consumption is the higher the cardiac output. - The cardiac output is the sum of all tissues blood flow, during exercise there is more oxygen consumption and more blood flow to skeletal muscles so the cardiac output increases during exercise. - Flow (cardiac output)= p/r (Ohm s law): * p: is the pressure difference between the aorta and the right atrium. The aortic pressure that we use on the equation is the mean arterial pressure (MAP) which is affected by systole and diastole. The mean arterial pressure= 1/3 systolic pressure+ 2/3 diastolic pressure. Why we took 2/3 of the diastolic pressure and only 1/3 of systolic pressure? that is because the duration of diastole equals 0.5s while the duration of the systole is 0.3s so diastole contributes more to the MAP. so p= 1/3 systolic pressure+2/3 diastolic pressure right atrium pressure (which is almost zero). * R is the total peripheral resistance: which equals all the resistance in all the vessels from aorta until reach the right atrium. If we rewrite the equation in another form it will be like this: 2 P a g e

3 Flow (CO)=The mean arterial pressure (MAP)/ the total peripheral resistance. MAP= CO* total peripheral resistance. - MAP of any person should always stay constant (homeostasis), if it increases our system will try to decrease it and vice versa. - From the previous equation we can conclude that we can change the MAP by changing CO or by changing Total peripheral resistance: 1- you can change the cardiac output by changing the stroke volume or heart rate or both. 2- You can change total peripheral resistance by vasodilation (decrease resistance) or vasoconstriction (increases resistance). -Normally the cardiac output is almost 5L, when during exercise there is an increase in the cardiac output and this increase in the cardiac output is mainly due to the increase in the blood flow to the cardiac muscles. Note : exercise can increase CO up to 700% ( almost 35 L). Note: the skeletal muscles usually constitute 40% of our weight and they normally receive about 1 L of blood/min, so 20% of our cardiac output goes to 40% of out body. But during exercise the blood flow reaches 8L per min. 3 P a g e

4 -Also, during exercise, the blood flow to the skin increases due to water loss. And the blood flow to the digestive system is reduced. -There are variations in tissue blood flow. And that the heart has one of the highest blood flow relative to its body weight (around 70ml/min/100gm). -Other tissues have higher blood flow but this is not for oxygen consumption, it's for filtration like in the kidney. While the heart receives good amount of blood flow only for oxygen consumption. -Other tissues like adrenal and thyroid glands have very high blood flow, they are small glands, the blood that is going to them is much higher than they need. 4 P a g e

5 - Cardiac output= Stroke volume* Heart Rate: Heart rate is controlled by sympathetic (positive chronotropic) and parasympathetic (negative chronotropic). Stroke volume is controlled intrinsically by End diastolic volume (Frank starling law) (increase venous return increase EDV contractility stroke volume), or extrinsically by sympathetic stimulation (positive inotropic). Now let s talk about the cardiac output curve: -The cardiac output curve relates the right atrium pressure to the cardiac output, and it is a mathematical representation of Frank-starling law. -The right atrium pressure is an indicator for EDV, the higher the EDV is, the higher the right atrium pressure. 5 P a g e

6 -The cardiac output is an indicator for the intraventricular pressure -keep this in your mind When the pressure in the right atrium equals zero the cardiac output will be 5L. * Cardiac reserve : Maximal % increase in CO in response to increase body needs -Normally, according to this curve the cardiac reserve is 10L. Remember: cardiac reserve= maximum CO- normal CO (15-5=10L). - The cardiac output curve might be shifted upward to the left: positive inotropic effect which is usually due to sympathetic stimulation, so very high sympathetic stimulation might shift the curve upward to the left and the is what we call HYPEREFFECTIVE HEART. Note: Athletes might have hyper effective heart, in this case they have hypertrophy of ventricles. -HYPOEFFECTIVE HEART the curve shifted downward to the right and it might occur because of sympathetic inhibition or myocardial infarction. - Hence that the normal curve represents normal sympathetic stimulation, the hypereffective curve represents maximum sympathetic stimulation and hypoeffective represents minimal (Zero) sympathetic stimulation. 6 P a g e

7 Maximum sympathetic stimulation: shifted upward to the left. Zero sympathetic stimulation: Shifted downward to the right. Parasympathetic stimulation: not very important because usually it does not affect. Effect of the intra-plural pressure on the cardiac output: -The heart is in the chest and it is surrounded by the lungs, and the lungs is surrounded by the pleura. -The pressure inside the pericardium is equal to the pressure inside the pleura. - The intra-plural pressure is always negative** around -5mmHg that s why the lungs are distended and there is a vacuum around them. ** remember that we considered the atmospheric pressure zero, so a negative pressure will be less than the atmospheric pressure. The atmospheric pressure is our reference point that is why it is 7 P a g e

8 considered zero, but it does not equal zero it equals 760mmHg so the pressure in the pleura will be 760-5= 755mmHg. - Normally the right atrium pressure is zero (760mmHg) when the pleural pressure around it is -5 (755mmHg). - In case of pleural effusion, the pleural pressure increases from -5 to -3(-5+2), this increase in the intra-pleural pressure will be reflected on the heart and the pressure will change in the right atrium from zero to +2 (zero+2) and this means that in order to fill the atrium we will need higher pressure gradient. This will shift the cardiac output curve to the right. - If the pleural pressure increases from -5 to zero ( -5+5) the right atrium pressure will become +5 (Zero+5), shifted to the right. - If the intra pleural pressure decreases, a decrease in the right atrial pressure is seen. - It is important to notice that in case of increase/decrease in IPP the whole curve will be shifted to the right/left and the maximum cardiac output according to Frank-Starling will 8 P a g e

9 be the same it will not be affected!! But it is shifted.( very important) - According to the figure above: 1- Let s consider the normal intrapleural pressure is (-4 mmhg) at this value the right atrium pressure (RAP) will be zero and the cardiac output at that pressure equals 5L and the maximum cardiac output is 15L. 2- When the intrapleural pressure is decreased to - 5.5mmHg the pressure in the right atrium will be reduced to -1.5mmHg and the cardiac output at that pressure will be equal to 5L and the maximum CO will be 15L. (shifted to the left). in this case the heart is working at less pressure 3- When the IPP increases to 2 (like in the case of pleural effusion) the pressure in the right atrium will be +6 and the CO at that pressure will be 5L and the maximum CO will remain 15L. (shifted to the right) in this case the heart is working on higher pressure. Hence that the normal CO and the maximum CO did not change they were only shifted!! That is because the Cardiac muscle is not affected directly because the pleura is far from the heart muscle (not on direct contact with it). - In the case of Cardiac tamponade pericardial effusion : The increase in the pericardium pressure will directly affect the heart muscle and it will prevent filling of the blood, thus reaching the maximum CO will become very difficult (we will need very high pressure to reach the maximum CO). From the figure above: -When the interpleural pressure was -4 mmhg we needed almost 2 mmhg to reach the maximum cardiac output. less severe. - However, when the interpleural was -4 mmhg and there was pericardial effusion we needed almost 8 mmhg to reach the maximum Co. more severe. 9 P a g e

10 As a conclusion because the pleural is not in direct contact with the heart muscle (far from it ), in case of pleural effusion the effect will not be severe. But because the pericardium is in direct contact with the heart muscle the pericardial effusion will have more sever effect. - If the cardiac tamponade becomes very severe, the cardiac output might not reach the maximum CO and it might reach 0 since the heart is unable to pump blood anymore and this eventually will cause heart failure. - So cardiac tamponade is an emergency case and it needs to be relieved by cutting through the chest using a sharp object. - cardiac tamponade --- increase RIGHT ATRIAL PRESSURE shift the curve to the right and sometimes downward Returning to our main subject which is the cardiac output curve: - Plateau of CO curve determined by heart strength (contractility + HR): 1- sympathetic stimulation raises the plateau up and shifts the curve to the left. hypereffective heart. 2-parasympathatic mostly does not have any significant effect. 3-Heart hypertrophy raises the plateau up and shifts the curve to the left. Hypereffective heart. 4- Myocardial infarction lowers the plateau and shifts the curve to the right due to mass decrease. Hypoeffective heart. 5- Valvular disease lowers the plateau and shifts the curve to the right due to decrease in the cardiac output, examples are stenosis or regurgitation, in case of regurgitation because of the valve (AV valve) incompetence some of the blood goes back to the atria from the ventricle, in case of semilunar valve incompetence some of the blood returns 10 P a g e

11 from the aorta to the ventricle in the case of aortic stenosis is a narrowing of the aortic valve opening. Aortic stenosis restricts the blood flow from the left ventricle to the aorta you can consider it as an increase in the resistance to blood flow due to the narrowing of the orifice and this leads to decrease in stroke volume and eventually decrease in cardiac output. 6- Myocarditis lowers the plateau because it affects the myocardium leading to reduction in the function of the myocardium (contractility). 7- Cardiac tamponade (pericardial effusion) it will prevent the filling of the ventricle, so it decreases cardiac output and thus lowers the plateau of the curve. 8- Metabolic damage also lowers the plateau. Factors that affects cardiac output: Cardiac output=heart rate * stroke volume *Heart rate is controlled by the Autonomic nervous system (sympathetic or parasympathetic) or Hormones (Thyroxin and catecholamines). *Stroke volume =End diastolic volume-end systolic volume 1-The increase in the End diastolic volume is called increase in preload and this is Frank-Starling law. 2-The decrease in the End systolic Volume is mainly due to positive inotropic and the increase in ESV in due to negative inotropic. a- EDV is mainly affected by: -The venous return (how much blood return back to the heart). Increase in venous return increases EDV increases preload. --The venous return = CO= RAP ( under physiological conditions) 11 P a g e

12 -Filling time, which is affected by the heart rate, increasing the heart rate leads to decrease in the cardiac output due to the decrease in the duration of ventricular diastole and this reduces the filling time of the ventricle. During exercise the heart reaches to its maximum heart rate and this is dangerous, you should not exceed 80% of your maximum heart rate, because the increase in heart rate leads to reduced stroke volume and thus decrease in cardiac output and eventually might lead to myocardial ischemia. There is a test called exercise stress test which is used to determine how well your heart responds during times when it s working its hardest. During the test, you ll be asked to exercise typically on a treadmill while you re hooked up to an electrocardiogram (EKG) machine. This allows your doctor to monitor your heart rate. If the ECG showed depression in the ST segment, the doctors will tell you to stop running and this depression is due to coronary obstruction (stenosis) which might lead to ischemia. b- ESV is affected by: - Contractility: Decrease in contractility increases ESV. - Vasoconstriction, increases the pressure, increases the resistance and thus decreasing the blood flow (cardiac output) by decreasing stroke volume. Vasoconstriction causes an increase in the afterload and increase in the ESV. 12 P a g e

13 *vasodilation decreases the afterload. - Contractility is increased by Epinephrine, Norepinephrine, Glucagon, Thyroid hormone. ** These figures are very important 13 P a g e

14 Regulation of Preload: -Increase in the venous pressure means increase in p: The difference between the venous pressure and the right atrium pressure. 14 P a g e

15 Regulation of afterload (contractility): - Main factor that controls contractility is sympathetic stimulation or inhibition. -Cardiac contractility is measured by measuring the maximum change in pressure per time (dp/dt). -Excess K+ decreases contractility. 15 P a g e

16 - Excess Ca++ increases contractility. Measurement of cardiac output: Direct methods: 1- - In animals you cut the aorta, collect the blood ejected per min, this gives you cardiac output. Obviously, we can't do this in humans. Indirect methods: 1- Electromagnetic flowmeter it is indirect but is done directly in heart surgery. 2- Indicator dilution (dye such as cardiogreen) 3- Thermal dilution 4- Oxygen Fick Method CO = (O2consumption / (A-V O2 difference) **remember that the cardiac output is the amount of blood ejected from the aorta per min. 1- Electromagnetic flowmeter: We have two poles of magnate (north and south). When a charged flow passes between the two poles, an electrical current is formed and it is proportional to the flow, the current can be followed up by a calibrated galvanometer. Because blood is full of electrolytes, It is a charged flow, and the current that would be formed (we can also call it voltage difference or potential difference) between the magnate is proportional to the flow. If we measure this flow per min, we can calculate the cardiac output. This method can be used around any artery, and many times, (only used during cardiac surgery). 2- Fick Method (oxygen consumption): -The blood coming from the right ventricle to the lungs through pulmonary artery. And it is deoxygenated. -The amount of blood that comes from the right ventricle to the lungs through the pulmonary artery per min is called Cardiac output. - The blood that come to the left ventricle by pulmonary veins is equal to CO. 16 P a g e

17 - the amount of oxygen that comes to the lung per minute equals cardiac output multiplied by oxygen concentration in the blood. - The amount of oxygen that come to left ventricle from the lungs by pulmonary veins = the cardiac output* the concentration of oxygen in the arterial blood. Which equals the concentration of oxygen in the blood that entered the lungs + the amount of oxygen which was up taken by the lungs. -Q1= Cardiac output*concentration of O2 in venous blood. -Q2= amount of Oxygen uptake by the lungs which can be measured by spirometer. -Q3= Cardiac output * (The concentration of O2 in the venous blood+ The concentration of oxygen uptake). Or the Cardiac output * the concentration of O2 in arterial blood. -Oxygen uptake= CO *(C arterial O2 C venous O2). -Cardiac output= Oxygen uptake/ (C arterial O2 C venous O2). THE END WORK HARD DREAM BIG 17 P a g e