Presentation on theme: "Measurement of cardiac output by the Fick principle"— Presentation transcript:
1Measurement of cardiac output by the Fick principle ‑The Fick principle can be expressed by the following equation:Cardiac output = O2 Consumption / pulmonary vein ‑pulmonary artery
2‑The equation can be solved as follows: 1. Oxygen consumption for the whole body can be measured.2. Pulmonary vein  can be measured in a peripheral artery.3. Pulmonary artery  can be measured in mixed systemic venous blood.‑For example, a man has a resting O2 consumption of 250 ml/min, a peripheral arterial O2 content of 0.20 ml O2/ml of blood, and a mixed venous O2 content of 0.15 ml O2/ml of blood. What is his cardiac output?
3Cardiac output = 250 ml/min / (0. 20 ml O2/ml‑ 0 Cardiac output = 250 ml/min / (0.20 ml O2/ml‑ 0.15 ml O2/ml) = 5000 ml/min or 5.0 L/min (typical value for a 70‑kg male)
4Definitions Preload Afterload Contractility amount of stretch on the ventricular myocardium prior to contractionAfterloadthe arterial pressure (or some other measure of the force) that a ventricle must overcome while it contracts during ejectionImpedance/resistance to ventricular ejectionContractilitymyocardium’s intrinsic ability to efficiently contract and empty the ventricle(independent of preload & afterload)Preload can be simply stated as the volume stretching the ventricular muscle prior to ejection. Afterload is the resistance to flow from the circulatory system.Contractility has historically been the most difficult parameter to measure in the clinical setting. It clearly is the most important parameter that is affected by cardiac pathology and cardioactive medications
5Determinants of Cardiac Output (CO) ContractilityStroke VolumePreloadAfterloadCardiac output is a function of the interplay of multiple physiologic parameters.Stroke volume is influenced in a predictable order:1. Preload first influences contractility.2. The combined effect of preload and contractility then influences the afterload response.3. Only after the stroke volume is established does the heart rate respond to adjust the final cardiac output.Heart RateCardiac Output
6Contractility. This is a change in contractile energy of the heart that is not due to changes in fibre length, but rather to external factors such as SNS activity or drugs.-is also called inotropism.‑can be estimated by the ejection fraction (stroke volume / end-diastolic volume), which is normally 0.55 (55%).‑Agents that produce an increase in contractility have a positive inotropic effect.‑Agents that produce a decrease in contractility have a negative inotropic effect.
7Factors that increase contractility (positive inotropic effects) a. Increased heart rate‑more action potentials per unit time ->Ca2 + entry into the myocardial cell-> Ca2 + released from the SR-> greater tension produced during contraction.b. Sympathetic stimulation (catecholamines) via beta1 receptorsc. Cardiac glycosides (digitalis)‑increase the strength ofcontraction by inhibitingNa+,K+ ATPase in the cardiacmuscle cell membraneSympathetic stimulation (catecholamines) via beta1 receptors‑increases the strength of contraction by two mechanisms:(1) It increases the entry of Ca2 + into the cell during the plateau of each cardiac action potential.(2) It increases the activity of the Ca2+ pump of the SR (phospholambam); therefore, more Ca2+ will be accumulated and thus will be available for release in subsequent beats.
8Factors that decrease contractility (negative inotropic effects) ‑Parasympathetic stimulation (ACh) via muscarinic receptors decreases the strength of contraction in atria by decreasing Ca2+ entry into the cell during the plateau of the cardiac action potential (inward Ca2+ current).
9Changes in contractility shift the Frank-Starling curve upward (increased contractility) or downward (decreased contractility).a. Increases in contractility cause an increase in cardiac output for any level of venous pressure, right atrial pressure, or end-diastolic volume.b. Decreases in contractility cause a decrease in cardiac output for any level of venous pressure, right atrial pressure, or end-diastolic volume.
11Afterload and Cardiac Performance Presentation InformationAfterload and Cardiac PerformanceAfterload: all the factors that impede fiber shortening, in this case it would be all the factors that impede the ejection of blood from the ventricle. What the heart has to pump againstVolume of blood in the arterial circulationPressure in aorta at onset of ejection (DAP)Compliance of aortaSize of outflow orificeCONFIDENTIAL
12Presentation Information The Diastolic Arterial Pressure (DAP) is the major component that governs afterload in the normal individual because it is the only factor subject to moment to moment changes.CONFIDENTIAL
13Conditions that Increase Afterload Presentation InformationConditions that Increase AfterloadHypertensionAortic stenosisIncreased HrIn chronic pathological conditions these can lead to chronic pressure overload of the heartCONFIDENTIAL
14Myocardial Hypertrophy Presentation InformationMyocardial HypertrophyCross sectional area of a muscle increases when repeatedly exposed to an elevated work load over a sustained period of timeIn cardiac muscle this can be the result of increased wall tension caused by increased preload, increased afterload or increased heart rate.Some hormones have also been implicated in the processNorepi, angiotensin II, and thyroxinphysiologyCONFIDENTIAL
15Three Types of Hypertrophy Presentation InformationThree Types of Hypertrophy1) Physiological – occurs in athletes in response to long term endurance exercise.there is a symmetrical enlargement2) Concentric – occurs as a result of long standing pressure overload. Thickness ratio is increased, ventricle lumen size can be unchanged or reduced.3) Eccentric – occurs as a result of long standing volume overload. Hypertrophies away from lumen, enlarging lumen size and the thickness ratio is reduced.physiologyCONFIDENTIAL
16Swollen legsA 47 year old woman was brought to the hospital because of severe shortness ofbreath and swelling of her lower body. Over the last year *she had noticed periodsof shortness of breath while doing her housework (exertional dyspnea). She alsohad shortness of breath while lying down (orthopnea). The patient often awoke atnight with a sensation of not getting enough air and she had to sit or stand toobtain relief (paroxysmal nocturnal dyspnea). #More recently she noticed swellingfirst of her lower extremities and then of her lower abdomen. The swelling wasworse through the day and decreased overnight. She reported awakening three tofour times a night to urinate. The patient did not remember any ill health beforethese problems began.Physical examination revealed a woman sitting up in bed in mild to moderaterespiratory distress. Her blood pressure was 100/70, pulse was 120 and weak.Respirations were 26 per minute and labored. There was jugular venousdistension, even while she was sitting. Palpation of the sternum revealed arestrosternal lift. Auscultation of the heart revealed an opening snap and a longdiastolic rumble at the apex. Auscultation of the lungs revealed crackles halfwayup the lungs. There was also severe lower extremity edema.During her hospitalization, as part the work-up, the following studies were done.PatientNormalO2 consumption(VO2)188 ml/minmL/minArterial-venous O2 content difference5.3 ml/dl bloodml/dl bloodHeart rate122beats/minMean Pulmonary Capillary Wedge Pressure25 mm Hg<15 mmHgRight Ventricular Systolic pressureEnd-Diastolic pressure80 mm Hg16 mm Hg<28mmHg<8mmHgRight Ventricular End Diastolic volume140 ml/m260-88mL/m2Use the data in the table above to calculate cardiac output and ejection fraction· Evaluate the mean electrical axis of the heart using the ECG shown overleaf
18C. Regulation of CO and Venous Return (VR) “ VR determines CO”, but since VR is not an independent variable, and is largely determined by Central Venous Pressure (CVP), so it is more accurate to say that CVP determines COCVP is affected by blood volume (BV), vasoconstriction and arteriolar vasoconstriction When VR becomes higher than the heart can pump (e.g. exercise), then the contractility of the heart is adjusted () by SNS, so that CO is matched to the VR
19Quantitative Analysis of CO Regulation Two primary factors are related to CO regulation: 1. The pumping ability of the heart (represented by CO curves that we discussed); and 2. The factors that affect CVP, and consequently VR. These are represented by the vascular function curves (also known as the venous return curves)Vascular Function Curves: VR is determined by P between central veins and the right atrium. The grater P the larger VR and vice versa The lower the pressure in RA, the greater the pressure gradient between the veins and RA, and vice versa (as RAP, VR )
21Mean Systemic Filling Pressure (MSFP) The graph shows that as RAP, VR. The slope is very steep, and this is due to the fact that veins are very compliant (distensible)When RAP is ~7 mm Hg, the VR is zero, i.e. there is no pressure gradient between RA and the veins to drive the blood back to the heart. This pressure is referred to as mean systemic filling pressureThe value of MSFP is 7 mm Hg and not zero because it depends on the volume of blood in the vascular system and its overall distensibilityThe overall distensibility or compliance of vascular system depends on the degree of venomotor tone as well as artriolar toneThe factors affectingg MSFP are: Blood volume, Venomotor tone, Arteriolar resistance