Parallel Circulation Cardiac Output Why is this important Why is this important Why is this important

Parallel Circulation Cardiac Output Why is this important Why is this important Why is this important

Parallel Circulation Cardiac Output Why is this important Why is this important Why is this important

Rogers, Jeff, Host has reference to this Academic Journal, PHwiki organized this Journal Parallel CirculationKarim Rafaat, M.D.The basic issue with “parallel” circulation is achieving the proper balance between the pulmonary in addition to systemic circulationsQp:QsToday, we focus on how to do it prior to definitive surgical correctionBe as long as e that, however, we have to underst in addition to some basics How to calculate Qp in addition to Qs from a cath diagramHow to calculate Qp:Qs ratioI have to apologize as long as the speed with which I am going to go over the different cardiac lesionsMy focus will be only how they lay in the spectrum of complete mixing lesions, in addition to so, how we must deal with the problems they present with relation to their systemic in addition to pulmonary circulations

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Cardiac OutputAn amount, I, of an indicator, can be added to an unknown fluid quantity, QThe concentration be as long as e the indicator is added is Ci, in addition to after, CfFluid quantity, QInitial sampleCiFinal sample, CfIndicator, amount is IQ x Cf – Q x Ci = I the amount of added indicator is equal to the amount of stuff in the fluid after minus the stuff in the fluid be as long as e Q = I Cf – Ci Upstream sample,Indicator concentrationCiDownstream sample,Indicator concentrationCfSteady state flow, QIndicator infusion (constant over time)IQ = I Cf – Ci This is the basic as long as m of the Fick Principle.

Fick principleUsed to calculate flow when it cannot be measured directlyWe can measure it indirectly by way of an indicatorThere are a few ways to use this concept, depending on the indicators that are usedThermodilution MethodThe indicator is temperatureBolus injected in RA, temp measured by thermistor in PA (usually)Degree of cooling is inversely proportional to the magnitude of flow in addition to directly proportional to amount of “cold”As an aside The sharper the curvethe quicker the return to normal blood tempso the less in addition to quicker influence of the set amount of “cold”Cf – Ci (integrated over time) is smaller .there as long as e, the higher the cardiac output.

When oxygen is the indicator, the Fick Principle is more directly applicableThe rate of change of the indicator (I) is Oxygen ConsumptionCan be directly measured (impossible practically)Commonly taken from a tableThe concentration is the Oxygen Content Then, to calculate Qp or Qs, you have to pick your points around which you are going to measure the “change in concentration”So, as long as Qp: pulmonary veins – pulmonary arteriesQs: aorta – mixed venous

Oxygen Content = (13.6 x Hgb x %sat) + (0.003 x pO2)1.36 is O2 carrying capacity of hgb in mL/gHgb is in g/dLO2 content, though, is measured in ml/LSo, you use 13.6 in the equation above Qp = Oxygen Consumption C pulmonary vein O2 – C pulmonary artery O2Qs = Oxygen Consumption C aorta O2 – C mixed venous O2DORV

Let’s calculate some ratios, then .Qp = Oxygen Consumption C pulmonary vein O2 – C pulmonary artery O2 = 172 (13.6 x 16 x 0.94) – (13.6 x 16 x 0.84) = 172 204 – 183 = 7.9 L/min/m2Qs = Oxygen Consumption C aorta O2 – C mixed venous O2 = 172 (13.6 x 16 x 0.72) – (13.6 x 16 x 0.49) = 172 156 – 106 = 3.4 L/min/m2So, Qp:Qs7.9/3.4 = 2.4Math trick Qp = Oxygen Consumption C pulmonary vein O2 – C pulmonary artery O2Qs = Oxygen Consumption C aorta O2 – C mixed venous O2Qp:Qs = C aorta O2 – C mixed venous O2 C pulmonary vein O2 – C pulmonary artery O2 = Sat aorta – Sat mixed venous Sat pulmonary vein – Sat pulmonary artery = 72 – 49 = 23 94 – 84 10 = 2.3 !!!!

Why is this importantIn lesions with parallel circulation, the total CO of the usually single ventricle is shared between pulmonary in addition to systemic circulationsThe ratio of Qp:Qs describes the relative amount of pulmonary in addition to systemic blood flowThe absolute value, however, is a representation of total cardiac outputWhy is this importantPhysiology with a high Qp:Qs brings with it a relatively low systemic oxygen deliveryLow systemic DO2 leads to tissue hypoxia, anaerobic metabolism, in addition to eventual end organ damage Why is this importantThe goal, then, of our management, is the optimization of systemic oxygen delivery (DO2)Not maximize SaO2This requires the maintenance of cardiac inotropy while balancing Qp:Qs.

Why is Qp:Qs importantThis is a theoretical graph of systemic O2 availability versus Qp:Qs, at different CO’sThe dashed line represents the max O2 deliveryWhy is this importantMax O2 delivery occurs at a Qp:Qs between 0.5 in addition to 1Not at 2.3 Increasing CO, increases systemic O2 deliveryWith more of a difference made at Qp:Qs ratios less than 1Why is this importantThe slope of each curve is steepest around point of maximal O2 deliverySuggesting small changes in Qp:Qs can be associated with large changes in oxygen delivery

Rogers, Jeff WMGY-AM Host

What does this meanWith complete mixing lesions, the ventricular output is the SUM of Qp in addition to QsCause there’s, effectively, one ventricleThe higher the ratio, the higher the dem in addition to on the heartSo, a Qp:Qs of 2.3 means that the heart is pumping about 3 “cardiac outputs”It must maintain such a high output in an attempt to allow as long as acceptable systemic oxygen deliveryWhat does this meanVentricular wall tension in addition to myocardial oxygen dem in addition to are increased in the dilated, volume overloaded ventricleLeads to myocardial dysfunction in addition to AV valve regurgitationProlonged increased pulmonary volume will lead to pulmonary vascular bed remodeling can lead to increased pulmonary vascular resistance, which makes single ventricle surgical repair impossibleWhen must we think of these thingsA wide variety of lesions, usually associated with atresia of an AV valve, have the common physiology of complete mixingWhile most of them are commonly dealt with in the NICU, there are a few that we will routinely see

HLHSThe most common is Hypoplastic Left Heart Syndrome1. PFO2. hypoplastic aorta3. Patent PDA4. aortic atresia5. Hypoplastic left ventricleMixing occurs via a patent PDAHLHS post Norwood Stage IWe see this lesion usually after the stage 1 Norwood operationBTS supplies pulmonary flowAtrial septectomyPulmonary trunk disconnected from MPAMPA in addition to Aorta anastomosed to as long as m a neo-aorta DORVDouble Outlet Right VentricleBoth the aorta in addition to pulmonary artery arise from the RVAccompanied by a VSD

Steih et al, in a retrospective evaluation of 72 patients with HLHS, found that in hospital mortality decreased from 65% to 13% with a shift in preoperative management from ventilation to increase PVR, to pharmacologic management to decrease SVRPreoperative organ dysfunction was higher in those patients who were ventilated versus those who received afterload reduction in the as long as m of phenoxybenzamineBibliographyChang et al, Pediatric Cardiac Intensive Care, LWW, 1998Steih J, et al, Impact of preoperative treatment strategies on the early perioperative outcome in neonates with hypoplastic left heart syndrome, Journal of Thoracic in addition to cardiovascular surgery, May 2006; 1122-9Graham E, Preoperative management of hypoplastic left heart syndrome, Expert Opinion in Pharmacotherapy, 2005 6:687-693Schwartz S et al, Single Ventricle Physiology, Critical Care Clinics 2003;19:393-411George M. Hoffman, Venous saturation in addition to the anaerobic threshold in neonates after the Norwood procedure as long as hypoplastic left heart syndrome, The Annals of Thoracic Surgery, Volume 70, Issue 5, , November 2000, Pages 1515-1520.

Rogers, Jeff Host

Rogers, Jeff is from United States and they belong to WMGY-AM and they are from  Montgomery, United States got related to this Particular Journal. and Rogers, Jeff deal with the subjects like Religious/Gospel

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