Intermediate Cardiac Physiology Flashcards
Myocardial action potentials include phases:
0-3
What is phase 0 of the myocardial action potential?
Phase 0 is the upstroke caused by activation of fast Na+ channels.
What is phase 1 of the myocardial action potential?
Phase 1 is early rapid repolarization, characterized by fast Na+ channel inactivation and an increase in K+ permeability.
What is phase 2 of the action potential?
Phase 2, or the plateau phase is caused by Ca2+ channels opening, prolonging the action potential.
What is phase 3 of the action potential?
Phase 3, represents the closing of the Ca2+ channels and increased K+ permeability.
Ventricular myocytes have which phases compared to the SA node?
SA nodal cells have a phase 0, followed by 3, then 4 (not present in ventricular cells) characterized by a slow leak of Ca2+and Na+ into the cell that sets of a subsequent action potential.
What do volatile agents do to the SA node?
characterized by a slow leak of Ca2+and Na+ into the cell that sets of a subsequent action potential.
Intracellular calcium held in the sarcoplasmic reticulum is released into the cytoplasm following:
A. Release of troponin from the Actin/ Myosin complex
B. Calcium removal from the cell via the Na/K ATPase
C. Mitochondrial depolarization
D. Calcium inflow across the ryanodine receptor
is: D: Calcium inflow across the ryanodine receptor
Contraction of myocardial cells starts with the action potential that activates Ca2+ inflow across dihydropyridine receptors on T-tubules. The increased Ca2+ levels activate ryanodine channels on the sarcoplasmic reticulum to open and allow proportionately enormous amounts of calcium into the cell. The calcium binds to troponin C allowing actin/ myosin contraction, followed by ATPase dependent relaxation. Relaxation is characterized by uptake of Ca2+ back into the sarcoplasmic reticulum, an ATPase dependent process.
Volatile agents’ depression of myocardial contractility probably involves:
Decreased calcium release by the sarcoplasmic reticulum
Volatile agents likely depress contractility by indirectly decreasing the release of calcium from the sarcoplasmic reticulum.
Interruption of the right vagus nerve would most likely affect the:
A. Conduction velocities from SA to AV node
B. Automaticity of the SA node
C. Conduction delay at the AV node
D. Presynaptic regulation of the stellate ganglion
How are SA node and AV node innervated?
How is the heart innervated?
B: Automaticity of the SA node
Cardiac autonomic innervation tends to have the SA node supplied from the right vagus and sympathetic chain, and the AV node from the left. Parasympathetic innervation comes by way of the vagus nerve, whereas sympathetic innervation arises from T1-4 and innervates the heart by way of stellate ganglion to cardiac nerves.
Also note that this means that during SVT treatment, right carotid massage is more likely to inhibit sinus discharge and left carotid massage slows the AV node.
Does AS need more or less preload? What kind of hypertrophy does AS have?
Aortic stenosis represents a high afterload state, necessitating an increase in preload to maintain cardiac output (Starlings Law of the Heart, see above). Furthermore, concentric hypertrophy associated with aortic stenosis requires increased pressures for a given volume (less compliant, diastolic dysfunction).
Wedge pressure equals pulmonary venous pressure, which very nearly equals left atrial pressures, which very nearly equals left ventricular end diastolic pressure (LVEDP).
Yes.
In normal hearts, wedge pressure is an accurate measure of LVEDP, but not necessarily ______ .
because the pressure volume relationship is non-linear. That is to say that as volume increases, pressure may proportionately rise more (or less). Not necessarily volume. Why?
Which of the following factors account for systemic vascular resistance (SVR) being an imperfect measure for afterload:
A: It does not include elastic properties of the aorta nor viscosity of the blood
Concentric hyoertrophy is associated with:
High pressures
Which of the following are NOT consistent with left ventricular diastolic dysfunction?
A. Decreased left ventricular end diastolic pressures (LVEDP)
B. Left ventricular concentric hypertrophy
C. Elevated brain natriuretic peptide in the setting of preserved systolic ejection fraction
D. E to A ratio of < 0.8 (E is less than A)
E. Pulmonary oedema
Decreased left ventricular end diastolic pressures (LVEDP)
Diastolic dysfunction is characterized by a stiff ventricle that poorly relaxes, requiring a higher LVEDP (not lower) for filling. The higher LVEDP are transmitted back to the pulmonary system which can manifest as pulmonary oedema. Diastolic dysfunction is more likely associated with concentric hypertrophy (resulting from high pressures, rather than eccentric hypertrophy (resulting from high volumes). Doppler evaluation across the mitral valve demonstrates characteristic patterns of early diastolic flow (E) and peak atrial flow (A). Although various patterns exist, a situation with an A wave larger than an E wave is only consistent with impaired relaxation.
Which of the following are compensatory mechanisms to maintain blood pressure when changing from a supine position to standing:
A. Autotransfusion from lower extremities
B. Renin-angiotensin-aldosterone system
C. Increased vasoconstriction
D. Sodium retention
C: Increased vasoconstriction
Immediate, short term mechanisms controlling blood pressure are a function of the autonomic nervous system. Controlling vasomotor tone (resistance), heart rate & contractility (cardiac output). Recall that blood pressure is essentially cardiac output multiplied by resistance (V= I X R, Ohm’s Law). Baroreceptors at carotid sinus (bulb) and aortic arch decrease discharge in response to dropping blood pressure, which lessens the inhibition of the sympathetic system, and increases inhibition of vagal tone. The carotid sinus communicates with the brainstem via Herings nerve (part of glosopharyngeal). The opposite is true when the BP is high: the receptors discharge increases, which increases its inhibition of the sympathetic nervous system. The pathways within the brainstem are complex and we do not think you’ll be expected to know them. Renin-angiotensin-aldosterone system and sodium retention are intermediate and long-term mechanism of blood pressure control and take minutes to days for full effect. A full description is found in the renal section and is discussed in the Basic Cardiac Physiology section as well. Autotransfusion from lower extremities may occur when changing from standing to supine, or in trendelenberg position.
How would Acute mitral regurgitation (MR) due to anterior papillary muscle ischaemia present?
The posterior mitral papillary muscle is typically solely supplied by the PDA; whereas the anterior papillary muscle has dual supply from left circumflex and LAD. This would present with flash pulmonary oedema, low cardiac output, and large bizarre V waves on wedged PA catheter tracing.
In times of hypoxia, NO is released (among other factors) which vasodilate coronaries further (unless there is stenosis!).
True
Who is more likely to suffer ischemia-endocardium or epicardium?
The endocardium is more likely to suffer ischemia, presenting with ST depressions than the epicardium. Typically when the epicardium is ischaemic, both the epi- and endo-cardium is ischaemic, presenting with ST elevations.
NSTEMI is a what?
To be clear, most NSTEMIs are the result of supply and demand with coronary disease below the threshold requiring intervention.
Match the best treatment with the clinical presentation:
1 Defibrilation with biphasic 200 J 2 Cardioversion with biphasic 120 J 3 6 mg Adenosine IV push 4 Diltiazem drip 5 Trans-cutaneous pacing CHOICES
A) Pt with sudden onset AV nodal re-entry, HR 160, BP 110/ 50
B) Pt with atrial fibrillation (A-Fib) with HR 170, BP 55/ 38
C) Pt with widened QRS, HR 39, BP 63 / 44
D) Pt with A-fib, HR 147, BP 153/ 78
E) Pt with ventricular fibrillation, no pulse or BP
- E. Pts with ventricular fibrillation should receive chest compressions, defibrillation at 360 J monophasic or 200 J biphasic, and epinephrine per ACLS protocols 2. B. The patient has unstable A-fib and will require emergent cardioversion to escape the grips of death 3. A. SVTs can often be broke by 6 mg of adenosine. 12 mg should be tried next twice over before cardioversion is attempted in a patient with a stable BP 4. D. A-fib with rapid ventricular rates (RVR) and stable BP can be effectively treated with B-blockers, Ca-channel blockers, and adenosine. A patient with a stable BP does not require emergent cardioversion, although it remains a viable option if the A-Fib has persisted less than 48 hours. 5. C. This patient likely has a 3rd degree heart block and an unstable BP. Immediate percutaneous pacing should be employed while a more permanent solution is sought.
What are the major cardiac risk factors?
These are: unstable or severe angina, myocardial infarction (MI) within a month, heart blocks (mobitz II or type III), major ventricular arrhythmias, supraventricular arrhythmias (such as a-fib/ flutter) with rapid ventricular rate (RVR), active or severe heart failure, or severe valvular stenotic disease. If any of these are present they need to be addressed prior to surgery.
If a patient can’t do METs due to physical impediments, but it’s not a major surgery-then what?
Now we have to further stratify him by “clinical risk factors,” formally called “intermediate risk factors,” back when the guidelines were more straight forward. Clinical risk factors are: ischaemic heart disease, compensated heart failure, diabetes (especially insulin dependent), renal insufficiency (especially CKD with creatinine greater than 2.0), and CVA. If the patient has none of these risk factors, he is deemed good to go without further cardiac evaluation (may need pulmonary evaluation still, but that’s a different story). A patient with 1-2 of these clinical risk factors qualify for a stress test, should the patient and cardiologist feel it will change management (versus continuing medical management with heart rate control).
A septum bulging towards the left ventricle indicates:
high pulmonary artery pressures and volume backup into the right ventricle
Which type of dysfunction is more common in patients with hypertension?
Diastolic dysfunction, not systolic dysfunction, is commonly seen in patients with HTN.
Type of hypertrophy in patients with heart problems
Long standing increases in afterload result in increased pressure work for the ventricle, leading to concentric hypertrophy.
Handgrip is the same as saying:
Increased SVR
MR results in which type of hypertrophy and why?
Eccentric due to VOLUME overload
Explain MS-what characterizes it? What’s normal valve area and gradient? What does HR and CO do to the gradient?
MS is characterized by a reduced valve area (normal 5 cm, severe 1 cm). To maintain cardiac output, blood must flow quicker through the stenotic valve as compared to a normal one, causing a pressure gradient (< 2 mm Hg normal, >12 mm Hg severe). Therefore, the greater the cardiac output (more blood), or higher the heart rate (shorter filling time), the higher the gradient. Atrial kick can account for 30% of ventricular filling; so therefore, loss of atrial kick (common in MS) would, if anything, increase the gradient needed to maintain cardiac output (assuming the same cardiac output). Slowing the HR with a beta blocker would probably not increase the gradient. The higher the gradient, the higher left atrial pressures (by definition) must be. High atrial pressures require elevated pulmonary vasculature pressures and pulmonary oedema is common. Fluid management is difficult as the patient cannot tolerate significant increases or decreases in intravascular volumes.
patient with severe mitral stenosis (MS) has an increase in HR from 60 to 120, with a reduction in systolic BP from 130 to 75 following tracheal intubation. Intraoperative ECG demonstrates p waves followed by narrow complex QRS’s. Which of the following is the best next treatment:
A. Immediate cardioversion
B. Esmolol
C. Propofol
The correct answer is: B: Esmolol
This is a question without good options, and none-of-the-above is not an option…you’ll see these on the boards. Of the available options, slowing the HR with a titratable, short acting agent such as esmolol would be the best option. Phenylephrine may be an even better choice, but was not listed. By decreasing the HR, the transvalvular gradient can be decreased to promote ventricular filling. The patient is in sinus rhythm, so cardioversion is not an option. Propofol will only worsen the hypotension. NTG may decrease vascular tone to the point of cardiovascular collapse. Nicardipine, an afterload reducer, has no place here, and may worsen the tachycardia.
Describe the gradients of AS to me:
Distal to the valve, aortic pressures are significantly lower (hence the transvalvular pressure gradient). Decreasing SVR, if anything, may widen the transvalvular gradient, not decrease it.
So patients with AS depend on atrial kick?
Yes
An anesthetized 45 year old patient with severe aortic stenosis (AS) develops atrial fibrillation (from sinus rhythm) at a rate of 70, the non-invasive blood pressure cuff cycles but continues to ‘time out.’ Peripheral pulses are thready and weak and were not assessed prior to surgery. The next best action is:
A. Immediate bolus of amiodorone B. Beta-blockade to HR of 60 C. Immediate cardioversion D. Phenylephrine E. Chest compressions
C: Immediate cardioversion
Patients with AS operate at elevated left ventricular end diastolic pressures and rely on atrial kick for ventricular filling. Rapid decompensation with loss of sinus rhythm is possible as cardiac output rapidly falls. Phenylephrine may temporarily help with myocardial perfusion, but the underlying problem is loss of sinus rhythm making cardioversion a more attractive option. Amiodarone (chemical cardioversion) can take hours for cardioversion. Beta blockade may slow the HR (which is not fast to begin with), favoring diastolic filling, avoiding rapid ventricular rates, and increasing the time for ventricular emptying, but again does not address the problem of loss of sinus rhythm and may also depress needed contractility. Chest compressions should not be performed on patients with pulses.
HOCM-explain what it is. What makes it worse? Why do they have the bisferiens pulse?
B: Decreased outflow obstruction
Patients with hypertrophic cardiomyopathy tend to have hypertrophic sub-aortic stenosis caused by overgrowth of the ventricular muscle. Both sporadic and hereditary forms exist. Increased contractility causes the sub-aortic myocardium to obstruct blood flow in the aortic outflow tract. This is further exacerbated by hypovolaemia and low LV afterload. Beta blockers and calcium channel blockers can decrease contractility as well as decrease heart rate. The bisferiens pulse is characteristic of this disease with the early rapid peak representing unobstructed flow and the subsequent peak is a result of the ‘dynamic’ obstruction. If anything, beta blockers would decrease this.
Why does phenylephrine work for TOF?
TOF includes right ventricular obstruction (typically infundibular stenosis), right ventricular hypertrophy (RVH), VSD, and an “over-riding” aorta. Due to the RV outflow obstruction, RV pressures are high and in the case where LV pressures decrease, an increased portion of deoxygenated blood from the RV crosses through the VSD to the lower pressures in the LV. This situation occurs with drops in SVR and systemic hypotension. Administration of phenylephrine increases SVR and therefore LV pressures, decreasing the shunt fraction from right to left (cyanosis). Propanolol can be used as a chronic treatment to decrease infindibular spasm (and therefore RV pressures), but has no place in acute hypoxia in the setting of hypotension. Indomethacin will antagonize prostaglandin mediated PDA patency. With severe RV outflow stenosis, aortic flow to the PDA and then through the pulmonary artery is responsible for the majority of pulmonary blood flow. Closure would be disastrous.
Strong indications for pacemaker/EP study
3rd degree block with escape rate < 40, symptomatic bradycardia, periods of systole > 3 s, certain conditions with AV block that are expected to worsen over time (myotonic muscular dystrophy, etc).
Which things prevent a pacemaker from exciting the myocardium?
A functioning pacemaker cannot excite the myocardium in some circumstances such as (extreme) hypokalaemia, hypocarbia, hypothermia, myocardial infarction, antidysrythmic drugs (possible), and fibrotic buildup around the electrodes
Which of the following is not part of the cardiopulmonary bypass (CPB) circuit:
A. Venous filter B. Venous reservoir C. Oxygenator D. Pump E. Heat Exchanger
And what is the order that blood goes through in the CPB machine?
Venous filter
The CPB circuit is as follows: Patient’s venous return flows from venous cannulas in the right atrium to the venous reservoir. From there blood is sent to the oxygenator and heat exchanger. The oxygenator oxygenates the blood as well as adds or removes CO2. Older oxygenators used small O2 bubbles for oxygen exchange but modern day CPB uses membrane oxygenators, as it is less traumatic to the blood. The heat exchanger can heat or cool blood. Next blood enters the main pump, which can be a roller pump or centrifugal. Roller pumps are generally more traumatic to RBCs, and have a hand crank in case power is interrupted. Centrifugal pumps are pressure dependent and require a flow meter to monitor output. Before returning to the patient, blood passes through the arterial filter removing thrombi, calcium, debris, and fat. The blood returns to the patient through the aortic cannula. Reread this a couple times. You have to know it.
Does hypothermia increase or decrease gas solubility? Explain pH stat. What’s the CO2 level?
Increases gas solubility-this can lead to an elevated pH (because CO2 gets absorbed), and it will look like-NOT ACTUALLY IS a respiratory alkalosis.
Therefore CO2 has to be added to the patient’s blood to replace the amount that is dissolved, keeping the pH static. Furthermore, when the blood is warmed up in the blood gas analyzer to 37 C, the added CO2 causes a respiratory acidosis picture
Temperature uncorrectef ABG=
Warm
Which one has worse neurological outcomes? pH stat or alpha stat?
pH stat
pH stat is adding CO2
True
Match the following clinical findings for a patient immediately coming off cardiopulmonary bypass (CPB) with the best treatment option
< BP// HR CO //Wedge // SVR TEE findings
1 80/50 // 105 2.5 // 6 // 1300 None Available
2 80/50 // 90 2.0 // 18 // 1300 Global hypokenesis
3 160/90 // 80 3.5 // 12 // 2600 Hyperdynamic
CHOICES
A) Intervascular volume administration
B) Nicardipine gtt
C) Balloon pump
A. 1=A; 2=C; 3=B
B. 1=C; 2=A; 3=B
C. 1=A; 2=B; 3=C
A: 1=A; 2=C; 3=B
Very common boards type question, interpreting PA cath or TEE findings and administering treatment. 1) Pt has low LVEDP, low CO and hypotension, most commonly this is a volume problem, but consider right heart failure as well. 2) Pt has low CO, hypotension in the setting of an elevated LVEDP, this is indicative of myocardial ischaemia, stunned myocardium, and hypervolaemia. Global hypokenesis is consistent with stunned myocardium, acidosis, electrolyte abnormality, and global ischaemia. Dobutamine, epinephrine, balloon pump, and going back on bypass are commonly thought of in this situation. If there is no evidence of metabolic problems or graft problems that can be resolved on bypass, a balloon pump can effectively reduce afterload and strain on the heart as well as maintain perfusion to essential organs. 3) CO is moderately low with high SVR and blood pressure. Nicardipine, a calcium channel blocker and afterload reducer, is an excellent choice to encourage forward flow.
Which of the following patients is the best candidate for intraaortic balloon pump:
A. 65 year old man following STEMI with coronary stent placement, now with 30% EF, BP 70/ 40, and paced rhythm of 60.
B. 50 year old woman with acute aortic insufficiency, vigorous LV function on TTE, BP 70/ 20, HR 110
C. 60 year old woman with acute Dailey type A aortic dissection, BP 70/40, HR 110
D. 60 year old man failing to wean from CPB, CO 1.0, TEE reveals new akenesis of septal, and anterior walls
65 year old man following STEMI with coronary stent placement, now with 30% EF, BP 70/ 40, and paced rhythm of 60.
Patients with low cardiac outputs can benefit from balloon pump as described above. Balloon pumps should be placed in the thoracic aorta distal to the left subclavian artery and timed to the dicrotic notch to increase diastolic blood flow to essential organs, including coronary perfusion. During systole the balloon deflates leaving a low afterload state for effective ventricular emptying. Balloon pumps should be avoided in patients with aortic insufficiency, mobile aortic plaques, and aortic dissection as it can worsen the underlying diseases. The patient in answer D has an overtly failing myocardium, possibly due to graft failure (LAD distribution) and should be returned back on to CPB for further evaluation. Ballon pumps decrease afterload (as the balloon deflates a vacuum effect is created) and increases coronary perfusion (balloon inflation during diastole). The net effect of ballon pumps are increased stroke volume, improved coronary perfusion, but no real change in survival.
Major complications of thoracic aortic repair:
Which artery is responsible? Which functions are controlled vi perfusion to that artery? Which ones are sometimes spared because of ____? Treatment? Other complications?
Lower extremity paralysis complicates up to 10% of thoracic aneurysm repairs and remains permanent in about half the cases. The typical presentation is anterior spinal artery syndrome where arteries feeding the anterior spinal artery off the aorta are interrupted or hypoperfused, especially the artery of Adamkiewicz. The artery of Adamkiewicz often is the primary source of blood flow for the lumbar and low thoracic anterior spinal cord. The anterior spinal cord includes tracks for motor, light touch, pain, and temperature; therefore, interruption of blood supply results in loss of these functions in the lower extremities. Proprioception, deep touch, and vibratory sense are often spared (supplied by paired posterior spinal cord arteries). Pressure monitoring distal to the cross clamp and neurological monitors (SSEPs) are used to identify when spinal cord ischaemia may be occurring. The primary treatment is deep hypothermia (decreasing cellular oxygen consumption), but intercostal reimplantation and shunts can be used to increase blood flow to the anterior spinal artery (increasing oxygen delivery). Since perfusion of the spinal cord is dependent on a pressure gradient between anterior spinal artery pressure and CSF pressure, a spinal drain can also be placed to decrease CSF pressures. Other common complications of aortic surgery (other than the usual suspects of bleeding, infection, etc) include myocardial ischaemia, renal failure, ARDS, and gut ischaemia.
Explain tamponade, which descent is absent?
During inspiration right ventricular filling is enhanced, moving the interventricular septum towards the left, decreasing left ventricular end-diastolic volumes. This normal process is enhanced in cardiac tamponade manifesting as pulses paradoxus. With cardiac tamponade, IV fluids should be given aggressively to maintain preload. The ‘y’ descent is absent in the CVP tracing, not the ‘x’ descent. Due to external pressure on the ventricles, ventricular filling and stroke volume are essentially fixed, making cardiac output heart rate dependent. Therefore decreasing heart rate will decrease cardiac output. Cardiac tamponade can be diagnosed by clinical presentation, echocardiogram, PA catheter (classically equalization of diastolic pressures within the heart), and surgically.
A 25 year old man in a motor vehicle collision is found to have aortic dissection and hypertension (170/85). Medical management is employed in the ICU. What is the best, first treatment:
And what’s the pathophys behind why aortic dissection is bad?
Aortic dissection is exacerbated by shear forces, resulting from the shear force of blood ejected by the left ventricle. Shear forces are increased with increased heart rates and cardiac output. Beta blockers reduce heart rate and contractility and are an ideal first line therapy. Nicardipine or nitroprusside can be added later, but when used alone can increase both heart rate and cardiac output. Traumatic aortic dissection typically occurs at the aortic isthmus in blunt trauma, presenting with hypotension and widened mediastinum.
Match whether each factor is a major, intermediate, or minor risk factor of increased cardiovascular risk (according to the American Heart Association):
1 Diabetes, IDDM
2 Left bundle branch block on ECG
3 Atrial-fibrilation, HR = 64
4 Atrial-fibrilation, HR = 122
5 Myocardial Infarction 1 year ago, EF =45%
6 Mitral Stenosis, Restrictive gradient of 14 mm Hg
CHOICES
A) Active Cardiac Condition
B) Clinical Risk Factor
C) Minor Risk Factor
A. 1=A; 2=B; 3=B; 4=A; 5=C; 6=A
B. 1=B; 2=A; 3=C; 4=A; 5=B; 6=B
C. 1=B; 2=C; 3=C; 4=A; 5=B; 6=A
D. 1=A; 2=C; 3=B; 4=B; 5=C; 6=A
s: C: 1=B; 2=C; 3=C; 4=A; 5=B; 6=A
Risk factors for cardiovascular risk are categorized as high risk (active cardiac conditions), intermediate risk (clinical risk factors) and minor risk (which aren’t used in the algorithm for preoperative cardiac evaluation any more). Active risk factors are: acute/ recent MI; unstable or severe angina; high grade AV block (mobitz 2 or complete); symptomatic ventricular arrhythmias; SVTs with uncontrolled ventricular rate; & severe valvular disease; and decompensated or new heart failure. (and now these aren’t used anymore either!) Multiple clinical risk factors in the absence of exercise capacity may warrant stress testing or coronary catheterization in some cases and include: ischaemic heart disease; compensated CHF; mild angina; diabetes (especially IDDM); CVA; and renal insufficiency. Minor risk factors (which are no longer recognized but helpful to know what they were so you do not get confused with them being clinical risk factors) are abnormal ECG (not including specific signs of ischaemia); low functional capacity, uncontrolled hypertension, arrhythmias with controlled ventricular rate, and advanced age. Why ask this question? Its important that you understand what patient characteristics traditionally represent an increased risk. As ACC/AHA guidelines evolve to essentially become completely ambiguous, I feel you need to have a reference point to deal with the ambiguity.
Ao clamp placed above splanchnic supraceliac
Afterload? Preload? EF? CO? Venous capacitance?
In a supraceliac clamp of the aorta, blood ejected by the LV will be redistributed above the clamp (heart, lungs, brain). That means that the heart will have increased venous return, increased after load, and variable changes in cardiac output (usually decreased). Also there is a surge of catecholamine release which will affect venous capacitance. Since venous tone will increase with high catecholamine levels, there will be additional venous return. With aortic cross-clamp both systolic and diastolic blood pressure will increase. Left end-diastolic ventricular pressures (LVEDPs) and wall motion abnormalities increase, and ejection fraction decreases. The reduction in EF is likely from reduced subendocardial perfusion exacerbated by a very elevated LVEDP (remember perfusion is Aortic diastolic pressure - LVEDP). So in this case the increase in preload (venous return) is exacerbating the reduction in CO. Its also worth saying that the reduction in CO is far less predictable than the increase in venous return.
So placed below splanchnic circulation:
the clamp is placed below the splanchnic circulation things get more complex. Now blood ejected by the LV will also be circulating in the gut. The haemodynamic response to this depends on the venous capacitance of the splanchnic circulation. If, at the time of the clamp, the splanchnic venous tone is high (low capacitance), the cross-clamp will result in a situation similar to that of a supra-celiac clamp, with increased venous return to the heart. If the splanchnic venous tone is low (high capacitance) venous return decreases as blood volume distributes to the highly compliant splanchnic vasculature. Changes in left end-diastolic ventricular pressures, wall motion abnormalities increase, and decreases in ejection fraction are less pronounced than with supraceliac. Perfusion distal to the clamp is pressure dependent and relies, of course, on collateral circulation. Increasing cardiac output does not increase perfusion distal to the cross clamp and is dependent on the pre-clamp aortic pressures (because physically only so much collateral flow is possible).
