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Cardiac Physiology PowerPoint Presentation

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Description : Check out this medical PowerPoint presentation titled "Cardiac Physiology" by Sohin Patel, M.D.

This medical PowerPoint presentation talks about basic cardiac physiology, the effect of common anesthetics on the normal and diseased heart and an anesthetic plan based on disease-specific hemodynamic goals.

Tags : Cardiac Physiology, anesthetics, anesthetic plan, disease-specific hemodynamic goals, Anesthesiology

Published on : Mar 16, 2023 | Views : 917 | Downloads : 1

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Slide 1-

Cardiac Physiology A Case-based Review By Sohin Patel, M.D.
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Learning Objectives Understand basic cardiac physiology. Describe the effect of common anesthetics on the normal and diseased heart. Devise an anesthetic plan based on disease-specific hemodynamic goals.
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Teaching Objectives Guide the student through the slide presentation, answering any questions that may arise. Allow the medical student to answer the questions asked within the slides and, with the assistance of the slides following the question, go over the relevant physiology and pathophysiology. The cases are all independent of each other and should each take about 5-10 minutes to review. If a question remains unanswered, an attending or textbook should be consulted.
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CASE 1 A 23 year old medical student with no PMH presents for a laparoscopic appendectomy. He is currently learning about cardiac physiology and has many questions. He turns to you and asks, “ What drugs are you planning on using to put me under and how will they effect my mean arterial pressure?”
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CASE 1 The most common drugs used to induce anesthesia include benzodiazepines, opioids, induction agents, paralytics, and inhalational anesthetics. MAP=COxSVR. SVR is primarily affected by ANS activity. What independent variables determine affect CO?
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CASE 1 CO = SV x HR. SV = EDV – ESV and thus is affected by preload, afterload and contractility. ddah.org.uk
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CASE 1 Preload reflects the stretch of ventricular myofilaments produced by the LVEDV. Afterload is the pressure against which the LV must propel blood. This pressure is affected by the distensibility of the aorta, resistance of peripheral arterial vasculature, and actions of relected waves on central aortic circulation. Contractility is the intrinsic force of myocardial contraction independent of preload, afterload, or HR.
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CASE 1 Anesthetic agents alter MAP by effecting one or more of the variables just discussed. Benzodiazepines generally have no effect on hemodynamics. Opiods decrease SNS activity, decreasing SVR and HR. The effect on CO is most obvious in patients who are volume depleted and negligible in patients with normal volume status and no other medications. Most commonly used paralytic agents do not effect hemodynamics. Some cause histamine release, resulting in mild hypotension. Pancuronium, however, increases HR, BP and CO due to a possible vagolytic and sympathomimetic effect.
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CASE 1 Induction agents generally decrease SVR and preload. Etomidate effects these parameters the least and is therefore used to maintain HD stability. Most inhalational agents decrease SVR and increase HR, causing little change in CO. Halothane, however, decreases CO by direct myocardial depressant effects. Barash, Clinical Anesthesia (6th ed.)
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CASE 1 After answering his questions, you give him 2mg of midazolam, which promptly brings a smile to his face and precludes him from asking any more medical questions. Induction is uneventful with fentanyl, lidocaine, propofol and rocuronium. You maintain anesthesia with sevoflurane, and reverse his paralysis with neostigmine and glycopyrrolate. After a few hours of vomiting in the PACU, he is discharged home without any other complications.
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CASE 2 A 60 year old gentleman with a PMH of dyslipidemia and HTN presents for an elective shoulder arthroscopy. He is an avid tennis player, but his play has been limited due to shoulder pain. While examining him prior to surgery, you hear a systolic murmur radiating to the carotids, best heard at the right upper sternal border. There is also a delay between the 1st heart sound and the carotid pulse. An EKG shows the following….
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http://cardiophile.org
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CASE 2 EKG shows LVH with strain and left atrial enlargement. Investigating further, he tells you that prior to quitting tennis because of shoulder pain, he experienced some tightness in his chest when playing hard, but it ceased if he rested. He also experienced two episodes of syncope in the past year. You present this information to your attending, who asks you what you are concerned about and whether you should go ahead with surgery?
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CASE 2 Given the concern for severe AS, the elective case is cancelled and further workup is performed. TTE confirms your suspicion of severe AS. The AVA is 0.8cm2 and the valve is bicuspid. There is concentric LVH and moderate LAE. No other abnormalities are identified and preoperative cardiac cath shows normal coronaries. The pt is scheduled for aortic valve replacement. You happen to be scheduled for this case and your attending asks how you plan to manage his hemodynamics pre-bypass to maintain cardiac output and avoid myocardial ischemia?
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CASE 2 Barash, Clinical Anesthesia (6th ed.) Pathophysiology of Aortic Stenosis
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CASE 2 Based on your stated goals, what anesthetic agents would be appropriate for this patient and why? Barash, Clinical Anesthesia (6th ed.)
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CASE 2 Anesthesia is induced with a high dose fentanyl, lidocaine and etomidate. The patient is paralyzed with rocuronium and anesthesia is maintained with isoflurane. Some time after induction, you notice the EKG tracing below on your monitor. The BP drops precipitously. Your attending asks you why might this be an unstable rhythm in our patient and what you would like to do about it? drsvenkatesan.wordpress.com
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CASE 2 Atrial fibrillation with rapid ventricular response can cause decreased BP in this pt for several reasons. Ventricular hypertrophy increases MVO2 because of increased muscle mass ( basal demand) and increased intraventricular systolic pressure ( demand per beat). Ventricular hypertrophy also decreases diastolic compliance, increasing the atrial kick’s contribution to LVEDV from 10% to 30-40%. So, the current rhythm will cause decreased CO secondary to decreased SV and tachycardia can cause myocardial ischemia with resulting systolic dysfunction. You decide to cardiovert the patient. How many joules and what mode would you use?
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CASE 2 After successfully cardioverting with biphasic 100J in sync mode, the pt is initially in SB with a HR in the 40s. Because stroke volume does not increase sufficiently with bradycardia and diastolic dysfunction, the CO and MAP remain low, but improved from before. You give a small dose of ephedrine, improving both the HR and BP. The rest of the case proceeds uneventfully and the pt is discharged from the hospital 4 days later.
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CASE 3 A 72yo gentleman with a h/o HTN, dyslipidemia, and 50pk-yr smoking history presents to the ER with chest pain radiating to the L shoulder. His BP is 190/100 and an EKG shows 2mm ST elevations in all precordial leads and I and aVL. He is given supplemental O2, morphine, and nitroglycerin. The pain subsides somewhat but does not resolve completely and EKG is unchanged. Based on the EKG findings, which coronary artery is involved and what walls of the LV does this correlate with?
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CASE 3 There are three main coronary arteries, the left anterior descending, circumflex, and right. The LAD and circumflex arise from the left main. V1 and V2 correlate with the septum; V3-V4 with the anterior wall; V5, V6, I and aVL with the lateral wall; and II, III, and aVF with the inferior. The septum and anterior wall are supplied by the LAD, the lateral wall by the left circumflex, and the inferior wall by the right coronary. http://www.cvphysiology.com http://radiology.rsna.org
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CASE 3 The pt is taken to the cath lab and angiography shows 90% left main, 50% mid LAD, and 60% left circumflex lesions. An IABP in inserted and the pt is taken for urgent CABG. As you are preparing for the case, your attending asks you, “What are the principal determinants of myocardial oxygen demand and coronary artery blood supply?”
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CASE 3 Of the determinants of O2 consumption, tachycardia generates more demand than increases in contractility and wall stress. The LV is perfused during diastole. RV perfusion is continuous. Tachycardia also decreases diastolic filling time, leading to decreased SV, CO and coronary artery perfusion. Barash, Clinical Anesthesia (6th ed.)
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CASE 3 Pressure relationships. 1-Aortic pressure 2- LV pressure 1a- decreased pressure distal to stenosis 2a- increased LVEDP Barash, Clinical Anesthesia (6th ed.) Coronary vascular reserve is normally 3-5 times higher than basal flow. Intramyocardial arterioles regulate diastolic vascular resistance. With stenosis in epicardial vessels, intramyocardial vessels dilate to maintain basal flow, decreasing reserve. Metabolic factors mostly determine coronary vascular tone, not SNS or stretch receptors. The LV subendocardial layer is most susceptible to ischemia because of increased systolic intraventricular pressure.
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CASE 3 Your pt arrives to the OR and you notice the above blood pressure tracing. He is no longer having chest pain. What does point B represent and why did the IABP relieve our patient’s chest pain? http://www.nurse411.com
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CASE 3 A- Assisted systole B- Dicrotic notch C- Diastolic augmentation D- Assisted aortic EDP E- Unassisted systole F- Unassisted aortic EDP - Increased coronary artery perfusion - Reduced myocardial O2 demand http://www.nurse411.com The intraaortic balloon pump is positioned between the left subclavian artery and renal artery takeoffs. The above tracing shows the IABP set at 2:1. The balloon inflates when the aortic valve closes, increasing AoDP, and deflates just prior to opening of the aortic valve. As can be seen by the highlighted portions of the curve above, the IABP increases coronary artery perfusion and decreases myocardial O2 demand.
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CASE 3 After attaching all monitors to the patient, obtaining adequate IV access and pre-oxygenating, you are ready to induce anesthesia. What agents would you use and what are your hemodynamic goals in terms of preload, afterload, contractility, rate and rhythm?
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CASE 3 Barash, Clinical Anesthesia (6th ed.)
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CASE 3 To maintain HD stability on induction, high dose opioids are important due to their lack of myocardial depression, reduction in HR, and blunting of sympathetic response from laryngoscopy. Lidocaine also blunts the response to laryngoscopy, although doses of 2mg/kg must be used for this effect. Of the induction agents, etomidate maintains the most stable BP. Propofol, however, can also be used with concurrently administered phenylephrine to prevent the drop in SVR and MAP. Of the volatile anesthetics, isoflurane dilates coronary arteries the most, although the clinical significance at <1 MAC is negligible. Volatile anesthetics have the added benefit of protecting the myocardium from ischemia and reperfusion injury and decreasing MI size.
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CASE 4 You are evaluating a patient for scheduled MVR tomorrow. The pt is 45 yrs old with a h/o bacterial endocarditis and remote IVDA. According to old records, he initially presented to the ER 6 yrs ago with pulmonary edema. TTE showed 1-2+ MR with valvular vegetations and EF of 60% with no other abnl. TTE 2 weeks ago showed 3+ MR, left atrial enlargement, LVESD of 45mm, and EF 55%. EKG showed…
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CASE 4 Ispub.com
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CASE 4 You call your attending, who has a reputation for “pimping,” to discuss the case. As expected, he has a list of questions he wants you to answer. 1. What is the difference between LVH in AS vs. MR? 2. What classes of agents would you use to treat acute MR? 3. Why has this patient’s MR worsened over time even though his infective endocarditis was treated appropriately?
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CASE 4 In chronic mitral regurgitation, eccentric hypertrophy of the LV develops, as opposed to the concentric hypertrophy of AS. http://www.cvphysiology.com http://scielo.br
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CASE 4 Acute MR, as may present with bacterial endocarditis, MV prolapse, or ruptured chordae leads to increased volume in the LV and LA. A certain percentage of the stroke volume, the regurgitant fraction, is directed from the LV to the LA. The increased LAP from the increased volume is transmitted to the pulmonary vasculature, causing pulmonary HTN and edema. http://www.h4heart.com
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CASE 4 To medically treat acute MR, the goals would be to increase forward flow and decrease LA and LV volume, and hence LV and LA pressures. If BP tolerates, afterload reducers such as SNP, diuretics such as lasix, and inotropes such as dobutamine or milrinone would all be helpful. A mildly tachycardic and hypotensive patient would be ideal. If the acute MR is able to be treated medically, pt’s may live for years without any symptoms. The MR, however, worsens over time. At first, during the compensated phase, ever-increasing LV volume dilates the LV. Progressive dilatation eventually leads to LV dysfunction and worsening MR. The MR worsens because progressive dilation of the LV and LA increases the MV annulus, causing the leaflets to no longer coapt.
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CASE 4 Ideally, as in our patient, MVR should take place in the transitional phase of MR, prior to development of permanent LV dysfunction. http://heartnet.bjmu.edu.cn
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CASE 4 The next day, you induce the pt successfully, being careful to keep him slightly tachycardic and mildly hypotensive. The valve is replaced successfully, however, when attempting to come off bypass, the pt is hypotensive. You give phenylephrine, which does not improve the BP. Your attending is not surprised and asks you why you think it is difficult to separate this pt from bypass despite successful MVR.
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CASE 4 You realize that with the MV now fixed, the LV no longer has a low-pressure vent (into the LA) during systole. The increased afterload uncovers the existing LV dysfunction. You start the pt on an inotrope and are now able to separate from bypass without much difficulty. The rest of the case is uneventful and your pt’s LV function improves over the next few days.