Apex Unit 3 Cardiovascular Flashcards

Question

Which finding is MOST likely to occur in a patient with congestive heart failure? Decreased natriuretic peptide Decreased left ventricular end diastolic pressure Increased renal blood flow Increased sympathetic tone

Answer 1

Increased sympathetic tone Patients with CHF rely on elevated levels of circulating catecholamines (increased SNS tone). Anesthetic techniques that interrupt this mechanism can precipitate cardiovascular collapse. For example, a standard propofol induction (2 mg/kg) is likely to cause issues as it reduces SNS tone while simultaneously reducing myocardial contractility. Ketamine preserves SNS tone, making it a smarter choice in the patient with congestive heart failure. CHF reduces renal blood flow, and this is the primary mechanism that increases RAAS activation. Atrial natriuretic peptide is increased in patients with CHF, as a result of atrial dilation. Remember that ANP causes natriuresis (Na+ & water excretion).

Answer 2

Decreased diastolic filling time Hypertension increases afterload. The LV must generate a higher amount of wall tension in order to open the aortic valve. In the chronically hypertensive patient, the left ventricle remodels concentrically because a greater mass augments the heart's ability to perform work. The problem is that more tissue means a higher need for oxygen ( ↑ MVO2). Additionally, a thicker heart suffers from reduced compliance and diastolic dysfunction (decreased lusitropy) is a downstream consequence of this. There is a tipping point where the heart requires more oxygen than what is delivered to it. This is when the patient is at the greatest risk for dysrhythmias or CHF. By itself, hypertension does not alter diastolic filling time. This parameter is determined by the heart rate.

Answer 3

Renal artery stenosis Secondary hypertension has an identifiable cause. It only accounts for 5% of hypertensive diagnoses, but there are many etiologies. The most common cause of secondary hypertension is renal artery stenosis. The most likely explanation is that a narrowed renal artery (atherosclerosis or fibromuscular dysplasia) delivers less blood to the affected kidney. In an attempt to increase GFR, the kidney activates the RAAS system. Definitive treatment includes renal artery endarterectomy or nephrectomy. Do NOT give an ACEI to a patient with bilateral renal artery stenosis, as this can significantly reduce GFR and precipitate renal failure.

Answer 4

Nisoldipine + Calcium channel blocker Terazosin + Alpha adrenergic receptor blocker Eprosartan + Angiotensin II receptor antagonist Perindopril + Angiotensin converting enzyme inhibitor We intentionally threw in some uncommon antihypertensive agents. We didn't do this to show you how smart we are, but rather to teach you to look to the suffix if you're unsure about a drug. You could've answered this question correctly based on the suffix alone. Angiotensin II receptor antagonist: -sartan ACE inhibitor: -pril Calcium channel blocker (dihydropyridines): - dipine Alpha adrenergic receptor blocker: - zosin Beta adrenergic receptor blocker: -lol

Answer 5

Diltiazem Calcium channel blockers reduce Ca+2 in cardiac and vascular smooth muscle. Some of these drugs target the myocardium, some affect the vasculature, and others do both. It's important to understand these nuances when selecting the best CCB for a given situation. Let's go to the next page to learn more.

Answer 6

Kussmaul's sign is usually present Bradycardia should be avoided Constrictive pericarditis limits the heart's ability to move within the pericardial sac. This reduces myocardial compliance and limits diastolic filling. Kussmaul's sign is a paradoxical rise in CVP and jugular venous distension during inspiration. It's the result of a right ventricular filling defect - in this case impaired RV compliance. Since stroke volume is reduced, cardiac output must be maintained with an adequate heart rate. Avoid bradycardia. BP = CO x SVR. If CO is limited, the BP must be maintained by SVR. Do not reduce afterload. Acute (not constrictive) pericarditis is usually caused by a virus.

Answer 7

Muffled heart tones Jugular venous distension Hypotension Pericardial tamponade can occur when the pericardium fills with fluid. This restricts myocardial movement and impairs its ability to fill and function as a pump. Beck's triad: Fluid accumulation in the pericardial sac → muffled heart tones Decreased venous return to the right heart → jugular venous distention Decreased stroke volume → hypotension

Answer 8

Ketamine The patient with pericardial tamponade relies upon the SNS to maintain blood pressure. Since most general anesthetics cause myocardial depression and reduce afterload (both of which contribute to CV collapse), local anesthesia is the preferred technique for pericardiocentesis. If general anesthesia must be performed, then ketamine is the best option. Recall that ketamine activates the SNS, which increases heart rate, contractility, and afterload. Benzodiazepines, etomidate, nitrous oxide, and opioids are preferred over volatile agents, because they produce less myocardial depression and vasodilation. Even so, ketamine is the best choice in the context of pericardial tamponade. Neuraxial anesthesia, propofol, and thiopental reduce afterload and are best avoided.

Answer 9

Dental implant Patients at risk for endocarditis (valve replacements, complex congenital heart disease, and previous endocarditis) that are scheduled for "dirty" procedures associated with transient bacteremia should receive preoperative antibiotics.

Answer 10

Nitroglycerin Hypertrophic cardiomyopathy is associated with left ventricular outflow tract obstruction. There are three determinants of blood flow through the LVOT: 1. Systolic LV volume 2. Force of LV contraction 3. Transmural pressure As a general rule, things that distend the LVOT are good, while things that narrow the LVOT are bad. Nitroglycerin reduces preload. This reduces systolic LV volume and causes the LVOT to narrow, thereby worsening the obstruction. A 500 mL 0.9% NaCl bolus would have the opposite effect. A slower heart rate extends LV filling time, so esmolol increases systolic LV volume. Additionally, it reduces contractility which helps improve LVOT obstruction. Phenylephrine increases aortic pressure, which increases the transmural pressure. This opens the LVOT.

Answer 11

30 days Patients with cardiac stents are prescribed dual antiplatelet therapy (aspirin + clopidogrel or ticlopidine). Premature discontinuation of these medications increases the risk of stent thrombosis. In the patient with a bare metal stent, elective surgery should be delayed for a minimum of 30 days. What if the patient has a drug eluting stent? Read on ...

Answer 12

Microvascular flow Because the CBP bypass circuit becomes an extension of the patient's circulation, it must be primed with enough volume to de-air the pump. The priming solution can be a balanced salt solution or blood. Priming with anything other than blood produces hemodilution, which has the following effects: ``` Decreased hematocrit Decreased plasma concentration of drugs and plasma proteins Decreased oxygen carrying capacity Decreased blood viscosity Increased microvascular flow ```

Answer 13

Sternotomy Awareness is most common during sternotomy (due to intense surgical stimulation).

Answer 14

It inflates during diastole and increases myocardial O2 supply It's contraindicated in severe aortic insufficiency The intra-aortic balloon pump improves myocardial oxygen supply while simultaneously reducing demand. It inflates during diastole. This increases coronary perfusion pressure (increased supply). It deflates during systole. This reduces afterload (decreased demand). The tip of the balloon should be positioned 2 cm distal to the left subclavian artery. A more proximal position causes the balloon to occlude perfusion of the left common carotid, and/or the brachiocephalic arteries. The IABP is contraindicated in the patient with aortic insufficiency. Balloon inflation would force blood retrograde into the left ventricle. This wouldn't be good!

Answer 15

The Crawford system classifies thoracoabdominal aortic aneurysms based on their location. There are four types. Type II aneurysms present the most significant risk for paraplegia and/or renal failure following surgery. This is because there’s a mandatory period of stopping blood flow to the renal arteries and some of the radicular arteries that perfuse the anterior spinal cord (possibly including the artery of Adamkiewicz). It’s recommended that methods to reduce the risk of ischemic injury (to be covered shortly) be used in these patients.

Answer 16

Back pain and hypotension suggest rupture Surgical intervention is recommended when the diameter is > 5.5 cm The law of Laplace (not Poiseuille) states that increased diameter increases wall tension. The greater the wall tension, the greater the risk of rupture. Surgery is indicated when aneurysmal diameter exceeds ~ 5.5 cm. Independent risk factors include cigarette smoking, gender (male > female), and advanced age. Acute onset of back pain and hypotension suggest rupture.

Answer 17

Pulmonary vascular resistance Total body oxygen consumption When the aortic clamp is released, ischemic tissues release acid and vasoactive substances into the systemic circulation. This increases pulmonary vascular resistance and pulmonary artery pressure. Removal of the aortic cross clamp increases the size of the vascular tank, so venous return falls. Hypotension reduces coronary blood flow. This topic brings so many physiologic concepts to life. If you understand and can apply the ideas on the next page, you're in great shape.

Answer 18

Loss of proprioception The artery of Adamkiewicz is the largest radicular spinal artery. It is the major blood supply to the thoracolumbar region of the spinal cord. An aortic cross clamp placed above the Adamkiewicz can cause ischemia to the lower portion of the anterior spinal cord. This can result in anterior spinal artery syndrome – otherwise known as Beck’s syndrome. We tend to generalize that the anterior cord contains motor neurons and the posterior cord contains sensory neurons. Sadly, it's not so cut and dry. We’ll explain exactly what you need to know on the next page.

Answer 19

Awake patient While cerebral oximetry, transcranial Doppler, and electroencephalography are useful monitors of neurologic integrity during CEA, an awake patient (who is minimally sedated) is the best monitor of all.

Answer 20

Right vertebral artery to the right subclavian artery Ok...so only a very small group of you will ever come across this in practice, let alone the NCE. But if you do, you'll be glad you learned about it.

Answer 21

Increasing potassium conductance Three things cause the SA node to increase its firing rate. The slope of spontaneous phase 4 depolarization increases. Threshold potential becomes more negative (shorter distance between RMP and TP). Resting membrane potential becomes more positive (shorter distance between RMP and TP). PNS stimulation increases potassium conductance. Since more potassium (a positive ion) exits the myocyte, its interior becomes more negative. This increases the distance between RMP and TP, so it takes longer for the cell to reach TP. This slows the heart rate.

Answer 22

Since you could use 1.32 - 1.39 as the theoretical maximum for oxygen binding, we accepted 4 - 5 mL/dL. The arteriovenous oxygen difference is a global measure of the amount of oxygen that is consumed by the body. It is the difference between the O2 content in the arterioles and the O2 content in the venules. Normal values: CaO2 = 20 mL O2/dL blood CvO2 = 15 mL O2/ dL/ blood Ca-v difference = 5 mL O2/dL blood Ca-v difference = (1.34 x Hgb x SpO2) - (1.34 x Hgb x SvO2) (1. 34 x 14 x 0.98) - (1.34 x 14 x 0.75) 18. 38 - 14.07 4. 31 mL O2/dL blood

Answer 23

Phase 0 = Na+ conductance is greatest Phase 1 = Cl- conductance is greatest Phase 2 = Ca+2 conductance is greatest Phase 3 = K+ conductance is greatest

Answer 24

80 SVR = MAP - CVP x 80 CO 80 is the conversion factor that changes L/min to dynes/sec/cm^-5. 1. 34 is the amount of molecular oxygen in mL that can be carried by 1 gram of hemoglobin. 0. 003 is the solubility coefficient for dissolved oxygen. Henry's law anyone? 10. ..well 10 is used for all sorts of things, but it's not used here.

Answer 25

Neither preload or afterload Contractility is the ability of the sarcomeres to shorten and perform work. This is independent of both preload and afterload. An increased contractility reflects a greater ventricular output for a given LVEDV. A decreased contractility reflects a lower ventricular output for a given LVEDV. Remember, that Chemicals affect Contractility - particularly Calcium. Don't forget that contractility (inotropy) is different than the Frank-Starling mechanism.

Answer 26

By convention, when we learn about pressure-volume loops we are looking at the left ventricle. Blood enters via the mitral valve and exits through the aortic valve. Each can assume 2 positions: open or closed At each corner of the loop, 1 valve either opens or closes: The aortic valve moves at the top of the loop. It opens on the top right corner and closes on the top left corner. The mitral valve moves at the bottom of the loop. It opens on the bottom left corner and closes on the bottom right corner.

Answer 27

Rapid ventricular filling Diastasis Atrial systole The cardiac cycle is divided into 6 phases (systole = 2 and diastole = 4). ``` Systole Isovolumic ventricular contraction (M = closed, A = closed) Ventricular ejection (M = closed, A = open) ``` ``` Diastole Isovolumic ventricular relaxation (M = closed, A = closed) Rapid ventricular filling (M = open, A = closed) Reduced ventricular filling or diastasis (M = open, A = closed) Atrial systole (M = open, A = closed) ```

Answer 28

B C Diastole B = Isovolumetric relaxation C = Rapid & late ventricular filling and atrial kick Systole D = Isovolumetric contraction A = Ventricular ejection

Answer 29

Leads II, III, and aVF monitor the right coronary artery The SA nodal artery most commonly arises from the right coronary artery The left anterior descending artery perfuses the anterior 2/3s of the septum The aorta gives rise to two coronary arteries: LCA and RCA. The RCA most commonly gives rise to the SA nodal artery. The coronary vessel that feeds the PDA determines dominance: ``` RCA supplies PDA → Right dominance (~80% of population) CxA supplies PDA → Left dominance RCA & CxA supply PDA → Co-dominance The LAD (not Cx) perfuses the left bundle. It also supplies the apex. ```

Answer 30

5% Resting coronary blood flow is 5% of cardiac output or about 225 mL/min. This increases by a factor of 3 - 4 during exercise

Answer 31

Adenosine Though all of the examples are vasodilators, adenosine is the most potent local vasodilator released by the cardiac cells. Adenosine is a byproduct of metabolism, so it should make sense that metabolically active tissue produces adenosine to increase local blood flow

Answer 32

Hyperkalemia increases resting membrane potential Like neural cells, myocytes are capable of generating a membrane potential. This quality makes them excitable or able to respond to an electrical stimulus. Resting membrane potential is determined by the difference in electrical potential inside and outside of the cell. At rest, the inside of the cell is relatively negative, and the outside of the cell is relatively positive. In the myocyte, the RMP is -90 mV. We want you to associate RMP with potassium. You must understand how potassium affects RMP! Hyperkalemia increases resting membrane potential. Hypokalemia decreases resting membrane potential. Threshold potential is the internal voltage at which the cell depolarizes. Depolarization is an all-or-none phenomenon, so once it begins, it cannot be stopped. When you think about TP, we want you to think about calcium. Hypercalcemia raises TP Hypocalcemia lowers TP Now that we understand how K+ and Ca+2 affect RMP and TP, let's look at the big picture. When RMP is closer to TP, the cell is more likely to depolarize. When RMP is further away from TP, the cell is less likely to depolarize. Given this information, you should understand why IV calcium stabilizes the myocardium in the patient with hyperkalemia. Also, it should make sense why patients with hypocalcemia are prone to muscle spasm and tetany.

Answer 33

20-30% Atrial contraction (atrial kick) contributes to 20-30% of the final LVEDP. Loss of atrial kick is particularly problematic for the patient with a poorly compliant ventricle. Without a higher atrial pressure to prime the ventricle, cardiac output suffers.

Answer 34

The absolute refractory period is when the cell is completely resistant to depolarization. This occurs between: The QRS complex and the top of the T wave Phase 0 through the middle of phase 3 The relative refractory period is when the cell can be depolarized, but it requires a larger than normal stimulus. This occurs between: The top of the T wave and the end of the T wave The middle of phase 3 to beginning of phase 4 Electrical stimulation timed with the T wave can lead to VT/VF.

Answer 35

Calcium stimulates the ryanodine receptor. Myocardial contraction begins when Ca+2 flows through the dihydropyridine receptors at the T-tubules. This occurs during phase 2 of the myocyte action potential. Ca+2 activates the ryanodine receptor (RyR2), which releases a large quantity of Ca+2 from the sarcoplasmic reticulum. This is called calcium-induced calcium-release. Next, Ca+2 binds to troponin C on the actin/myosin complex, and this causes muscle contraction. Relaxation occurs when Ca+2 unbinds from troponin C. The SERCA2 pump returns Ca+2 to the sarcoplasmic reticulum. Once inside, the Ca+2 is bound to a protein called calsequestrin.

Answer 36

SA node automaticity There are 2 vagus nerves: one right and one left. The right vagus n. innervates the SA node, so transection of this nerve will affect SA node automaticity. The left vagus n. innervates the AV node. The bundle of Kent is an abnormal accessory pathway between the atria and the ventricles in patients with Wolff-Parkinson White syndrome.

Answer 37

33 percent The ejection fraction is a measure of contractility. There are several ways to calculate EF, so we'll make sure to cover each of these. In this question, you were given a stroke volume of 30 mL and end-diastolic volume of 90 mL. EF = (SV / EDV) x 100% Since EF is a percentage, we have to multiply our answer by 100%. EF = (30 mL / 90 mL) x 100% = 33% A normal EF is 60 - 70% and an EF < 40% suggests significant LV dysfunction.

Answer 38

55 percent Since you weren't given the stroke volume, you had to calculate it. SV = EDV - ESV Then insert this into the EF equation. EF = [(EDV - ESV) / EDV] x 100 EF = [(110 - 50) / 110] x 100 = 55% A normal EF is 60 - 70% and an EF < 40% suggests significant LV dysfunction.

Answer 39

69 percent Don't think for a moment that all of the calculation questions are going to simply ask you to input numbers into a formula. There will be times where you have to interpret data before you can use it. Obviously these types of questions are harder. Answer them correctly, and you'll be rewarded. EF = (SV / EDV) x 100% The width of the pressure-volume loop is the stroke volume. So... SV = 130 - 40 = 90 mL EF = [(130 - 40) / 130) x 100 = 69%

Answer 40

79 - 81 mmHg Because the final answer depends on the formula you used, we accepted a range of answers. They are supposed to do this on the NCE as well. MAP = DBP + (SBP - DBP / 3) or (1/3 SBP) + (2/3 DBP) MAP = 65 + (110 - 65 / 3) = 80 mmHg

Answer 41

90 mmHg This one requires a little algebraic manipulation to arrive at the answer. In fact, on the NCE it is quite possible that you'll have to rearrange formulas that you already know to calculate the correct variable. You should get used to doing this before you sit for the exam. Many of you probably know this formula: MAP = CO x SVR If you input the numbers, you'd get 7200. How can this be? You know you have the correct formula, however this answer is absurd! It is an issue of units: CO is measured as L/min and SVR is measured as dynes/sec/cm-5. To get the units to agree, you'll have to divide 7200 by 80. MAP = (CO x SVR) / 80 = 90 mmHg If the question also gave you CVP, you would add this to MAP. For example, if the CVP is 10 mm

Answer 42

580 dynes/sec/cm-5 At the bedside, we use SVR as a rough estimate of afterload. It's important to consider that this calculation does not take ventricular wall tension into consideration. For example, the afterload of the patient with critical aortic stenosis is set at the valve (not the circulation). In this patient, this calculation greatly underestimates the true afterload that the LV is working against. SVR = [(MAP - CVP) / CO] x 80 SVR = [(60 - 2) / 8] x 80 = 580 dynes/sec/cm-5 The normal SVR is 900 - 1400 dynes/sec/cm-5.

Answer 43

208 dynes/sec/cm-5 If you know how to calculate SVR, then you also know how to calculate PVR. All you have to do is change the variables. SVR = [(MAP - CVP) / CO] x 80 PVR = [(MeanPAP - PAOP) / CO] x 80 PVR = [(25 - 12) / 5] x 80 = 208 dynes/sec/cm-5 The normal PVR is 150 - 250 dynes/sec/cm-5.

Answer 44

5.7 L/min In nursing school, you learned that cardiac output is the product of heart rate and stroke volume. We had to make it at least a little more difficult than that! CO = HR x SV or HR x (EDV - ESV) CO = 95 x (110 - 50) = 5,700 mL/min which converts to 5.7 L/min The average cardiac output is about 5 L/min.

Answer 45

2.53 L/min Any time you are asked about an index, all you have to do is divide the final variable by the body surface area. CO = HR x SV CI = (HR x SV) / BSA CI = (70 x 65) / 1.8 = 2,527 mL/min converts to 2.53 L/min The normal cardiac index is 2.8 - 4.2 L/min.

Answer 46

4.5 L/min As you can see, there are a variety of ways the NCE question writers can assess your knowledge of cardiac output. The pressure-volume loop does not measure time, so it cannot measure any variable that occurs over time such as heart rate or cardiac output. CO = HR x SV The width of the pressure-volume loop is the stroke volume. Once you have this number, plug it into the equation. CO = 50 x 90 = 4,500 mL/min converts to 4.50 L/min

Answer 47

Parallel replication of sarcomeres in the left atrium Mitral stenosis creates parallel replication of sarcomeres in the left atrium. Since the left atrium must generate a higher pressure to push blood past a stenotic mitral valve, the LA (not the LV) hypertrophies to satisfy the demand. The heart compensates for pressure overload with concentric hypertrophy (parallel replication of sarcomeres). The LV is chronically underfilled in mitral stenosis, so there is no reason for the chamber to increase in diameter. Serial replication of sarcomeres is called eccentric hypertrophy. It is seen with volume overload.

Answer 48

Bicuspid aortic valve The most common causes of aortic stenosis are a bicuspid valve and calcification. In fact, a bi-leaflet aortic valve calcifies earlier than a tri-leaflet valve. Rheumatic fever probably jumped out at you. We would probably select this answer for any other valvular lesion aside from AS. You have to be careful with this approach, as some of these classic teachings are ripe for questions where they become a distractor. With this in mind, rheumatic fever is a possible cause of AS, although it is far from the most common. Infective endocarditis causes AS, but again it's not the most common cause. A ruptured papillary muscle leads to acute mitral regurgitation (not AS).

Answer 49

Systemic vascular resistance = 1500 dynes/sec/cm-5 Pulmonary artery occlusion pressure = 12 mmHg This patient has aortic stenosis. You should be concerned with rate, volume, and afterload. Rate: Maintain NSR. Tachycardia reduces filling time and bradycardia creates LV distension. Volume: Increase preload. Keep CVP and PAOP at high/normal. Afterload: Afterload is set by the stenotic aortic valve. SVR must be kept high to help perfuse the coronary arteries (CPP = AoDBP - LVEDP).

Answer 50

Pressure overload Stenosis ``` Stenosis: Pressure overload Concentric hypertrophy Chamber becomes thicker to generate more pressure Sarcomeres in parallel "Slow, full, and tight" ``` ``` Regurgitation: Volume overload Eccentric hypertrophy Chamber dilates to accept more volume Sarcomeres in series "Full, fast, and forward" ```

Answer 51

The aortic valve closes at the upper left corner of the pressure-volume loop, therefore the period of isovolumetric relaxation is affected. The line slants to the right as the ventricle accepts preload during this time. Said another way, end diastolic volume is higher than end-systolic volume. You should envision the letter "A" in this region of the pressure volume loop in the patient with AI.

Answer 52

Aortic stenosis We find it SAD that the triad of Syncope, Angina, and Dyspnea on exertion are the hallmark symptoms of aortic stenosis. The average time of survival that corresponds with the onset of each of these symptoms is three, five, and two years respectively. Mitral stenosis presents with pulmonary congestion and a-fib. Chronic mitral regurgitation presents with DOE, paroxysmal nocturnal dyspnea, and a-fib. Acute aortic insufficiency presents with severe pulmonary edema and CHF.

Answer 53

Nitroprusside Dobutamine Systolic anterior motion (SAM) is a complication of mitral valve repair. In this condition, the left ventricular outflow tract becomes occluded. The risk of SAM is increased when the anterior leaflet is longer than the posterior leaflet or when there is a narrow angle between the mitral annulus and aortic annulus. Pharmacologic treatment is the same as hypertrophic cardiomyopathy. Vasodilators and inotropes (nitroprusside and dobutamine) make SAM worse. Vasoconstrictors and volume expansion (phenylephrine and NaCl bolus) tend to make SAM better. "I do not like that SAM I am..."

Answer 54

Vasopressin This patient should be treated with a pure vasoconstrictor (vasopressin), because it does not increase heart rate. Phenylephrine would've been the first best choice. We tried to make the question a little more difficult by omitting it as an answer choice. An increased heart rate could be detrimental with MS, as it reduces diastolic filling time, increased left atrial volume and pressure, and increases the risk of pulmonary edema. Ephedrine, epinephrine, and dobutamine increase heart rate.

Answer 55

Ketamine A large ventricle tends to reduce MV prolapse, while a small ventricle tends to increase MV prolapse. For this reason, the primary management goal for MVP is to prevent excessive cardiac emptying. To Keep the Heart Full, You’ll Want to Avoid: SNS stimulation → myocardial contractility Decreased SVR Hypovolemia Upright posture (reverse Trendelenburg or sitting position) You probably noticed that we said to avoid SNS stimulation (which increases SVR) as well as anything that reduces SVR. Think Goldilocks anesthesia…right in the middle. Pharmacologic Considerations: Ketamine is avoided, because it activates the SNS, increases myocardial contractility, and augments LV emptying. Etomidate provides cardiostability, making it a reasonable choice. Volatile anesthetics + N2O and/or opioids help minimize SNS stimulation, but they must be titrated to prevent a significant decrease in systemic vascular resistance. Phenylephrine is useful for hypotension. There is no contraindication to regional anesthesia.

Answer 56

Judicious fluid administration In the patient with severe mitral stenosis, any condition that increases left atrial volume can precipitate pulmonary edema. Of all of the answer choices, judicious fluid administration is least likely to significantly raise left atrial pressure. Both uterine contraction and Trendelenburg position increase preload. Atrial fibrillation reduces cardiac output and increases back pressure in the pulmonary circulation.

Answer 57

In the left heart, systolic murmurs are caused by aortic stenosis or mitral regurgitation, while diastolic murmurs are caused by aortic insufficiency or mitral stenosis. Mitral stenosis and regurgitation are best heard at the apex or left axilla. MS creates an opening snap with a low intensity murmur during diastole. MR causes a loud swishing sound during systole. This is the correct answer to the question. Aortic stenosis and insufficiency are best heard at the right sternal border. AS creates a harsh and noisy murmur during systole. AI causes a high pitch blowing murmur during diastole.

Answer 58

42 mmHg Coronary perfusion pressure = Aortic DBP - LVEDP CPP = 60 - 18 = 42 mmHg In this case, you had to use the a-line DBP as a surrogate for aortic DBP and also PAD as a surrogate for PAOP. You are expected to be able to make these assumptions on boards, so if you didn't get this correct, you've identified a knowledge gap you'll need to fill before the big day. You get extra credit if you noticed there was no SpO2 waveform.

Answer 59

Class I + Asymptomatic Class II + Symptomatic with moderate activity Class III + Symptomatic with mild activity Class IV + Symptomatic at rest

Answer 60

Increase heart rate to maximize cardiac output. The hallmark of systolic heart failure is a decreased ejection fraction with an increased end-diastolic volume (the ventricle does not empty well). The amount of systolic failure is quantified with the ejection fraction: EF = (Stroke volume / End-diastolic volume) x 100 where... SV = End-diastolic volume - End-systolic volume Know how to complete this calculation using both methods. Also, know how to calculate it from an illustration of a pressure-volume loop (the SV is the width of the loop). Since the heart can’t squeeze well, a greater volume of blood remains in the ventricle after each contraction. The body compensates with SNS activation – this increases the heart rate. Said another way, if the stroke volume is reduced, the only way to maintain cardiac output is to increase heart rate. Additionally, decreased renal blood flow activates the renin-angiotensin-aldosterone system. Anesthetic considerations for systolic dysfunction include: Preload: It’s already high, so don’t let it get higher Afterload: Decrease to reduce the LV workload Heart rate: Maintain high/normal range Contractility: Inotropic support as needed

Answer 61

Aortic stenosis Ischemic heart disease Essential hypertension Diastolic failure is associated with decreased ventricular compliance; the heart is unable to relax to accept the incoming volume. Said another way, the ventricle doesn't fill properly. This explains why the end-diastolic pressure overestimates the end-diastolic volume. The defining characteristic of diastolic dysfunction is symptomatic heart failure with a normal ejection fraction. Contractility is generally preserved until the late stage of the disease. An S4 may be heard. The most common causes of diastolic heart failure include aortic stenosis, ischemic heart disease, and long-standing essential hypertension. Diastolic dysfunction is also associated with: ``` Concentric hypertrophy Old age Valve stenosis Hypertrophic cardiomyopathy Cor pulmonale Obesity Diastolic heart failure can co-exist with systolic heart failure, which explains why you'll see some overlapping etiologies between the two. ```

Answer 62

Enalapril Spironolactone The failing heart changes its size, shape, and function in an attempt to preserve cardiac output. This is known as cardiac remodeling. Overtime, these compensatory mechanisms create problems of their own, and a decline in myocardial function ensues. The heart becomes thicker (concentric hypertrophy) in response to pressure overload. The heart becomes dilated (eccentric hypertrophy) in response to volume overload. Cardiac remodeling can be reversed by ACE inhibitors (-pril drugs) and aldosterone inhibitors (spironolactone). Indeed, these are first line agents in the patient with heart failure.

Answer 63

Elementary, my dear Watson. Diastolic compliance describes the ventricular filling pressure that results from a given end-diastolic volume. C ventricle = Ventricular volume / Ventricular pressur Decreased Cv results from conditions that cause a stiff heart. The curve shifts up and left. Increased Cv results from conditions that dilate the heart. The curve shifts down and right. Now is where it gets fun… The arterial waveform in the image illustrates a bisferiens pulse, and this can occur in the patient with aortic insufficiency (increased Cv). Take note of the sharp upstroke, low diastolic pressure, wide pulse pressure, and most importantly, the biphasic systolic peaks. See the Cardiac II Valvular Heart Disease question 6 for more detail. Notice how this one question pulls from several content areas? Expect the NCE to do the same.

Answer 64

Left ventricular subendocardium The left ventricular subendocardium is primarily perfused during diastole (there is very little perfusion during systole). As aortic pressure increases, the LV tissue compresses its own blood supply and reduces its own blood flow. The high compressive pressures in the LV subendocardium coupled with a decreased coronary blood flow during systole increase coronary vascular resistance and predispose this region to ischemia. Because the epicardial vessels lay on top of the heart, they are not compressed during systole and are perfused throughout the cardiac cycle. The subendocardium of the RV is also well perfused throughout the cardiac cycle. This is because the RV has a thinner wall and does not generate pressures high enough to occlude its circulation.

Answer 65

Myocardial infarction A cell requires oxygen and energy to maintain the integrity of its cell membrane. A cell that dies as a result of inadequate oxygenation is no longer able to maintain the integrity of its cell membrane. As a consequence, intracellular components are released into the circulation. Infarcted myocardium releases 3 key biomarkers that you should understand: Creatine Kinase-MB and Troponin I and T. ``` Creatine Kinase-MB (CK-MB): Initial elevation = 3-12 hrs Peak elevation = 24 hrs Return to baseline = 48-72 hrs Troponin I: Initial elevation = 3-12 hrs Peak elevation = 24 hrs Return to baseline = 5-10 days Troponin T: Initial elevation = 3-12 hrs Peak elevation = 12-48 hrs Return to baseline = 5-14 days Cardiac troponins are more sensitive than CK-MB for the diagnosis of myocardial infarction. These values must be evaluated in the context of the patient's EKG. ```

Answer 66

Open aortic aneurysm repair + High risk Carotid endarterectomy + Intermediate risk Temporal artery biopsy + Low risk In patients with co-existing coronary artery disease, you should be able to apply the AHA/American College of Cardiology guidelines to stratify cardiac risk by the type of surgical procedure. Risk is defined as perioperative myocardial infarction or death. ``` High (Risk > 5 percent): Emergency surgery (especially in the elderly) Open aortic surgery Peripheral vascular surgery Long surgical procedures with significant volume shifts and/or blood loss Intermediate (Risk = 1-5 percent): Carotid endarterectomy Head and neck surgery Intrathoracic or intraperitoneal surgery Orthopedic surgery Prostate surgery Low (Risk <1 percent): Endoscopic procedures Cataract surgery Superficial procedures Breast surgery Ambulatory procedures ```

Answer 67

P50 Diastolic time The heart is unique in that it has a very high basal oxygen consumption (8 - 10 mL O2/min) with an extraction ratio of 65-70 percent. This means that the heart is highly sensitive to an O2 supply/demand imbalance. Myocardial oxygenation is a function of how much oxygen is delivered and how much is consumed. Ischemia occurs when the demand becomes too great and/or the supply too low. Myocardial oxygen SUPPLY is a function of: Heart rate (diastolic time - the LV circulation only perfuses during diastole) Aortic diastolic blood pressure Coronary blood flow (CPP = AoDBP - PAOP) Oxygen content Oxygen extraction (P50 determines O2 offloading from Hgb) Myocardial oxygen DEMAND is a function of: Heart rate Preload Afterload Contractility (inotropy) *Notice that heart rate is on both sides of the equation.

Answer 68

Heart rate Pressure work Some cardiac activities require more oxygen than others. This is useful to understand when thinking of ways to improve the cardiac O2 supply/demand balance. We’ve ranked each from the highest O2 consumption activity to the lowest O2 consumption activity: Heart rate ~ Pressure work > Contractility > Wall stress > Volume work

Answer 69

Metoprolol Morphine Let's apply what we already know about cardiac pharmacology with what we reviewed in the last few questions. Metoprolol improves O2 supply and demand by attenuating HR and contractility. Morphine also improves the O2 supply/demand balance. Remember from ACLS, "MONA greets chest pain patients at the door." ``` Morphine Oxygen Nitroglycerine Aspirin Atropine increases heart rate. You must know that this increases O2 demand while simultaneously decreases O2 supply. ``` Dobutamine increases heart rate as well as myocardial contractility.

Answer 70

Alpha-1 subunit of the L-type calcium channel There are three types of voltage-gated calcium channels: ``` L-type = Long lasting or slow channel N-type = Neural T-type = Transient All of the clinically used CCBs bind to the alpha-1- subunit of the L-type calcium channel. This prevents calcium from entering cardiac and vascular smooth muscle cells. ``` Dihydropyridines target vascular smooth muscle Non-dihydropyridines target the myocardium Using this knowledge, we can predict the cardiovascular effects of calcium channel blockers based on their classes: Dihydropyridines primarily target vascular smooth muscle: Vascular smooth muscle relaxation → ↓ SVR Non-dihydropyridines primarily target the myocardium: ``` ↓ Chronotropy (heart rate) ↓ Inotropy (contractility) ↓ Dromotropy (speed of conduction) ↓ Coronary vascular resistance As you’ll see in the next few questions, not all CCBs are created equally. ```

Answer 71

Nicardipine + Dihydropyridine Verapamil + Phenylalkylamine Diltiazem + Benzothiazepine Just like there are three types of voltage-gated calcium channels, there are 3 classes of calcium channel blockers. Remember, all of these bind to the alpha-1 subunit of the L-type calcium channel, although each binds to the channel in a slightly different way. Dihydropyridines: Cellular target: Vascular smooth muscle Binding site: Binds to the outside of the channel (modulates channel function) Key examples: Nifedipine, nicardipine, nimodipine, amlodipine Phenylalkylamines: Cellular target: Myocardium Binding site: Binds to the inside of the channel (occludes the ion conducting pore) Key example = Verapamil Benzothiazepines: Cellular target: Myocardium Binding site: Poorly understood Key example: Diltiazem

Answer 72

Nicardipine Nicardipine and nifedipine are potent vasodilators, however only nicardipine is available for IV administration. They are best used to decrease SVR and/or relieve angina. Verapamil reduces heart rate and contractility. It also exhibits mild coronary vasodilating properties. It is primarily used for controlling supraventricular tachycardia and/or angina. It causes little systemic vasodilation. Nimodipine is a potent cerebral vasodilator. It’s high lipid solubility enhances its passage into the brain, which explains why it’s the most efficacious CCB in preventing/relieving cerebral vasospasm that occurs as a consequence of subarachnoid hemorrhage. Nimodipine can only be given orally. There is a black box warning that states IV administration can be fatal.

Answer 73

Viral infection The pericardium surrounds the heart and provides a minimal friction environment in which the heart can move with ease. It is composed of two layers that are separated by 10-50 mL of clear fluid: The visceral layer is attached to the myocardium. The parietal layer is anchored in the mediastinum. You must know three conditions that affect the pericardium. All of them limit the heart’s ability to move within the pericardial sac. ``` Acute pericarditis (most common cause = viral infection) Constrictive pericarditis (most common cause = radiation or previous cardiac surgery) Cardiac tamponade ```

Answer 74

Kussmaul’s sign Pulsus paradoxus Atrial dysrhythmias Constrictive pericarditis is caused by fibrosis or any condition where the pericardium becomes thicker. The ventricles cannot fully relax during diastole, and this limits filling by reducing ventricular compliance. S/sx of constrictive pericarditis include: Kussmaul's sign Pulsus paradoxus Atrial dysrhythmias Pericardial knock Increased venous pressure Acute pericarditis is usually the result of inflammation. It does not impair diastolic filling unless inflammation leads to constrictive pericarditis or cardiac tamponade. ``` S/sx of acute pericarditis include: Acute chest pain (pain increases with inspiration) Fever Pericardial friction rub ST elevation ```

Answer 75

Jugular venous pressure During inspiration, the negative pressure in the thoracic cavity augments blood flow into the right ventricle. This reduces jugular venous pressure during inspiration. Kussmaul sign is a paradoxical rise in jugular venous pressure during inspiration. It’s caused by a restriction in RV filling, and the high right-sided heart pressure is reflected back to the jugular veins. On the CVP waveform, the x and y descents are often exaggerated. Kussmaul’s sign is highly suggestive of constrictive pericarditis.

Answer 76

Pulsus paradoxus The pericardium is a fluid filled sac that surrounds the heart. We know that too much fluid can be a problem, but what’s the difference between effusion and tamponade? Pericardial effusion is the accumulation of fluid inside the pericardial sac, but it is not enough to impair cardiac filling. Pericardial tamponade is also an accumulation of fluid inside the pericardial sac. The key distinction is that it does impair cardiac filling. Said another way, the external compressive effect is enough to compress the cardiac chambers and impair the heart’s ability to act like a pump. Since cardiac filling is a problem, it has a predictable effect on cardiac output and blood pressure. Pulsus paradoxus is also called paradoxical pulse, and it is highlyconsistent with pericardial tamponade. Although there are other causes, we want you to know this specific association. So what is pulsus paradoxus? Normally the systolic BP decreases a little during inspiration (a few mmHg), but in the patient with pulsus paradoxus, the SBP decreases by 10 mmHg (or more). The other pulse abnormalities are covered in detail in Cardiac II Valvular Heart Disease.

Answer 77

Prosthetic heart valve Unrepaired cyanotic heart disease The following conditions are associated with the highest risk for developing infective endocarditis. Depending on the surgical procedure, these patients should be considered for pre-operative antibiotic prophylaxis (more on surgical procedures in the next question). History of infective endocarditis Prosthetic heart valve Heart transplant with valvuloplasty Unrepaired cyanotic congenital heart disease Repaired congenital heart disease if the repair is < 6 months old Repaired congenital heart disease with residual defects that have impaired endothelialization at the graft site Antibiotic prophylaxis is NOT indicated for patients with a history of: Mitral valve prolapse CABG Coronary stent placement Unrepaired cardiac valve disease

Answer 78

Bronchoscopy with biopsy In addition to knowing which patients are at high risk of developing infective endocarditis, you must also understand which procedures carry a high risk for this patient population. High risk procedures are thought to be "dirty" procedures, where the risk of bacteremia outweighs the risk of antibiotic therapy. As a general rule, these procedures injure tissue allowing pathogens direct entry into the systemic circulation. Examples include: Dental procedures involving gingival manipulation and/or damage to mucosa lining. Respiratory procedures that perforate the mucosal lining with incision or biopsy. Biopsy of infective lesions on the skin or muscle. Antibiotic prophylaxis is NOT recommended for:GI endoscopic procedures in the absence of active infection GU procedures in the absence of active infection

Answer 79

Dilated cardiomyopathy Hypertrophic cardiomyopathy is the most common genetic cardiac disorder, and it is the most common cause of sudden cardiac death in young athletes. This disease process goes by several names, and you never know which one might appear on boards. For this reason, we recommend that you learn all of them: Obstructive hypertrophic cardiomyopathy (OHCM) Hypertrophic obstructive cardiomyopathy (HOCM) Idiopathic hypertrophic subaortic stenosis (IHSS) Asymmetric septal hypertrophy (ASH)

Answer 80

Valsalva maneuver Ephedrine Nitroprusside In the patient with hypertrophic cardiomyopathy, we are always concerned about left ventricular outflow tract obstruction. ``` There are 4 conditions that increase the risk of LVOT obstruction: decreased preload, decreased afterload, increased heart rate, and increased contractility. 1. Conditions that Decrease Preload: Vasodilators Neuraxial anesthesia Hypovolemia Postural changes (reverse T-burg) Positive pressure ventilation Valsalva maneuver ``` ``` 2. Conditions that Decrease Afterload: Vasodilators Neuraxial anesthesia Oxytocin 3. Conditions that Increase Heart Rate: Beta-agonists Ketamine Pancuronium Desflurane Oxytocin Light anesthesia Histamine releasing drugs (morphine, meperidine, thiopental, atracurium) 4. Conditions that Increase Contractility: Beta-agonists Digoxin Light anesthesia ```

Answer 81

Hashimoto's disease Hypertension without an identifiable etiology is called primary hypertension. We call it secondary hypertension when we can pinpoint the cause of the patient's hypertension. In patients with secondary hypertension, treating this cause usually restores blood pressure to a normal range. Renal artery disease is the most common cause of secondary hypertension. Other examples include: Hyperaldosteronism (Conn's disease – too much aldosterone) Hyperadrenocorticism (Cushing's syndrome – too much glucocorticoid) Pheochromocytoma (catecholamine secreting tumor – usually in the adrenal gland) Coarctation of the aorta Pregnancy-induced hypertension Hashimoto's disease is an autoimmune disease that attacks the thyroid gland. It causes hypothyroidism.

Answer 82

Law of Laplace Tension is a pulling force that stretches or elongates something. For a cylinder (like the aorta), the law of Laplace states that tension is the product of pressure and radius (T = P x R). Both the aorta and the aneurysm are exposed to mean arterial pressure. According to the law of Laplace, if the pressure is constant and the radius is increased, tension must increase as a result. If this patient becomes hypertensive, the tension on the aneurysm rises, possibly leading to rupture. Poiseuille's law describes laminar flow through a tube. Flow is directly proportional to the radius raised to the fourth power and the pressure difference along the tube (P1 - P2). Flow is inversely proportional to viscosity and the length of the tube. Bernoulli's principle describes flow through a constriction. At the site of constriction, the fluid’s velocity increases, creating a pressure drop at the point of constriction. Henry's law describes the solubility of gas in a solution.

Answer 83

Spinothalamic tract impairment The spinal cord’s blood supply consists of: 2 posterior spinal arteries (dorsal cord = sensory) 1 anterior spinal artery (anterior cord = motor) The anterior spinal artery is supplied by the vertebral arteries as well as 6-8 radicular arteries that arise from the aorta. Collateralization is poor, making much of the anterior spinal cord depended on a single blood supply. The artery of Adamkiewicz perfuses much of the thoracolumbar cord, making it the most important radicular artery. It arises between T8-T12 in 75% of the population. Aortic cross clamping can impair flow through the artery of Adamkiewicz, and because collateralization in this region is poor, there is an increased risk of spinal cord ischemia or infarction. This can cause anterior spinal artery syndrome (Beck’s syndrome). S/sx include: Flaccid paralysis of the lower extremities (impaired motor tracts) Bowel and bladder dysfunction (impaired motor tracts) Loss of temperature and pain sensation (impaired spinothalamic tract) Touch and proprioception are preserved (intact dorsal column) Beck's TRIAD (distended jugular veins, hypotension, muffled heart sounds) occurs as a consequence of cardiac tamponade. Don't get this confused with Beck's SYNDROME.

Answer 84

Cerebrospinal fluid drainage A thoracic cross clamp time that exceeds 30 minutes poses a significant threat to spinal cord perfusion. Protective strategies include: CSF drainage – CSF shunting from the brain towards the spinal column during clamping can exert excess pressure on the spinal cord. Draining CSF improves spinal cord perfusion (spinal cord perfusion = MAP – CSF pressure). Moderate hypothermia (30 – 32 degrees C). Proximal hypertension during cross clamp (MAP ~ 100 mmHg). Avoidance of hyperglycemia. Partial CPB (left atrium to femoral artery). Drugs - corticosteroids, calcium channel blockers, and/or mannitol.

Answer 85

Preload Mixed venous oxygen saturation Mixed venous oxygen saturation increases as a function of decreased oxygen consumption. You are putting the same quantity of oxygen into the lungs, but cells distal to the aortic clamp don't receive or consume it. Preload increases because the blood volume is shifted proximal to the clamp. This increases cardiac filling pressures and wall stress. The contractile function of the myocardium and the increase in afterload determine cardiac output. CO is usually unchanged in the healthy heart and decreased in patients with reduced cardiac reserve. Renal blood flow decreases even if an infra-renal clamp is used.

Answer 86

Carotid denervation reduces the ventilatory response to hypoxia If a hematoma causes airway compromise, the anesthetist should remove the sutures from the incision site You must know the potential complications that can arise following carotid endarterectomy. Hematoma at the surgical site can compromise airway patency. This is an airway emergency. In an ideal world, the surgeon is present to remove the sutures and decompress the site. If the surgeon isn't available, you'll need to do it yourself. Cricothyroidotomy or tracheostomy may be required in the direst situations. Ipsilateral recurrent laryngeal nerve injury can occur during CEA. Remember, the RLN innervates all of the intrinsic laryngeal muscles except for the cricothyroid muscle. Unilateral RLN injury paralyzes the ipsilateral vocal cord and may result in hoarseness and inspiratory stridor. Bilateral injury can cause complete airway obstruction. Hemodynamic instability can occur after the baroreceptors are exposed to the patient's true blood pressure (after the plaque is removed). Hyper- and hypotension are common, but hypertension is more common. Both usually subside within 24 hours. Hypertension can lead to reperfusion injury, cerebral edema, and hematoma at the surgical site. Hypotension can reduce cerebral perfusion pressure. Postoperative stroke is usually the result of an embolic phenomena (not hyper- or hypotension). Carotid body denervation reduces the ventilatory response to hypoxia. This is further complicated by narcotics and/or bilateral CEA.

Answer 87

Bradycardia is better treated with isoproterenol than with atropine Although we covered the denervated heart in the ANS Tutorial, a little review never hurts... The transplanted heart is severed from autonomic influence, so the heart rate is determined by the intrinsic rate of phase 4 depolarization of the SA node (100 - 120 bpm). Said another way, the heart rate is relatively fixed. Since the heart rate is fixed, cardiac output is preload dependent. Cardiac output adjusts according to the position on the Starling curve – increasing preload augments cardiac output until a point is reached where the ventricular myocytes become over stretched and cardiac output falls. Atropine reduces vagal tone by acting as a competitive antagonist of the M2 receptor. In the absence of vagal input, atropine has no effect. Only direct acting drugs, such as epinephrine or isoproterenol, can be used to manipulate the heart rate. Although cholinesterase inhibitors won't cause bradycardia, they will still cause s/sx of PNS activation elsewhere in the body. You'll need to administer an anticholinergic with reversal of neuromuscular blockade to prevent these issues. You may see two P waves on the EKG; one corresponds to the recipient’s intrinsic SA node and one from the donor heart. The SA node of the native heart may still react to fluctuations in autonomic input, but this will not affect cardiac function.

Answer 88

Six months How long should you delay elective surgery after a coronary stent has been placed? Bare metal stent = 30 days DES = 6 months (current gen DES) or 12 months (1st gen DES) A patient with a stent that undergoes non-cardiac surgery too soon after stent placement is at risk for: coronary stent thrombosis, hemorrhage, perioperative MI, and death.

Answer 89

Infection Sepsis (infection) is the most common cause of death in the patient with an LVAD. Aseptic technique and prophylactic antibiotics are mandatory. Gastrointestinal bleeding is common in this population.

Answer 90

Acute respiratory distress syndrome: ↓ CVP + ↑ PADP + normal PAO Left ventricular failure: Normal CVP + ↑ PADP + ↑ PAOP Cardiac tamponade: ↑ CVP + ↑ PADP + ↑ PAOP Pulmonary hypertension: ↑ CVP + ↑ PADP + Normal PAOP

Answer 91

Kawasaki's disease Kawasaki’s Disease: Occurs primarily in children. S/sx: Fever, vasculitis, red “strawberry” tongue, conjunctivitis, inflammation of mucus membranes, cervical lymphadenopathy, and swollen hands and feet. Affects coronary arteries and medium size arteries. At risk for coronary artery aneurysm and myocardial ischemia. “Name game” → Mucocutaneous lymph node syndrome. Wegener's Granulomatosis: Necrotizing granulomas lead to vasculitis (inflamed arteries) in the airway, lungs, CNS, and kidneys. Friable, necrotic tissue in the airway bleeds easily. Tracheal granulomas reduce tracheal diameter. Be careful during airway management and downsize the endotracheal tube. Lung granulomas can cause hypoxemia. Takayasu’s Arteritis: Occlusive disease of the proximal aorta and its main branches. “Name game” → pulseless disease or occlusive thromboaortopathy or aortic arch syndrome. Thromboangiitis Obliterans: Inflammatory vasculitis that ultimately occludes the small and medium-sized arteries and veins in the extremities (it obliterates the blood vessels). This leads to Raynaud’s-like symptoms. A cold environment can impair perfusion, leading to ischemia of the affected extremities; maintenance of normothermia is critical. Be very careful with padding and positioning. Smoking is the most common cause and smoking cessation is the best treatment. “Name game” → Buerger’s disease.

Answer 92

Subclavian steal syndrome Subclavian steal syndrome occurs when there is an occlusion of the subclavian or innominate artery proximal to the origin of the ipsilateral vertebral artery. This causes flow reversal through the vertebral artery, and it creates a big problem. Blood that would usually travel to the posterior cerebral circulation (via the vertebral artery) is stolen by the ipsilateral arm. This is a function of altered pressure gradients in the arterial circulation. Symptoms of subclavian steal include ataxia, vertigo, syncope, and hemiplegia. Blood pressure measured in the affected arm is significantly lower than the contralateral arm. Distal pulses may be diminished or absent. Treatment is subclavian endarterectomy.

Answer 93

100 mmHg Before a patient can be placed on cardiopulmonary bypass, the aorta must be cannulated. Hypertension during cannulation can lead to aortic dissection, so it is imperative that the systolic blood pressure be below 100 mmHg during this time (Ideal range: SBP = 90 – 100 mmHg or MAP < 70 mmHg). Additionally, the patient should be heparinized prior to aortic cannulation.

Answer 94

400 seconds The patient must be adequately heparinized before transitioning to cardiopulmonary bypass. This is defined as an activated clotting time (ACT) > 400 seconds.

Answer 95

The goal of myocardial preservation is to reduce myocardial damage that occurs during cardiopulmonary bypass. Cardioplegia is introduced into the aortic root, where the solution then enters the coronary arteries. For this to occur, the aortic valve must be competent (no AI) and the aorta clamped. Alternatively, retrograde cardioplegia may be administered through a cannula placed in the coronary sinus. Potassium in the cardioplegia solution arrests the heart in diastole. Recall that K+ increases resting membrane potential. This initially activates the voltage-gated Na+ channels, but then it maintains the Na+ channels in an inactive state. Said another way, the voltage-gated Na+ channels are unable to depolarize again until the RMP returns to normal. When the surgical procedure is complete, the heart is "restarted" by infusing the coronary circulation with warm, normokalemic blood. Heart block (after the heart is restarted) is a side effect of the cardioplegia solution. For this reason, the heart is often paced in the post-bypass period.

Answer 96

300 mg Protamine is used to reverse heparin at the conclusion of cardiopulmonary bypass. It does this via a neutralization reaction (it forms an acid/base complex with heparin). As a general rule, 1 mg of protamine will reverse every 100 units of heparin that was given. If 30,000 units of heparin remain in the patient’s circulation, then the calculated dose of protamine is 300 mg. There are two ways to calculate the protamine dose: It is calculated from the initial heparin dose or... It is calculated from the amount of heparin that is predicted to remain in the patient’s circulation at the conclusion of cardiopulmonary bypass. Because protamine has anticoagulant properties, basing the protamine dose from the initial heparin dose (not what remains after CBP) may contribute to protamine overdose (prolonged ACT). Administering protamine over 10-15 minutes reduces the likelihood of systemic vasodilation as well as pulmonary vasoconstriction (both side effects of protamine). The rate of administration does not impact the probability of anaphylaxis.

Answer 97

Is more sensitive to increased afterload Cardiopulmonary bypass allows the surgeon to operate on an immobile heart. Once the blood flows into the bypass circuit, oxygen is added and CO2 is removed, so that the blood returning to the patient resembles arterial blood. Since it functions as an artificial heart, the CPB machine requires a method of pumping blood throughout the patient's circulation. This can be accomplished with a centrifugal pump or roller pump. Both methods produce non-pulsatile flow. A roller pump compresses the blood tubing, which creates an occlusion point and mechanically pushes the blood forward. This is traumatic to blood cells. Additionally, pump flow remains constant regardless of the patient's afterload, so if the arterial inflow line is camped, the pump continues pushing blood forward. This can rupture the inflow tubing. Last, a roller pump is more likely to entrain air if the venous reservoir runs dry, which can lead to air embolism. A centrifugal pump is nonocclusive - it uses gravity and spins the blood through a cone. This reduces trauma to the blood cells passing through. Since a centrifugal pump can't produce excessive negative pressure, it tends not to entrain air, thus reducing the risk of air embolism. Additionally, this type of pump is unable to produce excessively high positive pressure either, so pump flow decreases when it is confronted by excessive afterload. This reduces the risk of line rupture if the arterial inflow line is clamped. For all of these reasons, a centrifugal pump is preferred over a roller pump. One disadvantage of the centrifugal configuration is the lack of an occlusion point - if there is an excessively high afterload, blood backs up towards the venous circulation, which reduces the patient's circulating blood volume.

Answer 98

Membrane oxygenator The oxygenator is the component of the CPB machine where gas exchange occurs. There are two types of oxygenators: membrane and bubble. The bubble oxygenator carries an unacceptable high risk of cerebral emboli. For this reason, the membrane oxygenator is preferred for cardiopulmonary bypass. The oxygen diffusion oxygenator and the oxygen/ carbon dioxide exchangers are fictitious - we made them up.

Answer 99

The intra-aortic balloon pump improves myocardial oxygen supply while simultaneously reducing demand. It inflates during diastole. This increases coronary perfusion pressure (increased supply). It deflates during systole. This reduces afterload (decreased demand).