Apex Unit 3 Cardiovascular Flashcards

Question 1

Q

Identify the statements that BEST describe ventricular myocytes. (Select 3.)

They contain more mitochondria than skeletal myocytes.
Resting membrane potential is -90 mV.
Hypokalemia decreases resting membrane potential.
Hyperkalemia increases threshold potential.
T-tubules spread the wave of depolarization throughout the myocardium.
Sodium conductance is greater than potassium conductance at rest.

Answer

A

Resting membrane potential is -90 mV
Hypokalemia decreases resting membrane potential
They contain more mitochondria than skeletal myocytes

When thinking about the electrical potential of ventricular myocytes, you must understand resting membrane potential and threshold potential.

Resting membrane potential:
Normal = -90 mV.
Primarily regulated by potassium.
Hypokalemia decreases RMP, while hyperkalemia raises RMP.

Threshold potential:
Normal = -70 mV.
Primarily regulated by calcium.
Hypocalcemia decreases TP, while hypercalcemia raises TP.

What about sodium?
At rest, sodium conductance is low. It increases dramatically when the voltage gated sodium channels open in response to depolarization. The wave of depolarization throughout the heart is facilitated by gap junctions (not t-tubules).

Ventricular myocytes contain more mitochondria than skeletal myocytes.

Question 2

Q

Click on the region of the ventricular action potential where calcium conductance is the greatest.

Answer

A

The most important ion currents during each phase of the ventricular action potential:

Phase 0  = Sodium in
Phase 1  =  Chloride in
Phase 2  =  Calcium in
Phase 3  =  Potassium out
Phase 4  =  Sodium out

Question 3

Q

Which current is responsible for slow phase four depolarization in the SA node?

I-K
I-f
I-Na
I-Ca

Answer

A

I-f

The funny current (I-f) is the primary determinant of the pacemaker’s intrinsic heart rate. Said another way, it sets the rate of spontaneous phase four depolarization in the SA node.

Question 4

Q

What is the normal oxygen delivery in a 70-kg adult?

250 mL/min
15 mL/dL
20 mL/dL
1000 mL/min

Answer

A

1000 mL/min

To some of you, this may look like a list of unrelated numbers. Others quickly identified them as key reference points for CaO2, DO2, VO2, and CvO2.

You must commit these values to memory:

CaO2: Arterial oxygen content = 20 mL/O2/dL
DO2: Oxygen delivery = 1000 mL/min
VO2: Oxygen consumption = 250 mL/min
CvO2: Venous oxygen content = 15 mL/dL

Question 5

Q

Blood flow is inversely proportional to:
arteriovenous pressure difference.
vessel diameter.
body temperature.
hematocrit.

Answer

A

Hematocrit

We can’t have a rational discussion of hemodynamics without a deep understanding of Poiseuille’s law. This law says that flow is directly proportional to vessel radius and the AV pressure difference. It also says that flow is inversely proportional to viscosity and the length of the tube.

Knowing this should’ve helped you narrow down the choices to hematocrit and body temperature. Both affect viscosity, so now you need to determine how.

Changes in body temperature:
Increased temp = Decreased viscosity and increased flow
Decreased temp = Increased viscosity and decreased flow

Changes in hematocrit:
Increased hct = Increased viscosity and decreased flow
Decreased hct = Decreased viscosity and increased flow

Therefore, as hct increases, blood flow decreases (an inverse relationship).

Question 6

Q

Match each hemodynamic variable with its mathematical equation.

Answer

A

Stroke volume = CO x (1000 / HR)

Ejection fraction = [(EDV - ESV) / EDV] x 100

Systemic vascular resistance = [(MAP - CVP) / CO] x 80

Mean arterial blood pressure = [(CO x SVR) / 80] + CVP

Question 7

Q

Which variables are related by the Frank-Starling mechanism?

Left ventricular end diastolic pressure and systemic vascular resistance
Central venous pressure and mean arterial pressure
Pulmonary artery occlusion pressure and stroke volume
Contractility and cardiac output

Answer

A

Pulmonary artery occlusion pressure and stroke volume

Once again, there are a number of possible answers for this. The NCE likes to challenge you with different names for the same thing.

The Frank-Starling mechanism relates ventricular volume to ventricular output. In this question, the best choice is pulmonary artery occlusion pressure (ventricular volume) and stroke volume (ventricular output).

Each of the distractors contain hemodynamic parameters that you are familiar with, however none of them are good surrogates for ventricular volume and/or ventricular output.

Question 8

Q

Which conditions impair myocardial contractility? (Select 3.)

Hyperthermia
Hypovolemia
Hypoxia
Hyperkalemia
Hypercalcemia
Hypercapnia

Answer

A

Hypoxia
Hypercapnia
Hyperkalemia

Contractility is the ability of the myocardial sarcomeres to perform work (shorten and produce force). It is independent of preload and afterload.

Hypoxia and acidosis impair contractility. In the absence of oxygen, the cardiac myocytes convert to anaerobic metabolism. In this situation, intracellular lactate increases leading to acidosis and impaired enzymatic function. The net result is decreased contractility.

Hypercapnia is the result of accumulation of volatile acids. Again, acidosis impairs contractility.
Hyperkalemia increases resting membrane potential. Remember that the voltage gated sodium channels fire in response to depolarization, but they can’t fire again until the cell has repolarized. If the RMP rises to a level that exceeds where these channels would otherwise repolarize, they’ll get stuck in the closed and inactive state. The myocyte that can’t be depolarized can’t contract.

There are plenty of other factors that impact contractility, so read on…

Question 9

Q

A decrease in which of the following would most likely cause stroke volume to increase?

Contractility
Mean arterial blood pressure
Preload
Afterload

Answer

A

Afterload

Afterload is the tension that the heart must overcome to eject its stroke volume. It is usually set by systemic vascular resistance (mainly at the arterioles).

Stroke volume is decreased by:
Decreased preload
Decreased contractility
Decreased serum calcium
Increased afterload

Question 10

Q

Which phase of the cardiac cycle is characterized by an open mitral valve and closed aortic valve? (Select three.)

Isovolumetric contraction
Isovolumetric relaxation
Atrial systole
Ventricular ejection
Rapid ventricular filling
Diastasis

Answer

A

Rapid ventricular filling
Diastasis
Atrial systole

An open mitral valve and a closed aortic valve occur during rapid ventricular filling, diastasis (middle third of diastole), and atrial systole.

Questions like these demand a strong command of the cardiac cycle. You would be wise to understand the ins and outs of the Wiggers diagram on the next page.

Question 11

Q

Click on the area of the pressure volume loop where the mitral valve closes.

Answer

A

The LV sits between two valves, and each valve can assume two different positions (open or closed).

There are four corners on the LV pressure volume loop. At each corner, one of the valves assumes a new position.

Mitral valve:
Opens in the bottom left corner
Closes in the bottom right corner

Aortic valve:
Opens in the upper right corner
Closes in the upper left corner

Question 12

Q

Calculate the stroke volume.

(Enter your answer in mL)

Answer

A

70 mL

If you are given a pressure volume loop, then the stroke volume is equal to the width of the loop.

Stroke volume = LV end-diastolic volume - LV end-systolic volume

120 mL - 50 mL = 70 mL

Question 13

Q

Click on the region of the myocardium that is supplied by the circumflex artery.

Answer

A

When using TEE, the midpapillary muscle level in short axis provides the best view for diagnosing myocardial ischemia.

The circumflex a. supplies the left lateral wall of the LV.

The left anterior descending a. supplies the anterior wall of the LV, anterior two thirds of the septum and a small portion of the anterior RV.

The right coronary a. supplies the posterior wall of the LV, most of the RV, and the posterior third of the septum.

Question 14

Q

Causes of coronary vasodilation include: (elect two)

hypocapnia.

alpha-1 stimulation.

adenosine.

beta-2 stimulation.

Answer

A

Adenosine
Beta-2 stimulation

Adenosine and beta-2 stimulation cause coronary vasodilation.

Alpha-1 stimulation and hypocapnia cause coronary vasoconstriction.

Question 15

Q

Which conditions increase myocardial oxygen consumption?

Decreased diastolic filling time
Decreased P50
Decreased end-diastolic volume
Decreased aortic diastolic blood pressure

Answer

A

Decreased diastolic filling time

You must absolutely know which factors alter myocardial oxygenation! It’s best to organized these as conditions that influence O2 supply, O2 demand, or both. We have a table on the next page that will help you.

An increased heart rate reduces oxygen supply while simultaneously increasing oxygen demand. A decreased diastolic filling time is another way of saying increased heart rate.

Decreased end-diastolic volume reduces wall stress and decreases demand.

Decreased P50 shifts the OxyHgb curve to the left (left = love). Less oxygen is released to the myocardium, which decreases supply.

Decreased aortic diastolic blood pressure reduces coronary perfusion pressure, which also reduces oxygen supply.

Question 16

Q

Inhaled nitric oxide: (select two)

is inactivated by hemoglobin.
causes hypotension.
reduces right ventricular afterload.
stimulates cAMP production.

Answer

A

Reduces right ventricular afterload
Is inactivated by hemoglobin

Nitric oxide increases cGMP (not cAMP) synthesis in vascular smooth muscle. This reduces intracellular calcium and contributes to pulmonary vasodilation. By reducing pulmonary vascular resistance, inhaled nitric oxide reduces RV afterload.

Nitric oxide is inactivated by hemoglobin. This explains its ultra-short half time (~ 5 seconds). NO doesn’t cause hypotension, because it’s inactivated before it enters the systemic circulation.

Question 17

Q

Which valvular diseases are associated with eccentric hypertrophy? (Select 2.)

Mitral stenosis
Mitral regurgitation
Aortic stenosis
Aortic regurgitation

Answer

A

Mitral regurgitation

Aortic regurgitation

Regurgitant lesions tend to produce volume overload. The heart compensates with eccentric hypertrophy (thin wall + dilated chamber).

Stenotic lesions tend to produce pressure overload. The heart compensates with concentric hypertrophy (thick wall + smaller chamber).

Question 18

Q

Following aortic valve replacement for aortic stenosis, the left ventricular end-systolic volume will be:

increased due to afterload reduction.
increased due to decreased transvalvular gradient.
decreased due to a reduction in impedance to ventricular ejection.
unchanged.

Answer

A

Decreased due to a reduction in impedance to ventricular ejection

In the patient with aortic stenosis, the afterload is set at the valve itself. Replacing the valve restores a more normal physiology, where the systemic vascular resistance reestablishes itself as the primary regulator of afterload.

Since the new valve reduces the impedance to LV ejection (afterload), the heart naturally ejects a larger amount of blood with each beat (stroke volume increases). Since more blood leaves the heart, less blood remains at the end of systole. Said another way, left ventricular end-systolic volume decreases.

The transvalvular gradient (LV to Ao) is very high with aortic stenosis. Aortic valve replacement reduces (not increases) the transvalvular gradient.

Question 19

Q

Which drugs are most likely to contribute to hemodynamic instability in the patient who is symptomatic from severe mitral stenosis?  (Select 2.))
Nitrous oxide
Phenylephrine
Ephedrine
Furosemide

Answer

A

Ephedrine
Nitrous oxide

The anesthetic goals for mitral stenosis are “full, slow, and constricted.”

Any condition that increases cardiac output or heart rate (ephedrine) will increase left atrial pressure and may precipitate pulmonary edema.

Nitrous oxide increases PVR, increasing the workload of the right ventricle.

Phenylephrine supports afterload, which is useful in the patient with mitral stenosis.

Furosemide minimizes pulmonary congestion by reducing preload and left atrial volume.

Question 20

Q

After suffering a myocardial infarction, a patient presents with a left ventricular papillary muscle rupture and mitral regurgitation. Which of the following will worsen this patient’s condition? (Select 3.)

Increased heart rate
Decreased heart rate
Increased systemic vascular resistance
Decreased systemic vascular resistance
Increased LV to LA pressure gradient
Decreased LV to LA pressure gradient

Answer

A

Decreased heart rate
Increased systemic vascular resistance
Increased LV to LA pressure gradient

The anesthetic goals for mitral regurgitation are “full, fast, and forward.” The idea is to minimize the regurgitant volume (the amount of blood that travels through the mitral valve during LV systole).

The regurgitant volume is made worse by bradycardia, an increased LV to LA pressure gradient, and an increased SVR.

All of the distractors would improve this patient’s mitral regurgitation.

Question 21

Q

Which valvular disorders are associated with a systolic murmur?  (Select 2.)
Aortic insufficiency
Mitral stenosis
Aortic stenosis
Mitral insufficiency

Answer

A

Aortic stenosis
Mitral insufficiency

Now that we’ve reviewed the most important valvular lesions, you should be able to reason your way through this question. A murmur is caused by turbulent blood flow, so think about when the lesion causes turbulent flow during the cardiac cycle.

Blood becomes turbulent as it passes through a tight aortic valve during the ejection phase of systole.

Mitral regurgitation is an issue during isovolumetric contraction during systole.

Aortic regurgitation is an issue during isovolumetric relaxation of the LV during diastole.

Mitral stenosis is problematic during atrial systole (atrial kick), which occurs during ventricular diastole.

Question 22

Q

Which surgical procedure presents the HIGHEST risk of cardiovascular morbidity and mortality for the patient with coronary artery disease?
Open reduction and internal fixation of a femur fracture
Carotid endarterectomy
Open abdominal aortic aneurysm repair
Video assisted lung thoracoscopy

Answer

A

Open abdominal aortic aneurysm repair

The AHA/American College of Cardiology guidelines stratify cardiac risk by the type of surgical procedure. Risk is defined as perioperative myocardial infarction, CHF, or death.

High risk procedures include:

Emergency surgery (especially in the elderly)
Open aortic surgery
Peripheral vascular surgery
Long surgical procedures with significant volume shifts and/or blood loss

Question 23

Q

Use the data set to calculate the coronary perfusion pressure.
Heart rate = 50 bpm
Systolic blood pressure = 100 mmHg
Diastolic blood pressure = 55 mmHg
Pulmonary artery occlusion pressure = 15 mmHg
Central venous pressure = 10 mmHg

(Enter your answer in mmHg)

Answer

A

40 mmHg

Coronary Perfusion Pressure = Aortic diastolic pressure - LVEDP

You will see these types of equations on the NCE, but you may not always be provided the variables you’re accustomed to using. For example, we didn’t give you LVEDP, but if you know that PAOP is a surrogate for LVEDP, then you should recognize that this is the best option of those provided.

In this question:
CPP = DBP - PAOP
CPP = 55 mmHg - 15 mmHg = 40 mmHg

Question 24

Q

Click on the curve that BEST represents the ventricular compliance of the patient with aortic stenosis.

Answer

A

If you just completed the Valvular Heart Disease Tutorial, you’ll remember that aortic stenosis causes pressure overload and concentric hypertrophy.

The extra thickness impairs the ventricle’s ability to relax, reducing its compliance (the curve shifts up and left).

Question 25

Q

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

A

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).

Question 26

Q

Pathophysiologic complications related to chronic hypertension include all of the following EXCEPT:

decreased diastolic filling time.
left ventricular hypertrophy.
increased myocardial oxygen consumption.
dysrhythmias.

Answer

A

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.

Question 27

Q

What is the MOST common cause of secondary hypertension?
Pregnancy induced hypertension
Coarctation of the aorta
Renal artery stenosis
Cigarette smoking

Answer

A

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.

Question 28

Q

Match each antihypertensive medication to its drug class.

Answer

A

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

Question 29

Q

A patient with a history of coronary artery disease and an ejection fraction of 35 percent has developed atrial fibrillation with a rapid ventricular rate. Select the BEST treatment for this patient.

Verapamil
Diltiazem
Nicardipine
Nifedipine

Answer

A

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.

Question 30

Q

Select the statements that best describe constrictive pericarditis. (Select 2.)

Afterload should be reduced.
Bradycardia should be avoided.
Kussmaul’s sign is usually present.
It is most commonly caused by a virus.

Answer

A

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.

Question 31

Q

Which of the following are components of Beck’s triad? (Select 3.)
Muffled heart tones
Mill wheel murmur
Tachycardia
Jugular venous distension
Increased pulmonary artery occlusion pressure
Hypotension

Answer

A

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

Question 32

Q

Select the BEST induction agent for the patient with pericardial tamponade.
Midazolam
Ketamine
Propofol
Etomidate

Answer

A

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.

Question 33

Q

A patient presents to the preoperative clinic with a previous history of infective endocarditis. Which procedure puts this patient at the HIGHEST risk of an adverse outcome?
Cystoscopy
Colonoscopy
Coronary stent placement
Dental implant

Answer

A

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.

Question 34

Q

All of the following reduce outflow obstruction in obstructive hypertrophic cardiomyopathy EXCEPT:

nitroglycerin.
phenylephrine.
esmolol.
500 mL 0.9% NaCl bolus.

Answer

A

Nitroglycerin

Hypertrophic cardiomyopathy is associated with left ventricular outflow tract obstruction.

There are three determinants of blood flow through the LVOT:

Systolic LV volume
Force of LV contraction
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.

Question 35

Q

A patient with a bare metal cardiac stent presents for a bunionectomy. What is the MINIMAL amount of time that the patient should wait before she undergoes surgery?

(Enter your answer in days)

Answer

A

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 …

Question 36

Q

Priming the cardiopulmonary bypass machine with a balanced salt solution reduces all of the following EXCEPT:

plasma drug concentration.
oxygen carrying capacity.
blood viscosity.

Answer

A

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

Question 37

Q

When is awareness MOST likely to occur during coronary artery bypass graft surgery?
Prebypass period
Induction of anesthesia
Sternotomy
Rewarming

Answer

A

Sternotomy

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

Question 38

Q

Pick the statements that MOST accurately describe an intra-aortic balloon pump. (Select 2.)
The tip of the balloon should be positioned 2 cm proximal to the brachiocephalic artery.
It inflates during diastole and increases myocardial oxygen supply.
It is contraindicated in severe aortic insufficiency.
It inflates during systole and reduces afterload.

Answer

A

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!

Question 39

Q

Click on the thoracoabdominal aneurysm that is associated with the HIGHEST incidence of paraplegia following open surgical repair.

Answer

A

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.

Question 40

Q

Identify the statement that MOST accurately describes the patient with an abdominal aortic aneurysm. (Select 2.)
Back pain and hypotension suggest rupture.
Risk of aneurysmal rupture is best described by Poiseuille’s law.
It is more common in females.
Surgical intervention is recommended when the diameter is > 5.5 cm.

Answer

A

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.

Question 41

Q

Which of the following are expected to increase following cross clamp removal during abdominal aortic aneurysm repair? (Select 2.)

Pulmonary vascular resistance
Total body oxygen consumption
Coronary blood flow
Venous return

Answer

A

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.

Question 42

Q

Occlusion of the artery of Adamkiewicz during thoracic aneurysm repair may result in all of the following EXCEPT:

loss of proprioception.
flaccid paralysis of the lower extremities.
loss of temperature and pain sensation.
bowel and bladder dysfunction.

Answer

A

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.

Question 43

Q

Identify the BEST monitor of neurologic integrity during carotid endarterectomy.
Electroencephalography
Transcranial Doppler
Cerebral oximetry
Awake patient

Answer

A

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.

Question 44

Q

In the patient with right subclavian steal syndrome, arterial flow is diverted from the:
right subclavian artery to the left subclavian artery.
right vertebral artery to the right subclavian artery.
left subclavian artery to the right subclavian artery.
left vertebral artery to the right subclavian artery.

Answer

A

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.

Question 45

Q

Bradycardia is caused by:
increasing potassium conductance.
increasing the slope of phase 4 depolarization.
making the threshold potential more negative.
making the resting membrane potential more positive.

Answer

A

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.

Question 46

Q

Calculate the arteriovenous oxygen difference.
Hgb = 14 gm/dL
SpO2 = 98%
SvO2 = 75%

(Round your answer to the nearest whole number, and enter as mL/dL)

Answer

A

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

Question 47

Q

Click on the region of the ventricular action potential where potassium conductance is the GREATEST.

Answer

A

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

Question 48

Q

When calculating systemic vascular resistance, what is the conversion factor to change L/min to dynes/sec/cm^-5?

0.003
1.34
10
80

Answer

A

80

SVR = MAP - CVP x 80
CO
80 is the conversion factor that changes L/min to dynes/sec/cm^-5.

34 is the amount of molecular oxygen in mL that can be carried by 1 gram of hemoglobin.
003 is the solubility coefficient for dissolved oxygen. Henry’s law anyone?
..well 10 is used for all sorts of things, but it’s not used here.

Question 49

Q

Contractility is dependent on:

preload.
afterload.
both preload and afterload.
neither preload nor afterload.

Answer

A

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.

Question 50

Q

Click on the area of the pressure-volume loop where the aortic valve opens.

Answer

A

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.

Question 51

Q

Which phases of the cardiac cycle are associated with an open mitral valve and a closed aortic valve? (Select 3.)

Diastasis
Isovolumic ventricular contraction
Ventricular ejection
Rapid ventricular filling
Isovolumic ventricular relaxation
Atrial systole

Answer

A

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)

Question 52

Q

Which letters correspond with diastole? (Select 2.)

A
B
C
D

Answer

A

B
C

Diastole
B = Isovolumetric relaxation
C = Rapid & late ventricular filling and atrial kick

Systole
D = Isovolumetric contraction
A = Ventricular ejection

Question 53

Q

Choose the statements that most accurately describe the coronary circulation. (Select 3.)

The left anterior descending artery perfuses the anterior 2/3rds of the septum.
The SA nodal artery most commonly arises from the right coronary artery.
Left coronary artery dominance occurs in 80% of the population.
The right coronary artery perfuses the apex of the heart.
Leads II, III, and AVF monitor the right coronary artery.
The left circumflex artery supplies the left bundle branch.

Answer

A

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.

Question 54

Q

How much of the cardiac output does the myocardium receive at rest?

5%
10%
15%
20%

Answer

A

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

Question 55

Q

What is the MOST potent local vasodilator substance released by cardiac myocytes?
Prostacyclin
Adenosine
Carbon dioxide
Nitric oxide

Answer

A

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

Question 56

Q

Which statement MOST accurately describes resting membrane potential in the cardiac myocyte?

Hypercalcemia decreases resting membrane potential.
Hyperkalemia increases resting membrane potential.
Cardiac myocytes only generate a threshold potential.
When resting membrane potential is closer to threshold potential, the cell is more resistant to depolarization.

Answer

A

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.

Question 57

Q

How much does atrial contraction contribute to cardiac output?

(Enter your answer as a percentage

Answer

A

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.

Question 58

Q

Click on the region that represents the relative refractory period.

Answer

A

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.

Question 59

Q

The sarcoplasmic reticulum releases calcium when:

calcium stimulates the ryanodine receptor.
the SERCA2 pump is turned on.
repolarization occurs
troponin binds to the actin/myosin complex.

Answer

A

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.

Question 60

Q

Transection of the right vagus nerve would MOST likely affect:

AV node conduction delay.
the bundle of Kent.
the conduction velocity between the SA and AV node.
SA node automaticity.

Answer

A

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.

Question 61

Q

Calculate the ejection fraction given the following parameters:

Stroke volume: 30 mL
End-diastolic volume: 90 mL

(Enter your answer as the nearest whole percent)

Answer

A

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.

Question 62

Q

A patient has an end-systolic volume of 50 mL and an end-diastolic volume of 110 mL. What is the ejection fraction?

(Enter your answer as the nearest whole percent)

Answer

A

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.

Question 63

Q

Calculate the ejection fraction from the following data.

Enter your answer as the nearest whole percent
edv 130
sv = 40
esv =70

Answer

A

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%

Question 64

Q

A patient’s blood pressure is 110/65 mmHg. What is the mean arterial blood pressure?

(Enter your answer as a whole number in mmHg)

Answer

A

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 65

A

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 66

A

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 67

A

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 68

A

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 69

A

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 70

A

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 71

A

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 72

A

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 73

A

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 74

A

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 75

A

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 76

A

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 77

A

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 78

A

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 79

A

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 80

A

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 81

A

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 82

A

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 83

A

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

Answer 84

A

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 85

A

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 86

A

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 87

A

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 88

A

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 89

A

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 90

A

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 91

A

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 92

A

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 93

A

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 94

A

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 95

A

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 96

A

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 97

A

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 98

A

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 99

A

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 100

A

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 101

A

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 102

A

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 103

A

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 104

A

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 105

A

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 106

A

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 107

A

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 108

A

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 109

A

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 110

A

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 111

A

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 112

A

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 113

A

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 114

A

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 115

A

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 116

A

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 117

A

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 118

A

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 119

A

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 120

A

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 121

A

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 122

A

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 123

A

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).