Apex Unit 3 Cardiovascular Flashcards
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.
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.
Click on the region of the ventricular action potential where calcium conductance is the greatest.
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
Which current is responsible for slow phase four depolarization in the SA node?
I-K
I-f
I-Na
I-Ca
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.
What is the normal oxygen delivery in a 70-kg adult?
250 mL/min
15 mL/dL
20 mL/dL
1000 mL/min
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
Blood flow is inversely proportional to: arteriovenous pressure difference. vessel diameter. body temperature. hematocrit.
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).
Match each hemodynamic variable with its mathematical equation.
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
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
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.
Which conditions impair myocardial contractility? (Select 3.)
Hyperthermia Hypovolemia Hypoxia Hyperkalemia Hypercalcemia Hypercapnia
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…
A decrease in which of the following would most likely cause stroke volume to increase?
Contractility
Mean arterial blood pressure
Preload
Afterload
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
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
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.
Click on the area of the pressure volume loop where the mitral valve closes.
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
Calculate the stroke volume.
(Enter your answer in mL)
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
Click on the region of the myocardium that is supplied by the circumflex artery.
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.
Causes of coronary vasodilation include: (elect two)
hypocapnia.
alpha-1 stimulation.
adenosine.
beta-2 stimulation.
Adenosine
Beta-2 stimulation
Adenosine and beta-2 stimulation cause coronary vasodilation.
Alpha-1 stimulation and hypocapnia cause coronary vasoconstriction.
Which conditions increase myocardial oxygen consumption?
Decreased diastolic filling time
Decreased P50
Decreased end-diastolic volume
Decreased aortic diastolic blood pressure
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.
Inhaled nitric oxide: (select two)
is inactivated by hemoglobin.
causes hypotension.
reduces right ventricular afterload.
stimulates cAMP production.
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.
Which valvular diseases are associated with eccentric hypertrophy? (Select 2.)
Mitral stenosis
Mitral regurgitation
Aortic stenosis
Aortic regurgitation
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).
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.
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.
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
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.
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
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.
Which valvular disorders are associated with a systolic murmur? (Select 2.) Aortic insufficiency Mitral stenosis Aortic stenosis Mitral insufficiency
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.
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
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
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)
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
Click on the curve that BEST represents the ventricular compliance of the patient with aortic stenosis.
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).
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
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).
Pathophysiologic complications related to chronic hypertension include all of the following EXCEPT:
decreased diastolic filling time.
left ventricular hypertrophy.
increased myocardial oxygen consumption.
dysrhythmias.
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.
What is the MOST common cause of secondary hypertension? Pregnancy induced hypertension Coarctation of the aorta Renal artery stenosis Cigarette smoking
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.
Match each antihypertensive medication to its drug class.
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
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
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.
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.
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.
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
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
Select the BEST induction agent for the patient with pericardial tamponade. Midazolam Ketamine Propofol Etomidate
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.
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
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.
All of the following reduce outflow obstruction in obstructive hypertrophic cardiomyopathy EXCEPT:
nitroglycerin.
phenylephrine.
esmolol.
500 mL 0.9% NaCl bolus.
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.
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)
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 …
Priming the cardiopulmonary bypass machine with a balanced salt solution reduces all of the following EXCEPT:
plasma drug concentration.
oxygen carrying capacity.
blood viscosity.
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
When is awareness MOST likely to occur during coronary artery bypass graft surgery? Prebypass period Induction of anesthesia Sternotomy Rewarming
Sternotomy
Awareness is most common during sternotomy (due to intense surgical stimulation).
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.
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!
Click on the thoracoabdominal aneurysm that is associated with the HIGHEST incidence of paraplegia following open surgical repair.
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.
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.
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.
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
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.
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.
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.
Identify the BEST monitor of neurologic integrity during carotid endarterectomy. Electroencephalography Transcranial Doppler Cerebral oximetry Awake patient
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.
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.
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.
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.
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.
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)
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
Click on the region of the ventricular action potential where potassium conductance is the GREATEST.
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
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
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.
Contractility is dependent on:
preload.
afterload.
both preload and afterload.
neither preload nor afterload.
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.
