APEX CARDIAC
Play the pathophysiologic steps of thrombus formation in the correct order: Plaques break through vascular endothelium Positive feedback initiated a critical thrombin levels Platelets adhere to rough surfaces Fibrin fibers enmesh platelets, RBCs, & plasma
1. Plaques break through vascular endothelium 2. Platelets adhere to rough surfaces 3. Fibrin fibers enmesh platelets, RBCs, & plasma 4. Positive feedback initiated a critical thrombin levels
During open cardiac surgery, what is the highest systolic blood pressure or the aorta can be safely cannulated?
100mmHg 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 is less than 100 during this time ideal range SBP 90 to 100 OR MAP <70 Additionally, the patient should be heparinized before able to cannulation with an ACT minimum of 400
Patient was administered 30,000 units of IV heparin during CPB. How much Protamine should be administered to return the activated clotting time to baseline?
300mg Protamine is used to reverse heparin at the end of CPB it does this via a neutralization reaction. 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 than 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 circulation at the conclusion of CPB Because protamine has anticoagulant properties, basing the protamine dose from the initial heparin dose, and not what remains after CPP may contribute to protamine overdose (prolonged ACT) Administering protamine over 10 to 15 minutes reduces the likelihood of systemic vasodilation, as well as pulmonary vasoconstriction. The rate of administration does not impact the probability of anaphylaxis.
A pt w/ moderate cardiac disease & LE claudication, is scheduled for revascularization of the LLE under epidural anesthesia. identify concerns regarding management of her anesthetic. Select 3 The procedure should be delayed until after coronary surgical intervention is performed A preoperative exercise stress test is not recommended Myocardial ischemia is the number one perioperative risk factor GA should replace epidural Epidural should be placed no sooner than 1hr prior to intraop heparin
A preoperative exercise stress test is not recommended Myocardial ischemia is the number one perioperative risk factor Epidural should be placed no sooner than 1hr prior to intraop heparin A peripheral vascular procedure should alert CRNA of potential cardiac disease myocardial ischemia tops, the list of perioperative risk factors, and patients undergoing revascularization procedures. Individualized anesthetic technique for each patient. you may choose a GA for longer cases, or those with significant anticoagulation. Neuraxial techniques offer the advantage of increased graft flow, fewer respiratory complications, and postoperative analgesia. Be aware of the coagulation status of the patient when employing a regional block; if you choose a neuraxial block, insert the spinal or epidural at least one hour prior to intraoperative heparinization to decrease the chance of bleeding in the neuraxial space.
Calcium channel blockers produce their cardiovascular effects by binding to the: A. Alpha-1 subunit of the L-type calcium channel. B. Alpha-1 subunit of the T-type calcium channel. C. Beta subunit on the L-type calcium channel. D. Beta subunit on the T-type calcium channel.
A. Alpha-1 subunit of the L-type calcium channel. (This prevents calcium from entering, cardiac and vascular, smooth muscle cells) There are three types of voltage gated calcium channels : L-type: long-lasting or slow channel N-type: neural T-type: transient Dihydropyridine's primarily target vascular smooth muscle : Vascular smooth muscle relaxation = decreased, SVR Non-dihydropyridines primarily target the myocardium: Decrease chronotropy (HR), decreased inotropy (contractility), decreased dromotropy (speed of conduction), decreased coronary, vascular resistance
A patient has a prosthetic aortic valve. Which surgical procedure presents an indication for antibiotic prophylaxis against endocarditis? A. Bronchoscopy with biopsy. B. Colonoscopy C. EGD. D. Cystoscopy.
A. Bronchoscopy with biopsy. Hi, Iris procedures are thought to be dirty procedures were 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 mucosal lining Respiratory procedures that perforate the mucosal lining with incision or biopsy Biopsy of infected lesions on the skin or muscle Antibiotic prophylaxis is not recommended for : G.I. endoscopic procedures in the absence of active infection GU procedures in the absence of active infection
All of the following diseases, cause secondary hypertension, EXCEPT: A. Hashimoto's. B. Conns disease C. Coarctation of the aorta. D. Cushing's syndrome.
A. Hashimoto's. Hypertension, without an identifiable, ideology is called primary hypertension. We call it secondary hypertension when we can pinpoint the cause of the patients hypertension. And the 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 (Conns Ds) Hyperadrenocorticism (Cushing) Pheochromocytoma Coarctation of the aorta Pregnancy induced hypertension Hashimoto's disease is an autoimmune disease that attacks the thyroid gland. It causes hypothyroidism.
Anesthetic considerations for the patient with heart failure with reduced ejection fraction includes: A. Increased heart rate to maximize cardiac output. B. Increase preload to stretch a non-compliant ventricle. C. Avoidance of inotropes to reduce myocardial oxygen demand. D. Increased afterload to perfuse hypertrophic myocardium
A. Increased heart rate to maximize cardiac output. The hallmark of heart failure with reduced ejection fraction (Systolic failure), is a decreased ejection fraction with an increased end-diastolic volume; the ventricle does not empty well. The ejection fraction quantifies the degree of heart failure : EF= (SV/EDV) x100 SV= EDV-ESV Since the heart can't squeeze well, a greater volume of blood remains on the ventricle after each contraction. The body compensates with SMS activation. This increases the heart rate. Set another way if the stroke volume is reduce, the only way to maintain, cardiac output is to increase the heart rate. Additionally, decreased Reno blood flow activates the RAAS 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
Compared to the cardiopulmonary bypass machine with a roller clamp, the CBP machine with a centrifugal pump: A. Is more sensitive to increase afterload B. Causes more trauma to blood cells. C. Is more likely to entrain air. D. Is more likely to rupture if the arterial inflow line is clamped.
A. Is more sensitive to increase afterload 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 clamped, 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 spends the blood through the cone. This reduces trauma to the blood cells passing through. Since a centrifugal pump cannot produce excessive negative pressure, it tends to not 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.
Which of the following is LEAST likely to precipitate pulmonary edema with mitral stenosis? A. Judicious fluid administration. B. Uterine contraction C. Atrial fibrillation D. Trendelenburg position
A. Judicious fluid administration. In a patient with severe mitral stenosis, any condition that increases left atrial volume can precipitate, pulmonary edema of all the answer choices. Judicious fluid administration is least likely to raise, left atrial pressure significantly. Both uterine contraction and Trendelenburg position increased preload. Atrial fibrillation reduces cardiac output and increases back pressure in the pulmonary circulation.
Which law explains why an abdominal aneurysm is more likely to rupture during a period of hypertension? A. Laplace B. Bernoulli's. C. Henry. D. Poiseulles
A. 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= Px 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 . POISEULLE: describes laminar flow through a tube. Flow is directly proportional to the radius, raised to the fourth power, and the pressure difference along tube (P1-P2). Flow is inversely proportional to viscosity and the length of the tube. Bernoullis: describes flow through constriction. At the side of constriction the fluids velocity increases, creating a pressure drop at the point of constriction Henry: describes the solubility of a gas in a solution
Select the safest type of oxygenator for the cardiopulmonary bypass machine A. Membrane oxygenator. B. Oxygen diffusion oxygenator C. Bubble oxygenator. D. Oxygen/carbon dioxide exchanger
A. Membrane oxygenator. The oxygenator is the component of the CPB machine where gas exchange occurs. There are two types of oxygenators: membrane & bubble The bubble oxygenator carries an unacceptably high risk of cerebral emboli. For this reason the membrane oxygenator is preferred.
Patient presents with diaphoresis, chest pain, and shortness of breath. His blood pressure is 220/110. select the best intravenous drug for this patient. A. Nicardipine B. Verapamil C. Nimodipine D. Nifedipine
A. Nicardipine Nicardipine & nifedipine are potent vasodilators. However, only Nacardipine is available for IV administration. They are best used to decrease SVR and relieve angina. Verapamil reduce his heart rate in contractility. Also exhibits mild coronary vasodilating properties. It is primarily used to control, supeaventricular tachycardia, and/or angina; it causes little systemic vasodilation. Nimodipine is a potent cerebral vasodilator. It's high, lipid solubility enhances It's 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. It can only be given orally. There is a black box warning that states IV administration can be fatal.
Which condition is the most likely to increase the regurgitant volume in a patient with mitral regurgitation? A. Reduction in heart rate. B. Increased myocardial contractility C. Decreased left ventricular afterload. D. Increase in left atrial pressure.
A. Reduction in heart rate. The magnitude of regurgitate volume in mitral regurgitation is a function of: 1) the size of the valve orifice 2) the pressure differential between the LA and LV and 3) the duration of the regurgitation cycle. We cannot change #1 but various interventions can alter #2 & 3. Reductions in heart rate, lengthen diastole, and the duration of regurgitation. A longer duration of diastole, will increase the regurgitate volume Any increase in SVR will increase the volume of blood refluxed towards the lower pressure outflow tract: The enlarged mitral valve and left atrium. Increases in LA pressure will also decrease Regurgitant flow. Unless this condition is Foley decompensated LV contractility is typically maintained which contributes to a stable forward flow.
Match each diagnosis what is characteristic hemodynamic data: Cardiac Tamponade Pulmonary hypertension ARDS Left ventricular failure Increase CVP, increased PADP, normal PAOP Normal CVP, increased PADP, increased PAOP Increased CVP, increased PADP, increased PAOP Decreased CVP, increased PADP, normal PAO
ARDS: Decreased CVP, increased PADP, normal PAOP LV FAILURE: Normal CVP, increased PADP, increased PAOP Cardiac Tamponade: Increased CVP, increased PADP, increased PAOP Pulm HTN: Increase CVP, increased PADP, normal PAOP
Which anatomic features are most responsible for the risk of sudden death in a patient with hypertrophic obstructive cardiomyopathy? Select 2 Anterior motion of mitral valve during systole Papillary muscle rupture Coexisting mitral valve regurgitation Interventricular septal hypertrophy
Anterior motion of mitral valve during systole Interventricular septal hypertrophy The anatomy of hypertrophic obstructive cardiomyopathy includes a hypertrophic enlarged interventricular septum that bulges into the left ventricle during systole anatomically. This bulge occurs just proximal to the LV outflow tract, obstructing LV ejection. In about 20 to 30% of these patients the leaflets of the mitral valve move anteriorly at the end of systole also blocking the LV outflow tract. These events, whether isolated or together further starve, the LV muscle of oxygenated blood contributing to ischemia, cardiac dysrhythmias and sudden loss of cardiac output . While hypertrophic obstructive cardiomyopathy may be associated with some degree of mitral regurgitation mitral regurgitation is not the primary cause of sudden death
Which features of carvedilol contribute to its efficacy for the treatment of heart failure? Select 3 Antioxidant activity Alpha-2 adrenergic antagonism Anti-inflammatory action Alpha-1 adrenergic antagonism Intrinsic sympathomimetic activity Non-hepatic metabolism
Antioxidant activity Anti-inflammatory action Alpha-1 adrenergic antagonism Carvedilol is a nonselective, beta blocker, antagonizing, B1, B2, and A1 adrenergic receptors producing vasodilation this facilitates offloading of the left ventricle, a key component of treating heart failure, and the beta blockade prevents the development of reflex tachycardia carvedilol, also suppresses production of reactive oxygen species, scavenges free radicals (antioxidant activity), and reduces the uptake of LDL into coronary endothelium (anti-inflammatory activity) Overall carvedilol is the drug of choice in patients with heart failure. Carvedilol like labetalol, has membrane stabilizing activity, an attribute that contributes to the antiarrhythmic affects of beta blockers this feature rarely contributes to the clinical relevance of beta blockers Carvedilol does not block A2 adrenergic receptors
Which findings are most closely associated with heart failure with preserved ejection fraction select 3: Dilated cardiomyopathy Aortic stenosis Ischemic, heart disease Tricuspid regurgitation Essential, hypertension S3. Heart sound
Aortic stenosis Ischemic, heart disease Essential, hypertension Heart failure with preserved ejection fraction (diastolic failure) is associated with decreased ventricular compliance. The ventricle doesn't feel properly. Poor compliance 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 heart sound suggest poor ventricular compliance. 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 pulmonal obesity
What are EARLY classic signs & symptoms of pericardial constriction? Select 3 Chest pain Ascites JVD Peripheral edema High output heart failure Pulmonary congestion
Ascites JVD Peripheral edema Pericardial construction impairs, atrial and right ventricular filling. early indications associated with constructive pericarditis, include signs of right ventricular failure, such as peripheral edema, ascites, and jugular vein distention. Other signs and symptoms include fatigue, dyspnea, pulses, paradox, and a positive Kussmaul sign. Even in the presence of low, cardiac output, pulmonary congestion is typically absent. High output, heart failure is not a feature of constricted myocardium, but of conditions with excess blood, such as anemia, AV fistulas, or severe hyperthyroidism
What genomics, variance or biomarkers are associated with increased cardiovascular risk and post operative morbidity? Select 2 Apolipoprotein E4 genotype B-type natriuretic peptide High sensitivity C-reactive protein HMGCOA reductase variant
B-type natriuretic peptide High sensitivity C-reactive protein Elevated HSCRP and BNP are both predictors of cardiovascular risk and postoperative morbidity across the spectrum of healthy patients to those with decompensated heart failure Patients with the ApoLipoprotein E4 genotype are more likely to experience post operative delirium after major surgery . The E4 allele is also associated with higher risk of acute kidney injury post CABG. Patients with the risk variant of HMGCOA reductase demonstrate at 2 to 3 mg/dL variability in LDL cholesterol. for each 1mg/dL decrease in LDL cholesterol in the plasma, there is about a 2% decrease in mortality from Atherosclerotic, heart disease
During general anesthesia, a cRNA witnesses that her patient has several episodes of an unidentifiable dysrhythmia. What immediate action can be taken to determine the cardiovascular stability of the patient? A. Cycle the noninvasive blood pressure monitor. B. Assess presence or absence of a pulse deficit. C. Initiate transesophageal echocardiography. D. Auscultate for breath and heart sounds.
B. Assess presence or absence of a pulse deficit. Palpating for a peripheral pulse is the fastest method to determine the presence of adequate peripheral perfusion In the presence of an electrical abnormality in the ECG tracing, the most important assessment is determine whether the impulse is effectively translated into a ventricular contraction capable of peripheral perfusion. a simple finger on the pulse allows determination of a pulse deficit; when the pulse rate is less than the heart rate A pulse deficit can occur during a rapid heart rate, such as ventricular tachycardia, or atrial fibrillation when ventricular filling time is limited during a shorten diastole. the failure to detect a pulse also occurs during electromechanical dissociation and pulseless electrical activity
Kuszmaul sign is associated with an increased: A. PAOP. B. Jugular, venous pressure C. Right ventricular compliance D. Stroke, volume.
B. 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. Who's mall sign is a paradoxical rise in jugular venous pressure during inspiration. It caused by restriction an RV filling & the high right sided heart pressure reflect to the jugular veins. On the CVP waveform, the x & y descents are often exaggerated. Kussmauls sign is highly suggestive of constrictive pericarditis
Which disease is common in children, presents with a strawberry tongue, and is associated with an increased risk of coronary artery aneurysm? A., thromboangiitis obliterans B. Kawasaki's disease. C. Tokayasu's arteritis. D. Wegener's granulomatosis
B. Kawasaki disease Occurs primarily on children. signs and symptoms include fever, vasculitis, red strawberry, tongue, conjunctivitis, inflammation of mucous membranes, cervical lymphadenopathy and swollen hands and feet Affects coronary arteries and medium size arteries. At risk for coronary artery aneurysm, and myocardial ischemia. Mucocutaneous lymph node syndrome Wegener's granulomatosis : Necrotizing granuloma's 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 ETT. Lung granulomas can cause hypoxemia. Takayasu's arteritis: Occlusive disease of the proximal aorta and its main branches. Pulseless disease, or occlusive thromboaortopathy, or aortic arch syndrome Thromboangiitis obliterans : Inflammatory vasculitis, that ultimately includes the small and medium sized arteries and veins in the extremities 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. Smoking cessation is the best treatment. A.k.a. Buergers Ds
Which intervention is most likely to precipitate hemodynamic instability in the patient with obstructive hypertrophic cardiomyopathy? A. Esmolol B. Nitroglycerin C. Phenylephrine D. 500cc bolus
B. Nitroglycerin Hypertrophic cardiomyopathy is associated with left ventricular outflow tract obstruction . Three things determine 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 well things that narrow the LVOT are bad . Nitroglycerin reduces preload reduces systolic LV, volume narrows, LVOT, and worsen the obstruction ; fluid administration has the opposite effect A slower Heart rate extends LV filling time so esmolol increases systolic LV volume additionally reduces contractility, which helps improve LVOT obstruction Phenylephrine increases aortic pressure, which increases transmural pressure. This opens LVOT.
Mitral stenosis causes: A. Parallel replication of sarcomeres in the left ventricle. B. Parallel replication of sarcomeres in the left atrium. C. Serial replication of sarcomeres in the left ventricle. D. Serial replication of sarcomeres in the left atrium.
B. 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 LV) hypertrophies to satisfy the demand. The heart compensates for pressure overload with concentric hypertrophy (parallel replication of sarcomeres). The LV is chronically under filled in mitral stenosis, so there's no reason for the chamber to increase in diameter. Serial replication of sarcomeres is called eccentric hypertrophy. It is seen with volume overload.
Why does maternal fetal circulation decrease the effect of maternally administered anesthetic drugs on the fetus? A. Post ductal blood delivers lower drug concentration to fetal brain B. The umbilical vein delivers the drug initially to the fetal liver C. Drugs are sequestered in the intervillous space of the maternal placenta. D. The foreman ovale allows the drug to bypass fetal systemic circulation.
B. The umbilical vein delivers the drug initially to the fetal liver The fetal liver is the first organ perfused by oxygenated maternal arterial blood from the placenta via the umbilical vein about 75 to 80% of umbilical vein. Blood does undergoes first pass, fetal metabolism. This effectively reduces fetal brain exposure to anesthetic drugs. Post ductal blood combines oxygenated blood with the venous return from the SVC perfusing the fetal trunk and lower extremities The foreman ovale, directs, a.k.a. Shunts, highly oxygenated blood preferentially into the left heart, such that the coronary and cerebral vascular circuits receive it
Tx of hypertrophic cardiomyopathy
BB, CCB, fluids, Phenylephrine
Match the component of the cardiac conduction pathway with its normal conduction time: Bundle branches to Purkinje fibers Atrioventricular bundle Atrioventricular node Internodal SA to AV node pathways 0.04 secs 0.06 secs 0.09 secs 0.03 secs
Bundle branches to Purkinje fibers: 0.06 Atrioventricular bundle: 0.04 Atrioventricular node: 0.09 Internodal SA to AV node pathways: 0.03
A patient presents with a history of angina, syncope and dyspnea. What is the most likely diagnosis? A. Acute Aortic insufficiency. B. Mitral stenosis. C. Aortic stenosis D. Chronic mitral regurgitation.
C. Aortic stenosis We find it SAD that the triad of Syncope, Angina and Dyspnea on exertion are Hallmark symptoms of aortic stenosis. The estimated survival time corresponding to the onset of the symptoms is 3, 5, and 2 years respectively. Mitral stenosis presents with pulmonary congestion, and afib Chronic mitral regurgitation presents with DOE, paroxysmal nocturnal dyspnea,& afib Acute aortic insufficiency presents with severe pulmonary edema & CHF
What is the most common cause of aortic stenosis? A. Ruptured papillary muscle. B. Infective endocarditis C. Bicuspid aortic valve. D. Rheumatic fever
C. Bicuspid, aortic valve. The most common causes of aortic stenosis are bicuspid valve and calcification. I bi-leaflet aortic valve calcifies earlier than a trileaflet valve. Romantic fever probably jump out at you. You have to be careful because question riders will take advantage of knee-jerk reactions. 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 is not the most common cause A ruptured papillary muscle leads to acute mitral regurgitation
What are the anesthetic implications for a heart transplant Recipient scheduled for elective surgery? A. An anticholinergic is not required when antagonizing neuromuscular blockade. B. P waves will be absent on the electrocardiogram. C. Bradycardia is better treated with isoproterenol, then with atropine. D. Heart rate is the primary determinant of cardiac output.
C. Bradycardia is better treated with isoproterenol, then with atropine. The transplanted heart is suffered from autonomic influence, so the heart rate is determined by the intrinsic rate of phase for depolarization of the SA node (100-120) heart rate is relatively fixed Since the heart rate is fixed, cardiac output is preload dependent. Cardiac output, adjust according to the position of the starling curve. Increasing prelude augments, cardiac output, until the point is reached where the ventricular myocytes become overstretched and cardiac output fails. 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 Epi or isoproterenol, can be used to manipulate the heart rate. Although cholinesterase inhibitors won't cause bradycardia, they will still cause signs and symptoms of PNS, activation elsewhere in the body. You'll need to administer an anticholinergic with reversal of neuromuscular blocking to prevent these issues. You may see 2 P waves on the EKG. One corresponds to the recipients, 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.
What is the best way to preserve spinal cord blood flow during an ascending aortic aneurysm repair? A. Patient warming to 38°C. B. Controlled hypotension C. CSF drainage. D. Induced hypoglycemia.
C. CSF drainage. Thoracic cross clamp time that exceeds 30 minutes poses a significant threat to spinal cord perfusion. Protective strategies include.: CSF drainage. CSF chanting from the brain towards the spinal column during clamping can exert excess pressure on the spinal cord. Training CSF improves spinal cord perfusion Moderate hypothermia, 30-32°C Proximal hypertension during cross clamp MAP of 100 AVOIDANCE OF HYPERGLYCEMIA PARTIAL CBP (LEFT ATRIUM TO FEM ARTERY) Drugs: corticosteroids, calcium channel, blockers, and/or mannitol
Potential acute consequences of a thoracic, aortic cross clamp include: A. Becks triad. B. Spastic paralysis of lower extremities. C. Spinothalamic tract impairment. D. Loss of proprioception.
C. Spinothalamic tract impairment. The spinal cord 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 to 8 radicular arteries that arise from the aorta. Collaterization is poor, making much of the anterior spinal cord dependent on a single blood supply. The artery of Adamkiewicz perfuses much of the thoracolumbar cord, making it the most important radicular artery. In arise between T8-12 in 75% of the population. Aortic cross, clamping can impair blood flow through the artery of Adamkiewitz and because of collaterization in this region being poor, there is an increase risk of spinal cord ischemia or infarction. This can cause anterior spinal artery syndrome, (BECKS syndrome) signs and symptoms include: Flaccid paralysis of the lower extremities (impaired motor tracts) note: chronic spinal cord injury, presents with spastic paralysis Bowel and bladder dysfunction (impaired motor tracts) Loss of temperature & pain sensation (impaired spinothalamic tract) Touch and proprioception are preserved (intact dorsal column) Becks triad (distended, jugular veins, hypotension, muffled heart sounds) occurs as a consequence of cardiac Tampanade; don't confuse it with BECKS syndrome
Blood flow reversal through the vertebral artery is caused by: A. Innominate artery steal syndrome. B. Basilar artery steal syndrome C. Subclavian steal syndrome. D. Carotid artery steal syndrome.
C. Subclavian steal syndrome. Subclavian, steal syndrome occurs when there is an occlusion of 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 of the other vertebral artery is stolen by the ipsilateral arm. This is a function of altered pressure gradient in 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.
Select the best treatment for the hypotensive patient with mitral stenosis A. Dobutamine B. Epi C. Vasopressin. D. Ephedrine
C. Vasopressin An increased heart rate could be detrimental with mitral stenosis, because it reduces diastolic feeling time, increases left atrial volume and pressure, and increases the risk of pulmonary edema. Epi, ephedrine, & dobutamine increase heart rate. The patient should be treated with a pure vasoconstrictor vasopressin, because it does not increase heart rate. Although phenylephrine would've been the first best choice, we made the question a little more difficult by omitting it as an answer.
Use the AHA/American College of cardiology guidelines to determine the degree of cardiac risk for a patient with coronary artery disease scheduled for each procedure: Carotid, endarterectomy Temporal artery biopsy Open aortic aneurysm repair
Carotid, endarterectomy: intermediate risk Temporal artery biopsy: low risk Open aortic aneurysm repair: high risk High risk (>5%): 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%): Carotid, endarterectomy Head and neck surgery Intrathoracic or intraperitoneal surgery Orthopedic surgery Prostate surgery Low risk (<1%): Endoscopic procedure's cataract surgery Superficial procedures Breast surgery Ambulatory procedures
Match the congenital heart defect with its major physiologic sequelae: Coarctation of aorta VSD Truncus arteriosis TOF Increase pulmonary blood flow Ventricular pressure overload Common mixing chamber Decrease pulmonary blood flow
Coarctation of aorta: Ventricular pressure overload VSD: Increased pulmonary blood flow Truncus arteriosis: common mixing chamber TOF: Decreased pulmonary blood flow Anesthesia management of patients with congenital heart disease involves not only understanding the specific anatomic defects but more importantly, appreciating the resulting physiologic consequences in particular, what features of the anomaly are present or absent that allow for the maintenance of blood flow to the lungs and the aorta Congenital heart defects can be classified into for resulting physiologic outcomes : 1. Increased pulmonary blood flow resulting from fluid overload (VSD) 2. Cyanosis resulting from obstruction and or decrease pulmonary blood flow (TOF) 3. Pressure overload of the ventricle (CoA) 4. Cyanosis due to a common mixing chamber (Truncus arteriosis)
The atrioventricular delay during cardiac conduction facilitates: select 2 Completion of atrial contraction Calcium accumulation in cardiac muscle cells Backward conduction into the atria Adequate ventricular filling
Completion of atrial contraction Adequate ventricular filling
Synonyms for idiopathic hypertrophic, subaortic stenosis, include all of the following, EXCEPT: A. Asymmetric septal hypertrophy. B. Obstructive hypertrophic cardiomyopathy C. Hypertrophic obstructive cardiomyopathy D. Dilated cardiomyopathy
D. Dilated cardiomyopathy Hypertrophic cardiomyopathy is the most common genetic cardiac disorder. It's the most common cause of sudden, cardiac death and 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: Asymmetric septal hypertrophy. Obstructive hypertrophic cardiomyopathy Hypertrophic obstructive cardiomyopathy idiopathic hypertrophic, subaortic stenosis
Which cell type is largely responsible for initiating thrombosis? A. Hepatocyte. B. Platelet. C. Reticular. D. Endothelial.
D. Endothelial Vascular endothelium is metabolically active tissue and is largely responsible for inhibiting vascular thrombosis. It's negative charge repels platelets, and it produces platelet inhibitors like prostacyclin I2, and nitric oxide. However, the balance of thrombus inhibition versus generation can be shifted when the vascular endothelium is damaged endothelial damage exposes the extra cellular matrix to which platelets bind, and the complex clotting process is initiated
What are the signs and symptoms of angina pectoris? A. Pain in the radial surface of the arm. B. Rapid, shallow breaths. C. Acute chest pain lasting seconds. D. Epigastric discomfort.
D. Epigastric discomfort. Retrosternal, pain, discomfort, or pressure Jaw pain Pain radiating down the neck Pain radiating down the arms, specifically the ulnar surface of the forearm and hand Epigastric discomfort Shortness of breath Some patients confuse the symptoms of chess construction for just now you can differentiate the two by observing the patient's respiratory pattern taking deep breaths, and not Shiloh rapid rest, differentiates angina pectoris from other causes Angina normally last minute not seconds or hours it has a crescendo/decrescendo cycle. So if someone complains of sharp pain lasting a few seconds or adult, constant chest egg lasting hours, it is most likely something else.
Anesthestic considerations for the pt with HFrEF includes a/an: A. Avoidance of inotropes to reduce myocardial oxygen demand B. Increased preload to stretch a noncompliant ventricle C. Increased afterload to perfuse hypertrophied myocardium D. Increased HR to maximize CO.
D. Increased HR to maximize CO. The hallmark of HF with reduced EF (systolic failure) is a decreased ejection fraction with an increased end-diastolic volume (the ventricle does not empty well). Since the heart can't squeeze well, greater volume of blood remains in the ventricle after each contraction. The body compensates with/ SNS activation—this increases the HR. If SV is reduced the only way to maintain CO is to increase HR. Additionally decreased renal BF, activates RAAS. Anesthetic considerations for systolic dysfunction include: Preload: it's already high to don't let it get higher Afterload: Decrease to reduce LV workload Heart Rate: maintain high/normal range Contractility: inotropic support as needed
Which drug is most likely to increase the degree of prolapse and the patient with mitral valve prolapse? A. Phenylephrine B. Sevoflurane C. Etomidate D. Ketamine
D. Ketamine A large ventricle tends to reduce MD prolapse, while a small ventricle tends to increase in the prolapse. For this reason, the primary management goal for MVP is to prevent excessive, cardiac emptying. To keep the heart FULL, you want to avoid: SNS stimulation, myocardial contractility Decreased SVR Hypovolemia Upright posture (RT or sitting) Pharmacological considerations : Ketamine is avoided because it activates the S&S increases myocardial contractility and augments LV emptying Etomidate provides cardiostability, making it a reasonable choice Volatile anesthetics plus nitrous, and or opioids help minimize SNS stimulation, but they must be titrated to prevent a significant decrease in SVR Phenylephrine is useful for hypotension There is no contraindication to regional anesthesia
Sudden death and hypertrophic cardiomyopathy is due to: A. Excessive left ventricular afterload B. Accelerated diastolic relaxation C. Dysfunctional, cardiac myocytes. D. Left ventricular outlet obstruction.
D. Left ventricular outlet obstruction. Hypertrophic cardiomyopathy is characterized by subaortic stenosis during systole which obstructs Elzhi outflow thus decreasing cardiac output in blood pressure. It's especially tough to maintain adequate coronary oxygenation in the presence of hypotension and LVH, so myocardial ischemia may present even at rest. Although HCM is a genetic mutation, the most common form is asymmetric, interventricular, septal hypertrophy HCM is rarely a primary dysfunction of cardiac myocytes and is not associated with increased LV afterload Due to LV hyper trophy, HCM is associated with impaired, not accelerated, diastolic relaxation
Which region of the myocardium receives the least amount of perfusion during systole? A. Right ventricular epicardium B. Right ventricular subendocardium C. Left ventrcircular epicardium. D. Left ventricular subendocardium.
D. Left ventricular subendocardium. They left ventricular sub endocardium is primarily perfused during diastole. As I ordered pressure increases the LV tissue compresses it's blood supply and reduces it's 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 compress during systole The sub endocardium of the RV is also well profuse throughout the cardiac cycle. The RV has a thinner wall, and does not generate pressures high enough to occlude its circulation.
An elevated creatinine kinase-MB is most consistent with: A. Aortic stenosis. B. Rheumatic fever C. Congestive heart failure D. Myocardial infarction
D. Myocardial infarction A cell requires oxygen and energy to maintain the integrity of a cell membrane. When that sell dies due to the lack of oxygen, it releases its intracellular components into the system of circulation. Infarcted myocardium releases, three key biomarkers: CK-MB: Initial elevation 3-12hrs Peak elevation 24hrs Return to baseline 48-72hrs Troponin I: Initial elevation 3-12hrs Peak elevation 24hrs Return to baseline 5-10 days Troponin T: Initial elevation 3-12hrs Peak elevation 12-48hrs Return to baseline 5-14days Cardiac troponins are more sensitive than CKMB for the diagnosis of myocardial infarction. These values must be evaluated in the context of the patient EKG.
What is the primary anatomic determinant of atrial and right ventricular filling in a non-diseased heart? A. Myocardial wall stiffness. B. Volume of pericardial fluid. C. Atrial chamber size D. Non-compliant pericardium.
D. Non-compliant pericardium. This is not an issue of pericardial tamponade or constrictive pericarditis. The low compliance pericardium surrounding the RA, LA, & RV provides the most significant barrier to the filling of these high compliance structures. In fact, pericardial constraint is the main factor of the diastolic pressure volume relations of these chambers . Atrial chambers are compliant and can chronically enlarge, but remain limited in their ability to expand due to pericardial restriction. Myocardial muscle is thin in the low pressure atria and right ventricle; in the normal heart, myocardial compliance in these areas is relatively high. pericardial fluid volume is typically between 15 to 30mls and is not an impedance to filling
Which abnormality is most likely to occur in a patient with pericardial tamponade? A. Pulsus parvus B. Pulsus alternans C. Pulsus tardus D. Pulsus paradoxus.
D. Pulsus paradoxus. Normally, the systolic blood pressure decreases a little during inspiration, but in the patient with pulses paradoxus the systolic blood pressure decreases by 10 or more
What is the most common cause of acute pericarditis? A. Rheumatoid arthritis. B. Systemic, lupus C. Radiation D. Viral infection
D. Viral infection. The pericardium surrounds the heart and provides a minimal friction environment in which the heart to move with ease. It is composed of two layers that are separated by 10 to 15ml 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 hearts ability to move within the pericardial sac Acute pericarditis (most common cause is a viral infection) Constrictive pericarditis (most common cause is radiation or previous cardiac surgery) Cardiac Tampanade
Conditions that worsen LVOT:
Decreased preload Increased contractility Decreased afterload
Which drugs reverse left ventricular remodeling in the patient with heart failure select 2 Enalapril Spironolactone Esmolol Clonidine
Enalapril Spironolactone The failing heart changes, its size shape and function in an attempt to preserve cardiac output. This is called cardiac remodeling. Overtime these compensatory mechanisms become maladaptive and lead to a decline in myocardial function Pressure overload -myocardium get thicker concentric hypertrophy Volume overload-myocardium becomes dilated Eccentric hypertrophy Cardiac remodeling can be reversed by ACE inhibitors and aldosterone inhibitors. Indeed, these are the first line agents in the patients with heart failure.
Which conditions are associated with an increased incidence of silent myocardial ischemia? Select 2 Parkinson's Essential, hypertension Gillian-barre Diabetes mellitus
Essential, hypertension Diabetes mellitus Diabetes accelerates. The Arthur is Lorado process affecting multiple organ systems including the heart diabetic patients have an increased risk for coronary artery disease, silent myocardial, ischemia, and myocardial infarction hypertensive. Patient also have an increased incidence of silent ischemia and infarction.
Beck's syndrome (anterior spinal artery syndrome)
Flaccid paralysis of LE (corticospinal tract is affected) Bowel & bladder dysfunction (autonomic nerve fibers affected) Loss of temperature & pain sensation (spinalthalamic tract affected) Touch & proprioception intact (dorsal column preserved)
An increase in which factor is associated with the highest increase in myocardial oxygen consumption, select 2. Pressure work Wall stress Heart rate Volume work
HR & pressure work
Which congenital heart conditions require a patent ductus arteriosus to maintain systemic perfusion? Select 2 Hypoplastic left heart Tricuspid atresia Ventricular septal defect Tetralogy of Fallot
Hypoplastic left heart Tricuspid atresia Conditions that impede blood flow to the systemic circulation require the maintenance of an open ductus arteriosus. These congenital heart conditions include: hypoplastic LV, aortic stenosis, coarctation of the aorta, and tricuspid or aortic atresia. The maintenance of patent ductus allows blood from the pulmonary artery to be directed (shunted) into the systemic circulation, which would otherwise be starved for oxygen and nutrients. Use of 21% oxygen should be considered in lieu of higher FiO2 in order to assist in keeping this sensitive ductal shunt patent.
What medications precipitate pharmacologic closure of the ductus arteriosus? Select 2 Nitric oxide Ibuprofen Indomethacin Prostaglandin E2
Ibuprofen Indomethacin Normally increases in arterial oxygen levels (PaO2 >50) following delivery and rapid decreases in prostaglandin E2 (vasodilator) contribute to the functional closure of the PDA. This process begins at 10 to 15 hours post delivery and is typically complete in 48 hours. Both indomethacin and ibuprofen may be administered to precipitate closure of the PD; however, the former is associated with more (primarily renal) side effects. Aspirin is much less effective than indomethacin. Nitric oxide is a potent, smooth muscle vasodilator, not a vasoconstrictor.
Identify the statements that best describe the postoperative complications. Following carotid endarterectomy, select 2. If a hematoma causes airway compromise, The Anesthetist should remove the sutures from the incision site. Carotid denervation reduces the ventilatory response to hypoxia Hypotension is the most common postoperative complication Injury to the superior laryngeal nerve may result in hoarseness & inspiratory stridor
If a hematoma causes airway compromise, The Anesthetist should remove the sutures from the incision site. & Carotid denervation reduces the ventilatory response to hypoxia Potential complications, following carotid endarterectomy: Hematoma at the surgical site : can compromise the airway patency. This is an airway emergency. And 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 in 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 plaque 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 phenomenon. Carotid body denervation reduces the ventilatory response to hypoxia. This is further complicated by narcotics, and or bilateral CEA.
What medications precipitate pharm closure of PDA? Select 2 Indomethacin Ibuprofen Nitric oxide Prostaglandin E2
Indomethacin Ibuprofen Normally increases in arterial oxygen levels (Pa>50) following delivery and rapid decreases in prostaglandin E2 (vasodilator) contribute to the functional closure of the PDA. This process begins at 10-15hrs post-delivery and is complete in 48hrs. Both indomethacin and ibuprofen may be administered to precipitate closure of the PDA; however the former is associated with more (primarily renal) side effects. ASA is much less effective than indomethacin. Nitric oxide is a potent smooth muscle vasodilator (not constrictor).
Which findings are MOST closely associated with HFpEF? Select 3. Tricuspid regurgitation Dilated cardiomyopathy Ischemic heart disease S3 heart sound Essential HTN Aortic stenosis
Ischemic heart disease Essential HTN Aortic stenosis Heart failure preserved ejection fraction diastolic failure is associated with decreased ventricular compliance ventricle doesn't feel properly. Poor compliance explains why the end, diastolic pressure over estimates the end, diastolic volume. Defining characteristic of diastolic dysfunction as symptomatic heart failure with a normal ejection fraction. contractility is generally preserved until the late stage of the disease. An S4 heart sound suggest poor ventricular compliance. The most common causes of diastolic heart failure include aortic stenosis, ischemic heart disease, and long standing essential HTN. Diastolic dysfunction is also associated with: Concentric hypertrophy Old age Valve stenosis Hypertrophic cardiomyopathy Cor pulmonale Obesity
Left ventricular perfusion occurs at which point in the cardiac cycle? Select 2 Isovolumetric relaxation Systole Isovolumetric contraction Diastole
Isovolumetric relaxation Diastole Perfusion of any vascular bad is dependent on driving pressure coronary arteries are located upon the epicardial surface of the heart and give rise to branches that penetrate into the myocardial muscle. These branches are exposed to the extravascular pressure of cardiac contraction. During early diastole, isovolumetric relaxation, the pressure gradient from the aortic root, is maximized against the now Minimal extravascular compression of the epicardial vessels. Coronary vascular resistance is also decreased at this time LV myocardial blood flow is at its peak.
What are early classic signs and symptoms of pericardial construction? Select 3 Jugular vein, distention Peripheral edema Pulmonary congestion High output heart failure Ascites Chest pain
Jugular vein, distention Peripheral edema Ascites Pericardial construction impairs atrial and right ventricular filling early indications associated with constrictive pericarditis include signs of right ventricular failure, such as peripheral edema, ascites and jugular vein distention. Other signs and symptoms include fatigue, dyspnea, pulsus paradoxus, and a positive Kuszmaul sign. Even in the presence of low cardiac output, pulmonary congestion is typically absent. High output Heart failure is not a feature of constricted myocardium, but of conditions with excess blood volume such as anemia, AV fistulas, or severe hyperthyroidism.
When compared to acute pericarditis, which of the following are more likely to occur with constrictive pericarditis, select 3. Atrial dysrhythmias Pulses paradoxus Fever Pericardial friction rub Kussmauls sign Chest pain
Kuszmaul sign Pulsus paradoxus Atrial dysrhythmias Constrictive pericarditis is caused by fibrosis, or any condition where the pericardium becomes sticker. The ventricles cannot fully relax during diastole, and this limits filling by reducing ventricular compliance. signs and symptoms of constrictive pericarditis include. : Kuszmaul 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 Tampanade. Signs and symptoms of acute pericarditis include: Acute chest pain increases with inspiration Fever Pericardial friction rub ST elevation
Which Pharmalogical agents, reduce myocardial oxygen demand, select 2 Metoprolol Morphine Atropine Dobutamine
Metoprolol Morphine Metoprolol improves 02 supply, and demand by attenuating heart rate and contractility Morphine also improves the O2 supply demand balance
Where is mitral regurgitation her best?
Mitral regurgitation and stenosis 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. 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.
Match the calcium channel blocker with its chemical classification: Nicardipine Verapamil Diltiazem Phenylalkylamine Dihydropyridine Benzothiazepine
Nicardipine: Dihydropyridine Cellular target: vascular, smooth muscle Binding site: binds to the outside of the channel modulates channel function Key examples: Nifidipine, Nicardipine, Nimodipine, Amlodipine Verapamil: Phenylalkylamine Cellular target: myocardium Binding site: binds to the inside of the channel, occludes the ion conducting pore. Diltiazem: Benzothiazepine Cellular target: myocardium Binding site: poorly understood Just like there are three types of voltage gated calcium channels. There are three classes of calcium channel blockers. Remember CCBs bind to the alpha-1 subunit of the L-type calcium channel, although each binds to the channel in a slightly different way.
Following mitral valve repair, you observe systolic anterior motion of the anterior leaflet on the TEE. This patient MOST likely received. Select two. Nitroprusside Phenylephrine Dobutamine 500ml NACL Bolus
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. Pharmacological treatment is the same as hypertrophic cardiomyopathy: Vasodilators and inotropes make SAM worse (nitroprusside, and dobutamine) Vasoconstrictors in volume expansion tend to make SAM better (phenylephrine & NS bolus)
Which interventions reduce stroke volume in the pt with hypertrophic cardiomyopathy? Select 3 Nitroprusside Ephedrine Esmolol Phenylephrine Hypervolemia Valsava maneuver
Nitroprussude Ephedrine Valsava maneuver Always concerned with LVOT obstruction 4 conditions that increase risk of LVOT obstruction: decreased preload, decreased afterload, increased HR, & increased contractility Conditions that decrease preload: Vasodilators Neuraxial anesthesia Hypovolemia Postural changes (RT) PPV Valsava maneuver Conditions that decrease afterload: Vasodilators Neuraxial anesthesia Oxytocin Conditions that increase HR: Beta agonists Ketamine Pancuronium Desflurane Oxytocin Light anesthesia Histamine releasing drugs (morphine, meperidine, thiopental, atracurium) Conditions that's increase contractility: Beta agonists Digoxin Light anesthesia
The best pharmacological choices for treating a hypotensive patient with aortic stenosis include: select 2 EPI Norepinephrine Phenylephrine Nitroprusside
Norepinephrine Phenylephrine In aortic stenosis, avoidance of negative inotropy, Tachycardia, and vasodilation is key to my maintenance of adequate forward flow through a tight, stiff valve. the goals for managing a patient with aortic stenosis include: Maintenance of a low to normal heart rate Normal, cardiac contractility Normal LV outflow resistance (SVR) Norepinephrine has potent alpha-1, and beta-1 effects increasing both arterial vasoconstriction and myocardial contractility. It has minimal effects upon beta-2 receptors. Phenylephrine is a direct, acting, alpha-1 agonist; it constricts venous capacitance vessels and produces renal vasoconstriction resulting in an increased LV preload, and afterload which increases arterial pressure. dosing may produce baroreceptor mediated decreasing heart rate. Epi increases HR
hypertrophic cardiomyopathy (AKAs:)
Obstructive hypertrophic cardiomyopathy (OHCM) Hypertrophic obstructive cardiomyopathy (HOCM) Asymmetric septal hypertrophy (ASH) Idiopathic hypertrophic subaortic stenosis (IHSS)
Which factors primarily affect myocardial oxygen supply, select 2 P 50 Wall tension Inotropy Diastolic time
P 50 and diastolic time The heart has a very high basil oxygen consumption (8-10mlO2/min) with an extraction ratio of 65 to 70%. 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 is too low Determinants of myocardial oxygen SUPPLY: Heart rate (diastolic time-LV circulation only perfuses during diastole) Aortic diastolic blood pressure Coronary blood flow Oxygen content Oxygen extraction (P 50 determines 02 offloading from hemoglobin) Determinants of myocardial oxygen DEMAND: Heart rate Preload Afterload Contractility (inotropy) Notice that heart rate is on both sides of the equation
Which are true statements regarding acute pericarditis, as it relates to myocardial ischemia? Select 2 There are reciprocal, ST segment changes present PR segment depression is absent Pain is relieved with positional changes Symptoms last longer
Pain is relieved with positional changes Symptoms last longer Differential of acute pericarditis and myocardial ischemia: Acute pericarditis: Retrosternal, acute pain, relief with leaning forward, worsens with inspiration PR depression Pericardial friction rub No reciprocal ST changes Duration of signs and symptoms last hours to days Myocardial ischemia: Retrosternal pressure no relief with positional changes No PR depression No pericardial friction rub There are reciprocal ST changes Duration of symptoms: minutes to hours
Which are TRUE statements regarding acute pericarditis as it relates to myocardial ischemia? Select 2 PR segment depression is absent Pain is relieved with positional changes There are reciprocal ST-segment changes present Symptoms last longer
Pain is relieved with positional changes Symptoms last longer Acute pericarditis: Retrosternal acute pain, relief with leaning forward, worsens with inspiration PR depression Pericardial friction rub No reciprocal ST changes Duration: hours to days MI: Retrosternal pressure, no relief with positional changes No PR depression No pericardial friction rub Reciprocal ST changes Duration: minutes to hours
Which data set is consistent with a diagnosis of moderate aortic stenosis? Select 3. Peak velocity of 3.5m/s Peak velocity of 2.9m/s Mean gradient of 28mmhg Mean gradient of 19mmhg Aortic valve area of 1.3cm Aortic valve area of 0.6cm
Peak velocity of 3.5 Mean gradient of 28 Aortic valve of 1.3 Moderate aortic stenosis: Peak velocity of 3-4m/s Mean gradient of 20-40mmhg Valve area from 1-1.5cm Severe AS: Peak velocity >4.0 Mean gradient >40 Valve area <1.0 Mild AS: Peak velocity 2.6-2.9m/s Mean gradient <20mmhg Valve area >1.5cm
Which data set is consistent with a diagnosis of moderate aortic stenosis? Select 3 Peak velocity of 3.5 m/s Peak velocity of 2.9 m/s Mean gradient of 28mmhg Mean gradient of 19mmhg Aortic valve area of 1.3cm^2 Aortic valve area of 0.6cm^2
Peak velocity of 3.5 m/s Mean gradient of 28mmhg Aortic valve area of 1.3cm^2 Aortic stenosis is defined by peak velocity of 3-4 m/s, mean gradient of 20-40mmHg, and valve area from 1-1.5cm^2 In severe AS: peak aortic flow velocity >/= 4.0 m/s mean gradient >40mmhg aortic valve area <1.0cm^2 In Mild AS: Peak velocity 2.6-2.9 m/s Mean gradient <20mmHg Valve area >1.5cm^2 Aortic stenosis may be asymptomatic and chest auscultation is not reliable until AS quite severe; placing the patient in left lateral decubitus position During auscultation of the apical impulse may increase detection. Aortic stenosis impedes ventricular ejection, which increases afterload. This increases left ventricular wall stress and LV oxygen demand leading to LV Hypertrophy. clinical S/S of AS include: chest pain or fatigue on exertion, shortness of breath, syncope and systolic heart failure.
The BEST pharm choices for treating hypotension in pt with aortic stenosis include: select 2 Phenylephrine Epinephrine Nitroprusside Norepinephrine
Phenylephrine Norepinephrine And aortic stenosis, avoidance of negative anatomy, tachycardia, and vasodilation is key to the maintenance of adequate forward flow through a stiff tight valve. The goals for managing a patient with aortic stenosis include. : Maintenance of low to normal HR Normal cardiac contractility Normal LV outflow resistance (SVR) Norepinephrine has potent, alpha-1 and beta-1 effect, increasing both arterial vasoconstriction and myocardial contractility, and has minimal effects upon beta-2 receptors Phenylephrine is a direct-acting, alpha-1 agonist; it constricts venous capacitance vessels and produces renal vasoconstriction, resulting in an increased LV preload and afterload, which increases arterial pressure. Dosing may produce baroreceptor-mediated decrease in heart rate
Which physiological factors increase after placement of an infra-renal aortic cross clamp, select 2. Cardiac output Reno blood flow Preload Mixed venous oxygen saturation
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 sells distal to the aortic cleanup 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 in the increase in after Lou determine cardiac output. Cardiac output is usually unchanged in a healthy heart, and decrease in patients with reduced cardiac reserve. Renal blood flow decreases, even if an infrarenal clamp is used
Which conditions promote myocardial remodeling through parallel replication of sarcomeres. Select 2 Ecentric hypertrophy Chamber dilation Pressure overload Stenosis
Pressure overload Stenosis STENOSIS: Pressure overload concentric hypertrophy Chambers become thicker to generate more pressure sarcomeres in parallel "slow, full, tight" REGURGITATION: Volume overload Ecentric hypertrophy Chambers dilate to accept more volume Sarcomeres in series "Full fast forward"
Antibiotic prophylaxis against endocarditis may be indicated if a patient has a history of select 2 Mitral prolapse Unrepaired, cyanotic, heart disease Cardiac stent placement Prosthetic heart valve
Prosthetic heart valve and 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 preoperative antibiotic prophylaxis : History of infective endocarditis Prosthetic heart valve Heart transplant with valvuloplasty Unrepaired, cyanotic, congenital, heart disease Repaired congenital heart disease, if the repair is less than six months old Repaired congenital heart disease with residual defects that have impaired endothelialization at the graft site Antibiotic prophylaxis is not indicated for the patient with a history of : MVP CABG Coronary stent placement Unrepaired, cardiac valve disease
A patient under general inhalation Anesthesia @ MAC is exhibiting signs of myocardial ischemia. Blood pressure is 125/70 & the heart rate is 100, SPO2 is 99% on 90% inspired oxygen. what are the most meaningful immediate interventionS? Select 2 Increase fraction of inspired oxygen Raise the agent concentration Provide balance, salt solution, fluid bolus Deliver short, acting beta blocker
Raise the agent concentration Deliver short, acting beta blocker The primary goal in the presence of myocardial ischemia is to reduce myocardial oxygen consumption determinants of MVO2 include heart rate, prelude, contractility, and afterload. Myocardial oxygen consumption is increased with an increase heart rate the primary intervention should be directed towards a reduction in the heart rate when it is elevated in the presence of ischemia. Use of a short acting intravenous, beta adrenergic antagonist will reduce the heart rate and decrease myocardial oxygen consumption Since all modern inhalation anesthetics decrease SVR the next best choice is to increase the agent concentration reduction of SVR, or left in circular afterload allows the ventricle to empty with less work there by decreasing myocardial O2 consumption. any increase in heart rate with Desflurane should be ameliorated by the beta blocker
In patient with aortic stenosis you should be concerned with rate, volume and afterload. Describe management of each:
Rate: Maintain NSR. Tachycardia reduces filling time, bradycardia creates LV distention 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)
What features characterize chronic, severe mitral regurgitation? Select 2 Regurgitant fraction > 50% Normal left atrial size Enlarged left ventricle Regurgitant volume >40ml/beat
Regurgitant fraction > 50% Enlarged left ventricle Severe mitral regurgitation is defined by regurgitant fraction >/= to 50%, Regurgitant volume >60 mL/beat and BOTH an enlarged left atrium and left ventricle. This can occur in both chronic compensated or a chronic decompensated case. In acute MR, no changes in LA or LV size occur, although left atrial pressure will increase in a V wave may be present on LAP tracings
Which coronary arteries perfuse the anterior wall of the right ventricle? Select 2 Left circumflex Posterior descending Right coronary Left anterior descending
Right coronary Left anterior descending Most of the right ventricle is perfused by the right coronary artery. however, distal diagonal and septal branches of the left anterior descending artery, also perfuse part of the RV anterior wall Occlusion of either RCA, or the LED can cause right ventricular ischemia, RV, infarction and ischemia and the sinoatrial and/or the atrioventricular node. presenting symptoms of nodal ischemia include Bradyarrhythmias or heart block
patients with which conditions should prompt a preoperative evaluation for pericarditis? Select 2 Systemic lupus Rheumatoid arthritis Osler-Weber-Rendu disease Pemphigus vulgaris
Systemic lupus Rheumatoid arthritis The fibrous pericardium outer layer is thick, connective tissue. Thus some connective tissue disorders are associated with pericarditis. In RA, a chronic autoimmune inflammatory disease, 20-50% of patients have pericarditis that can progress to restrictive pericarditis, and/or cardiac tamponade. In SLE, a complex disorder of altered innate & adaptive immunity, patients may present with pericarditis and pericardial effusions. Pemphigus vulgaris is an autoimmune blistering disease, and which IgG antibodies attacks skin and mucous membranes with oral lesions in 50 to 70% of patients. There is a significant risk of fluid and protein loss through the lesions along with risk of infection. Osler-Weber-Rendu disease, a.k.a. hereditary, hemorrhagic telangiectatic. Tasia is a hereditary autosomal dominant condition that affects skin, mucous membranes brain liver, and lungs bleeding during surgery is a high risk, and all patients should be a valuated for arteriovenous malformation prior to an anesthetic.
What are common symptoms of a patent ductus, arteriosus in a premature infant? Select 3 Narrow, pulse pressure Systolic murmur Respiratory failure Relative volume depletion Diastolic murmur Widened pulse pressure
Systolic murmur Respiratory failure Widened pulse pressure When SVR is greater than PVR, a patent ductus, arteriosus will direct blood into the pulmonary circulation, creating pulmonary congestion as blood flows from left (aorta) to right (pulmonary artery) and overload the pulmonary vasculature. The shock occurs during systole leading to a systolic, not diastolic, murmur. widened pulse pressure is due to the additional runoff of blood into the pulmonary vasculature during contraction . These premature infants will be volume overloaded, not volume depleted, and typically require fluid restriction & diuretic therapy
What are common symptoms of patent ductus arteriosus in a premature infant? Select 3. Narrow pulse pressure Systolic murmur Widened pulse pressure Respiratory failure Relative volume depletion Diastolic murmur
Systolic murmur Widened pulse pressure Respiratory failure When SVR is greater than PVR, a PDA will direct blood into the pulmonary circulation creating pulmonary congestion as blood flows from left (aorta) to right (pulmonary artery) and overloads the pulmonary vasculature. The shunt occurs during systole leading to a systolic murmur. Widened pulse pressure is due to the additional run-off of blood into the pulmonary vasculature. The premature infants will be volume overloaded and typically require fluid restriction and diuretic therapy
What are the most appropriate interventions for an anesthetized Patient who has developed symptomatic complete heart block? Select 2 Transcutaneous pacing Intravenous EPI Intravenous atropine Transesophageal pacing
Transcutaneous pacing Intravenous EPI Intravenous atropine blocks parasympathetic input to the SA and AV nodes but if the pacemaker is below the AV node, atropine will not be effective. Sympathetic innervation is more extensive and includes input to the SA and AV node, along with direct innervation of the atrial and ventricular muscle. The infusion of a potent Beta-1 catecholamine, such as EPI or isoproterenol can effectively increase ventricular contraction. Electrical pacing is also an expedient tool in this scenario, but the approach is key. transesophageal PM is an atrial PM, and for the same reasons that atropine is ineffective, nerve simulation above the area of blocked conduction will be ineffective in eliciting a ventricular response. On the other hand, a transcutaneous PM, can directly stimulate myocardial muscle. 45 or less HR w/ hypotension
Which congenital heart conditions require a PDA to maintain systemic perfusion? Select 2. TOF VSD Tricuspid atresia Hypoplastic left heart
Tricuspid atresia Hypoplastic left heart Conditions that impede blood flow to the systemic circulation require the maintenance of an open ductus arteriosis. These congenital heart conditions include: hypoplastic LV, aortic stenosis, coarctation of aorta, tricuspid or aortic atresia. The maintenance of a patent ductus allows blood from the pulmonary artery to be directed (shunted) into the systemic circulation, which would otherwise be starved for oxygen and nutrients. use of 21% oxygen should be considered in lieu of higher FiO2 in order to assist in keeping this sensitive duct shunt patent.
Match congenital heart defect with its major physiologic sequelae: VSD Truncus arteriosis TOF Coarctation of aorta Increased pulmonary blood flow Decreased pulmonary blood flow Ventricular pressure overload Common mixing chamber
VSD: increased pulmonary blood flow TOF: decreased pulmonary blood flow (cyanosis) Coarctation of aorta: ventricular pressure overload Truncus arteriosis: common mixing chamber (cyanosis)
Which interventions reduce stroke volume, in the patient with hypertrophic cardiomyopathy, select 3 Hypervolemia Esmolol Valsalva maneuver Phenylephrine Nitroprusside Ephedrine
Valsalva maneuver Ephedrine Nitroprusside In the patient with hypertrophic cardiomyopathy we are always concerned about left ventricular outflow tract obstruction There are four conditions that increase the risk of LVOT obstruction : decrease preload, decreased afterload, increased heart rate, and increased contractility Conditions that decrees preload: Vasodilators neuraxial Anesthesia Hypovolemia Postural changes (RT) Positive pressure ventilation Valsalva maneuver Conditions that decrease afterload: Vasodilators Neuraxial Anesthesia Oxytocin Conditions that increase heart rate : Beta agonist Ketamine Pancuronium Desflurane Oxytocin Light anesthesia Histamine, releasing drugs (morphine, meperidine, thiopental, atracurium) Conditions that increase contractility : Beta agonist Digoxin Light anesthesia
NYHA classification of HF
class 1 -no symptoms class 2 - symptoms w/ moderate activity class 3 - symptoms w/ minimal activity class 4 - symptoms at rest
Conditions that narrow the LVOT
these are bad! -decreased systolic LV volume (decreased preload or increased HR) -Force of contraction (increased contractility—inotropes) -Transmural pressure gradient (decreased aortic pressure —vasodilators)
Conditions that distend the LVOT:
these are good! -increased systolic LV volume (increase preload or decrease HR) -Force of contraction (decreased contractility) -Transmural pressure gradient (increased aortic pressure—pressure distends the OT)
