Cardiac Surgery CSC

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Your patient is still hypothermic with a temperature of 35º C on admission to ICU from the OR. You know that continued hypothermia has which of the following adverse effects: A. Causes platelet dysfunction and impairs the coagulation cascade which contributes to postoperative bleeding. B. Causes shivering which decreases tissue O2 consumption. C. Shortens the duration of action of anesthetic drugs and contributes to agitation. D. Causes peripheral vasodilation which increases SVR and myocardial O2 demand.

A. Hypothermia (temp < 36º C) can cause several adverse effects, including: -Peripheral vasoconstriction which increases SVR, afterload, and myocardial O2 requirements, and can cause hypertension. -Increased incidence of arrhythmias -Shivering which increases tissue O2 demand -Platelet and coagulation cascade dysfunction which increases the risk of bleeding -Prolongs the duration of action of anesthetic drugs and prolongs time to extubation -Increases the risk of wound infection

Postoperative hypertension following cardiac surgery can occur due to all of the following EXCEPT: A. Low cardiac output syndrome. B. Pain and agitation associated with awakening from anesthesia. C. Hypothermia. D. Hyperdynamic ventricular contractility.

A. CO = HR X SV, and SV is determined by preload, afterload, and contractility. Low cardiac output results in hypotension and can be due to inadequate preload, decreased ventricular contractility, increased afterload, or heart rate or rhythm abnormalities. BP = CO X SVR. High BP is due to either high CO or high SVR. Postoperative hypertension is usually due to increased SVR rather than to increased CO. Hypothermia causes peripheral vasoconstriction which increases SVR. Pain and agitation increase sympathetic nervous system activity which increases heart rate and contractility (determinants of CO), and causes peripheral vasoconstriction, which increases SVR. The use of vasopressor drugs can also contribute to an increase in SVR. Hyperdynamic ventricular contractility is more common in patients with left ventricular hypertrophy.

You are caring for a patient with an intra-aortic balloon pump and note blood in the tubing. Your initial action should be: A. Stop the balloon pump and notify the physician. B. Administer 100% oxygen to help displace the helium and notify the physician C. Leave the IABP running and notify the physician. D. Purge the IABP manually to clear the blood from the tubing.

A. Blood in the IABP tubing indicates a balloon rupture which can cause gas embolus. However, helium is thought to be easily absorbed in the presence of balloon rupture and oxygen is not generally indicated. The appropriate action is to disconnect the balloon from the console or turn it on standby so the movement of helium is stopped and notify the physician. The nurse will need to prepare for IABP removal and replacement if needed.

All of the following are Type I neurological complications following cardiac surgery EXCEPT: A. Memory loss. B. Stroke. C. Coma. D. TIA.

A. Memory loss and varying degrees of intellectual deterioration are classified as Type II deficits. Type I deficits include stroke, major focal neurological deficits TIA, and coma. CPB plays a major role in the risk for adverse neurological events, both type I and type II, due to the resultant inflammatory response to CPB and the risk for microembolization. Other risk factors for stroke include advanced age, atherosclerotic aortic disease, history of stroke, hypertension, female sex, and diabetes. Additional risk factors for type II complications include prior CABG, alcohol consumption, heart failure, arrhythmias, and metabolic abnormalities.

Your patient post CABG has a BP of 192/96. Which of the following drugs would be appropriate for BP control: A. Nitroprusside. B. Epinephrine. C. Milrinone. D. Norepinephrine.

A. Nitroprusside is a vasodilator that causes dilation of both arteries and veins, with somewhat more arterial than venous dilation. It is usually the drug of choice for management of postoperative hypertension because of its short onset and duration of action which makes it easy to titrate. Some patients are extremely sensitive to nitroprusside, so the infusion should be started at a very low dose and increased as tolerated for BP control. In the immediate postoperative period, hypertension can be due at least partially to hypothermia associated with CPB and anesthesia. The BP must be monitored continuously because as the patient rewarms, blood vessels will dilate and SVR and BP will begin to fall. Epinephrine and norepinephrine are commonly used after cardiac surgery to increase BP because they cause vasoconstriction and increased contractility. Milrinone (Primacor) is a vasodilator and a positive inotropic drug. Its vasodilation effects could help lower BP but the positive inotropic effect would increase contractility which could contribute to an increase in BP. A drug like nitroprusside with pure vasodilator effect would be preferable for BP control in a hypertensive patient.

You are caring for a post CABG patient who has developed a monomorphic wide QRS tachycardia seen in the lead III rhythm strip on top in this example. His BP is 110/70 and he is tolerating the rhythm, but there is disagreement among physicians as to the mechanism of the tachycardia. You obtain the unipolar atrial electrogram seen in the bottom strip. The atrial electrogram confirms the diagnosis of: (P WAVES AND QRS NOT CORRELATING) A. Atrial flutter. B. VT. C. Sinus tachycardia. D. SVT with aberrant conduction.

B. A unipolar atrial electrogram shows very large P waves because it is recorded directly from the atrium. In this AEG, the large spikes are the P waves and they are dissociated from the smaller and faster QRS complexes (these strips are not simultaneously recorded), confirming the diagnosis of ventricular tachycardia.

You are caring for a post CABG patient who received a large amount of contrast in the cardiac cath lab prior to going to surgery for urgent revascularization. You expect that this patient is likely to develop which of these postoperative complications: A. Acute respiratory failure. B. Acute kidney injury. C. Excessive mediastinal bleeding. D. Ischemic stroke.

B. Acute kidney injury (AKI) increases mortality following cardiac surgery, and any degree of preoperative renal dysfunction greatly increases the risk for developing AKI postoperatively. Patients who receive nephrotoxic agents, such as large amounts of contrast during diagnostic or interventional cardiac cath procedures, aminoglycosides, or metformin, are at increased risk for developing AKI. Other preoperative factors that increase this risk include cardiogenic shock, decompensated heart failure, or any preexisting renal disease. Medications that can contribute to development of AKI include NSAIDS, ACE inhibitors, antibiotics, furosemide, and cephalosporins. Postoperative sustained hypotension and low cardiac output syndrome, vasoconstriction due to vasopressor drugs, renal embolization related to IABP use, sepsis, and effects of nonpulsatile flow during CPB also increase the risk of postoperative AKI. Any cardiac surgery patient can develop mediastinal bleeding, respiratory failure, or have a stroke, so the nurse must be vigilant for signs of these complications as well as for AKI in all patients.

Which of the following patients should receive a transfusion of RBCs following cardiac surgery: A. A patient with a Hgb of 9 g/dL. B. A stable patient with a HCT of 22%. C. A patient who is bleeding and has a HCT of 24%. D. A 78 year old patient with prolonged bypass time and a HCT of 26%.

C. A bleeding patient should be transfused to maintain a HCT of >25%. A HCT of 22-24% is considered acceptable in stable patients (Bojar, 2011: Manual of perioperative care in adult cardiac surgery, 5th ed.) Transfusion guidelines from the Society of Thoracic Surgeons and the Society of Cardiovascular Anesthesiologists recommend RBCs when the Hgb is < 6g/dL as a lifesaving strategy and for most patients when the Hgb is < 7g/dL. It is reasonable to transfuse patients with higher Hgb levels if signs of end organ ischemia are present.

You are caring for a post CABG patient who has developed a monomorphic wide QRS tachycardia seen in the lead III rhythm strip on top in this example. His BP is 110/70 and he is tolerating the rhythm, but there is disagreement among physicians as to the mechanism of the tachycardia. You obtain the unipolar atrial electrogram seen in the bottom strip (p waves not followed by qrs waves). The atrial electrogram confirms the diagnosis of: A,. Sinus tachycardia. B. Atrial flutter. C. VT. D. SVT with aberrant conduction.

C. A unipolar atrial electrogram shows very large P waves because it is recorded directly from the atrium. In this AEG, the large spikes are the P waves and they are dissociated from the smaller and faster QRS complexes (these strips are not simultaneously recorded), confirming the diagnosis of ventricular tachycardia.

Atrial fibrillation is particularly dangerous in which of these patients: A. Patient with mitral valve replacement for mitral stenosis. B. Patient who had 5-vessel CABG. C. Patient with aortic valve replacement for aortic stenosis. D. Patient with preoperative LV dysfunction.

C. Aortic stenosis causes left ventricular hypertrophy with a stiff noncompliant LV and diastolic failure. A noncompliant LV depends on atrial kick for adequate preload and stroke volume. Sinus rhythm or AV pacing is especially important in this patient to maintain AV synchrony and adequate preload. Atrial fibrillation results in a loss of atrial kick and can lead to profound hemodynamic deterioration. Atrial fibrillation can occur in any post operative cardiac surgery patient and is especially common in mitral valve disease because of the increased atrial pressure and/or volume that occurs. However, it is better tolerated in patients who do not have LV diastolic dysfunction or LV hypertrophy.

In caring for a patient with chest tubes the nurse knows the following to be true concerning drainage: A. Aggressive stripping is necessary to keep the drainage tube patent. B. Dumping of blood into the chest tube with a position change is usually related to a new bleed. C. Chest tubes can safely be removed as long as the amount of drainage is < 500 ml per 8 hours. D. A patient with decreased breath sounds and increased inspiratory pressures on the ventilator but with no drainage in the chest tube might have a collection of undrained blood in the pleural space.

D. A change in patient condition, such as decreased breath sounds and increased inspiratory pressures on the ventilator alarm, may indicate blood in the pleural space that has not been effectively drained by the chest tube. Aggressive stripping of the chest tube can cause a negative pressure of over 300 cm of H2O and this can cause further bleeding and is painful for the patient. When a dumping of blood occurs with a position change this can represent either new or old blood. The color of the blood as well as other changes in the patient condition can be used to help assess the acuity of the bleeding. Chest tubes are typically not removed until the amount of drainage is less than 50 to 100 ml for a 24-hour period of time. After CABG surgery chest tubes are typically removed when drainage is less than 100 ml for eight hours.

All of the following are Type I neurological complications following cardiac surgery EXCEPT: A. TIA. B. Stroke. C. Coma. D. Memory loss.

D. Memory loss and varying degrees of intellectual deterioration are classified as Type II deficits. Type I deficits include stroke, major focal neurological deficits TIA, and coma. CPB plays a major role in the risk for adverse neurological events, both type I and type II, due to the resultant inflammatory response to CPB and the risk for microembolization. Other risk factors for stroke include advanced age, atherosclerotic aortic disease, history of stroke, hypertension, female sex, and diabetes. Additional risk factors for type II complications include prior CABG, alcohol consumption, heart failure, arrhythmias, and metabolic abnormalities.

In the immediate postoperative period following surgery with CPB, urine output is expected to be high: False True

True Hemodilution occurs when CBP is used which expands the extracellular volume and produces a high urine output in the immediate postoperative period. During the first 12 hours after surgery, cardiac output may be low as the heart recovers from the effects of CPB and surgery, which often results in transient oliguria (defined at urine output < 0.5 ml/kg/hr). Persistent oliguria usually indicates acute kidney injury.

Atrial fibrillation is particularly dangerous in which of these patients: A. Patient with preoperative LV dysfunction. B. Patient with mitral valve replacement for mitral stenosis. C. Patient with aortic valve replacement for aortic stenosis. D. Patient who had 5-vessel CABG.

C. Aortic stenosis causes left ventricular hypertrophy with a stiff noncompliant LV and diastolic failure. A noncompliant LV depends on atrial kick for adequate preload and stroke volume. Sinus rhythm or AV pacing is especially important in this patient to maintain AV synchrony and adequate preload. Atrial fibrillation results in a loss of atrial kick and can lead to profound hemodynamic deterioration. Atrial fibrillation can occur in any post operative cardiac surgery patient and is especially common in mitral valve disease because of the increased atrial pressure and/or volume that occurs. However, it is better tolerated in patients who do not have LV diastolic dysfunction or LV hypertrophy.

In a patient with an IABP, the first pulse to weaken or disappear if the balloon moves upward in the aorta is: A. Left radial. B. Left carotid. C. Left femoral. D. Right femoral.

A. The tip of the balloon should be below the left subclavian artery, which is the last major branch off the aortic arch. If the balloon moves upward in the aorta, the left radial pulse will weaken or disappear because the balloon will occlude the left subclavian artery which carries blood into the left arm. This is why monitoring the left radial pulse is part of routine assessment of a patient with an IABP.

In caring for a patient with chest tubes the nurse knows the following to be true concerning drainage: A. A patient with decreased breath sounds and increased inspiratory pressures on the ventilator but with no drainage in the chest tube might have a collection of undrained blood in the pleural space. B. Dumping of blood into the chest tube with a position change is usually related to a new bleed. C. Chest tubes can safely be removed as long as the amount of drainage is < 500 ml per 8 hours. D. Aggressive stripping is necessary to keep the drainage tube patent.

A. A change in patient condition, such as decreased breath sounds and increased inspiratory pressures on the ventilator alarm, may indicate blood in the pleural space that has not been effectively drained by the chest tube. Aggressive stripping of the chest tube can cause a negative pressure of over 300 cm of H2O and this can cause further bleeding and is painful for the patient. When a dumping of blood occurs with a position change this can represent either new or old blood. The color of the blood as well as other changes in the patient condition can be used to help assess the acuity of the bleeding. Chest tubes are typically not removed until the amount of drainage is less than 50 to 100 ml for a 24-hour period of time. After CABG surgery chest tubes are typically removed when drainage is less than 100 ml for eight hours.

You are caring for a post CABG patient who received a large amount of contrast in the cardiac cath lab prior to going to surgery for urgent revascularization. You expect that this patient is likely to develop which of these postoperative complications: A. Acute kidney injury. B. Excessive mediastinal bleeding. C. Acute respiratory failure. D. Ischemic stroke.

A. Acute kidney injury (AKI) increases mortality following cardiac surgery, and any degree of preoperative renal dysfunction greatly increases the risk for developing AKI postoperatively. Patients who receive nephrotoxic agents, such as large amounts of contrast during diagnostic or interventional cardiac cath procedures, aminoglycosides, or metformin, are at increased risk for developing AKI. Other preoperative factors that increase this risk include cardiogenic shock, decompensated heart failure, or any preexisting renal disease. Medications that can contribute to development of AKI include NSAIDS, ACE inhibitors, antibiotics, furosemide, and cephalosporins. Postoperative sustained hypotension and low cardiac output syndrome, vasoconstriction due to vasopressor drugs, renal embolization related to IABP use, sepsis, and effects of nonpulsatile flow during CPB also increase the risk of postoperative AKI. Any cardiac surgery patient can develop mediastinal bleeding, respiratory failure, or have a stroke, so the nurse must be vigilant for signs of these complications as well as for AKI in all patients.

Antifibrinolytic drugs used to reduce intraoperative or postoperative blood loss include: A. Amicar (aminocaproic acid) and cyclokapron (tranexaminic acid). B. Aprotinin and amicar. C. tPA (tissue plasminogen activator) and clopidogrel. D. Protamine and vitamin K.

A. Amicar and cyclokapron are antifibrinolytic drugs that inhibit the breakdown of fibrin. They are used in both on- and off-pump cases to reduce intraoperative bleeding and can be used in postoperative patients who are bleeding excessively. Aprotinin is another antifibrinolytic drug that was commonly used to reduce blood loss but it is no longer being manufactured because of the risk of renal dysfunction and increased mortality. Tissue plasminogen activator (tPA) is a thrombolytic drug used to break down clots in acute coronary syndromes and acute ischemic stroke. Bleeding is a common side effect of tPA and it is not indicated in cardiac surgery patients. Clopidogrel is a P2Y12 receptor inhibitor that inhibits platelet activation and is used in acute coronary syndromes and ischemic stroke. Bleeding is a side effect of P2Y12 inhibitors and they are not used in patients who are bleeding. Protamine is used to reverse heparin at the end of a cardiac surgical procedure and therefore is used to reduce the incidence of bleeding, but it is not an antifibrinolytic agent. Vitamin K is used to reverse the effects of warfarin and is not an antifibrinolytic agent.

Treatment of HIT involves discontinuing all heparin products (including heparin coated catheters) and using which of these drugs to manage intravascular clotting: A. Argatroban (Novastan), bivalirudin (Angiomax), or fondaparinux (Arixtra). B. Warfarin. C. Clopidogrel (Plavix) and ASA. D. LMWH: Enoxaparin (Lovenox) or dalteparin (Fragmin).

A. Argatroban and bivalirudin are direct thrombin inhibitors that bind directly to soluble and clot-bound thrombin and do not bind to platelet factor 4 as heparin does, therefore they do not cause HIT. Fondaparinux is an indirect factor Xa inhibitor that does not cause HIT. Newer oral factor Xa inhibitors (rivaroxaban and apixaban) and the oral thrombin inhibitor dabigatran should theoretically be effective as anticoagulants in patients with HIT, but at this time data is lacking on their use in treating patients with HIT. LMWH (low molecular weight heparin) can cause HIT but not as often as unfractionated heparin. However, all forms of heparin must be discontinued in the treatment of HIT. Warfarin is not indicated for managing intravascular clotting in HIT because its onset of action is delayed for 2-7 days until normal clotting factors are cleared from the circulation. Clopidogrel and ASA inhibit platelet activation but have no effect on thrombin so are not effective in managing intravascular clotting in HIT.

Your postoperative CABG patient has atrial fibrillation with a ventricular rate in the 40's. Atrial and ventricular epicardial pacing wires are in place. Which pacing mode is indicated to increase the heart rate in this patient: A. VVI. B. DDD. C. DVI. D. AAI.

A. Atrial fibrillation with a slow ventricular response requires VVI pacing to maintain an adequate ventricular rate. Atrial pacing and sensing are ineffective in atrial fibrillation, therefore any mode that utilizes atrial pacing or atrial sensing is not indicated. The AAI, DVI, and DDD modes all utilize atrial pacing or sensing and are not indicated for this patient.

Which of the following is not an appropriate nursing intervention in caring for a patient with a chest tube drainage system: A. Clamping the chest tube after disconnecting suction in a patient leaving the unit for a diagnostic test. B. Reporting new diminished or any absence of lung sounds. C. Reporting continuous bubbling in the waterseal chamber. D. Performing gentle milking when drainage is present.

A. Do not clamp chest tube for transport (can cause tension pneumothorax with pleural chest tubes or tamponade with mediastinal chest tubes). Use portable suction if available or transport on gravity drainage with tubing from suction chamber open to air. Leaving the tubing open to air allows a vent for the escape of air. If there is an order for suction and no portable suction is available then obtain an order to transport with gravity drainage. Maintaining patency is a key nursing intervention. Avoid dependent loops in the drainage tubing. Chest tube should be gently milked if there is drainage, but there should be no routine stripping. Aggressive stripping of a mediastinal chest tube can result in a negative 300 cmH2O pressure in the mediastinum and can aggravate bleeding. Reportable conditions in patients with chest tubes include: • Signs and symptoms of increased air leak (increased crepitus, bubbling in the water seal chamber) • Drainage of more than 100 ml in a hour • Tachypnea, hypoxemia, diminished or absent lung sounds • Signs and symptoms of tension pneumothorax or cardiac tamponade (hypotension, jugular venous distention, muffled heart sounds, deviation of the trachea).

The ability of heparin to bind to platelet factor 4 (PF4) can cause which of these potentially dangerous side effects: A. HIT (heparin induced thrombocytopenia). B. Osteoporosis. C. Uncontrolled bleeding. D. Heparin rebound.

A. Heparin binds with platelet factor 4, forming a heparin-PF4 complex that stimulates an immune reaction involving formation of antibodies against the complex. The heparin-PF4-antibody complex binds to platelets, causing platelet activation and thrombin generation that results in intravascular thrombosis. Activated platelets are removed from circulation, leading to thrombocytopenia. Bleeding and osteoporosis can be side effects of heparin but are not due to binding of heparin with PF4. Heparin rebound is the reappearance of anticoagulant activity after adequate neutralization of heparin with protamine at the end of cardiac surgery. A significant amount of heparin is bound to plasma proteins and tissues, and its slow release following surgery results in anticoagulation after protamine has worn off. Heparin rebound is not due to heparin binding with PF4.

Which of the following patients is likely to have the dangerous form of heparin induced thrombocytopenia: A. A patient who is 5 days post CABG whose platelet count has decreased by 60%. B. A patient who is 4 hours post CABG with a platelet count of 200,000. C. A patient who is 2 days post CABG with a platelet count of 100,000. D. Any patient post CABG with a 20% decrease in platelet count.

A. Heparin induced thrombocytopenia can be a life threatening clinical condition. However, thrombocytopenia is a common clinical condition for many patients after CABG due to a variety of factors including heparin administration and the effects of cardiopulmonary bypass and use of intra-aortic balloon pump therapy. There are two types of heparin induced thrombocytopenia (HIT), Type 1 and Type 2. Type 1 HIT is common, is not immune related, usually develops within 48 hours of administration, results in a mild reduction in platelets. Heparin therapy can usually be continued in Type 1 HIT. Type 2 HIT is immune mediated and typically results in a decrease in platelets by 50% or more starting 4 to 10 days after the initiation of therapy, or as soon as within 10 hours of administration if the patient has had heparin within the last 100 days. Type 2 HIT can result in a procoagulant state leading to both venous and arterial thrombosis. The mortality rate associated with type 2 heparin induced thrombocytopenia is approximately 20 to 30 %.

The use of protamine to reverse heparin at the end of a cardiac surgical procedure can result in which of the following complications: A. Anaphylaxis and heparin rebound. B. Acute kidney injury and SIRS. C. Arrhythmias and pulmonary hypertension. D. Perioperative MI and pulmonary edema.

A. Hypersensitivity reactions, including anaphylaxis, can occur following protamine administration. Hypotension, cardiovascular collapse, noncardiogenic pulmonary edema, pulmonary vasoconstriction, and pulmonary hypertension may occur. Patients with fish allergy and those using NPH insulin are at higher risk for a protamine reaction. Heparin rebound is the reappearance of anticoagulant activity after adequate neutralization of heparin with protamine at the end of surgery. Heparin that is bound to plasma proteins and tissues may not be completely neutralized by protamine. This protein and tissue-bound heparin is released slowly after surgery, producing the heparin rebound phenomenon after the effects of protamine are gone. Acute kidney injury is a potential complication of CABG that can be caused by multiple factors including intraoperative or postoperative hypotension, hemolysis, embolization to renal arteries (associated with aortic cross clamping during CPB), and exposure to contrast media prior to surgery. SIRS can occur secondary to the use of CPB during surgery. Protamine use is not directly associated with acute kidney injury or SIRS. Perioperative MI and arrhythmias are potential complications of CABG and can be due to multiple factors including intraoperative or postoperative hypotension, embolization to coronary arteries (associated with aortic cross clamping during CPB), acute graft closure, and inadequate myocardial protection during CPB. Protamine use is not directly associated with perioperative MI or arrhythmias. Severe protamine reactions can result in pulmonary vasoconstriction with elevated PA pressures, right ventricular dysfunction, and significant hypotension due to vasodilation.

Hypokalemia can occur after cardiac surgery because of the high urine output associated with hemodilution during CPB. The major adverse effects of hypokalemia after cardiac surgery are: A. Respiratory muscle weakness delaying extubation, and cardiac arrhythmias. B. Acute renal failure and delirium. C. Increased incidence of stroke and delirium. D. Increased incidence of perioperative MI and arrhythmias.

A. Hypokalemia can cause muscle weakness when K+ level is < 2.5 mEq/L. Respiratory muscle weakness can delay time to extubation. Muscle weakness can also involve the GI tract and skeletal muscles, leading to ileus and delaying ambulation. The most common manifestation of hypokalemia is cardiac arrhythmias, including both atrial and ventricular arrhythmias. Hypokalemia is a common cause of torsades de pointes. Potassium level is not directly related to the incidence of perioperative MI, stroke, or delirium. Acute renal failure would cause hyperkalemia, not hypokalemia.

Management of postoperative hypertension includes which of the following: A. Adequate sedation and pain management, and vasodilators. B. Dobutamine and beta blockers. C. Calcium channel blockers and inotropes. D. All of the above.

A. Pain and anxiety contribute to hypertension by causing increased sympathetic nervous system activity. Adequate pain control and sedation with drugs such as propofol, midazolam, morphine, or dexmedetomidine can be used to treat early postoperative hypertension, especially in the ventilated patient. However, antihypertensive agents are preferred over sedatives to facilitate early extubation. There are several drugs that can be used as antihypertensive agents: Nitroprusside is primarily an arterial dilator that causes relaxation of arterial smooth muscle to reduce SVR, but it also dilates veins and reduces preload. Calcium channel blockers, especially nicardipine and clevidipine, cause arterial vasodilation and decrease SVR. They also dilate coronary arteries and slow the heart rate which can be beneficial in improving myocardial perfusion and controlling hypertension. Beta blockers decrease blood pressure by decreasing myocardial contractility and heart rate, as well as decreasing renin activity. They are used to treat hypertension in patients whose cardiac output is adequate, especially if tachycardia and hyperdynamic contractility are present. Dobutamine is a positive inotropic agent and is not indicated in treatment of hypertension. Increased contractility that results from positive inotropes can increase BP, not decrease it.

A patient with epicardial atrial and ventricular pacing wires post cardiac surgery has a change in his rhythm on the bedside monitor. Which of the following connections would allow you to obtain an atrial electrogram to help diagnose the rhythm: A. Connect an atrial pacing wire to the chest lead on your monitor cable and record 'V' on the bedside monitor. B. Connect a ventricular pacing wire to the chest lead and record 'V' on the bedside monitor. C. Connect an atrial pacing wire to the right leg electrode and record "V" on the bedside monitor D. Connect an atrial pacing wire to the chest lead on your monitor cable and record lead II on the bedside monitor.

A. Recording an atrial electrogram directly from an atrial pacing wire allows easy identification of atrial activity (P waves or flutter/fib waves) and helps illustrate the relationship between P waves and QRS complexes when it is difficult to see on a surface lead. The easiest way to do this is to attach a monitoring electrode to the chest lead on a 5-wire monitor cable and wrap it tightly around the metal end of an atrial pacing wire, making sure that the metal end of the pacing wire is in the gel center of the electrode and touching the metal portion of the button under the gel. Then set the monitor to record 'V', which records from the chest lead that is now attached to the atrial pacing wire. This connection will provide a unipolar recording (using one atrial wire) with very large atrial deflections. The connection between the atrial pacing wire and the monitor lead can also be made using an alligator clip, but this method using a regular monitoring electrode doesn't require any special equipment. It is a good idea to simultaneously record a surface lead along with the atrial electrogram and to run the paper at double speed through the recorder to spread the tracing out for better visualization. Lead II on the monitor is recorded between the right arm and the left leg electrodes, not the chest lead. Connecting a ventricular pacing lead will only accentuate the QRS, not the P waves. This illustration shows the connection of the chest lead on the monitor to an atrial pacing wire using a regular monitoring electrode.

You are caring for a patient on post op day 3 after aortic valve surgery. His epicardial pacing wires were removed an hour ago. You know that a potential complication of pacing wire removal is: A. Cardiac tamponade. B. 3rd degree AV block. C. Ventricular tachycardia. D. Atrial fibrillation.

A. Removal of epicardial pacing wires can cause bleeding and result in cardiac tamponade. Following pacing wire removal, the patient must be assessed for signs of tamponade, which include hypotension, JVD, chest pain, tachycardia, pulsus paradoxus, and distant heart sounds. Vital signs should be assessed every 15 minutes for the first hour after pacing wires are removed and then hourly for a few hours since tamponade can occur immediately or may not be manifest for several hours. If tamponade is suspected, a STAT echocardiogram should be done and if tamponade is present, pericardiocentesis should be performed. All cardiac surgery patients need to be monitored for arrhythmias, but pacing wire removal is not directly a cause of arrhythmias. Patients who have had valve surgery more often need pacing for the first few days because of transient AV block associated with valve surgery. If conduction disturbances are still present after 3 days a permanent pacemaker should be considered.

Which of the following statements is accurate concerning SvO2 and SCvO2 monitoring: A. Both are affected by cardiac output, arterial O2 saturation, Hgb, and O2 consumption by tissues. B. Only SvO2 can be used to evaluate the balance between O2 delivery and consumption. C. They can both be obtained without the use of a pulmonary artery catheter. D. Normal SCvO2 is about 90% and normal SvO2 is 80%, but they trend together.

A. SvO2 measures mixed venous oxygen saturation from the pulmonary artery and includes blood returning to the heart from the whole body. SCvO2 measures venous oxygen saturation of blood from the superior vena cava and only includes blood from the head and upper extremities. SvO2 is obtained from the distal port of a pulmonary artery catheter, but SCvO2 only requires a CVP catheter placed in the superior vena cava. They both reflect the balance between O2 delivery (determined by cardiac output, arterial O2 saturation, and Hgb) and O2 consumption by the tissues. The SCvO2 is normally slightly lower than the SvO2 but can be up to 7% higher than SvO2 in critically ill patients. However, the two values tend to trend together. Normal SCvO2 is about 70%, normal SvO2 is 60-80%.

Atrial fibrillation is an arrhythmia often seen in post-operative patients undergoing CABG. Preoperative therapy for the reduction of post-operative atrial fibrillation includes the following: A. Preoperative administration of a beta blocker or amiodarone, and a statin. B. Preoperative administration of sotalol and amiodarone. C. Preoperative administration of a calcium channel blocker and a beta blocker. D. Preoperative administration of a statin and digoxin.

A. The standard therapy for the reduction of postoperative atrial fibrillation is the initiation of beta blockers preoperatively. Amiodarone can be used for prophylaxis in high risk patients who are unable to receive beta blockers, but due to inconsistent clinical trial results, amiodarone is not recommended as a routine strategy for the prevention of postoperative atrial fibrillation. Preoperative statin therapy is known to reduce the risk of postoperative atrial fibrillation and is also associated with a reduction in mortality associated with postoperative atrial fibrillation.

You are using a chest tube drainage system that requires fluid in the water seal chamber. What is an important nursing consideration: A. Assure that the amount of sterile fluid in the water seal and suction chambers is at the manufacturer recommended level. B. Assure that there is continuous bubbling in the water seal chamber. C. Report any tidaling of this chamber immediately. D. Invert the water seal system at least once every 4 hours.

A. The 2nd compartment is connected to the 1st and creates a water seal. A small amount of sterile water (per manufacturer directions) is injected into the water seal chamber before the drainage system is connected to the patient. The main purpose of the water seal is to allow air to exit from the pleural space on exhalation and prevent air from entering the pleural cavity or mediastinum on inhalation. Air that is allowed to pass through the water seal will bubble out the bottom of the chamber. The water seal chamber is calibrated and should be seen as the window into the pleural space. During gravity drainage the level of water reflects the intrapleural pressure. Some newer systems eliminate the water seal chamber and use a check-valve to serve its purpose. Assure that the amount of sterile fluid in the water seal and suction chambers is at the manufacturer recommended levels when wet systems are used. To maintain an adequate water seal in a wet system it is important to monitor the level of water in the water seal chamber and to keep the chest drainage unit upright at all times. Assess for air leak by checking water seal chamber for bubbles during inspiration. The water seal chamber may bubble gently with insertion, during expiration and with a cough. Continuous bubbling represents an air leak. Some water seal compartments have an air leak meter.

Which of the following are true about the surgical MAZE procedure: A. It involves ablation of the AV node and permanent pacemaker insertion. B. It is surgical amputation of the left atrial appendage. C. It is done to correct severe mitral stenosis. D. It is done to prevent recurrent atrial fibrillation.

A. The MAZE procedure creates multiple incisions in the right and left atria in order to interrupt the reentry pathways responsible for maintenance of atrial fibrillation. It usually includes amputation of the left atrial appendage as well, since this is the site of most thrombus formation in atrial fibrillation. AV node ablation with permanent pacemaker insertion is an electrophysiology procedure that can be performed in patients with chronic atrial fibrillation who are unresponsive to or intolerant of drug therapy. AV node ablation prevents the atrial fibrillation from conducting into the ventricle but requires a ventricular pacemaker to maintain an adequate ventricular rate.

Which of the following are true about the surgical MAZE procedure: A. It is done to prevent recurrent atrial fibrillation. B. It involves ablation of the AV node and permanent pacemaker insertion. C. It is surgical amputation of the left atrial appendage. D. It is done to correct severe mitral stenosis.

A. The MAZE procedure creates multiple incisions in the right and left atria in order to interrupt the reentry pathways responsible for maintenance of atrial fibrillation. It usually includes amputation of the left atrial appendage as well, since this is the site of most thrombus formation in atrial fibrillation. AV node ablation with permanent pacemaker insertion is an electrophysiology procedure that can be performed in patients with chronic atrial fibrillation who are unresponsive to or intolerant of drug therapy. AV node ablation prevents the atrial fibrillation from conducting into the ventricle but requires a ventricular pacemaker to maintain an adequate ventricular rate.

A patient with epicardial atrial and ventricular pacing wires post cardiac surgery displays the rhythm seen in the lead II strip (top strip) on the bedside monitor. The nurse on the previous shift documented the rhythm as junctional rhythm because no P waves were seen in Lead II on the monitor. You decide to obtain an atrial electrogram and record the bottom strip (labeled AEG). .(P WAVES BEFORE EVERY QRS) You document the rhythm as: A. Normal sinus rhythm. B. Atrial flutter. C. Junctional rhythm. D. Accelerated ventricular rhythm.

A. The atrial electrogram in the bottom strip clearly shows atrial activity preceding each QRS complex.

The diagnosis of perioperative MI in a cardiac surgery patient can be made by which of the following: A. New Q waves or LBBB on the postoperative ECG or new wall motion abnormalities on echocardiogram. B. Widespread ST depression on the postoperative ECG. C. Any troponin I or CK-MB elevation postoperatively. D. ST elevation on the post operative ECG.

A. The diagnosis of perioperative MI is often difficult to make after cardiac surgery because biomarkers (Troponin I, CK-MB) are usually elevated secondary to the surgical procedure, and ST elevation (the ECG sign of myocardial injury) can occur secondary to low graft flow or postoperative pericarditis. The Society of Thoracic Surgeons recommends the following definition of perioperative MI: 1) CKMB or troponin elevations > five times the 99th percentile of the normal reference range during the first 72 h following CABG, plus 2) New pathological Q waves or new LBBB, or angiographically documented new graft or native coronary artery occlusion, or imaging evidence of new loss of viable myocardium. ST depression is associated with myocardial ischemia or with non-ST elevation MI.

A post CABG patient with a normal BP and normal CO/CI, high PWP, and high SVR needs which of the following interventions: A. Diuretic or venous dilator. B. Vasopressor. C. Inotrope. D. Volume.

A. The first illustration shows the four clinical and hemodynamic subsets based on cardiac index (CI) as the perfusion indicator and wedge pressure (PWP) as the congestion indicator. Normal hemodynamics (subset I) = CI > 2.2 and PWP < 18. Backwards failure (subset II) = CI > 2.2 and PWP > 18 indicating adequate perfusion but pulmonary congestion. Forwards failure (subset III) = CI < 2.2 and PWP < 18, indicating hypoperfusion but no congestion. The shock box (subset IV) = CI < 2.2 and PWP > 18, indicating both hypoperfusion and pulmonary congestion. This patient is in subset II with an adequate CI but high PWP, indicating pulmonary congestion and backwards failure. The second illustration shows suggested therapies based on the clinical subsets. This patient has a normal CO/CI and normal BP with high PWP, indicating the need for preload reduction with diuretics or venous dilators. The SVR may be elevated due to compensatory vasoconstriction, which helps to maintain the BP. Volume would be indicated if the PWP was low, indicating hypovolemia. An inotrope would be indicated if the CO/CI was low in spite of adequate preload (PWP) and afterload (SVR) - the shaded portion of subset III. A vasopressor would be indicated if BP and CO/CI was low in the presence of a low SVR indicating vasodilation.

Multiple choice question When caring for a patient with a chest tube it is important for the nurse to understand that all of the following are true regarding the water seal chamber EXCEPT: A. Constant bubbling in the water seal chamber represents effective functioning. B. The water seal allows air to exit the pleural space but prevents air from entering during inhalation. C. It is important for the drainage unit to remain upright in order to maintain an adequate water seal. D. Lack of fluctuation (tidaling) with respiration may indicate a problem in the chamber.

A. The water seal chamber may bubble gently with insertion, during expiration and with a cough. However, continuous bubbling represents an air leak. The water seal chamber must contain the recommended amount of water to reach the appropriate level and the drainage unit must remain upright at all times in order to assure an adequate water seal. Tidaling (fluctuation with respiration) is normal. A lack of tidaling can indicate a kink. Lack of tidaling may also represent a fully expanded lung. The water seal allows air to exit from the pleural space on exhalation and prevents air from entering the pleural cavity or mediastinum on inhalation.

You are caring for a post CABG patient who is hypotensive with a BP that has fallen over the past hour from 136/76 to 98/64. His rhythm is sinus tachycardia at 110 beats/min. He has the following hemodynamic values: CO = 3.5 L/min, CI = 1.8 L/min/M2, CVP = 3 mmHg, PAP = 20/8, PWP = 6 mmHg, SVR = 1645 dynes. Based on these values, which of the following are likely to be present in this patient: A. Decreased urine output, increased chest tube drainage, flat neck veins, cool pale skin. B. Fever, warm and red sternal wound with drainage, warm pink skin, bounding pulses. C. Decreased chest tube drainage, jugular vein distention, increased inspiratory pressure on the ventilator. D. Jugular vein distention, bilateral rales in lungs, S3 gallop, decreased urine output.

A. This patient's hemodynamics are consistent with inadequate preload: low CO/CI, CVP and PWP; high SVR due to compensatory vasoconstriction. Inadequate preload can occur as a result of blood loss, diuresis associated with hypothermia during CPB, third-spacing due to increased capillary permeability associated with CPB. Other signs of hypovolemia are likely to include decreased urine output, increased chest tube drainage indicating bleeding as a likely cause of hypovolemia, flat neck veins, and cool pale skin due to compensatory peripheral vasoconstriction. Postoperative bleeding is common and can be caused by a variety of mechanisms including leaking at graft or incision sites, residual heparin effect after cardiopulmonary bypass, clotting factor depletion and platelet dysfunction, hypothermia, postoperative hypertension placing strain on graft incisions, and hemodilution with dilutional thrombocytopenia and coagulopathy. Jugular vein distention, bilateral rales in the lungs, S3 gallop, and decreased urine output are more consistent with left ventricular dysfunction which can occur for a variety of reasons after cardiac surgery. Causes of postoperative LV dysfunction include perioperative MI (which can be due to coronary artery graft occlusion, vasospasm, air or debris embolus), hypoxemia, acidosis, arrhythmias, inadequate myocardial protection during cross-clamping of the aorta, and preexisting heart failure. Decreased chest tube drainage, jugular vein distention, and increased inspiratory pressure on the ventilator are more likely to be associated with cardiac tamponade. Tamponade occurs when blood or clots accumulate in the mediastinum and compresses the right heart, reducing both right and left ventricular filling and resulting in decreased cardiac output. Pressure on the right heart reflects backwards into the neck veins, causing JVD and an elevated CVP. In tamponade, the CVP, PWP, and PA diastolic pressures elevate and equalize. A sudden decrease in mediastinal chest tube drainage can occur if clots accumulate in the mediastinum and occlude the chest tube. Tamponade can also increase intrathoracic pressure which can trigger the inspiratory pressure alarm on the ventilator. Tamponade is a life-threatening emergency that must be immediately recognized and corrected. Fever, warm and red sternal wound with drainage, warm pink skin, and bounding pulses are likely to occur with sternal wound infection and sepsis. In sepsis, CO and CI are elevated in the early stages and SVR is low due to peripheral vasodilation. Wound infections usually occur later in the postoperative course, often after the patient has been discharged.

Which of the following post-op CABG patients is NOT ready to be weaned from mechanical ventilation despite adequate ABGs: A. Patient requiring 10 cm H2O PEEP and FIO2 of 50% to maintain adequate PO2. B. Patient receiving dexmedetomidine. C. Patient with cardiac index of 2.4 L/min/m2, HR 100, chest tube drainage 30 ml/hr. D. Patient on SIMV rate of 6 and FIO2 40%.

A. Weaning criteria generally include the following: patient is awake with stimulation; not receiving neuromuscular blockade, long-acting or high dose narcotics, or Propofol (dexmedetomidine is OK because it provides anxiolysis and sedation without depressing respirations); hemodynamically stable with CI > 2.2 L/min/m2, HR < 120, systolic BP stable at 100-140 mmHg with or without medication; chest tube drainage < 50 ml/hr; ABGs on mechanical ventilation: PaO2 > 75 mmHg on < 50% FIO2, pCO2 < 50 mmHg, PEEP < 7.5 cm H2O.

Your patient has had an aortic valve replacement for severe aortic stenosis. She has been in sinus rhythm at a rate of 70 with adequate hemodynamics but has now gone in to 3rd degree AV block with a junctional rhythm at a rate of 40 beats per minute and is hypotensive. Atrial and ventricular epicardial pacing wires are present. What type of pacing would be best in this patient: A. DDD. B. DVI. C. AAI. D. VVI.

A.A patient with aortic stenosis has a stiff noncompliant LV that depends on atrial kick for much of its preload to maintain an adequate stroke volume. DDD pacing means that the pacemaker paces atria and ventricles (first D), senses in atria and ventricles (second D), and inhibits or triggers pacing depending on whether atrial or ventricular activity was sensed (third D). The DDD pacing mode allows the pacemaker to sense the patient's own P waves and paces the ventricle in response to those P waves, thus maintaining AV synchrony and improving LV preload. The DDD pacing mode always maintains AV synchrony regardless of what the underlying rhythm is. This patient is in third degree block, so pacing the atrium alone (AAI) will do no good since there is no AV conduction present. VVI pacing would increase the ventricular rate but would not maintain AV synchrony. DVI pacing paces both the atria and the ventricles but only senses in the ventricle, therefore it would not sense her intrinsic P waves but would pace both atria and ventricles at the minimum rate set in the pacemaker. Since this patient has an adequate sinus rhythm, the DDD mode is better because it will allow for atrial sensing and pace the ventricle in response to her intrinsic P waves. Both DDD and DVI modes preserve AV synchrony.

Prosthetic heart valves are associated with all of the following complications EXCEPT: A. High incidence of renal failure. B. Hemolytic anemia. C. Bleeding. D. Systemic embolization. E. Endocarditis.

A.Prosthetic valves are not directly associated with an increased risk of renal failure, although renal failure can occur for several reasons following any type of cardiac surgery. Systemic embolization can occur with both mechanical and biological valves as a result of thrombosis, vegetations, or left atrial thrombus (especially in the presence of atrial fibrillation). The risk is twice as high with valves in the mitral position than those in the aortic position. Bleeding risk is higher with mechanical valves because of the need for chronic anticoagulation. Infective endocarditis occurs with equal frequency on mechanical and bioprosthetic valves during the first postoperative year, but bioprosthetic valves have a higher risk after18 months. Hemolytic anemia due to mechanical damage to RBCs can occur with mechanical valves.

Your patient is a 56-year-old male s/p CABG now 4 hours post-op with the following: CMV with FIO2 50% and PEEP at 5 cm H2O. Chest tube drainage was initially 150-200 cc, down to 25 cc the last hour. Lung sounds are clear, skin is cool and dry. BP 80/60; sinus tachycardia at 110 bpm CI: 2.1 CVP 20 mmHg PA 36/23 mmHg PAOP 22 mmHg The most likely cause of this scenario is: A. Cardiogenic pulmonary edema. B. Cardiac tamponade. C. Hypovolemic shock. D. Non-cardiogenic pulmonary edema.

B. An acute drop in chest tube drainage can signal chest tube occlusion that can result in fluid/blood build-up around the heart, compressing it and preventing adequate filling. Hemodynamic values show equalization of right and left atrial filling pressures and PA diastolic pressure. In hypovolemic shock the filling pressures (CVP and PAOP) would be low. In non cardiogenic pulmonary edema there would be pulmonary congestion with normal LV filling pressures. Cardiogenic pulmonary edema could result in elevated PAOP as seen here but lungs would sound congested and the CVP would not likely be equal to PAOP.

Intra-aortic balloon pump (IABP) counterpulsation would be indicated in all of these patients EXCEPT: A. Refractory myocardial ischemia prior to emergent cardiac surgery. B. Acute aortic regurgitation. C. Acute mitral regurgitation. D. Cardiogenic shock. E. Postcardiotomy low cardiac output unresponsive to inotropic drugs.

B. Aortic regurgitation is a contraindication to IABP insertion. Balloon inflation during diastole would push blood back into the LV through the incompetent aortic valve. Other contraindications include aortic dissection and severe aortic or peripheral vascular atherosclerotic disease. IABP therapy is used to support CO, reduce afterload, and increase coronary artery perfusion in severe LV failure (cardiogenic shock), postcardiotomy low cardiac output states, or refractory myocardial ischemia. It is also useful as a mechanical afterload reducer in acute mitral regurgitation or ventricular septal defect.

Your postoperative CABG patient has atrial fibrillation with a ventricular rate in the 40's. Atrial and ventricular epicardial pacing wires are in place. Which pacing mode is indicated to increase the heart rate in this patient: A. DDD. B. VVI. C. DVI. D. AAI.

B. Atrial fibrillation with a slow ventricular response requires VVI pacing to maintain an adequate ventricular rate. Atrial pacing and sensing are ineffective in atrial fibrillation, therefore any mode that utilizes atrial pacing or atrial sensing is not indicated. The AAI, DVI, and DDD modes all utilize atrial pacing or sensing and are not indicated for this patient.

A post CABG patient with hypotension, satisfactory CO/ CI, adequate PWP, and low SVR needs which of the following interventions: A. Inotrope. B. Vasopressor. C. Vasodilator. D. Volume.

B. BP is CO X SVR. If BP is low but CO is normal, then the cause of low BP must be low SVR due to peripheral vasodilation. A vasopressor will cause peripheral constriction and elevate the SVR and BP. Volume is indicated when the preload is low due to hypovolemia. Inotropes are indicated when CO/CI is low due to decreased contractility. Vasodilators are indicated when BP and SVR are high.

Patients with prolonged CPB times are likely to experience: A. An increased likelihood of early extubation. B. An increase in coagulopathies. C. A decrease in total body fluid due to dehydration. D. A decrease in chest tube drainage.

B. Coagulopathy is present to some degree with all CPB. During CPB, blood contacts the non-physiological surfaces of the bypass circuit and an inflammatory response is initiated. A coagulopathy can develop from activation of platelets and the fibrinolytic system. Clotting factors, platelets, and RBCs are diluted during CPB. A longer pump time is associated with increased coagulopathies. Postoperatively, patients have an increased amount of total body fluid due to priming of the CPB pump and administration of fluids during surgery. Extra volume is given to the patient during cardiopulmonary bypass to assure adequate circulating volume through the cardiopulmonary circuit. Long pump times are associated with increased bleeding and therefore increased chest tube drainage, and prolongs time to extubation.

Which of the following is an indication for emergency chest reopening in the ICU in a post cardiac surgery patient: A. Hypotension, CVP < 3 mmHg, PWP or PA diastolic < 15 mmHg. B. Cardiac tamponade with imminent cardiac arrest or exsanguinating hemorrhage. C. Chest tube drainage > 300 ml/hour. D. All of the above.

B. Exsanguinating hemorrhage and cardiac tamponade with imminent cardiac arrest are indications for emergency reopening of the chest in the ICU. Cardiac tamponade is fatal if pressure around the heart is not relieved. Reopening the sternal incision may be enough to relieve pressure around the heart and allows identification of bleeding sites that can be controlled with pressure or suturing. Internal defibrillation can be done using internal defibrillation paddles placed directly on the heart if VF is present, and internal cardiac massage can be done if necessary. Chest tube drainage > 300 ml/hour for 2-3 hours indicates excessive bleeding and warrants a return trip to the OR but not reopening in the ICU unless cardiac arrest occurs. Hypotension with a low CVP and PA diastolic or PWP indicates hypovolemia and can be treated with fluids and/or blood product administration but does not require reopening of the chest.

When caring for a patient after CABG the nurse knows that the following will increase the patient's risk for acute saphenous vein graft closure: A. Hypothermia. B. Hypotension or poor left ventricular function after surgery. C. Low platelets as a result of cardiopulmonary bypass. D. All of the above.

B. Flow through vein grafts depends on an adequate driving pressure through the graft, therefore patients with hypotension and decreased left ventricular function after surgery are at increased risk for acute saphenous vein graft closure. Coagulopathies may develop as a result of the cardiopulmonary bypass circuit in all patients. This increases the risk of bleeding in the postoperative period but does not directly contribute to the risk of acute graft closure. Hypothermia also increases the risk of bleeding but not directly to graft closure.

The initial intervention to treat postoperative hypotension is: A. Ventricular pacing at a rate of 90 beats per minute to provide adequate heart rate. B. Fluid administration to provide adequate preload. C. Dobutamine to increase cardiac contractility. D. Norepinephrine or vasopressin to cause peripheral vasoconstriction.

B. Fluids are the initial intervention in postoperative hypotension. Cardiac surgery patients require higher filling pressures (CVP or PWP) because of decreased ventricular compliance that can result from use of CPB and cardioplegia, intraoperative ischemia and reperfusion, diastolic failure, or hypertrophy from prolonged pressure overload (i.e. aortic stenosis, chronic hypertension). Fluids are usually administered until the PA diastolic or PWP are in the 18-20 mmHg range (sometimes up to 25 mmHg in hypertrophied hearts). Additional causes of hypotension include the inflammatory response caused by CPB and the resulting capillary leak which causes loss of intravascular volume. Excessive bleeding can also be a cause of postoperative hypotension and requires fluid administration in addition to treatment to stop bleeding. Dobutamine is used to increase contractility when cardiac output is low in spite of adequate filling pressures (preload) and normal SVR (afterload) and heart rate. Remember that cardiac output is determined by heart rate, preload, afterload, and contractility; so when CO is still low in the presence of normal preload, afterload and heart rate, then decreased contractility is the culprit and dobutamine (or other inotropic agents) can be beneficial. Norepinephrine and vasopressin are vasoconstrictors and are indicated for hypotension that is due to peripheral vasodilation (low SVR). Vasodilation can occur during rewarming or from use of vasodilator drugs like nitroglycerin, nitroprusside, or ACE inhibitors. Analgesic and anxiolytic drugs also cause vasodilation and can contribute to hypotension. Ventricular pacing can be used when bradycardia is the cause for hypotension, but atrial pacing (in the presence of normal AV conduction) or dual chamber pacing are better options to maintain AV synchrony and atrial kick.

Your patient is a 56-year-old male s/p CABG now 4 hours post-op with the following: CMV with FIO2 50% and PEEP at 5 CM H2O. Chest tube drainage was initially 150-200 cc, down to 25 cc the last hour. Lung sounds are clear, skin is cool and dry. BP 80/60; sinus tachycardia at 110 bpm CI: 2.1 CVP 22 mmHg PA 36/23 mmHg PAOP 22 mmHg Your best initial actions would be all of the following EXCEPT: A. Milk the chest tube. B. Furosemide. C. Notify the physician and prepare to return to the OR. D. Normal saline IV.

B. Furosemide would not be indicated because the problem is reduced ventricular filling due to tamponade and furosemide would further decrease volume and filling pressure. Normal saline might help increase right and left ventricular filling and improve cardiac output. Milking the chest tube could dislodge a clot that is occluding drainage and relieve the tamponade. Milking of chest tubes on a routine basis is not recommended because it can generate dangerously high negative pressures. However, in this situation where a sudden decrease in chest tube drainage is accompanied by signs of tamponade, milking the chest tube would be a reasonable action to try to dislodge an obstruction to drainage. If this doesn't work then notify the physician and prepare to return the patient to the OR to locate the bleeding.

Which of the following describes proper timing of IABP inflation and deflation: A. Balloon only inflates or deflates when HR is regular. B. Balloon inflates during diastole and deflates during systole. C. Balloon inflates during systole and deflates during diastole. D. Balloon inflation and deflation is regulated by patient systolic BP as measured at the tip of the IABP catheter.

B. Inflation of the balloon occurs at the beginning of diastole and is timed to occur at the dicrotic notch of the arterial waveform. Balloon inflation during diastole augments diastolic pressure in the aorta and displaces blood backwards into the root of the aorta where the coronary arteries arise, increasing coronary artery perfusion. Inflation also displaces blood forwards towards the renal arteries and peripheral arteries and improves forwards flow. Balloon deflation should occur at the end diastolic dip just prior to systole. The deflation point should be set to achieve two goals: balloon assisted diastolic pressure lower than patient diastolic pressure; and balloon assisted patient systolic pressure lower than patient systolic pressure. This illustration show proper inflation and deflation with appropriate hemodynamic effects.

The term OPCAB refers to: A. combination open heart surgery and percutaneous procedure. B. CABG surgery without the use of cardiopulmonary bypass (CPB). C. the use of thoracotomy instead of sternotomy. D. patients who are fast tracked to be discharged in less than 5 days.

B. OPCAB refers to off-pump coronary artery bypass. Surgery is done without CPB but it still involves a median sternotomy. MIDCAB (minimally invasive direct coronary artery bypass) is performed on a beating heart without CPB and without the use of a median sternotomy. MIDCAB is commonly done through an anterior thoracotomy incision and is used to bypass the mid to distal LAD with a left internal mammary artery (LIMA) graft. A ministernotomy can also be used to gain access during MIDCAB.

You are caring for a cardiac surgery patient who was transferred from the ICU to the progressive care unit earlier today after being extubated about 8 hours ago. The patient is uncooperative when asked to use the incentive spirometer and to cough and deep breathe due to pain. Which of the following would be appropriate approaches to this patient: A. Tell him that pain is expected after this type of surgery and that he can't let a little pain interfere with his care. B. Explain the benefits of coughing, deep breathing, using the spirometer, and ambulating in preventing pulmonary complications postoperatively, and work with him to develop a schedule of pain medication that will keep him comfortable. C. Tell him that if he doesn't deep breathe and cough he will get pneumonia and won't be able to go home. D. Medicate the patient for pain and tell him he needs his rest and to go to sleep.

B. Pain is a major reason patients don't want to participate in the activities that are meant to prevent pulmonary and other complications, like use of the incentive spirometer, coughing, deep breathing, and early ambulation. Pain management should be proactive so that pain can be avoided or minimized by routine medication rather than waiting until the pain is bad enough that the patient has to ask for medication. Involving the patient in his care by working together on a pain medication schedule and reinforcing the benefits of what he is being asked to do is more likely to result in cooperation and improved outcomes.

Your patient had an aortic valve replacement done and is now post op day 3. His epicardial pacing wires were removed an hour ago and he has been stable until now. He is tachycardic, hypotensive and complaining of SOB. His neck veins are elevated, lungs are clear, and his heart sounds are distant. You suspect which of the following: A. Acute aortic regurgitation due to failed valve. B. Cardiac tamponade. C. 3rd degree AV block. D. Acute myocardial infarction.

B. Removal of epicardial pacing wires can cause bleeding and result in cardiac tamponade. Tamponade can occur immediately or may not become manifest for several hours. Signs of tamponade include hypotension, JVD, chest pain, tachycardia, pulsus paradoxus, and distant heart sounds. If tamponade is suspected, a STAT echocardiogram should be done and if present, pericardiocentesis should be performed. 3rd degree AV block would present with bradycardia, not tachycardia, Acute aortic valve regurgitation would present with a diastolic murmur and acute pulmonary edema. Acute MI could present with chest pain, hypotension and tachycardia, and right ventricular MI could present with JVD and clear lungs. Distant heart sounds are not usually present during acute MI. It is much more likely that this is tamponade following pacing wire removal. A 12 lead ECG would be a good idea in this patient.

Post-operative wound infection is a serious complication resulting in increased post-operative mortality. Patient characteristics that place the patient at high risk for the development of post-operative wound infections include all of the following EXCEPT: A. Excessive use of electrocautery. B. Race. C. Obesity. D. Diabetes. E. End stage renal disease.

B. Risk factors for the development of infection include: obesity, diabetes, end stage renal disease, re-operation, excessive use of electrocautery, prolonged mechanical ventilation, and use of both internal mammary arteries (decreased blood flow to the sternum).

Which of the following patients is at highest risk for neurological complications after CABG? A. A 63-year- old patient with a BMI of 30 undergoing OPCAB B. A 85-year-old patient with an atherosclerotic aorta undergoing CPB C. A previously healthy 50-year-old woman undergoing CPB D. A 67-year-old man having a MIDCAB to the LAD with no known history of hypertension

B. Severe atherosclerosis of the aorta, advanced age, use of CPB, aortic cross-clamping, diabetes, hypertension, female sex, and history of stroke place patients at high risk for neurological complications following cardiac surgery. Other factors contributing to neurological complications include alcohol abuse, heart failure, arrhythmias, and hyperglycemia.

What is correct nursing knowledge regarding the chest tube drainage systems and suction: A. Wet suction units regulate the amount of suction by the suction from the wall unit and not by the height of a column of water in the suction chamber. B. Wet suction units regulate the amount of suction by the height of a column of water in the suction chamber not by the suction from the wall unit. C. Usually -80 cm H2O should be applied to a chest tube drainage system. D. Robust bubbling is needed in order to have an adequate amount of suction.

B. The 3rd compartment of a chest drainage system is connected to the first two sections and provides suction. There are two types of suction units: wet and dry. Wet suction units regulate the amount of suction by the height of a column of water in the suction chamber not by the suction from the wall unit. When a water column is used, only gentle bubbling should occur in the suction chamber. The source of suction should be adjusted to prevent loud bubbling of the water. Excessive external suction results in evacuation of water from the control chamber. The system valve controls the amount of suction and should normally be adjusted to achieve -20 cm H2O of suction. Lower levels of suction may be indicated for patients with friable lung tissue. The goal is to have an adequate amount of suction to keep open the pleural space, but not an excessive amount that will cause damage to the lung tissue. No more than -40 cm H2O should be applied to a chest tube drainage system. Many disposable chest tubes today have a dry suction regulator. This means there is no water in the suction chamber. A mechanical regulator within the unit is used to set the amount of suction applied to the system. The wall vacuum regulator is set at minus 80 cmH2O but the regulator on the unit is set to limit the suction to typically minus 20 cmH2O.

The diagnosis of perioperative MI in a cardiac surgery patient can be made by which of the following: A. Widespread ST depression on the postoperative ECG. B. New Q waves or LBBB on the postoperative ECG or new wall motion abnormalities on echocardiogram. C. Any troponin I or CK-MB elevation postoperatively. D. ST elevation on the post operative ECG.

B. The diagnosis of perioperative MI is often difficult to make after cardiac surgery because biomarkers (Troponin I, CK-MB) are usually elevated secondary to the surgical procedure, and ST elevation (the ECG sign of myocardial injury) can occur secondary to low graft flow or postoperative pericarditis. The Society of Thoracic Surgeons recommends the following definition of perioperative MI: 1) CKMB or troponin elevations > five times the 99th percentile of the normal reference range during the first 72 h following CABG, plus 2) New pathological Q waves or new LBBB, or angiographically documented new graft or native coronary artery occlusion, or imaging evidence of new loss of viable myocardium. ST depression is associated with myocardial ischemia or with non-ST elevation MI.

A post CABG patient with a high BP, low CO/CI, high PWP, and high SVR needs which of the following interventions: A. Vasopressor. B. Vasodilator. C. Inotrope. D. Volume.

B. The first illustration shows the four clinical and hemodynamic subsets based on cardiac index (CI) as the perfusion indicator and wedge pressure (PWP) as the congestion indicator. Normal hemodynamics (subset I) = CI > 2.2 and PWP < 18. Backwards failure (subset II) = CI > 2.2 and PWP > 18 indicating adequate perfusion but pulmonary congestion. Forwards failure (subset III) = CI < 2.2 and PWP < 18, indicating hypoperfusion but no congestion. The shock box (subset IV) = CI < 2.2 and PWP > 18, indicating both hypoperfusion and pulmonary congestion. This patient is in subset IV with a low CI, high PWP, and high SVR and BP. The second illustration shows suggested therapies based on the clinical subsets. This patient has a low CO/CI with high preload (PWP) and high afterload (SVR) with elevated BP indicating the need for afterload reduction with an arterial vasodilator. Afterload reduction allows the ventricle to eject more blood using less O2, and will result in a decrease in preload and BP. Volume is indicated when the preload is low due to hypovolemia. Inotropes are indicated when CO/CI is low due to decreased contractility (low CI in the presence of adequate preload and afterload - shaded portion of subset III). Vasopressors are indicated when hypotension does not respond to volume or when SVR is low due to peripheral vasodilation.

When caring for a patient with a chest tube it is important for the nurse to understand that all of the following are true regarding the water seal chamber EXCEPT: A. Lack of fluctuation (tidaling) with respiration may indicate a problem in the chamber. B. Constant bubbling in the water seal chamber represents effective functioning. C. The water seal allows air to exit the pleural space but prevents air from entering during inhalation. D. It is important for the drainage unit to remain upright in order to maintain an adequate water seal.

B. The water seal chamber may bubble gently with insertion, during expiration and with a cough. However, continuous bubbling represents an air leak. The water seal chamber must contain the recommended amount of water to reach the appropriate level and the drainage unit must remain upright at all times in order to assure an adequate water seal. Tidaling (fluctuation with respiration) is normal. A lack of tidaling can indicate a kink. Lack of tidaling may also represent a fully expanded lung. The water seal allows air to exit from the pleural space on exhalation and prevents air from entering the pleural cavity or mediastinum on inhalation.

Causes of hypotension due to vasodilation in the postoperative patient can include all of the following EXCEPT: A. Rewarming after hypothermia. B. Infusion of norepinephrine or epinephrine. C. Inflammatory response or sepsis. D. Infusion of nitroglycerin or nitroprusside.

B. Vasodilation can occur from an inflammatory response due to contact of blood with tubing in the CPB machine. Full blown sepsis is rare but would also result in peripheral vasodilation and hypotension. Nitroglycerin and nitroprusside both cause vasodilation and can result in hypotension. Nitroglycerine is primarily a venous dilator, while nitroprusside causes both arterial and venous dilation. Hypothermia causes peripheral vasoconstriction; rewarming causes vasodilation that can lead to hypotension.

Treatment of HIT involves discontinuing all heparin products (including heparin coated catheters) and using which of these drugs to manage intravascular clotting: A. Clopidogrel (Plavix) and ASA. B. LMWH: Enoxaparin (Lovenox) or dalteparin (Fragmin). C. Argatroban (Novastan), bivalirudin (Angiomax), or fondaparinux (Arixtra). D. Warfarin.

C. Argatroban and bivalirudin are direct thrombin inhibitors that bind directly to soluble and clot-bound thrombin and do not bind to platelet factor 4 as heparin does, therefore they do not cause HIT. Fondaparinux is an indirect factor Xa inhibitor that does not cause HIT. Newer oral factor Xa inhibitors (rivaroxaban and apixaban) and the oral thrombin inhibitor dabigatran should theoretically be effective as anticoagulants in patients with HIT, but at this time data is lacking on their use in treating patients with HIT. LMWH (low molecular weight heparin) can cause HIT but not as often as unfractionated heparin. However, all forms of heparin must be discontinued in the treatment of HIT. Warfarin is not indicated for managing intravascular clotting in HIT because its onset of action is delayed for 2-7 days until normal clotting factors are cleared from the circulation. Clopidogrel and ASA inhibit platelet activation but have no effect on thrombin so are not effective in managing intravascular clotting in HIT.

A complication seen in patients who have received a CABG using the LIMA or a radial artery graft that is not seen with saphenous vein grafts is: A. Graft aneurysm. B. Bleeding at graft suture lines. C. Graft spasm. D. Acute MI due to graft thrombosis.

C. Arterial conduits, such as the LIMA, RIMA, or radial artery are prone to spasm because of their thicker arterial walls. All grafts can thrombose or bleed at suture lines, and aneurysm formation is more common in veins harvested from the arms. IMA grafts have excellent long term patency and are preferred conduits in most patients.

Which of the following is the most common post operative cardiac arrhythmia following any kind of cardiac surgery: A. Sinus bradycardia. B. Second or third degree AV block. C. Atrial fibrillation. D. Ventricular tachycardia.

C. Atrial fibrillation (AF) occurs in up to 40% of patients after CABG, up to 50% after valve surgery, and up to 60% after CABG plus valve surgery. Most atrial fibrillation occurs on postoperative day 2 or 3, and is associated with increased morbidity and prolonged hospital stay. Risk factors for developing post operative atrial fibrillation include advanced age, previous history of AF, mitral valvular disease, increased left atrial size, cardiomegaly, long bypass and aortic cross-clamp times, previous cardiac surgery, COPD, obesity, and severe RCA stenosis. Nonsustained ventricular tachycardia is common after cardiac surgery but not as common as AF. VT is thought to be reperfusion-induced, but hypokalemia and hypomagnesemia can also contribute. Heart block is more common after valve surgery because both the aortic and mitral valves are close to the conduction system. Heart block can be related to direct surgical injury and edema of the conduction system.

Which of the following is the most common post operative cardiac arrhythmia following any kind of cardiac surgery: A. Ventricular tachycardia. B. Second or third degree AV block. C. Atrial fibrillation. D. Sinus bradycardia.

C. Atrial fibrillation (AF) occurs in up to 40% of patients after CABG, up to 50% after valve surgery, and up to 60% after CABG plus valve surgery. Most atrial fibrillation occurs on postoperative day 2 or 3, and is associated with increased morbidity and prolonged hospital stay. Risk factors for developing post operative atrial fibrillation include advanced age, previous history of AF, mitral valvular disease, increased left atrial size, cardiomegaly, long bypass and aortic cross-clamp times, previous cardiac surgery, COPD, obesity, and severe RCA stenosis. Nonsustained ventricular tachycardia is common after cardiac surgery but not as common as AF. VT is thought to be reperfusion-induced, but hypokalemia and hypomagnesemia can also contribute. Heart block is more common after valve surgery because both the aortic and mitral valves are close to the conduction system. Heart block can be related to direct surgical injury and edema of the conduction system.

Your CABG patient POD 2 develops atrial fibrillation with a heart rate of 120 beats per minute. You recognized that to avoid the need for long term anticoagulation which of the following medications may be used for rhythm control in this patient: A. Digoxin. B. Metoprolol. C. Amiodarone. D. Diltiazem.

C. Beta blockers, calcium channel blockers, and digoxin can be used for ventricular rate control in atria fibrillation. Amiodarone also affects heart rate but additionally can be used for pharmacological conversion of atrial fibrillation to sinus rhythm (rhythm control). Amiodarone is often given initially to convert to sinus rhythm and continued post operatively for a period of time to maintain sinus rhythm throughout the recovery period..

The first line strategy to maintain an adequate cardiac index in the immediate postoperative period includes: A. Administering a vasodilator. B. Administering a vasopressor. C. Optimizing pre-load with volume administration. D. Administering an inotrope.

C. Cardiac index (CI) is dependent on HR, preload, afterload and contractility. Preload must be adequate before an inotrope or a vasopressor will work. 'You have to fill the tank before you step on the gas.' Volume administration is usually the first therapy when CI is low unless preload indicators (CVP, PWP) are very high, or stroke volume variation (SVV) or pulse pressure variation (PPV) are low. An inotrope would be indicated if the CI is low in the presence of adequate preload (normal CVP, PWP) and normal afterload (SVR not low or excessively elevated). A vasodilator would be indicated if the CI is low in the presence excessively high afterload (increased SVR) and hypertension. When vasodilators are used, volume administration is often needed to fill the larger vascular space that results from vasodilation. A vasopressor would be indicated if the CI is low in the presence of adequate preload and significant vasodilation (low SVR).

All of the following are true regarding the cardiopulmonary bypass machine (heart / lung machine) EXCEPT for: A. Cardiopulmonary bypass provides perfusion to the other organs of the body during surgery. B. Cardiopulmonary bypass allows for surgery to be performed on a still and bloodless heart. C. Blood is drained from the aorta and reentered into the right atrium allowing for a high pressure flow through the circuit. D. The circuit contains an arterial line filter to remove microemboli before returning blood to the patient.

C. Cardiopulmonary bypass allows for surgery to be performed on a still and bloodless heart while at the same time providing perfusion to other organs of the body. Blood is drained (usually by gravity) from the right atrium into a venous reservoir. From there blood is oxygenated, cooled or warmed, and returned to the patient through an arterial cannula usually placed in the ascending aorta. The circuit contains an arterial line filter to remove microemboli before returning blood to the patient. Microemboli can consist of air, blood, fat, and platelet microaggregates.

Proper chest tube care in a cardiac surgery patient includes which of the following: A. Irrigate chest tubes with antibiotic solution to prevent infection. B. Increase suction if chest tube drainage falls below 100 cc/hr C. Attach chest tubes to a drainage system with -20 cm of H2O suction. D. Strip chest tubes hourly to prevent clotting in tubes.

C. Chest tubes are attached to a drainage system with -20 cm H2O suction. Patency can be maintained with gentle milking or tapping of chest tubes. Stripping creates high negative pressure and can cause lung damage and increase bleeding. Chest tube output should be recorded hourly until it is < 30 ml/hour and is expected to be < 100 ml/hour. If drainage is persistently >100 ml/hr, the patient should be evaluated for a surgical source of bleeding and a stat PT, PTT, and platelets should be drawn to assess for a medical cause of bleeding. Irrigation of chest tubes is not recommended because of the risk of infection.

Preoperative clopidogrel should be held for how many days in the elective surgery patient: A.It does not need to be held. B. 1-2 days. C. 5-7 days. D. 30 days.

C. Clopidogrel inhibits the P2Y12 receptor on the platelet for the lifetime of the platelet (10 days). Inhibited platelets cannot participate in clotting, so the risk of bleeding increases with antiplatelet drugs. Most clinical trials have identified an increased risk in bleeding, transfusion, and re-exploration when clopidogrel is taken within 5 days of surgery, and no increase in bleeding or transfusions when clopidogrel is stopped for > 5 days prior to surgery. Therefore, clopidogrel should be stopped for 5 to 7 days prior to elective surgery. Emergent surgery can be done regardless of when the last dose of clopidogrel was taken, but will be associated with increased bleeding and need for platelet transfusions.

Your post-op CABG/ AVR patient develops 2nd degree type II AV block with an associated drop in systolic blood pressure. The patient has atrial and ventricular epicardial pacing wires. The best pacing mode in this situation would be: A. AAI. B. DVI. C. DDD. D. VVI.

C. DDD pacing mode is the best option because it maintains AV synchrony. This mode allows for tracking of atrial activity when it is present and paces the ventricle after every sensed P wave. It also paces the atrium when the sinus rate is too low. AAI is an atrial pacing mode and requires intact AV conduction. This patient is experiencing an AV conduction disturbance, so pacing the atrium will do no good. While a VVI mode would provide an adequate ventricular rate, this is not the best option since you have both atrial and ventricular wires. If you have the ability to provide AV synchrony, as you do with DDD pacing, then you should do this when there is an AV conduction abnormality. DVI mode only senses in the ventricle, therefore it would not sense atrial activity and maintain AV synchrony in the presence of AV block.

An early sign of HIT (heparin induced thrombocytopenia) is: A. Stroke, MI, or DVT. B. Massive organ failure. C. Drop in platelet count by about 50%. D. Excessive bleeding from gums, puncture sites, GI system.

C. Drop in platelet count by about 50%. Platelet count usually falls by 50% or more from baseline, usually within 4-10 days after heparin is started. Excessive bleeding can occur with any anticoagulant therapy but is not associated with HIT. HIT results in arterial and venous thrombosis that can cause DVT, pulmonary embolism, limb gangrene, stroke, MI and other organ failure - but these events occur after the initial drop in platelet count.

When caring for a patient immediately post CABG the nurse recognizes that the most likely cause of hypotension in the immediate post-operative period is A. Decreased circulating volume requiring no intervention unless persistent > 12 hours. B. LV failure requiring an inotrope as first line treatment for any hypotension. C. Decreased circulating volume representing the need for increased fluid administration. D. LV failure requiring an assist device.

C. Hypotension in the immediate postoperative period is usually caused by low circulating volume and responds to treatment with fluids. Volume is the first line treatment for hypotension. If there is no immediate response to volume administration, 500 mg of IV calcium chloride is often given. Existing vasopressors, such as norepinephrine, can also be adjusted. It is important for hypotension to be promptly treated. Persistent hypotension can result in hypoperfusion and end organ damage. LV failure is not the most common cause of hypotension in the immediate post-operative period and therefore inotropic agents are not first line agents used in the treatment of hypotension. Hypotension that does not respond to fluid administration may require an inotrope.

You are admitting a cardiac surgery patient from the OR to the ICU. As the patient is being placed on the ventilator, ECG leads are attached to the bedside monitor, chest tubes are connected to suction, and the arterial line transducer is attached to the bedside monitor, you note that the arterial line BP displayed on the monitor is 80/56. You know that in order for the arterial line pressure to be accurate, which of the following must be verified: A. The system was correctly zeroed in the OR. B. The pressure bag around the fluid source is pumped up to 150 mmHg. C. The arterial catheter is not kinked and there is no air in the tubing. D. The transducer is placed at the tip of the arterial catheter. E. All of the above.

C. In order for an arterial line to correctly monitor the patient's BP, all of the following must be verified: -The arterial catheter and monitoring tubing is not kinked -There is no air or blood in the monitoring tubing -The transducer is level with the patient's phlebostatic axis (4th intercostal space, mid anterior-posterior chest) -The transducer is re-zeroed whenever the cables are disconnected for any reason, including transport from the OR to the ICU monitoring system. - The pressure bag around the fluid source needs to be pumped up to 300 mmHg in order to overcome the resistance in the transducer and keep the line open

A characteristic of a fast-track pathway after CABG would include: A. anticipated discharge between post-op days 7 and 8. B. a defined medication strategy to prevent postoperative atrial fibrillation. C. liberal use of opioid medications to increase patient comfort during the ventilator weaning process. D. extubation by the third post-op day

C. Low-risk patients can be selected for fast tracking after CABG. These patients are targeted for early extubation, early ambulation, and early discharge. Patients who are fast tracked receive sedation and analgesia to allow for early extubation. Pharmacological strategies to prevent atrial fibrillation and early phase I cardiac rehabilitation are also key components of fast tracking.

The risk of sternal wound infection is increased by which of the following: A. Early extubation and pneumonia. B. Diabetes and obesity. C. Prolonged CPB and renal dysfunction. D. Hypoglycemia and advanced age.

C. Major risk factors for sternal wound infection include diabetes and obesity. Diabetes is a risk factor because hyperglycemia impairs the immune system. Patients with diabetes have impaired chemotaxis (the process that draws white blood cells to the site of an infection) and phagocytosis (the process of ingestion of bacteria by white blood cells). Obesity results in increased force applied to the incision which affects the collagen fibers and inhibits healing. Patient factors that increase risk include: Diabetes mellitus, obesity, COPD, advanced age, and protein calorie malnutrition. Surgical factors that increase risk include: prolonged cardiopulmonary bypass time, prolonged intubation time, reoperation or surgical re-exploration. and use of both internal mammary arteries.

Your postoperative AVR patient is confused, disoriented, sleeps during the day and is awake all night, lethargic at times and combative at other times. This is a typical manifestation of: A. Acute kidney injury. B. Acute ischemic stroke. C. Postoperative delirium. D. Low cardiac output syndrome.

C. Manifestations of delirium include disorientation, confusion, attention deficits, agitation, lethargy, disturbed sleep-wake cycles, memory loss, paranoia, and hallucinations. These symptoms can alternate with times of apparent lucidity Low cardiac output states can contribute to delirium but present with hemodynamic abnormalities, hypotension, and hypoperfusion. Acute ischemic stroke often presents with focal deficits such as unilateral paralysis or aphasia, although it can include some of the same symptoms as delirium. Acute kidney injury presents with electrolyte and metabolic abnormalities, oliguria, and often hemodynamic abnormalities which can be a cause of AKI.

Your patient has received a mechanical valve to replace his severely stenotic aortic valve. You know the following to be true: A. Infective endocarditis only occurs with biological valves. B. Mechanical valves do not require anticoagulation but biological valves do. C. Mechanical valves are more durable but require lifelong anticoagulation, while biological valves do not. D. Biological valves have a lower rate of structural failure than mechanical valves.

C. Mechanical valves are manufactured from manmade materials and usually have a tilting disk or bileaflet design. Biological valves are made from living tissue and include porcine or bovine tissue, or are transplanted from other humans (homografts) or from the same patient (autografts). Mechanical valves have a very low rate of structural failure but require life-long anticoagulation therapy, usually with warfarin. Bioprosthetic valves usually do not require long term anticoagulation unless there are other risk factors (like atrial fibrillation), but have a higher rate of structural failure requiring a second valve replacement within 10-15 years. Infective endocarditis occurs with equal frequency on mechanical and bioprosthetic valves during the first postoperative year, but bioprosthetic valves have a higher risk after 18 months.

Which of the following is true concerning the use of aspirin following CABG surgery: A. ASA is contraindicated because of the increased risk of bleeding from new grafts. B. ASA is indicated for all CABG patients as an analgesic for postoperative pain control. C. ASA is indicated for all CABG patients because of its antiplatelet effects and for secondary prevention of coronary disease. D. ASA is indicated for patients receiving arterial grafts but not venous grafts.

C. The use of ASA in the early postoperative period is used to offset platelet activation and aggregation in the early postop period. ASA may result in improved graft patency; decrease the incidence of perioperative MI, stroke, and acute kidney injury; and reduce mortality. It is recommended that ASA be started within 6 hours postoperatively (after mediastinal bleeding has stopped) and continued indefinitely for secondary prevention in all CABG patients who do not have a contraindication to ASA.

The following measures can be used to manage hypothermia and its effects in the postoperative period: A. Administration of sedation and pain medications to keep the patient asleep until they warm up. B. Use of vasoconstrictor and inotropic medications to keep the BP and cardiac output high enough to pump warm blood to the periphery. C. Use of forced air warming systems (e.g. Bair Hugger) to increase the rate of rewarming and meperidine or dexmedetomidine to control shivering. D. All of the above.

C. Methods to facilitate rewarming include use of forced air warming systems (e.g. Bair Hugger), warm blankets, warmed IV fluids, and heated humidifiers in the ventilator circuit. Vasodilator drugs can help redistribute core heat to the periphery but may also lower the BP and may not be tolerated. Shivering is an adverse effect of hypothermia that increases tissue and myocardial O2 demand. It can be controlled with meperidine or dexmedetomidine. Administering sedation and pain medication is important to facilitate emergence from anesthesia and for comfort once the patient is awake, and to facilitate use of incentive spirometer and ambulation. Sedation and pain medication is not used to keep patients asleep until they warm up. The sooner patients awaken the earlier they can be extubated, and early extubation leads to improved outcomes after cardiac surgery. Vasoconstrictor and inotropic drugs are indicated for BP support and support of cardiac contractility in patients with hypotension or reduced LV function, but they also increase myocardial O2 demands and are not used as rewarming drugs. Vasoconstriction is already present in the hypothermic patient and prolongs rewarming by preventing warm blood from reaching peripheral tissues.

Inotropic support is often needed for the first few hours following CABG surgery when there is left ventricular dysfunction present. Which of the following drugs are appropriate for inotropic support: A. Nitroglycerine or nitroprusside. B. Norepinephrine or vasopressin. C. Milrinone, dobutamine, dopamine, or epinephrine. D. Esmolol, metoprolol, or nicardipine.

C. Milrinone, dobutamine, dopamine, and epinephrine all increase contractility. Milrinone is also a vasodilator so would be indicated when inotropic support is needed in the presence of a high SVR. Dobutamine, dopamine, and epinephrine all have beta adrenergic effects to increase contractility. Epinephrine is often the preferred inotropic agent because it causes less tachycardia than dopamine or dobutamine and also has some peripheral vasoconstrictor effects that can help support the blood pressure. Nitroglycerin and nitroprusside are both vasodilators with no inotropic effect. Nitroglycerin is primarily a venous dilator and is used for preload reduction. Nitroprusside has both venous and arterial vasodilating effects with somewhat more arterial effect and is used to manage postoperative hypertension. Esmolol and metoprolol are beta blockers and nicardipine is a calcium channel blocker. Beta blockers and calcium channel blockers are negative inotropic drugs and decrease contractility. Nicardipine is also a peripheral vasodilator and can be used to treat postoperative hypertension.

Management of postoperative hypertension includes which of the following: A. Calcium channel blockers and inotropes. B. Dobutamine and beta blockers. C. Adequate sedation and pain management, and vasodilators. D. All of the above.

C. Pain and anxiety contribute to hypertension by causing increased sympathetic nervous system activity. Adequate pain control and sedation with drugs such as propofol, midazolam, morphine, or dexmedetomidine can be used to treat early postoperative hypertension, especially in the ventilated patient. However, antihypertensive agents are preferred over sedatives to facilitate early extubation. There are several drugs that can be used as antihypertensive agents: Nitroprusside is primarily an arterial dilator that causes relaxation of arterial smooth muscle to reduce SVR, but it also dilates veins and reduces preload. Calcium channel blockers, especially nicardipine and clevidipine, cause arterial vasodilation and decrease SVR. They also dilate coronary arteries and slow the heart rate which can be beneficial in improving myocardial perfusion and controlling hypertension. Beta blockers decrease blood pressure by decreasing myocardial contractility and heart rate, as well as decreasing renin activity. They are used to treat hypertension in patients whose cardiac output is adequate, especially if tachycardia and hyperdynamic contractility are present. Dobutamine is a positive inotropic agent and is not indicated in treatment of hypertension. Increased contractility that results from positive inotropes can increase BP, not decrease it.

Which of the following is true concerning the use of aspirin following CABG surgery: A. ASA is contraindicated because of the increased risk of bleeding from new grafts. B. ASA is indicated for all CABG patients because of its antiplatelet effects and for secondary prevention of coronary disease. C. ASA is indicated for patients receiving arterial grafts but not venous grafts. D. ASA is indicated for all CABG patients as an analgesic for postoperative pain control.

C. The use of ASA in the early postoperative period is used to offset platelet activation and aggregation in the early postop period. ASA may result in improved graft patency; decrease the incidence of perioperative MI, stroke, and acute kidney injury; and reduce mortality. It is recommended that ASA be started within 6 hours postoperatively (after mediastinal bleeding has stopped) and continued indefinitely for secondary prevention in all CABG patients who do not have a contraindication to ASA.

You are evaluating a patient on the progressive care unit who is 2 weeks post triple CABG surgery. She is admitted for chest pain, fever, and fatigue. She has been having chest pain for several days and describes it as similar to the angina she had prior to surgery but it sometimes feels better with changes in position. Her ECG shows diffuse ST segment elevation in many leads. Her vital signs are stable but she has a fever of 101 degrees (38 centigrade). Her heart sounds are distant, she has bibasilar rales in her lungs, neck veins are visible but not especially elevated. You suspect the following diagnosis: A. Pneumonia. B. Acute MI due to graft closure. C. Postpericardiotomy syndrome. D. Heart failure.

C. Postpericardiotomy syndrome is pericarditis with or without a pericardial effusion resulting from injury to the pericardium during surgery. Acute pericarditis can occur immediately following surgery. When the pericarditis is delayed for several weeks to months after surgery it is termed postpericardiotomy syndrome. Chest pain is the most common symptom and can mimic the pain of angina or MI. Because of the inflammation that occurs, fever, leukocytosis, and an elevated erythrocyte sedimentation rate are usually seen. The ECG typically shows widespread ST elevation and often depression of the PR segment. A pericardial friction rub may be heard, although if pericardial effusion is present the rub is usually not heard. Pericardial effusion is common and can vary in size, usually reaching its maximum size at about 10 days. Small effusions usually resolve spontaneously, but an echocardiogram should be done to assess effusion size and rule out tamponade. Acute MI would present with ST elevation is specific leads facing the infarcted area, not diffuse ST elevation as seen in this patient. The pain of infarction is not relieved by changes in position, while the pain of pericarditis is often relieved by leaning forward. Pneumonia would not cause this type of chest pain or the ST elevations on the ECG. Cardiac tamponade can be a complication of postpericardiotomy syndrome but would cause elevated neck veins, hypotension, and hemodynamic instability not seen in this patient. Heart failure could cause rales in the lungs as seen here but would not necessarily cause the fever or the ECG changes present in this patient.

All of the following statements are true about use of antibiotics in cardiac surgery patients EXCEPT: A. Vancomycin is indicated for proven or suspected MRSA. B. Post-operative antibiotics are continued for 7 to 10 days after surgery. C. Preoperative IV prophylactic antibiotics should not be given until the patient is in the operating suite so the administration can be timed to be 30 to 60 minutes prior to the initial incision. D. A cephalosporin (typically cefazolin or cefuroxime) is the antibiotic of choice in patients without MRSA.

C. Preoperative intravenous prophylactic antibiotics are not given until the patient is in the operating suite so the administration can be timed to be 30 to 60 minutes prior to the initial incision. National quality standards require administration within one hour of incision time to insure adequate tissue levels at the time of incision. Postoperative antibiotics are given for 48 hours or less. A cephalosporin (typically cefazolin or cefuroxime) is the antibiotic of choice in patients without MRSA, and vancomycin, alone or in combination with other antibiotics, is recommended in patients with MRSA.

Prosthetic heart valves are associated with all of the following complications EXCEPT: A. Endocarditis. B. Systemic embolization. C. High incidence of renal failure. D. Hemolytic anemia. E. Bleeding.

C. Prosthetic valves are not directly associated with an increased risk of renal failure, although renal failure can occur for several reasons following any type of cardiac surgery. Systemic embolization can occur with both mechanical and biological valves as a result of thrombosis, vegetations, or left atrial thrombus (especially in the presence of atrial fibrillation). The risk is twice as high with valves in the mitral position than those in the aortic position. Bleeding risk is higher with mechanical valves because of the need for chronic anticoagulation. Infective endocarditis occurs with equal frequency on mechanical and bioprosthetic valves during the first postoperative year, but bioprosthetic valves have a higher risk after18 months. Hemolytic anemia due to mechanical damage to RBCs can occur with mechanical valves.

A patient with epicardial atrial and ventricular pacing wires post cardiac surgery has a change in his rhythm on the bedside monitor. Which of the following connections would allow you to obtain an atrial electrogram to help diagnose the rhythm: A. Connect an atrial pacing wire to the chest lead on your monitor cable and record lead II on the bedside monitor. B. Connect an atrial pacing wire to the right leg electrode and record "V" on the bedside monitor. C. Connect an atrial pacing wire to the chest lead on your monitor cable and record "V" on the bedside monitor. D. Connect a ventricular pacing wire to the chest lead and record "V" on the bedside monitor.

C. Recording an atrial electrogram directly from an atrial pacing wire allows easy identification of atrial activity (P waves or flutter/fib waves) and helps illustrate the relationship between P waves and QRS complexes when it is difficult to see on a surface lead. The easiest way to do this is to attach a monitoring electrode to the chest lead on a 5-wire monitor cable and wrap it tightly around the metal end of an atrial pacing wire, making sure that the metal end of the pacing wire is in the gel center of the electrode and touching the metal portion of the button under the gel. Then set the monitor to record "V", which records from the chest lead that is now attached to the atrial pacing wire. This connection will provide a unipolar recording (using one atrial wire) with very large atrial deflections. The connection between the atrial pacing wire and the monitor lead can also be made using an alligator clip, but this method using a regular monitoring electrode doesn't require any special equipment. It is a good idea to simultaneously record a surface lead along with the atrial electrogram and to run the paper at double speed through the recorder to spread the tracing out for better visualization. Lead II on the monitor is recorded between the right arm and the left leg electrodes, not the chest lead. Connecting a ventricular pacing lead will only accentuate the QRS, not the P waves. The right leg electrode is a ground electrode and does not participate in the direct recording of any lead. This illustration shows the connection of the chest lead on the monitor to an atrial pacing wire using a regular monitoring electrode.

Post-operative wound infection is a serious complication resulting in increased post-operative mortality. Patient characteristics that place the patient at high risk for the development of post-operative wound infections include all of the following EXCEPT: A. Diabetes. B. Obesity. C. Race. D. Excessive use of electrocautery. E. End stage renal disease.

C. Risk factors for the development of infection include: obesity, diabetes, end stage renal disease, re-operation, excessive use of electrocautery, prolonged mechanical ventilation, and use of both internal mammary arteries (decreased blood flow to the sternum).

Discharge medications for a patient following CABG who is in sinus rhythm usually include all of the following EXCEPT: A. ASA and clopidogrel. B. Beta blocker. C. Warfarin and antibiotics. D. Statin and ACEI.

C. Warfarin would be indicated in a patient with atrial fibrillation or a prosthetic valve but not for a CABG. Antibiotics are indicated for prophylaxis in patients who have prosthetic valves or grafts prior to dental work but are not routinely indicated beyond 48 hours in post surgical patients. ASA is indicated in all CABG patients for prevention of secondary coronary events and to improve graft patency. Clopidogrel is given in addition to ASA to patients who had CABG due to NSTEMI or had a recent stent. Statins are indicated for all patient with CAD to lower LDL cholesterol and for secondary prevention. They may also stabilize plaque and even promote plaque regression, and can slow the progression of saphenous vein graft disease. ACEI are indicated in patients with CAD, especially those with LV dysfunction or hypertension, and may have long-term mortality benefits. Beta blockers are indicated in all patients with CAD because of proven survival benefit in MI as well as CABG patients with or without MI.

You are caring for a patient who had an aortic valve replacement due to severe aortic stenosis causing left ventricular hypertrophy. His postoperative hemodynamic profile is: CO = 4.6 L/min, CI = 2.4 L/min/M2, CVP = 6 mmHg, PWP = 22 mmHg. His postoperative ejection fraction (EF) was 58%. You interpret this hemodynamic profile as indicating: A. Left ventricular systolic heart failure. B. Right heart failure. C. Left ventricular diastolic dysfunction. D. Normal hemodynamic values.

C. Severe aortic stenosis (AS) can cause left ventricular hypertrophy (LVH) and remodeling that is characterized by an increased LV wall thickness and normal or reduced LV cavity size. LVH can cause diastolic dysfunction in which the LV is stiff and non-distensible, resulting in a higher pressure for any given LV volume. A normal PWP is 8-12 mmHg when LV volume is normal, but in severe AS the same normal volume causes an increase in PWP because of the thick, stiff LV. Even though the aortic valve has been replaced, the underlying LV diastolic dysfunction remains, resulting in higher PWP than would be seen with a normal LV. Patients with LVH due to aortic stenosis or hypertrophic cardiomyopathy often require pulmonary artery wedge pressures higher than normal (e.g.18 to 22 mmHg) to maintain an adequate preload to support the cardiac output. Left ventricular systolic function, measured by ejection fraction, is usually normal in diastolic failure. A normal EF is around 60 - 75%, and a reduced EF is < 40%. This patient's EF of 58% indicates normal or near-normal systolic function. Right heart failure would present with elevated CVP. A CVP of 6 mmHg is normal. Left ventricular systolic heart failure would also cause an elevated PWP, but the cardiac output and cardiac index would be significantly reduced and the EF would be < 40%.

You are using a chest tube drainage system that requires fluid in the water seal chamber. What is an important nursing consideration: A. Report any tidaling of this chamber immediately. B. Invert the water seal system at least once every 4 hours. C. Assure that the amount of sterile fluid in the water seal and suction chambers is at the manufacturer recommended level. D. Assure that there is continuous bubbling in the water seal chamber.

C. The 2nd compartment is connected to the 1st and creates a water seal. A small amount of sterile water (per manufacturer directions) is injected into the water seal chamber before the drainage system is connected to the patient. The main purpose of the water seal is to allow air to exit from the pleural space on exhalation and prevent air from entering the pleural cavity or mediastinum on inhalation. Air that is allowed to pass through the water seal will bubble out the bottom of the chamber. The water seal chamber is calibrated and should be seen as the window into the pleural space. During gravity drainage the level of water reflects the intrapleural pressure. Some newer systems eliminate the water seal chamber and use a check-valve to serve its purpose. Assure that the amount of sterile fluid in the water seal and suction chambers is at the manufacturer recommended levels when wet systems are used. To maintain an adequate water seal in a wet system it is important to monitor the level of water in the water seal chamber and to keep the chest drainage unit upright at all times. Assess for air leak by checking water seal chamber for bubbles during inspiration. The water seal chamber may bubble gently with insertion, during expiration and with a cough. Continuous bubbling represents an air leak. Some water seal compartments have an air leak meter.

The AAI pacing mode would most likely be used in a postoperative cardiac surgery patient with which of the following situations resulting in hemodynamic compromise: A. 2nd degree type II heart block. B. Ventricular tachycardia. C. Sinus bradycardia. D. Complete heart block.

C. The AAI pacing mode is only utilized when there is intact AV conduction. In sinus bradycardia, the problem is the slow sinus rate - not AV block, so pacing the atrium would fix the problem. AAI mode is used most frequently in the post-operative cardiac patient to increase heart rate to enhance cardiac output when the risk of AV block is small. Whenever AV block is present, either DDD or VVI pacing can be used to assure an adequate ventricular rate - the advantage of DDD mode would be maintenance of AV synchrony. Antitachycardia pacing as part of an ICD could terminate VT, but Acai pacing would have no effect on VT.

A patient with epicardial atrial and ventricular pacing wires post cardiac surgery displays the rhythm seen in the lead II strip (top strip) on the bedside monitor. The nurse on the previous shift documented the rhythm as junctional rhythm because no P waves were seen in Lead II on the monitor. You decide to obtain an atrial electrogram and record the bottom strip (labeled AEG). You document the rhythm as: )P WAVES BEFORE QRS) A. Atrial flutter. B. Junctional rhythm. C. Normal sinus rhythm. D. Accelerated ventricular rhythm.

C. The atrial electrogram in the bottom strip clearly shows atrial activity preceding each QRS complex.

You are caring for a patient with an IABP. Which of the following are desired effects of IABP therapy: A. Increased HR, increased systolic aortic pressure, decreased LV wall tension. B. Increased diastolic aortic pressure, increased coronary artery perfusion, increased LV wall tension. C. Decreased HR, decreased afterload, increased coronary artery perfusion. D. Decreased HR, increased systolic aortic pressure, increased preload.

C. The goal of IABP therapy is to decrease the work load on the heart and improve coronary artery perfusion. Balloon inflation during diastole displaces blood backwards into the root of the aorta where the coronary arteries arise, increasing coronary artery perfusion. Inflation also displaces blood forwards towards the renal arteries and peripheral arteries and improves forwards flow. Balloon deflation during systole reduces afterload by decreasing systolic pressure in the aorta, which decreases myocardial work and myocardial O2 consumption. Heart rate decreases because balloon inflation stimulates the baroreceptors in the aortic arch, causing a reflex decrease in HR. Other hemodynamic effects of the IABP include increased diastolic aortic pressure, decreased systolic aortic pressure, decreased preload, and decreased LV wall tension.

When caring for a patient after CABG which of the following is NOT true regarding interventions to support stable hemodynamic status: A. A vasodilator such as nitroprusside can help improve cardiac output when SVR is elevated. B. Patients will have extra fluid needs during the period of time when they are rewarming after surgery. C. A vasopressor such as phenylephrine will optimize cardiac output in a patient with a cardiac index of 1.7. D. Epicardial pacing wires can be used to increase HR and improve cardiac output.

C. When cardiac index is low, a patient is likely to need either volume or inotropic support. The vasopressor phenylephrine does not have positive inotropic effects. Phenylephrine is a primary alpha-1 stimulator and causes vasoconstriction of peripheral blood vessels. Some vasopressors such a epinephrine, dopamine, and norepinephrine exhibit varying degrees of beta-1 stimulation (inotropic effect) in addition to alpha-1 stimulation. Optimizing preload and heart rate are first line strategies for maintaining an adequate cardiac output after CABG. Epicardial pacing wires can be used to maintain an adequate heart rate when bradycardia is present. As patients rewarm after CABG they will vasodilate and require extra fluid administration to assure adequate preload and cardiac output. When SVR is elevated (particularly in the presence of reduced left ventricular function) a vasodilator such as nitroprusside can be used to decrease SVR (afterload) and improve cardiac output.

Your patient arrived 2 hours ago from the OR following CABG surgery. His chest tube drainage was 200 ml the first hour, but has stopped now. His BP was 136/76 and when you check it now you get 110/60 during expiration and 88/54 during inspiration. His CVP is 17, PWP is 18, PA pressure is 32/18, neck veins are elevated. You suspect which of the following: A. Normal postoperative course. B. Low cardiac output syndrome due to perioperative MI. C. Cardiac tamponade. D. Hypovolemia due to bleeding from his grafts.

C.Cardiac tamponade is a life-threatening emergency that can occur immediately or within the first several hours after cardiac surgery. Tamponade occurs when blood or clot accumulates in the mediastinum and compresses the right heart. When the right heart is compressed the RV cannot adequately fill the left ventricle, so LV filling pressure is low, resulting in low cardiac output and hemodynamic instability. Signs and symptoms of cardiac tamponade include: 1) JVD and increased CVP reflecting elevated right heart pressure, 2) pulsus paradoxus (>10 mmHg drop in systolic BP during inspiration) that occurs when blood enters the compressed RV during inspiration and causes the septum to bulge into the LV, reducing LV filing and decreasing stroke volume further during inspiration; 3) hypotension due to decreased LV stroke volume, 4) equalization of CVP, PWP, and PA diastolic pressures, 5) sudden or significant decrease in chest tube drainage. Other signs may include decreased QRS voltage on the ECG, muffled heart sounds, widened mediastinum on chest X-ray, and tachycardia (although cardiac surgery patients receiving beta blockers or calcium channel blockers may not be able to mount a compensatory tachycardia). Beck's Triad is often associated with the clinical assessment findings of cardiac tamponade: hypotension, muffled heart sounds, and JVD. This patient's CVP is 17 and his PWP and PAD are both 18 indicating equalization of pressures. Hypovolemia due to bleeding from grafts can cause hypotension but would not cause JVD or pulsus paradoxus, and filling pressures (CVP and PWP) would be low. Perioperative MI can cause hypotension due to LV dysfunction but would not be associated with pulsus paradoxus or equalization of intracardiac pressures, and would not cause a sudden decrease in chest drainage.

Fresh frozen plasma or cryoprecipitate would most likely be administered to a post cardiac surgery patient who is bleeding from which of the following causes: A. Heparin rebound. B. A graft leak at the anastomosis site. C. Clotting factor depletion related to effects of prolonged CBP or liver dysfunction. D. Thrombocytopenia.

C.FFP is separated from the cellular components of blood (white cells, red cells, and platelets) and contains all of the coagulation factors and other proteins present in the original unit of blood. Cryoprecipitate is a small volume (10-15 ml) of insoluble protein from one unit of FFP and contains von Willebrand factor, factor VIII, factor XIII, fibrinogen, and fibrinonectin. When a patient is bleeding extensively, coagulation tests including platelet count, ACT, PTT, INR, and clotting factor levels should be done. If coagulopathy is due to clotting factor depletion, FFP and/or cryoprecipitate can be used. Bleeding due to heparin rebound can be treated with protamine. Bleeding from inadequate surgical hemostasis can be treated with antifibrinolytic medications such as aminocaproic acid (Amicar) or tranexamic acid (Cyclokapron), or blood transfusion if necessary. Returning to the OR may be necessary if hemorrhage cannot be controlled any other way. If bleeding is due to thrombocytopenia, platelets can be transfused.

Your patient, who is post aortic valve replacement, has developed atrial fibrillation. You know that atrial fibrillation in a patient with aortic stenosis or post aortic valve replacement is: A. Insignificant because the aortic valve is not connected to the atria. B. Poorly tolerated because of the slow ventricular rate. C. Poorly tolerated because of left ventricular diastolic dysfunction. D. Better tolerated than in a patient who is post CABG.

C.Significant aortic stenosis (AS) causes left ventricular hypertrophy and diastolic dysfunction due to the stiff noncompliant ventricle and reduced ventricular filling. Patients who have had aortic valve replacement still have the left ventricular dysfunction that existed before surgery. Atrial fibrillation can be a life-threatening arrhythmia in patients with severe AS because of the loss of atrial contraction and the rapid ventricular rate that often occurs with atrial fibrillation. Patients with diastolic dysfunction are more dependent on atrial contraction for ventricular filling because the stiff noncompliant ventricle is unable to relax sufficiently to fill well during the passive phase of ventricular filling. These patients also need a slower heart rate to allow adequate time for ventricular filling to occur. Both the loss of atrial contraction and the rapid ventricular rate that often occurs in atrial fibrillation make this a particularly dangerous arrhythmia following aortic valve surgery.

A post CABG patient with hypotension, low CO/CI, low PWP, and high SVR needs which of the following interventions: A. Inotrope. B. Vasodilator. C. Volume. D. Vasopressor.

C.The first illustration shows the four clinical and hemodynamic subsets based on cardiac index (CI) as the perfusion indicator, and wedge pressure (PWP) as the congestion indicator. Normal hemodynamics (subset I) = CI > 2.2 and PWP < 18. Backwards failure (subset II) = CI > 2.2 and PWP > 18 indicating adequate perfusion but pulmonary congestion. Forwards failure (subset III) = CI < 2.2 and PWP < 18, indicating hypoperfusion but no congestion. The shock box (subset IV) = CI < 2.2 and PWP > 18, indicating both hypoperfusion and pulmonary congestion. This patient is in subset III with a low CI, low PWP, and high SVR (indicating compensatory vasoconstriction due to decreased CO). The second illustration shows suggested therapies based on the clinical subsets. Patients in subset III are often hypovolemic, and volume is all that is needed to improve hemodynamics and move them to subset I. Hypovolemia can cause hypotension and reduce the cardiac output by decreasing filling pressures (PWP, CVP). Hypovolemia is treated with volume until CO and filling pressures improve. A PWP of around 15-18 mmHg is usually adequate if LV function is normal, but a higher PWP may be necessary with LV hypertrophy and diastolic dysfunction. An inotrope increases contractility and is indicated when low BP and CO/CI is due to decreased LV contractility. The shaded portion of subset III indicates decreased CI in the presence of adequate preload, a situation where inotropes would be indicated. A vasodilator is indicated when low cardiac output is due to elevated SVR. A vasopressor is indicated when BP is low and SVR is low due to peripheral vasodilation, such as sepsis or anaphylactic reactions.

Your patient has had an aortic valve replacement for severe aortic stenosis. She has been in sinus rhythm at a rate of 70 with adequate hemodynamics but has now gone in to 3rd degree AV block with a junctional rhythm at a rate of 40 beats per minute and is hypotensive. Atrial and ventricular epicardial pacing wires are present. What type of pacing would be best in this patient: A. VVI. B. AAI. C. DVI. D. DDD.

D. A patient with aortic stenosis has a stiff noncompliant LV that depends on atrial kick for much of its preload to maintain an adequate stroke volume. DDD pacing means that the pacemaker paces atria and ventricles (first D), senses in atria and ventricles (second D), and inhibits or triggers pacing depending on whether atrial or ventricular activity was sensed (third D). The DDD pacing mode allows the pacemaker to sense the patient's own P waves and paces the ventricle in response to those P waves, thus maintaining AV synchrony and improving LV preload. The DDD pacing mode always maintains AV synchrony regardless of what the underlying rhythm is. This patient is in third degree block, so pacing the atrium alone (AAI) will do no good since there is no AV conduction present. VVI pacing would increase the ventricular rate but would not maintain AV synchrony. DVI pacing paces both the atria and the ventricles but only senses in the ventricle, therefore it would not sense her intrinsic P waves but would pace both atria and ventricles at the minimum rate set in the pacemaker. Since this patient has an adequate sinus rhythm, the DDD mode is better because it will allow for atrial sensing and pace the ventricle in response to her intrinsic P waves. Both DDD and DVI modes preserve AV synchrony.

When you turn your post CABG patient you notice about 100 ml of dark blood dumping through the chest tubes. You should now do which of the following: A. Ignore it because it is normal for dumping to occur with position changes. B. Immediately notify the surgeon because this indicates acute and excessive bleeding that could require surgical intervention. C. Evaluate blood pressure and hemodynamic values and give a 500 cc fluid bolus. D. Assess blood pressure and hemodynamic values to evaluate patient's condition and observe chest tubes for additional drainage once patient is repositioned.

D. A significant volume of blood can collect in the mediastinum over time and drain through the chest tubes when the patient is turned. If the blood is dark rather than bright red and there is normal additional drainage after the patient is repositioned, it has most likely been accumulating over time and does not necessarily indicate active significant bleeding. Bright red blood that continues to drain in excessive amounts, and changes in the patients BP and hemodynamics would indicate ongoing bleeding and needs to be reported immediately. General guidelines for return to the OR for bleeding include: > 400 ml/hour for 1 hour, > 300 ml/hour for 2-3 hours, > 200 ml/hour for 4 hours. A fluid bolus would be appropriate if bleeding continues and the patient is hypotensive with low filling pressures (CVP, PWP).

Which of the following is NOT an indication for IABP therapy: A. Weaning from cardiopulmonary bypass. B. Unstable angina. C. Cardiogenic shock. D. Acute aortic regurgitation. E. Acute mitral regurgitation.

D. Acute aortic regurgitation is a contraindication for IABP therapy because balloon inflation during diastole makes the aortic regurgitation worse by pushing blood backwards through the incompetent aortic valve.

Which of the following medications should be held prior to cardiac surgery: A. ASA, beta blocker, IV insulin drip. B. Clopidogrel, beta blockers, oral hypoglycemic agents. C. Statin, beta blockers, prasugrel. D. Clopidogrel, ACE inhibitors, oral hypoglycemic agents, NSAIDS.

D. All antianginal, antihypertensive, and heart failure medications should be continued up until the time of surgery. Exceptions are ACE inhibitors and angiotensin receptor blockers, which should be held the morning of surgery. P2Y12 inhibitors (clopidogrel, prasugrel, ticagrelor) should be discontinued 5-7 days prior to surgery whenever possible to reduce the risk of post op bleeding. Oral hypoglycemic agents should be held for 24 hours prior to surgery. NSAIDS should be held a few days prior to surgery to decrease risk of bleeding and in patients with renal dysfunction. Beta blockers should be continued or started at least 24 hours prior to surgery to reduce the risk of postop atrial fibrillation. Statin therapy should be started at least one week prior to surgery, as they are associated with decreased incidence of stroke, atrial fibrillation, renal dysfunction and infection. ASA should not be discontinued in patients with acute coronary syndrome or critical coronary artery disease. If there is an increased risk for bleeding, or if the patient refuses blood transfusion, ASA can be held 3 days prior to surgery. If a patient is dependent on IV insulin to maintain glucose <180 mg/dL, the drip should be started preoperatively and continued through the first 24 hours postop.

A complication seen in patients who have received a CABG using the LIMA or a radial artery graft that is not seen with saphenous vein grafts is: A. Acute MI due to graft thrombosis. B. Bleeding at graft suture lines. C. Graft aneurysm. D. Graft spasm.

D. Arterial conduits, such as the LIMA, RIMA, or radial artery are prone to spasm because of their thicker arterial walls. All grafts can thrombose or bleed at suture lines, and aneurysm formation is more common in veins harvested from the arms. IMA grafts have excellent long term patency and are preferred conduits in most patients.

You are caring for a CABG patient who received a radial artery graft to the RCA. Which of the following drugs do you expect to administer to prevent spasm of the graft: A. Beta blockers. B. Nitroprusside. C. Amiodarone. D. Nitrates or calcium channel blockers.

D. Arterial grafts are prone to vasospasm because of their thick muscular wall. Calcium channel blockers and nitroglycerin are arterial dilators and can be used to prevent graft spasm. Beta blockers can leave alpha vasoconstrictor receptors unopposed and are not indicated for preventing arterial spasm. Nitroprusside is a potent arterial dilator but it is used as an afterload reducer and for managing hypertension, not for preventing arterial spasm. Amiodarone is an antiarrhythmic used for managing atrial fib and ventricular arrhythmias.

You are caring for a CABG patient who received a radial artery graft to the RCA. Which of the following drugs do you expect to administer to prevent spasm of the graft: A. Nitroprusside. B. Amiodarone. C. Beta blockers. D. Nitrates or calcium channel blockers.

D. Arterial grafts are prone to vasospasm because of their thick muscular wall. Calcium channel blockers and nitroglycerin are arterial dilators and can be used to prevent graft spasm. Beta blockers can leave alpha vasoconstrictor receptors unopposed and are not indicated for preventing arterial spasm. Nitroprusside is a potent arterial dilator but it is used as an afterload reducer and for managing hypertension, not for preventing arterial spasm. Amiodarone is an antiarrhythmic used for managing atrial fib and ventricular arrhythmias.

You are caring for a 72 yr old female patient who is readmitted for left pleural effusion three weeks after CABG surgery. On night shift she develops progressive dyspnea. Assessment reveals the following: HR 110 (sinus tachycardia), BP 104/70 mmHg, and the systolic falls to 88 mmHg with inspiration. Her radial pulse becomes weaker during inspiration. She has jugular venous distention, moderate peripheral edema, distant heart sounds, fine inspiratory crackles left lower lobe. What emergency situation must be ruled out based on these assessment findings: A. Increase in left pleural effusion causing tension pneumothorax. B. Spasm of a radial artery graft. C. Closure of one of the saphenous vein grafts. D. Cardiac tamponade.

D. Cardiac tamponade is a cause of obstructive shock. Signs and symptoms of tamponade include Beck's triad: hypotension, JVD, and muffled heart sounds. Other signs include abnormal pulsus paradoxus, which is a drop in systolic blood pressure during inspiration of > 12 mmHg and weak or absent pulses during inspiration. A patient who is post open-heart surgery has the potential risk of bleeding and development of tamponade. A tension pneumothorax can compress the heart and great vessels and cause obstructive shock and many of the same signs as cardiac tamponade. However, pleural effusion does not cause tension pneumothorax. In addition there are fine inspiratory crackles in the left low lobe, which is consistent with the admission diagnosis. Lung sounds do not provide any evidence of worsening pleural effusion. Closure of a saphenous vein graft or radial artery graft spasm would result in signs consistent with myocardial ischemia or infarction. Neither of these two cases would result in obstructive shock.

Mediastinal drainage in the following amount meets criteria for re-exploration: A. > 300 ml/hr for 2-3 hours. B. > 200 ml/hr for 4 hours. C. > 400 ml to 500 ml for 1 hour. D. All of the above.

D. Chest tube drainage criteria for surgical re-exploration: • > 400 to 500 ml for 1 hour • > 300 ml/hr for 2 to 3 hours • > 200 ml/hr for 4 hours • Acute onset of bleeding >300 ml/hr after period of stable and minimal bleeding

You are caring for a patient who had an aortic arch repair using deep hypothermic circulatory arrest (DHCA) instead of routine CPB. You expect which of the following in this patient compared to one who had routine CPB: A. Longer rewarming time. B. Higher risk of coagulopathy. C.Longer neurologic recovery time. D. All of the above.

D. DHCA is used when the aorta cannot be crossclamped due to severe atherosclerosis or calcification and is usually used in repair of type A aortic dissections and arch repairs. Patients are systemically cooled to a core temperature of 18º C, to achieve electroencephalographic silence. This low temperature can be maintained for about 45 minutes for cerebral protection while blood circulation is stopped. Methods of antegrade or retrograde cerebral perfusion can be utilized during DHCA to provide some blood flow to the brain. Following DHCA, patients take longer to rewarm, and use of forced air warming (i.e. Bair Hugger) is indicated in the ICU. Patients may take up to 24 hours to wake up, and there is often prolonged time on the ventilator as well. Coagulopathy is common due to hypothermia and patients often have bleeding problems postoperatively when DHCA is used.

Coagulopathies associated with CBP can include which of the following: A. DIC. B. HIT. C. Heparin rebound. D. All of the above.

D. DIC (disseminated intravascular coagulation) is a systemic process due to massive activation of the clotting cascade. Excessive thrombin production leads to widespread deposition of fibrin which results in intravascular clotting and tissue ischemia. This widespread intravascular coagulation consumes platelets and clotting factors, which then results in bleeding. In cardiac surgery involving the use of CPB, DIC can result from prolonged contact between the blood and the artificial surface of the bypass circuit which leads to activation of the clotting cascade. HIT (heparin induced thrombocytopenia) ) is an immune-mediated disorder in which antibodies are formed against the heparin-platelet factor 4 complex. Cardiac surgery patients receive large amounts of unfractionated heparin while on CPB. Heparin binds with platelet factor 4 released by activated platelets, forming a heparin- PF4 complex. The body makes antibodies to this heparin-PF 4 complex, forming a heparin-PF4-antibody complex on the platelet surface. These platelets aggregate and are removed prematurely from the circulation leading to thrombocytopenia which increases the risk of bleeding. Heparin rebound is the reappearance of anticoagulant activity after adequate neutralization of heparin with protamine at the end of surgery. A significant amount of heparin is bound to plasma proteins and tissues, and is not completely neutralized by protamine. This protein and tissue-bound heparin is released slowly after surgery, producing the heparin rebound phenomenon. Heparin rebound is one of the most common causes of postoperative bleeding after cardiac surgery.

Coagulopathies associated with CBP can include which of the following: A. Heparin rebound. B. HIT. C. DIC. D. All of the above.

D. DIC (disseminated intravascular coagulation) is a systemic process due to massive activation of the clotting cascade. Excessive thrombin production leads to widespread deposition of fibrin which results in intravascular clotting and tissue ischemia. This widespread intravascular coagulation consumes platelets and clotting factors, which then results in bleeding. In cardiac surgery involving the use of CPB, DIC can result from prolonged contact between the blood and the artificial surface of the bypass circuit which leads to activation of the clotting cascade. HIT (heparin induced thrombocytopenia) ) is an immune-mediated disorder in which antibodies are formed against the heparin-platelet factor 4 complex. Cardiac surgery patients receive large amounts of unfractionated heparin while on CPB. Heparin binds with platelet factor 4 released by activated platelets, forming a heparin- PF4 complex. The body makes antibodies to this heparin-PF 4 complex, forming a heparin-PF4-antibody complex on the platelet surface. These platelets aggregate and are removed prematurely from the circulation leading to thrombocytopenia which increases the risk of bleeding. Heparin rebound is the reappearance of anticoagulant activity after adequate neutralization of heparin with protamine at the end of surgery. A significant amount of heparin is bound to plasma proteins and tissues, and is not completely neutralized by protamine. This protein and tissue-bound heparin is released slowly after surgery, producing the heparin rebound phenomenon. Heparin rebound is one of the most common causes of postoperative bleeding after cardiac surgery.

Which of the following is not an appropriate nursing intervention in caring for a patient with a chest tube drainage system: A. Reporting continuous bubbling in the waterseal chamber. B. Reporting new diminished or any absence of lung sounds. C. Performing gentle milking when drainage is present. D. Clamping the chest tube after disconnecting suction in a patient leaving the unit for a diagnostic test.

D. Do not clamp chest tube for transport (can cause tension pneumothorax with pleural chest tubes or tamponade with mediastinal chest tubes). Use portable suction if available or transport on gravity drainage with tubing from suction chamber open to air. Leaving the tubing open to air allows a vent for the escape of air. If there is an order for suction and no portable suction is available then obtain an order to transport with gravity drainage. Maintaining patency is a key nursing intervention. Avoid dependent loops in the drainage tubing. Chest tube should be gently milked if there is drainage, but there should be no routine stripping. Aggressive stripping of a mediastinal chest tube can result in a negative 300 cmH2O pressure in the mediastinum and can aggravate bleeding. Reportable conditions in patients with chest tubes include: • Signs and symptoms of increased air leak (increased crepitus, bubbling in the water seal chamber) • Drainage of more than 100 ml in a hour • Tachypnea, hypoxemia, diminished or absent lung sounds • Signs and symptoms of tension pneumothorax or cardiac tamponade (hypotension, jugular venous distention, muffled heart sounds, deviation of the trachea).

You are caring for a patient who returned from CABG surgery 4 hours ago. You expect drainage from the mediastinal chest tubes to: A. Be at least 200 ml/hr for the first 2 hours. B. Drainage should have stopped by now. C. Be bright red with clots present. D. Be <100 ml per hour.

D. Drainage from chest tubes should be no more than 100 ml/hr on return from surgery and should gradually decrease over the first 3-4 hours. Bright red blood and clots or drainage >200 ml/hr can indicate surgical bleeding and should be reported. The patient will probably need to return to surgery if drainage is > 400 ml/hr, or > 300 ml/hr for 2-3 hours, or >200ml/hr for 4 hours. A sudden decrease in drainage can indicate the presence of clots obstructing chest tubes or can be a sign of tamponade. Chest tubes are usually removed in about 24 hours if drainage is <20 ml/hr

During the immediate postoperative period, the goal glucose level in the diabetic patient with an anticipated ICU LOS of less 48 hours is: A. < 250 mg/dl. B. Glucose control is not important in the post operative cardiac surgery patient. C. <120 mg/dl. D. < 180 mg/dl.

D. Due to potential hypoglycemic complications involved in therapy to maintain strict glycemic control, recent guidelines for glucose control in the patient undergoing CABG include the following parameters: Preoperative: HgbA1c assessed preoperatively in diabetics. Intraoperative: insulin infusion for diabetics intraoperatively, SQ insulin acceptable for non diabetics as long as glucose < 180 mg/dl. Postoperative: IV insulin drip for 24 hours in diabetics, SQ insulin acceptable for non-diabetics. Complex patients (ICU greater than 3 days) maintain glucose < 150 mg/dl.

Coagulopathy is present to some degree with all CPB. During CPB, blood contacts the non-physiological surfaces of the bypass circuit and an inflammatory response is initiated. A coagulopathy can develop from activation of platelets and the fibrinolytic system. Clotting factors, platelets, and RBCs are diluted during CPB. A longer pump time is associated with increased coagulopathies. Postoperatively, patients have an increased amount of total body fluid due to priming of the CPB pump and administration of fluids during surgery. Extra volume is given to the patient during cardiopulmonary bypass to assure adequate circulating volume through the cardiopulmonary circuit. A. Long pump times are associated with increased bleeding and therefore increased chest tube drainage, and prolongs time to extubation. B. The patient is excessively dry from the hemoconcentration that occurs during cardiopulmonary bypass. C. The patient is still vasoconstricted from being cool during the prolonged cardiopulmonary bypass time. D. The patient has capillary leak and fluid is shifting into the interstitial space. E. All of the above.

D. Failure of fluid challenges to raise preload may indicate the presence of capillary leak and fluid shifting into the interstitial space. Patients with longer CPB times are at greater risk for capillary leak. In patients with capillary leak, a large amount of fluid is required to maintain adequate circulating volume. Administration of large amounts of volume also increases the interstitial volume. Inotropes and vasopressors may also be needed for hemodynamic support in the patient with capillary leak. Vasoconstriction from hypothermia results in an increase in preload not a decrease. Venous vasodilation will result in decreased preload. Cardiopulmonary bypass results in hemodilution, not hemoconcentration. Extra volume is given to the patient during cardiopulmonary bypass to assure adequate circulating volume through the cardiopulmonary circuit.

Which of the following patients is likely to have the dangerous form of heparin induced thrombocytopenia: A. A patient who is 2 days post CABG with a platelet count of 100,000. B. Any patient post CABG with a 20% decrease in platelet count. C. A patient who is 4 hours post CABG with a platelet count of 200,000. D. A patient who is 5 days post CABG whose platelet count has decreased by 60%.

D. Heparin induced thrombocytopenia can be a life threatening clinical condition. However, thrombocytopenia is a common clinical condition for many patients after CABG due to a variety of factors including heparin administration and the effects of cardiopulmonary bypass and use of intra-aortic balloon pump therapy. There are two types of heparin induced thrombocytopenia (HIT), Type 1 and Type 2. Type 1 HIT is common, is not immune related, usually develops within 48 hours of administration, results in a mild reduction in platelets. Heparin therapy can usually be continued in Type 1 HIT. Type 2 HIT is immune mediated and typically results in a decrease in platelets by 50% or more starting 4 to 10 days after the initiation of therapy, or as soon as within 10 hours of administration if the patient has had heparin within the last 100 days. Type 2 HIT can result in a procoagulant state leading to both venous and arterial thrombosis. The mortality rate associated with type 2 heparin induced thrombocytopenia is approximately 20 to 30 %.

When caring for a patient who is post CABG the nurse knows the following is true regarding hypertension in the immediate post operative period: A. Hypertension increases myocardial oxygen demand. B. Hypertension increases left ventricular afterload. C. Hypertension increases the risk of bleeding. D. All of the above.

D. Hypertension increases the risk of graft dehiscence at the anastomoses site, bleeding, myocardial ischemia, stroke, and cardiac arrhythmias. Myocardial oxygen demand is affected by the same parameters that affect cardiac output (preload, afterload, contractility, and heart rate). An increase in any one of these four parameters will increase myocardial oxygen demand and consumption.

Low cardiac output following cardiac surgery is common and can be due to all of the following EXCEPT: A. Cardiac tamponade. B. Postoperative arrhythmias. C. Reduced preload due to bleeding or increased capillary permeability. D. Reduced afterload due to hypothermia. E. Use of CPB and cardioplegia during surgery.

D. Hypothermia causes peripheral vasoconstriction which increases afterload. A reduced afterload would cause vasodilation and allow the ventricle to eject against a lower resistance and therefore increases LV function and often increases cardiac output. Cardiac output is determined by four things: heart rate, preload, afterload, and contractility. A low cardiac output postoperatively can be caused by a heart rate that is too fast or too slow, low preload, high afterload, decreased contractility, or a combination of these factors. The use of CPB and cardioplegic arrest during surgery contributes to myocardial stunning which decreases LV contractility and can cause low cardiac output postoperatively. In addition, CPB alters coagulation factors and platelet function which contributes to the risk of bleeding as well as initiating an inflammatory response that causes increased capillary permeability and fluid shifts into the interstitial space - all of which contribute to reduced preload and low cardiac output. Postoperative arrhythmias, including bradycardia and tachycardias, can decrease cardiac output. Cardiac tamponade compresses the heart and causes decreased filling of the ventricles, resulting in decreased cardiac output.

You are caring for a post CABG patient who is hypotensive with a BP that has fallen over the past hour from 136/76 to 98/50. His rhythm is sinus tachycardia at 120 beats/min. He is receiving fluid at 150 ml/hour. He has the following hemodynamic values: CO = 8 L/min, CI = 4.4 L/min/M2, CVP = 6 mmHg, PAP = 25/14, PWP = 8 mmHg, SVR = 600 dynes. Which of the following is most likely the cause of this hemodynamic picture: A. Perioperative MI. B. Cardiac tamponade. C. Excessive postoperative pain. D. Sepsis. E. Excessive bleeding.

D. In early sepsis, cardiac output is often quite elevated as long as cardiac contractility is normal and adequate volume is being administered. Because of the many vasodilator substances released in sepsis, the SVR is low (normal is 900-1200 dynes) and BP is low due to peripheral vasodilation. Additionally, pulse pressure widens as the vasodilation occurs. Large amounts of volume are necessary to fill the enlarged vascular space, and if cardiac function is adequate the cardiac output can be very high in early sepsis. In cardiac tamponade the CVP, PWP, and PA diastolic pressures elevate and equalize because of pressure from accumulated blood trapped in the pericardium or mediastinum pushing on the heart and elevating intrathoracic pressure. SVR is usually high due to compensatory vasoconstriction. Perioperative MI would most likely cause a decrease in CO and CI due to left ventricular dysfunction. PWP is often elevated in acute MI due to decreased LV compliance and decreased contractility. The SVR would be high due to compensatory vasoconstriction when CO falls. Excessive bleeding would cause hypovolemia which would lead to a decrease in right and left ventricular filling pressures, resulting in low CVP and PWP. CO/CI would decrease due to decreased stroke volume secondary to hypovolemia. SVR would increase due to compensatory vasoconstriction. Excessive postoperative pain would most likely increase both heart rate and BP due to sympathetic nervous system stimulation. SVR would likely increase due to vasoconstriction caused by sympathetic stimulation.

The nurse caring for the post operative cardiac surgery patient recognizes the following as potential contributors to post-operative vasodilation that can cause hypotension: A. Cooling that occurs while on cardiopulmonary bypass, and use of vasodilators post op. B. Use of norepinephrine or dopamine to support BP immediately post-op. C. Inflammatory response due to CPB and use of norepinephrine to support BP D. Rewarming that occurs after return to the ICU, and the inflammatory response to use of cardiopulmonary bypass during surgery

D. Intraoperative cooling results in vasoconstriction; rewarming after surgery causes vasodilation and can contribute to hypotension if volume administration is inadequate for the increased size of the vascular space caused by vasodilation. The use of CPB stimulates an inflammatory response that results in vasodilation that contributes to hypotension. Norepinephrine and dopamine cause peripheral vasoconstriction, not vasodilation.

Your patient has received a mechanical valve to replace his severely stenotic aortic valve. You know the following to be true: A. Mechanical valves do not require anticoagulation but biological valves do. B. Infective endocarditis only occurs with biological valves. C. Biological valves have a lower rate of structural failure than mechanical valves. D. Mechanical valves are more durable but require lifelong anticoagulation, while biological valves do not.

D. Mechanical valves are manufactured from manmade materials and usually have a tilting disk or bileaflet design. Biological valves are made from living tissue and include porcine or bovine tissue, or are transplanted from other humans (homografts) or from the same patient (autografts). Mechanical valves have a very low rate of structural failure but require life-long anticoagulation therapy, usually with warfarin. Bioprosthetic valves usually do not require long term anticoagulation unless there are other risk factors (like atrial fibrillation), but have a higher rate of structural failure requiring a second valve replacement within 10-15 years. Infective endocarditis occurs with equal frequency on mechanical and bioprosthetic valves during the first postoperative year, but bioprosthetic valves have a higher risk after 18 months.

Important discharge teaching points for patients with mechanical prosthetic valves include: A. Warfarin can be discontinued if atrial fibrillation converts to sinus rhythm. B. Discontinue warfarin if there is any sign of bleeding. C. There is no need to discuss antibiotic prophylaxis prior to any dental procedure. D. Follow-up with an anticoagulation clinic or physician's office is critical to maintain therapeutic INR on warfarin.

D. Mechanical valves require lifelong anticoagulation with warfarin. (Newer anticoagulants such as rivaroxaban (Xarelto), dabigatran (Pradaxa), or apixaban (Eliquis) may eventually be used instead of warfarin, but at this time they are not approved for valve thrombosis prophylaxis.) Patients with mechanical valves should be told to NEVER discontinue their anticoagulant without a physician's order for any reason. Bleeding should be reported immediately and the dose adjusted accordingly, but the patient should never discontinue their own warfarin. Atrial fibrillation also requires lifelong anticoagulation. New oral anticoagulants, dabigatran (Pradaxa), a direct thrombin inhibitor, rivaroxaban (Xarelto) and apixaban (Eliquis), factor Xa inhibitors, have recently been approved by the FDA and are indicated for non-valvular atrial fibrillation. Antibiotic prophylaxis is recommended prior to dental procedures that involve manipulation of gingival tissue or the periapical region of teeth or perforation of the oral mucosa for patients with prosthetic valves. Antibiotics are no longer required for GI or GU procedures in these patients.

Myocardial stunning can be a cause of postoperative left ventricular dysfunction. Which of the following best describes stunning: A. Normal ventricular function in the presence of excessively high afterload. B. Intraoperative ischemia resulting in permanent left ventricular dysfunction. C. Transient ischemia followed by myocardial reperfusion and normal left ventricular function. D. Transient ischemia followed by myocardial reperfusion and left ventricular dysfunction of limited duration.

D. Myocardial stunning is transient post ischemic LV dysfunction that occurs after total or significant reduction of coronary blood flow, followed by reestablishment of coronary flow. The LV dysfunction is of limited duration and improves over time with support from inotropic agents or mechanical assist (i.e. IABP). In the cardiac surgery patient, stunning can occur when coronary flow is disrupted by CPB and then reestablished at the end of the procedure and is one of the causes of postoperative low cardiac output syndrome.

A 72-year-old male 4 days status post CABG complains of substernal chest pain when lying down. On cardiac auscultation you note a friction rub. What is the most likely cause of the patient's discomfort: A. Angina. B. Pulmonary embolism. C. Incisional pain. D. Pericarditis.

D. Pericarditis can occur early or late following cardiac surgery and presents as pain that can mimic angina in presentation. Pericardial pain is usually positional and can often be relieved by leaning the patient forward. The presence of a friction rub is indicative of the inflammation of pericarditis. Pericardial friction rubs are transient and only present about 50% of the time in pericarditis. Anginal pain can be similar to the pain of pericarditis but it is not positional and is not relieved by changes in position. Angina is not associated with a friction rub unless there happens to be pericarditis present as well. Incisional pain can be positional but is not associated with a friction rub. Pulmonary embolism can cause chest pain but is not associated with a cardiac friction rub.

An early sign of HIT (heparin induced thrombocytopenia) is: A. Massive organ failure. B. Excessive bleeding from gums, puncture sites, GI system. C. Stroke, MI, or DVT. D. Drop in platelet count by about 50%.

D. Platelet count usually falls by 50% or more from baseline, usually within 4-10 days after heparin is started. Excessive bleeding can occur with any anticoagulant therapy but is not associated with HIT. HIT results in arterial and venous thrombosis that can cause DVT, pulmonary embolism, limb gangrene, stroke, MI and other organ failure - but these events occur after the initial drop in platelet count.

Your patient had a CABG and mitral valve replacement yesterday. He has had a low cardiac output and signs of right ventricular failure since he arrived in the ICU and is still on the ventilator. Today he appears slightly jaundiced, his bilirubin and INR are elevated, and serum albumin is low. This is most likely indicative of which of the following: A. Pain and sedation medication effect. B. Acute respiratory failure. C. Anticoagulation overdose. D. Post pump hepatic dysfunction.

D. Postoperative hepatic dysfunction can result from reduced hepatic perfusion or from systemic congestion (usually associated with right heart failure). Reduced hepatic perfusion can occur during CPB or postoperatively in low cardiac output states, and is more common in patients with preexisting liver disease, multiple comorbidities (CHF, diabetes), preoperative cardiogenic shock, and prolonged pump time. The low serum albumin and high INR represent impaired liver synthesis of protein and clotting factors and is a marker for hepatic dysfunction. Pain and sedation medications can result in somnolence that prevents early extubation, and can cause hypotension that could contribute to a low cardiac output state. However, they would not elevate the bilirubin and INR or cause jaundice. Acute respiratory failure would certainly delay extubation and contribute to postoperative problems but would not elevate the bilirubin or INR, cause jaundice, or decrease albumin. Anticoagulation overdose would contribute to bleeding and prolong the INR but would not cause jaundice, elevate the bilirubin, or decrease albumin.

Treatment of postpericardiotomy syndrome includes: A. Vasodilators for associated hypertension. B. Emergent reopening of the sternum for drainage. C. Use of inotropes for decreased cardiac output. D. Use of ASA or NSAID for pain relief.

D. Postpericardiotomy syndrome (PPS) is an inflammatory response to cardiac injury or surgery, and in the cardiac surgery patient it can occur within the first week or not until weeks to months later. It usually presents with fever, pleuritic chest pain or pain that can mimic angina, elevated sedimentation rate, pericardial friction rub, and often pericardial or pleural effusions. Pain and inflammation can usually be relieved with ASA or a NSAID (i.e. ibuprofen). If a large effusion is present then pericardiocentesis is indicated. Emergent reopening of the sternum is not indicated for PPS. Hypertension and decreased cardiac output are not necessarily related to PPS and use of vasodilators or inotropes would not be indicated.

All of the following statements are true about use of antibiotics in cardiac surgery patients EXCEPT: A. A cephalosporin (typically cefazolin or cefuroxime) is the antibiotic of choice in patients without MRSA. B. Preoperative IV prophylactic antibiotics should not be given until the patient is in the operating suite so the administration can be timed to be 30 to 60 minutes prior to the initial incision. C. Vancomycin is indicated for proven or suspected MRSA. D. Post-operative antibiotics are continued for 7 to 10 days after surgery.

D. Preoperative intravenous prophylactic antibiotics are not given until the patient is in the operating suite so the administration can be timed to be 30 to 60 minutes prior to the initial incision. National quality standards require administration within one hour of incision time to insure adequate tissue levels at the time of incision. Postoperative antibiotics are given for 48 hours or less. A cephalosporin (typically cefazolin or cefuroxime) is the antibiotic of choice in patients without MRSA, and vancomycin, alone or in combination with other antibiotics, is recommended in patients with MRSA.

The use of cardiopulmonary bypass (CPB) during cardiac surgery is associated with which of the following effects: A. Increased vascular permeability and increased intravascular coagulation. B. Increased intravascular coagulation and hypovolemia. C. Hyperthermia and increased vascular permeability. D. Increased inflammatory response and hemodilution.

D. Prior to initiating CPB, the pump and its tubing are primed with about 1500 ml of fluid which causes hemodilution. Hemodilution is associated with a decrease in Hgb, Hct, platelets, clotting factors, serum albumin, and electrolytes. This can result in dilutional thrombocytopenia and coagulopathy that increases the risk of bleeding. Heparin is used during CPB to prevent clotting in the circuit, and this can contribute to bleeding. CPB also initiates a systemic inflammatory response as blood comes in contact with the foreign material in the bypass circuitry. This inflammatory response triggers the release of several substances that impair coagulation and the immune response, and cause increased vascular permeability leading to fluid shifts from the intravascular space to the interstitial space. Hypothermia is induced to protect the heart and reduce metabolic demands while the patient is on CPB. Hypothermia results in vasoconstriction which increases afterload, shivering which increases metabolic demand, and increases the risk of bleeding, arrhythmias, and organ dysfunction post operatively.

Right ventricular failure can be a cause of low cardiac output in post surgical patients due to which of the following conditions: A. Preexisting mitral stenosis. B. Preoperative or intraoperative right ventricular infarction. C. Preexisting pulmonary hypertension. D. All of the above.

D. Right ventricular infarction can cause RV failure by decreasing RV contractility. Mitral stenosis causes pulmonary hypertension which can precipitate RV failure when the RV must work against chronically high PA pressure. Pulmonary hypertension from any cause, including severe LV failure, mitral or aortic valve disease, or severe lung disease can contribute to post operative RV failure. Reduced RV contractility results in decreased LV filling which can cause a low cardiac output state postoperatively. Additionally, when the RV dilates it pushes the septum leftward into the LV cavity which further decreases LV filling and function.

Right ventricular failure can be a cause of low cardiac output in post surgical patients due to which of the following conditions: A. Preexisting pulmonary hypertension. B. Preexisting mitral stenosis. C. Preoperative or intraoperative right ventricular infarction. D. All of the above.

D. Right ventricular infarction can cause RV failure by decreasing RV contractility. Mitral stenosis causes pulmonary hypertension which can precipitate RV failure when the RV must work against chronically high PA pressure. Pulmonary hypertension from any cause, including severe LV failure, mitral or aortic valve disease, or severe lung disease can contribute to post operative RV failure. Reduced RV contractility results in decreased LV filling which can cause a low cardiac output state postoperatively. Additionally, when the RV dilates it pushes the septum leftward into the LV cavity which further decreases LV filling and function.

You are caring for a patient with a chest tube in place for treatment of a pneumothorax. What is true regarding the waterseal chamber: Continuous bubbling represents an air leak. A. The main purpose of the water seal is to allow air to exit from the pleural space on exhalation and prevent air from entering the pleural cavity or mediastinum on inhalation. B. The chamber may bubble gently during expiration. C. Lack of tidaling may indicate a kink. D. All of the above.

D. The 2nd compartment is connected to the 1st and creates a water seal. A small amount of sterile water (per manufacturer directions) is injected into the water seal chamber before the drainage system is connected to the patient. The main purpose of the water seal is to allow air to exit from the pleural space on exhalation and prevent air from entering the pleural cavity or mediastinum on inhalation. Air that is allowed to pass through the water seal will bubble out the bottom of the chamber. The water seal chamber is calibrated and should be seen as the window into the pleural space. During gravity drainage the level of water reflects the intrapleural pressure. Some newer systems eliminate the water seal chamber and use a check-valve to serve its purpose. Assure that the amount of sterile fluid in the water seal and suction chambers is at the manufacturer recommended levels when wet systems are used. To maintain an adequate water seal in a wet system it is important to monitor the level of water in the water seal chamber and to keep the chest drainage unit upright at all times. Assess for air leak by checking water seal chamber for bubbles during inspiration. The water seal chamber may bubble gently with insertion, during expiration and with a cough. Continuous bubbling represents an air leak. Some water seal compartments have an air leak meter. Check for system leaks by clamping before each connection (system may need to be replaced). Check for leak where tube enters chest. Check chest x-ray to assure last hole of chest tube is inside chest. Assess the water seal chamber for slight fluctuation. Slight fluctuation (tidaling) in the water seal level (rising during spontaneous inspiration and falling during expiration) is normal. Lack of fluctuation with respiration may indicate kinking or other problems interfering with drainage. A slow gradual rise in the water level is consistent with an increase in intrapleural pressure. This is a desired outcome as normal intrapleural pressure is restored and the lung re-expands.

What is correct nursing knowledge regarding the chest tube drainage systems and suction: A. Usually -80 cm H2O should be applied to a chest tube drainage system. B. Robust bubbling is needed in order to have an adequate amount of suction. C. Wet suction units regulate the amount of suction by the suction from the wall unit and not by the height of a column of water in the suction chamber. D. Wet suction units regulate the amount of suction by the height of a column of water in the suction chamber not by the suction from the wall unit.

D. The 3rd compartment of a chest drainage system is connected to the first two sections and provides suction. There are two types of suction units: wet and dry. Wet suction units regulate the amount of suction by the height of a column of water in the suction chamber not by the suction from the wall unit. When a water column is used, only gentle bubbling should occur in the suction chamber. The source of suction should be adjusted to prevent loud bubbling of the water. Excessive external suction results in evacuation of water from the control chamber. The system valve controls the amount of suction and should normally be adjusted to achieve -20 cm H2O of suction. Lower levels of suction may be indicated for patients with friable lung tissue. The goal is to have an adequate amount of suction to keep open the pleural space, but not an excessive amount that will cause damage to the lung tissue. No more than -40 cm H2O should be applied to a chest tube drainage system. Many disposable chest tubes today have a dry suction regulator. This means there is no water in the suction chamber. A mechanical regulator within the unit is used to set the amount of suction applied to the system. The wall vacuum regulator is set at minus 80 cmH2O but the regulator on the unit is set to limit the suction to typically minus 20 cmH2O.

Which of these procedures carries the highest risk for development of acute kidney injury (AKI) requiring dialysis: A. Mitral valve replacement (MVR). B. Aortic valve replacement + CABG. C. Aortic valve replacement (AVR). D. Mitral valve replacement (MVR) + CABG.

D. The Society of Thoracic Surgeons model for predicting the risk of needing dialysis after cardiac surgery assigns points for known risk factors and uses the total point score to predict the risk of AKI requiring dialysis. This model assigns 7 points for MVR + CABG, 5 points for AVR + CABG, 4 points for MVR alone, and 2 points for AVR alone. CABG alone receives no points in this model.

A post CABG patient with hypotension, low CO/ CI, high PWP, and high SVR needs which of the following interventions: A. Volume. B. Vasopressor. C. Vasodilator. D. Inotrope.

D. The first illustration shows the four clinical and hemodynamic subsets based on cardiac index (CI) as the perfusion indicator and wedge pressure (PWP) as the congestion indicator. Normal hemodynamics (subset I) = CI > 2.2 and PWP < 18. Backwards failure (subset II) = CI > 2.2 and PWP > 18 indicating adequate perfusion but pulmonary congestion. Forwards failure (subset III) = CI < 2.2 and PWP < 18, indicating hypoperfusion but no congestion. The shock box (subset IV) = CI < 2.2 and PWP > 18, indicating both hypoperfusion and pulmonary congestion. This patient is in subset IV with a low CI, high PWP, and hypotension. The second illustration shows suggested therapies based on the clinical subsets. Hypotension with low CO/CI and high PWP may respond to an inotropic agent to increase contractility. A high SVR is compensatory in the hypotensive patient, and a vasodilator is contraindicated in the presence of hypotension. If CO remains low despite adequate volume and inotropic support, IABP therapy may be indicated to improve CO and mechanically reduce afterload. Volume is indicated when the preload is low due to hypovolemia. Vasodilators are indicated when BP and SVR are high. Vasopressors are indicated when SVR is low. Volume status should be optimized before using either an inotrope or a vasopressor.

Which of the following describes proper IABP timing: A. Augmented diastolic pressure higher than patient's unassisted diastolic pressure, balloon assisted systolic pressure higher than patient's systolic pressure B. Augmented diastolic pressure lower than patient's unassisted diastolic pressure, balloon assisted systolic pressure higher than patient's unassisted systolic pressure. C. Augmented diastolic pressure lower than patient's unassisted systolic pressure, balloon assisted diastolic pressure higher than patient's diastolic pressure. D. Augmented diastolic pressure higher than patient's systolic pressure, balloon assisted diastolic pressure lower than patient's diastolic pressure, balloon assisted systolic pressure lower than patient's unassisted systolic pressure.

D. The goal of balloon inflation is to augment diastolic pressure in the aorta so that blood is displaced backwards into the coronary arteries and forwards into the peripheral arterial circulation. Proper inflation timing is aimed at producing an augmented diastolic pressure that is higher than the patient's systolic pressure. The goal of balloon deflation is to lower pressure in the aorta at the same time that ventricular systole occurs in order to afterload reduce the left ventricle. Proper deflation timing should cause balloon assisted aortic diastolic pressure to be lower than the patient's intrinsic aortic diastolic pressure. As a result of balloon deflation during ventricular systole, the systolic pressure in the aorta (balloon assisted systolic pressure) should be lower than the patient's own unassisted systolic pressure. This illustration shows proper timing and desired hemodynamic effects. The red lines represent the patient's own unassisted systolic and diastolic pressure. The green lines show the effect of the IABP on systolic and diastolic pressures (balloon assisted pressures). Balloon inflation occurs on the dicrotic notch and results in augmented diastolic pressure which improves perfusion. Balloon deflation occurs just prior to the next systole, resulting in afterload reduction.

When caring for a patient who had the radial artery harvested during CABG surgery the nurse is aware of the following: A. The radial artery is the first choice graft to use to bypass the LAD. B. The patient will need to be on immunosuppressive agents to prevent graft rejection. C. The radial artery harvest site will require skin grafting as soon as the patient is stable D. The patient will be on a nitrate or calcium channel blocker to prevent spasm.

D. The radial artery is a graft that has the advantage of being a long graft capable of reaching distal sites. The primary disadvantage is that it is thick and muscular and prone to spasm. For this reason perioperative nitrates or calcium channel blockers are indicated. Patients do not need immunosuppressants when native grafts are used. The harvesting sites for grafts involve puncture sites or incisions and do not require any type of skin grafting because skin is not removed.

When caring for a patient who had the radial artery harvested during CABG surgery the nurse is aware of the following: A. The radial artery is the first choice graft to use to bypass the LAD. B. The radial artery harvest site will require skin grafting as soon as the patient is stable C. The patient will need to be on immunosuppressive agents to prevent graft rejection. D. The patient will be on a nitrate or calcium channel blocker to prevent spasm.

D. The radial artery is a graft that has the advantage of being a long graft capable of reaching distal sites. The primary disadvantage is that it is thick and muscular and prone to spasm. For this reason perioperative nitrates or calcium channel blockers are indicated. Patients do not need immunosuppressants when native grafts are used. The harvesting sites for grafts involve puncture sites or incisions and do not require any type of skin grafting because skin is not removed.

Atrial fibrillation is an arrhythmia often seen in post-operative patients undergoing CABG. Preoperative therapy for the reduction of post-operative atrial fibrillation includes the following: A. Preoperative administration of a calcium channel blocker and a beta blocker. B. Preoperative administration of sotalol and amiodarone. C. Preoperative administration of a statin and digoxin. D. Preoperative administration of a beta blocker or amiodarone, and a statin.

D. The standard therapy for the reduction of postoperative atrial fibrillation is the initiation of beta blockers preoperatively. Amiodarone can be used for prophylaxis in high risk patients who are unable to receive beta blockers, but due to inconsistent clinical trial results, amiodarone is not recommended as a routine strategy for the prevention of postoperative atrial fibrillation. Preoperative statin therapy is known to reduce the risk of postoperative atrial fibrillation and is also associated with a reduction in mortality associated with postoperative atrial fibrillation.

Which of the following is the proper location of the intra-aortic balloon during IABP therapy: A. Abdominal aorta just above bifurcation of iliac arteries. B. Tip of the balloon in the aortic arch. C. Tip of balloon below renal arteries. D. Descending aorta between left subclavian artery and renal arteries.

D. The tip of the balloon should be below the left subclavian artery, usually around the 2nd to 3rd intercostal space, and above the renal arteries.

Diabetes increases the risk for postoperative complications in patients undergoing cardiac surgery. Which of the following are appropriate statements about glycemic control in diabetic patients: A. Insulin administration should begin in the ICU and be maintained for 12 hours. B. Intermittent subcutaneous administration of insulin is as effective as continuous insulin infusion in maintaining tight glycemic control. C. Intraoperative glycemic control is not necessary. D. Serum glucose level should be maintained < 180 mg/dL using continuous IV infusion that begins in the OR and is maintained for at least 24 hours postoperatively.

D.The Society of Thoracic Surgeons guidelines on blood glucose management in cardiac surgery patients state the following for diabetic patients: - Glycemic control is best achieved with continuous insulin infusions rather than intermittent subcutaneous insulin injections or intermittent IV insulin boluses. - All patients with diabetes undergoing cardiac surgical procedures should receive an insulin infusion in the operating room, and for at least 24 hours postoperatively to maintain serum glucose levels < 180 mg/dL.

When caring for a patient with a traditional 3-compartment chest tube unit, the nurse knows that: A. Turning up the external source of suction causes loud bubbles and increases the amount of suction applied to the system. The loud bubbles assure an adequate level of suction is being maintained. B. When transporting a patient and portable suction is not available it is important to clamp the chest tube. C. A system valve that is part of the chest tube controls the amount of suction. The amount of suction is limited by the height of the fluid column in the 3rd chamber. D. The typical amount of suction applied to a chest tube drainage system is negative 60 cm H2O.

D. The typical amount of suction applied to a chest tube is minus 20 cm H2O. Patients with very friable lung tissue may need less suction. The maximum amount of suction that should be applied is minus 40 cm H2O. Chest tubes that have been connected to suction should never be clamped for transport. If portable suction is not available, patients should be transported on water seal (on gravity drainage) with the tubing from the suction chamber open to air. Clamping a chest tube for transport can result in pneumothorax for pleural chest tubes or tamponade for mediastinal chest tubes. The source suction should be adjusted to produce only gentle bubbling in the suction control chamber. Excessive external suction causes loud bubbling, which can interfere with patient rest, and also increases the evaporation of water from the suction control chamber.

When caring for a patient with a traditional 3-compartment chest tube unit, the nurse knows that: A. When transporting a patient and portable suction is not available it is important to clamp the chest tube. B. Turning up the external source of suction causes loud bubbles and increases the amount of suction applied to the system. The loud bubbles assure an adequate level of suction is being maintained. C. The typical amount of suction applied to a chest tube drainage system is negative 60 cm H2O. D. A system valve that is part of the chest tube controls the amount of suction. The amount of suction is limited by the height of the fluid column in the 3rd chamber.

D. The typical amount of suction applied to a chest tube is minus 20 cm H2O. Patients with very friable lung tissue may need less suction. The maximum amount of suction that should be applied is minus 40 cm H2O. Chest tubes that have been connected to suction should never be clamped for transport. If portable suction is not available, patients should be transported on water seal (on gravity drainage) with the tubing from the suction chamber open to air. Clamping a chest tube for transport can result in pneumothorax for pleural chest tubes or tamponade for mediastinal chest tubes. The source suction should be adjusted to produce only gentle bubbling in the suction control chamber. Excessive external suction causes loud bubbling, which can interfere with patient rest, and also increases the evaporation of water from the suction control chamber.

Your patient who is day 2 post CABG has developed the rhythm seen here. He is unstable with a BP in the 80s systolic, SOB, and diaphoretic. Which of the following would be the most appropriate therapy for an unstable patient with this rhythm: (AFIB) A. Amiodarone. B. Immediate defibrillation. C. Adenosine. D. Synchronized cardioversion. E. Digoxin.

D. This is atrial fibrillation with a rapid ventricular response and the patient is hemodynamically unstable. Cardioversion is recommended as first line therapy for hemodynamically unstable AF. Defibrillation is appropriate for ventricular fibrillation or pulseless VT, not for atrial fibrillation. Digoxin might be appropriate for rate control in a patient with heart failure, but it takes time to work, and in an unstable patient cardioversion is the therapy of choice, then drug therapy to prevent recurrences. Amiodarone can be effective in terminating atrial fibrillation and may also slow the ventricular response, but it takes time to work and is not the first drug recommended for an unstable patient. Adenosine is a good drug for terminating AV nodal reentry tachycardia or accessory pathway tachycardias but it is not indicated for treating atrial fibrillation or flutter.

Which of the following can contribute to postoperative hyperkalemia: A. Use of ACE inhibitors or angiotensin receptor blockers (ARBs). B. Acute renal failure. C. Low cardiac output state and tissue ischemia. D. All of the above.

D. Tissue ischemia from low cardiac output or as a complication of IABP therapy or severe peripheral vascular disease results in cell breakdown with release of intracellular potassium. Medications like ACE inhibitors and ARBs result in potassium retention by the renal tubules. Acute renal failure prevents the kidneys from excreting potassium normally. In addition, use of high potassium cardioplegia during CPB can contribute to hyperkalemia in patients with renal dysfunction or oliguria.

Which of the following can contribute to postoperative hyperkalemia: A. Use of ACE inhibitors or angiotensin receptor blockers (ARBs). B. Low cardiac output state and tissue ischemia. C. Acute renal failure. D. All of the above.

D. Tissue ischemia from low cardiac output or as a complication of IABP therapy or severe peripheral vascular disease results in cell breakdown with release of intracellular potassium. Medications like ACE inhibitors and ARBs result in potassium retention by the renal tubules. Acute renal failure prevents the kidneys from excreting potassium normally. In addition, use of high potassium cardioplegia during CPB can contribute to hyperkalemia in patients with renal dysfunction or oliguria.

You are caring for an early post-operative CABG patient who remains hypotensive despite treatment with adequate fluid administration and an alpha constricting agent. You know that one potential post-operative complication responsible for this persistent hypotension could be: A. Acute kidney injury. B. Acute saphenous vein graft closure. C. Acute respiratory distress syndrome (ARDS). D. Vasoplegia.

D. Vasoplegia is a form of vasodilatory shock that can occur after separation from CPB. It is characterized by significant hypotension despite adequate fluid resuscitation, low SVR(due to vasodilation), and is resistant to vasopressors. When vasopressors (norepinephrine, epinephrine, high dose dopamine, or vasopressin) are not able to maintain blood pressure in the presence of adequate filling pressures, then vasoplegia may be present. There are several theories behind the cause of vasoplegia, including leukocyte activation and the release of pro-inflammatory mediators during cardiopulmonary bypass, and vasoplegia has been associated with long-term use of ACE inhibitors, calcium channel blockers, amiodarone, and heparin. Patients with EF <35%, heart failure and diabetes are at higher risk. Vasoplegia can also be seen after OPCAB. Acute respiratory distress syndrome (ARDS) and acute kidney failure can both be complications in the cardiac surgery patient, but do not typically occur early in the post-operative course and are not necessarily associated with hypotension and failure to respond to vasopressors. An acute saphenous vein occlusion can occur as a result of persistent hypotension. The most direct clinical signs of acute saphenous vein graft closure would be those of ischemia.

Management of postoperative RV dysfunction includes which of the following: A. Vasoconstrictors and inotropes. B. Beta blockers and venous dilators. C. Preload reduction with venous dilators and diuretics. D. Volume infusion and pulmonary vasodilators.

D. Volume infusion is indicated to optimize RV preload so that the RV can fill the LV. Overdistension of the RV can result in shifting of the septum toward the LV, so volume administration is done cautiously and the CVP should not go over 20 mmHg. Pulmonary vasodilators, such as inhaled nitric oxide, epoprostenol (Flolan), iloprost (Ventavis), and sildenafil (Viagra) result in pulmonary vasodilation and reduce pulmonary vascular resistance against which the RV has to work. Anything that reduces RV preload is contraindicated in RV failure because RV preload must be maintained or improved in order to support LV filling and function. Diuretics and venous dilators would reduce preload and are not indicated. AV synchrony must be maintained if possible because atrial kick contributes to preload and improved RV function. If pacing is needed, AV sequential pacing is preferred over ventricular pacing for this reason. Beta blockers decrease contractility and would not be helpful in supporting a failing RV. Inotropic drugs to increase contractility are indicated if RV function doesn't improve with volume. Milrinone has both inotropic and vasodilator effects and can improve RV contractility and reduce pulmonary artery pressure. Dobutamine may also be effective in supporting RV contractility.

The risk of sternal wound infection is increased by which of the following: A. Early extubation and pneumonia. B. Hypoglycemia and advanced age. C. Prolonged CPB and renal dysfunction. D. Diabetes and obesity.

D.Major risk factors for sternal wound infection include diabetes and obesity. Diabetes is a risk factor because hyperglycemia impairs the immune system. Patients with diabetes have impaired chemotaxis (the process that draws white blood cells to the site of an infection) and phagocytosis (the process of ingestion of bacteria by white blood cells). Obesity results in increased force applied to the incision which affects the collagen fibers and inhibits healing. Patient factors that increase risk include: Diabetes mellitus, obesity, COPD, advanced age, and protein calorie malnutrition. Surgical factors that increase risk include: prolonged cardiopulmonary bypass time, prolonged intubation time, reoperation or surgical re-exploration. and use of both internal mammary arteries.

Thrombocytopenia after CABG surgery is common due to the following contributing factors: A. Use of the intra aortic balloon pump. B. Platelet activation during cardiopulmonary bypass. C. Use of heparin during or after surgery. D. All of the above.

D.Multiple factors in the patient post CABG affect the platelet count. Intraoperative cardiopulmonary bypass reduces the platelet count through platelet activation and dilution. Any patient who requires supportive intra aortic balloon pump therapy will have a further decline in platelet count due to the effect of balloon inflation on blood components. Medications such as heparin add the additional potential to reduce the platelet count.

A patient with epicardial atrial and ventricular pacing wires post cardiac surgery has a change in his rhythm on the bedside monitor. Which of the following connections would allow you to obtain an atrial electrogram to help diagnose the rhythm: A. Connect a ventricular pacing wire to the chest lead and record 'V' on the bedside monitor. B. Connect an atrial pacing wire to the right leg electrode and record "V" on the bedside monitor C. Connect an atrial pacing wire to the chest lead on your monitor cable and record lead II on the bedside monitor. D. Connect an atrial pacing wire to the chest lead on your monitor cable and record 'V' on the bedside monitor.

D.Recording an atrial electrogram directly from an atrial pacing wire allows easy identification of atrial activity (P waves or flutter/fib waves) and helps illustrate the relationship between P waves and QRS complexes when it is difficult to see on a surface lead. The easiest way to do this is to attach a monitoring electrode to the chest lead on a 5-wire monitor cable and wrap it tightly around the metal end of an atrial pacing wire, making sure that the metal end of the pacing wire is in the gel center of the electrode and touching the metal portion of the button under the gel. Then set the monitor to record 'V', which records from the chest lead that is now attached to the atrial pacing wire. This connection will provide a unipolar recording (using one atrial wire) with very large atrial deflections. The connection between the atrial pacing wire and the monitor lead can also be made using an alligator clip, but this method using a regular monitoring electrode doesn't require any special equipment. It is a good idea to simultaneously record a surface lead along with the atrial electrogram and to run the paper at double speed through the recorder to spread the tracing out for better visualization. Lead II on the monitor is recorded between the right arm and the left leg electrodes, not the chest lead. Connecting a ventricular pacing lead will only accentuate the QRS, not the P waves. This illustration shows the connection of the chest lead on the monitor to an atrial pacing wire using a regular monitoring electrode.

Which of these patients is at highest risk for an adverse neurovascular complication after CABG: A. A previously healthy 50-year-old woman undergoing cardiopulmonary bypass. B. A patient undergoing OPCAB for bypass surgery using the LIMA and RIMA. C. A 67-year-old man having a MIDCAB to the LAD with no known history of hypertension. D. A patient with an atherosclerotic aorta undergoing emergent traditional on pump cardiopulmonary bypass graft surgery.

D.Traditional cardiopulmonary bypass graft surgery on pump involves cross-clamping of the aorta. Cross clamping of the aorta in the presence of atherosclerosis can result in an embolic event and resultant CVA. For this reason imaging of the aorta via epi-aortic or transesophageal echocardiography is required before cross-clamping the aorta. OPCAB (off pump coronary artery bypass graft surgery) is an option to do surgery on a beating heart and avoid the use of cardiopulmonary bypass and clamping of the aorta. If a saphenous vein graft is used during OPCAB, aortic cross clamping may still be needed while the graft is being sutured to the aorta. Patient factors which increase the risk for a neurological complication in any type of open heart surgery include advanced age and presence of preoperative hypertension.

You are caring for a patient with a chest tube in place for treatment of a pneumothorax. What is true regarding the waterseal chamber: A. The main purpose of the water seal is to allow air to exit from the pleural space on exhalation and prevent air from entering the pleural cavity or mediastinum on inhalation. B. Lack of tidaling may indicate a kink. C. Continuous bubbling represents an air leak. D. The chamber may bubble gently during expiration. E. All of the above.

E. The 2nd compartment is connected to the 1st and creates a water seal. A small amount of sterile water (per manufacturer directions) is injected into the water seal chamber before the drainage system is connected to the patient. The main purpose of the water seal is to allow air to exit from the pleural space on exhalation and prevent air from entering the pleural cavity or mediastinum on inhalation. Air that is allowed to pass through the water seal will bubble out the bottom of the chamber. The water seal chamber is calibrated and should be seen as the window into the pleural space. During gravity drainage the level of water reflects the intrapleural pressure. Some newer systems eliminate the water seal chamber and use a check-valve to serve its purpose. Assure that the amount of sterile fluid in the water seal and suction chambers is at the manufacturer recommended levels when wet systems are used. To maintain an adequate water seal in a wet system it is important to monitor the level of water in the water seal chamber and to keep the chest drainage unit upright at all times. Assess for air leak by checking water seal chamber for bubbles during inspiration. The water seal chamber may bubble gently with insertion, during expiration and with a cough. Continuous bubbling represents an air leak. Some water seal compartments have an air leak meter. Check for system leaks by clamping before each connection (system may need to be replaced). Check for leak where tube enters chest. Check chest x-ray to assure last hole of chest tube is inside chest. Assess the water seal chamber for slight fluctuation. Slight fluctuation (tidaling) in the water seal level (rising during spontaneous inspiration and falling during expiration) is normal. Lack of fluctuation with respiration may indicate kinking or other problems interfering with drainage. A slow gradual rise in the water level is consistent with an increase in intrapleural pressure. This is a desired outcome as normal intrapleural pressure is restored and the lung re-expands.

Your patient who is day 2 post CABG has developed the rhythm seen here. He is unstable with a BP in the 80s systolic, SOB, and diaphoretic. Which of the following would be the most appropriate therapy for an unstable patient with this rhythm: (AFIB WITH RVR) A. Immediate defibrillation B. Amiodarone. C. Digoxin. D. Adenosine. E. Synchronized cardioversion.

E. This is atrial fibrillation with a rapid ventricular response and the patient is hemodynamically unstable. Cardioversion is recommended as first line therapy for hemodynamically unstable AF. Defibrillation is appropriate for ventricular fibrillation or pulseless VT, not for atrial fibrillation. Digoxin might be appropriate for rate control in a patient with heart failure, but it takes time to work, and in an unstable patient cardioversion is the therapy of choice, then drug therapy to prevent recurrences. Amiodarone can be effective in terminating atrial fibrillation and may also slow the ventricular response, but it takes time to work and is not the first drug recommended for an unstable patient. Adenosine is a good drug for terminating AV nodal reentry tachycardia or accessory pathway tachycardias but it is not indicated for treating atrial fibrillation or flutter.

You are admitting a cardiac surgery patient from the OR to the ICU. After the patient has been transferred to the ICU bed, you note that the arterial line BP displayed on the monitor is 80/56. You have verified that the arterial line is not kinked and the tubing is free of air and blood, and that the transducer is correctly located at the patient's phlebostatic axis and has been correctly zeroed after connection to the bedside monitor. Which of the following should be evaluated to determine the cause of this patient's hypotension: A. Verify that chest tube drainage is not excessive. B. Verify that medication infusions have not become disconnected during transport and transfer to the ICU bed. C. Evaluate CVP, PWP (or PA diastolic pressure), CO, SVR, SaO2. D. Verify an adequate cardiac rhythm on the bedside monitor. E. All of the above.

E.Immediate postoperative hypotension is commonly due to inadvertent vasopressor infusion termination (i.e. disconnected lines or wrong infusion rate due to switching from one infusion pump to another) or hypovolemia due to excess bleeding. The nurse must make sure that all medication infusions are intact and running at the correct rate. If a vasodilator (nitroglycerin or nitroprusside) is running it should be turned off. Excessive chest tube drainage can indicate bleeding as a cause of hypotension. Other causes of postoperative hypotension can include cardiac arrhythmias, myocardial dysfunction or ischemia, cardiac tamponade, pneumothorax or hemothorax, or ventilation problems. Evaluation of hemodynamic monitoring parameters can help determine if hypotension is due to preload problems (low CVP and PWP), cardiac tamponade (equalization of CVP, PA diastolic, and PWP), or myocardial dysfunction (low cardiac index in presence of adequate preload and afterload). Bilateral breath sounds should be present and ventilator settings and function verified. A postoperative chest X-ray should be obtained to verify ET tube placement and absence of pneumothorax or hemothorax.


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