STS Benchmark - Cardiac Surgery General Mgmt Flashcards
In the penicillin-allergic patient undergoing elective coronary revascularization, what is a safe alternative that can cover MRSA?
How is it administered safely to avoid hypotension?
Vancomycin - provides safe and effective prophylaxis if administered slowly.
*Vancomycin was first used clinically in 1958 before the antistaphylococcal penicillins, such as methicillin, were developed. Despite introduction of the cephalosporins, vancomycin is still effective in methicillin-resistant staphylococcal infections, bacterial endocarditis in patients allergic to penicillin, and for prophylaxis of bacterial endocarditis in patients with prosthetic valves and penicillin allergy.
Its most serious side effect, hypotension, can usually be avoided if vancomycin is administered cautiously as a 0.5% solution over 30-60 minutes.
As with all perioperative antibiotic regimens, 48 hours of administration is sufficient. More prolonged administration predisposes to superinfection and provides no documented decrease in wound, lung, or urinary infections. The spectrum of vancomycin is limited to gram-positive organisms.*
Assuming no change in myocardial contractility, mean arterial pressure or heart rate, which of the following will increase the pulmonary capillary wedge pressure needed to maintain a cardiac index of 2.0 liters/min/m2 addition of positive end-expiratory pressure to positive pressure ventilation?
- myocardial edema
- removal of a functioning intra-aortic balloon pump
- conversion from sinus to junctional rhythm
- right atrial-pulmonary artery mechanical assist device
Right atrial-pulmonary artery mechanical assist device.
The determinants of left ventricular (LV) performance are heart rate, preload, afterload, and contractility. If all variables except preload are held constant, cardiac index (CI) will become dependent on left ventricular end-diastolic volume (LVEDV). Compliance relates LVEDV to wedge pressure. Positive end-expiratory pressure increases the wedge pressure required to maintain CI. Conversion from sinus to junctional rhythm removes the atrial kick, decreasing LVEDV and stroke volume and increasing wedge pressure to maintain Cl. Edema reduces compliance of the left ventricle and requires increased wedge pressure to maintain LVEDV and Cl. Pulmonary stenosis and tricuspid insufficiency increase right ventricular end-diastolic pressure and volume, pushing the interventricular septum to the left and distorting the LV. Wedge pressure must then be increased to maintain LVEDV and Cl. Right atrial-pulmonary artery mechanical bypass unloads the right ventricle and, by a mechanism opposite that above, will decrease the wedge pressure required to maintain LVEDV and CI.
The decline in myocardial contractility that occurs after coronary artery occlusion is due to both lack of substrates and accumulation of various metabolites.
What is the most important substrate?
*The most important substrate is oxygen. Within minutes intramyocardial oxygen tension falls to low levels.
The attendant decrease in myocardial contractility is also associated:
* increased rate of glycolysis
* increased cellular levels of cyclic AMP
* accelerated conversion of phosphorylase from the inactive “B” form to the more active “A” form
* ATP degradation
* decreased glycogen synthesis
Some of these effects may be especially important in regions of partial ischemia where a reduced capacity for aerobic energy production may support marginal levels of function.*
In an intubated, febrile multiple trauma patient, systemic therapy with what should be initiated if a CVP line tip culture shows Candida and fundoscopic examination is consistent with Candida endophthalmitis.
amphotericin B
Complex Intensive Care Unit patients are highly susceptible to fungal infections especially if they have been on broad spectrum antibiotics (which is the case in most patients with multi-system trauma). The question addresses the problem of when to initiate anti-fungal therapy for suspected systemic fungemia or systemic fungal infection. In general the surgical literature has been more aggressive in treating fungal infections than many of the infectious disease recommendations. Although a central venous pressure line tip which grows Candida in a febrile patient may or may not be the source of the fever, all patients who have fundoscopic evidence of Candida endophthalmitis have systemic fungemia by definition and need systemic therapy.
When should one start systemic antifungal therapy based on blood cultures?
What about for urine?
In general, one positive blood culture in a patient who has positive cultures from another source and who has a persistent fever, should be a stimulus to initiate systemic therapy. One should not wait for a second culture to begin therapy.
50,000 organisms in the urine with positive fundoscopic examination would be adequate stimulus for systemic therapy. However, merely having Candida with a Foley catheter in place does not necessarily imply that the urine is the source of the fever. 50,000 per/ml Candida in the urine without budding yeast may or may not suggest a systemic problem, although Candida is obviously present. Finally, empiric amphotericin therapy for systemic fungal infections in the absence of positive cultures is not warranted except in the immunosuppressed patient who is either status posttransplant or is on immunosuppressive chemotherapy. (Candida pneumonia is extremely rare in a non-immunologically suppressed host). Empiric anti-fungal therapy in a trauma patient is usually not warranted.
A 70 year old man with aortic insufficiency underwent cardiac catheterization. Ejection fraction was 50%, regurgitant fraction was 25% and end-diastolic volume was 200 ml. Heart rate was 100 beats/minute. What was his cardiac output?
7.5 L/min
Tumor necrosis factor (TNF), a low molecular weight polypeptide, is an early primary mediator of inflammation. For each of the following conditions, does TNF play a central role in the pathogenesis?
- cachexia.
- reperfusion injury.
- coma.
- septic shock.
- transplant rejection.
All except coma.
Tumor necrosis factor (TNF) is a low molecular weight polypeptide derived mainly from mononuclear phagocytes (monocytes and macrophages) and T-lymphocytes. To accomplish its biological functions, TNF must combine with specific receptor molecules on target cells. These TNF receptors are present on all cells except red blood cells. Soluble TNF receptors can be detected in the body fluids (serum and urine) of patients with sepsis, cancer, and fever. When TNF binds to cell receptors, gene upregulation and production of new protein follow. This communication, known as receptor signal transduction, results in the production of other cytokines that amplify and propagate the biological effects of TNF or change the host response to TNF. TNF is an early primary mediator of inflammation and plays a central role in the pathogenesis of cachexia, septic shock, tissue injury (including ischemia/reperfusion), transplant rejection, and tumor cytolysis. Biological effects of TNF on the central nervous system are fever, hypothalamic-pituitary release of corticotropin releasing factor and adrenocorticotropic hormone, anorexia, and meningeal inflammation.
The major physiologic mechanism that augments myocardial oxygen delivery during exercise is?
coronary vasodilatation
During exercise or any type of hemodynamic stress the major coronary reserve is vasodilatation. Under normal conditions, myocardium extracts 75% or more of the available oxygen in the blood, so the heart has little extraction reserve. Conversely, the normal coronary vascular resistance is three to six times the resistance of the vasculature when coronary vessels are maximally dilated, Thus, coronary arteriolar dilatation can increase myocardial oxygen delivery by up to 600%.
What tissue changes/effect does acute heart failure have on the following?
* ATP
* protein synthesis
* phosphocreatine
* mitochondrial mass
* lactate
decreased ATP levels
increased protein synthesis
decreased phosphocreatine
increased mitochondrial mass
increased lactate
The response of the heart to overload can be divided into three stages: acute short-term heart failure, compensatory hyperfunction, and cell death and fibrosis. In the first stage the reserves of the non-hypertrophied myocardium are exhausted and glycogen, ATP, and phosphocreatine levels are decreased. Lactate production (accelerated glycolysis), protein synthesis, and mitochondrial mass increase. Histologically there is edema of the ventricular wall and swelling and separation of the myofibrils. These changes lead to the second stage (i.e., hypertrophy) which is associated with the return of protein synthesis rates and RNA levels to normal. The final stage of heart failure occurs when muscle cells die and are replaced by connective tissue.
A 72-year-old man had a right carotid endarterectomy three days ago. Re-intubation was elected because of worsening stridor. Attempts to secure an airway by awake nasotracheal intubation after protracted use of aerosolized topical 4% lidocaine were not successful. Following cricothyroidotomy the patient was stabilized and moved to the ICU. The pulse oximeter indicates an oxygen saturation of 92% but an arterial blood gas reveals hypoxemia with a pO2 of 55 mmHg.
What is the workup and management?
Discordance b/w the O2 sat and pO2 should prompt a suspicion for MetHgb toxicity in the setting of topical lidocaine use. Determine if hx of G6PD defx or serotonergic drugs.
The blood gas should report methemoglobin levels.
* >5% is diagnostic.
* >30% is life threatening.
Mgmt:
* Stop offending agent.
* Support - supplement oxygen.
* If hx of G6PD def or serotonergic meds, use ascorbic acid (vit C).
* If no hx of above, use Methylene blue.
* If not working, re-evaluate and consider exchange transfusion or hyperbaric oxygen.
Iron contained in hemoglobin is usually in the ferrous form. Reduction of iron to the ferric form results in the formation of methemoglobin (MetHgb), and methemoglobinemia results from increased methemoglobin formation. Several chemicals and drugs can be responsible, including local anesthetics (cetacaine, benzocaine, or lidocaine as in this patient), nitrites and sulfonamides. Clinical effects are due to the inability of MetHgb to bind oxygen, resulting in a state of functional anemia and by an increase in the affinity of the remaining ferrous heme for oxygen. Signs and symptoms depend on the MetHb level. Levels greater than 15% are associated with cyanosis. Levels of 20-45% are associated with headache, lethargy, tachycardia, weakness and dizziness. Levels greater than 45% manifest dyspnea, acidosis, cardiac dysrhythmias, heart failure, seizures and coma. Oximetry overestimates O2 saturation when there is methemoglobinemia. CO-oximetry directly measures methemoglobin saturation and correctly yields O2 saturation. The drug of choice for treatment of methemoglobinemia is methylene blue, an electron donor that converts methemoglobin to hemoglobin. Methylene blue should be given in boluses of 1-2 mg/kg IV, anticipating an effect in 30-60 minutes. This dose can be repeated after one hour. Doses exceeding 15 mg/kg may actually cause methemoglobinemia by direct oxidation of Hgb to MetHgb. Patients with glucose 6-phosphate dehydrogenase (G6PD) deficiency will not respond to methylene blue due to decreased production of NADPH. Ascorbic acid works slowly so it is of little value. Transfusions, exchange transfusions and hyperbaric oxygen therapy are potential treatments for refractory failures of methylene blue but the other modalities have not been critically studied.
A 65-year-old man underwent a reoperative CABG x 4. His initial post-operative course was uneventful, but on POD# 3 thrombocytopenia was noted and examination revealed black toes and evidence of a cerebrovascular accident. An echocardiogram demonstrated thrombus in the left ventricle, and other workup confirmed the stroke and bilateral common iliac vein thromboses. HIT serologic testing was reported positive. In addition to stopping all unfractionated heparin, what else should be added?
an intravenous direct thrombin inhibitor
Heparin induced thrombocytopenia (HIT) was first described as an arterial thrombotic disease that is now usually called HITT (heparin induced thrombocytopenia and thrombosis). This entity was notable because the emboli were pale in color secondary to platelet domination (“white clot syndrome”). It is now recognized that thrombosis can occur in either the arterial or venous system, related to the underlying vascular damage and associated surgical risk factors. Reports suggest that HITT affects the venous system more commonly than the arterial system (4:1), but as this case illustrates, both systems can be affected simultaneously. HIT and HITT are immunological disorders in which heparin-IgG-platelet factor 4 complexes bind to platelet Fc receptors, which activate to cause aggregation and potential thrombosis. In addition to aggregation, patients may develop evidence of disseminated intravascular coagulation (DIC) during the acute thrombocytopenic episode. Evidence supporting the pro-thrombotic nature of HIT is apparent from complications that follow substitution of warfarin for discontinued heparin. This may cause an initial depletion in the level of protein C, a natural anticoagulant, and these patients can develop particularly aggressive and worsening thrombosis. Thrombin generation plays a pivotal role in the pathogenesis of HIT. Treatment must include stopping all heparin, but an intravenous direct thrombin inhibitor (lepirudin, bivalirudin, argatroban, and others) should be given. Warfarin can be started only after the platelet count has returned to normal. Thrombin inhibition is continued until warfarin is therapeutic. Utilization of a Factor 10 inhibitor (enoxaparin, other low molecular weight heparins [LMWH]) as a bridge for coumadin therapy or for prophylaxis may be efficacious, but these drugs pose a residual risk. Low molecular weight heparins may produce a positive test for HIT in patients with previous exposure or a history of HIT, and thrombocytopenia may occur. About one third of patients will demonstrate cross-reactivity to unfractionated heparin. If aggregation is demonstrated, then LMWH must not be used. Otherwise, daily platelet counts are indicated.
Diagnostic coronary angiography prior to elective aortic valve replacement demonstrates a small right coronary artery with a single posterior descending branch. The left anterior descending coronary artery is normal, but the circumflex coronary artery is not seen.
What are some credible explanations for this?
- short left main coronary artery with selective engagement of the left anterior descending coronary artery.
- separate origins of the left anterior descending and circumflex coronary arteries from the left aortic sinus.
- proximal occlusion of the circumflex coronary artery from atherosclerotic disease.
- anomalous origin of the circumflex coronary from the right coronary artery.
- NOT likely to be congenital absence of the circumflex coronary artery.
The proximal right coronary artery is the most common anomalous origin of the circumflex coronary artery. Congenital absence of the circumflex coronary artery is extremely rare, and the lack of visualization of the circumflex on coronary angiography should prompt a thorough search for the vessel. Proximal occlusion of the circumflex coronary artery can occur, but in most instances the distal vessel will fill by collaterals from the left anterior descending (LAD) coronary artery or right coronary artery. The circumflex coronary artery may not opacify if the left main coronary artery trunk is very short and the LAD is cannulated selectively or if separate origins of the LAD and circumflex exist.
Under normal conditions, left ventricular subendocardial blood flow is determined primarily by?
Under normal conditions when net coronary perfusion pressure is adequate, regional myocardial blood flow is primarily determined by regional arteriolar resistance which, in turn, is modulated by local metabolic demands.
During normal physiology, subendocardial blood flow autoregulates and is altered minimally in response to changing diastolic perfusion intervals, aortic diastolic pressures, ventricular end-diastolic pressures, and regional diastolic intramyocardial pressures. However, with maximal vasodilatation induced by hypoxia or other stimuli, regional myocardial perfusion becomes pressure and time dependent, and hemodynamic factors assume greater importance.
The majority of ventricular filling occurs in which phase of the cardiac cycle?
The first third of diastole.
Most ventricular filling occurs during the rapid filling phase in the first third of diastole. In fact, up to 50% of total filling occurs before ventricular pressure reaches the first diastolic minimum. The combination of a high atrioventricular pressure gradient upon mitral valve opening and active restorative forces associated with myocardial relaxation probably accounts for this finding.
Stunned myocardium is defined as a loss of myocardial contractile force following reperfusion of ischemic myocardium that does not develop necrosis.
What happens to diastolic compliance?
What happens to oxygen utilization efficiency?
Myocardial contractility decreases almost immediately after ischemia begins and remains depressed far longer than the duration of the ischemic period. Fifteen to twenty minutes of ischemia depresses myocardial contractility for several days. Thirty minutes of ischemia at 37 degrees C causes loss of mitochondrial dense granules, clearing of the matrix and fragmentation of cristae; yet after 120 minutes of reperfusion, mitochondrial architecture appears normal. Reversible ischemia reduces both systolic and diastolic function. Myocardial cells develop wide I bands consistent with myocardial creep. Diastolic compliance decreases and stunned myocardium is stiff. Oxygen consumption per unit of left ventricular work increases several fold in stunned myocardium. By definition, oxygen utilization efficiency is profoundly decreased.
Although the evidence is inconclusive, recovery of oxygen utilization efficiency precedes recovery of contractile function. The depression in oxygen utilization efficiency is five to ten times longer than the period of ischemia. During reversible ischemia, permeability of the sarcoplasmic reticulum membrane increases so that excess extracellular calcium enters the myocyte during reperfusion. Cellular calcium overload results and intracellular calcium contractile functions are depressed. Reperfusion with low calcium perfusates improves contractile function of stunned myocardium. However, myocardial stunning also produces oxygen free radicals and other metabolites which may also contribute to the delayed return of contractile force.
Discuss how protamine can have a contradictory effect on ACT levels at the end of a CPB case.
Excess protamine weakens clot structure and decreases platelet function. Therefore, an increased activated clotting time (ACT) after protamine reversal of heparin may be misinterpreted as residual heparin anticoagulation. Additional protamine administered to treat a prolonged ACT may further increase clotting time, reduce platelet aggregation, and potentially contribute to excess bleeding after CPB. In contrast, heparin antagonists, such as recombinant platelet factor 4 and hexadimethrine, exhibit heparin reversal activity without adversely affecting the activated clotting time
A 75-year-old man is in mild respiratory distress in the intensive care unit on POD# 3 following repair of an extent I thoracoabdominal aneurysm (CT and composite shown). Proximal control of the aorta was obtained just beyond the left common carotid artery. He is quite hoarse when he tries to speak and it is difficult for him to effectively cough. When he is given water to drink he clearly aspirates and coughs violently. The most likely explanation for this man’s symptoms is?
left recurrent nerve injury during the aneurysm repair
In addition to the usual concerns for central nervous system injury during thoracic aneurysm repair, injury to a number of intrathoracic nerves is a function of anatomy and the nature of the patient’s pathology. The left phrenic nerve can be injured when mobilizing the aortic arch in preparation for cross-clamping, during cannulation of the superior pulmonary vein or left atrial appendage for partial left heart bypass or during division of the diaphragm for exposure of aneurysms that extend below the diaphragm. Patients with impaired pulmonary function may struggle heroically (but often unsuccessfully) from a phrenic neuropraxia. A plain chest radiograph will usually reveal a markedly elevated left hemidiaphragm. Fortunately, this complication is quite rare because the nerve is usually easy to identify as it runs beneath the mediastinal pleura and along the pericardium. Left recurrent nerve injuries are a much more common problem. They occur in approximately 10% of cases and are usually due to nerve contusion or a traction injury rather than actual nerve transection. When this occurs, patients will be hoarse and will have difficulty generating a forceful cough. The risk of aspiration is substantial. This problem is much more common in descending or thoracoabdominal aneurysm repair where control of the aorta is obtained proximal to the left subclavian artery. It may also occur in cases similar to the one described, where total arch reconstruction is performed. Fortunately, only 15% of patients will require further intervention after the diagnosis is made.
Preoperative infusion of magnesium sulfate in patients undergoing revascularization for unstable angina results in?
Increasing clinical evidence suggests that perioperative infusion of magnesium sulfate has many beneficial effects in patients who undergo revascularization for unstable angina. Patients receiving perioperative infusion of magnesium sulfate have a significantly lower incidence of postoperative ventricular arrhythmias which require treatment, a decreased incidence of postoperative hypertension which requires nitroprusside infusion, improved left ventricular stroke work index and improved cardiac index with a decreased requirement for postoperative inotropic support.
The incidence of postoperative atrial fibrillation does not appear to be influenced by magnesium treatment. The only noticeable side effect of magnesium infusion is an increased time to resumption of normal sinus rhythm after release of the aortic crossclamp. However, new conduction abnormalities such as left or right bundle branch block do not result from, and are not favorably influenced by, magnesium infusion.
Chronic pulmonary venous hypertension can produce miliary nodules of hemosiderin laden macrophages scattered throughout the lung parenchyma. These result from punctate hemorrhages caused by venous hypertension. Are they a recognized cause of arteritis or altered pulmonary vascular resistance?
No.
High altitude pulmonary hypertension is caused by?
reduced inspired oxygen tension
Is hypertrophy of pulmonary arteriolar smooth muscle that progresses to intimal proliferation and hyperplasia is reversible in adults who remain at altitude?
No
Angiotensin converting enzyme (ACE) inhibitors are effective in reducing pulmonary hypertension?
No
Chronic pulmonary thromboembolism usually effects medium-sized and large pulmonary arteries and can cause severe right heart failure with liver congestion (cirrhosis, ascites, and severe swelling and stasis changes of the legs).
What surgical options are there?
Extended pulmonary endarterectomy has been shown to be effective and specific therapy for patients with chronic thromboembolic pulmonary vascular occlusive disease. The goals of the operation are complete removal of obstructing thrombus and reactive tissue, prevention of further emboli, and avoidance of cardiopulmonary bypass if possible.
Persistent large left-to-right shunts increase pulmonary arterial blood flow and produce hyperkinetic pulmonary hypertension. Eventually, the patient gets arteriolar proliferation and hyperplastic changes with loss of pulmonary vascular arborization. Because of the high pulmonary vascular resistance, the shunt typically reverses to right-to-left. Patients develop cyanosis, clubbing and polycythemia.
What is the eponym for this?
Is this reversible?
Eisenmenger’s syndrome.
Large pulmonary vessels develop medial smooth muscle hypertrophy and increased elastic tissue which regresses if the shunt is closed. Persistence of hyperkinetic pulmonary blood flow eventually produces Eisenmenger’s disease with its arteriolar proliferation and hyperplastic changes with loss of pulmonary vascular arborization. This condition is not reversible.