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.
What can increase the risk of protamine reaction?
Although not all factors are identified as significant in all studies, factors which have been shown to have a predictive influence on the risk of protamine reactions include history of fish or non-protamine allergic reaction, prior protamine exposure, and use of NPH insulin.
Protamine sulfate is a strongly cationic polypeptide that is used commonly in clinical medicine. It is administered regularly after cardiac catheterization, cardiothoracic and vascular surgical procedures, and less frequently after dialysis and leukapheresis because of its capacity to reverse the anticoagulant activity of heparin. In addition, because it delays the absorption of insulin, protamine is combined with insulin in protamine zinc insulin and neutral protamine Hagedorn insulin.
The incidence of significant protamine reactions at the end of cardiopulmonary bypass (CPB) has been reported to be as high as 10.7%. Cardiovascular effects vary in severity from mild hypotension to hemodynamic collapse, and a precipitous drop in blood pressure follows protamine administration in approximately 2% of CPB cases. Many putative risk factors for protamine reactions have arisen from anecdotal reports, and others derive from theoretical immunologic considerations.
Unfortunately, neither a positive skin test nor a positive IgE ELISA for antiprotamine antibody predicts that a patient will have a reaction. Management of protamine reactions may include volume loading, antihistamines, steroids, epinephrine or additional heparinization and reinstitution of cardiopulmonary bypass. Some additional alleged risk factors for protamine reactions include prior vasectomy, poor left ventricular function, and hemodynamic instability. A complex operation in a compromised patient that requires prolonged cardiopulmonary bypass may make separation from bypass challenging, but this is unrelated to the incidence of true protamine reactions. Alternative strategies for anticoagulation and for heparin reversal are needed.
What are some benefits of tight perioperative glucose control after CPB cases?
Studies show decreases in the prevalence of several complications including infections, prolonged inflammation, acute renal failure requiring dialysis or hemofiltration, critical illness polyneuropathy, and transfusion requirements. Patients receiving intensive insulin therapy are also less likely to require prolonged mechanical ventilation and intensive care. Attempts at tight glycemic control, however, do not seem to influence neurologic or behavioral outcomes.
Glycemic control is increasingly recognized as an important goal for perioperative patients and the critically ill. Hyperglycemia and insulin resistance are common in ICU patients, even when there is no history of diabetes. Multiple studies agree that patients who undergo cardiac surgery with hyperglycemia have increased morbidity rates (including wound and sternal infections). Mortality increases when such patients remain in the ICU more than five days. It is not clear, however, if elevated blood glucose is a marker or a pathogenic mechanism of disease in these patients. The exact mechanisms by which hyperglycemia, insulin resistance, or both contribute to complications remains under investigation. Leukocyte activity, immunoglobulin production, wound healing, collagen production, endothelial function, cardiac performance, and fluid balance are each impaired in the setting of hyperglycemia. The most recent recommendations for intensive insulin therapy include strict protocol-driven testing and management with a goal of serum glucose under 110mg/dL. Studies with a less ambitious endpoint were associated with decreases by at least half in the prevalence of several complications including infections, prolonged inflammation, acute renal failure requiring dialysis or hemofiltration, critical illness polyneuropathy, and transfusion requirements. Patients receiving intensive insulin therapy are also less likely to require prolonged mechanical ventilation and intensive care. 2009 Society of Thoracic Surgeons Recommendations are as follows: Patients with and without diabetes with persistently elevated serum glucose (180 mg/dL) should receive IV insulin infusions to maintain serum glucose 180 mg/dL for the duration of their ICU care (level of evidence A). All patients who require 3 days in the ICU because of ventilatory dependency or requiring the need for inotropes, intra-aortic balloon pump, or left ventricular assist device support, anti-arrhythmics, dialysis, or continuous veno-venous hemofiltration should have a continuous insulin infusion to keep blood glucose 150 mg/dL, regardless of diabetic status (level of evidence B). Before intravenous insulin infusions are discontinued, patients should be transitioned to a subcutaneous insulin schedule using institutional protocols (level of evidence B).
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
In patients with atherosclerotic coronary disease, myocardial blood flow at rest is?
The normal myocardial blood flow is approximately 90 ml per 100 gm heart muscle per minute, and values of 200 ml/100 gm/min are achieved only during extreme exercise or with maximal coronary vasodilatation. When the diameter of a coronary artery is narrowed by 50%, its luminal area is reduced by 75%, and this degree of stenosis may reduce resting blood flow depending on the coronary perfusion pressure. Myocardial “bridging” occurs during systole, and even though there is narrowing of the artery, this has little influence on coronary blood flow because most occurs during diastole. Most studies show little diminution in total left ventricular blood flow in patients with angina pectoris, whether it is stable or variant (unstable) angina. Patients with stable angina pectoris experience symptoms during exercise, and in such cases, coronary flow reserve may be inadequate to meet the myocardial demands. Resting blood flow, however, is normal.
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.
Patients w/ L to R shunt eventually develops cyanosis, clubbing and polycythemia. Cath reveals PVR 9 Woods units.
Discuss closure of the shunt.
Closure of the shunt in a patient with a pulmonary vascular resistance greater than 7 or 8 Woods units (after administration of a pulmonary vasodilator) does not stop progression of the disease and such an operation is extremely risky.
What hemodynamic changes to the pulmonary vascular can occur with MV disease or severe L side heart failure?
Elevated pulmonary venous pressures due to mitral valve disease or severe left heart failure increase pulmonary arterial pressure and may over time increase pulmonary vascular resistance. Hyperplastic changes in pulmonary arterioles may develop. Reduction of pulmonary venous pressures reduces pulmonary vascular resistance acutely and chronically.
Is surgery for MV disease contraindicated in patients with pulmonary hypertension due to increased pulmonary venous pressure?
Operation is not contraindicated in patients with pulmonary hypertension due to increased pulmonary venous pressure.
Which valvular pathology increases risk of sudden cardiac output collapse from being an autologous blood donor? Why?
Autologous blood donation reduces the need for homologous blood transfusions in cardiac surgery. Blood can be collected safely from most patients in whom a temporary decrement in intravascular volume can be tolerated.
Predonation is feasible in volume loading lesions such as aortic regurgitation, left ventricular aneurysms, and mitral valve disease.
In a patient with aortic stenosis a sudden decrement in blood volume could lead to a sudden decrease in cardiac output. Autologous blood donation should be avoided for a patient with this lesion.
At present, the estimated risk of seroconversion after a single human immunodeficiency virus contaminated needle stick is?
The risk of becoming infected with human immunodeficiency virus (HIV) after a single HIV-contaminated needle stick is less than 1%. However, in surgical specialties in which there is a high risk of glove puncture (e.g., orthopaedics), even this low risk translates into a significant long-term risk. In one study, the risk to an orthopaedic surgeon operating at the San Francisco General Hospital of becoming HIV-positive over five years was estimated to be 49% (40 sticks per year of which 33 % carry the HIV virus at risk of I% with each puncture).
Which physical finding can differentiate severe tricuspid stenosis from severe tricuspid regurgitation?
* accenuation of the murmur during inspiration
* jaundice
* hepatomegaly
* ascites
Jaundice and cirrhosis do not generally occur with tricuspid regurgitation
Tricuspid regurgitation features a high-pitched, blowing, holosystolic murmur. Tricuspid stenosis typically causes a low-pitched, rumbling diastolic murmur with a presystolic crescendo if the patient is in normal sinus rhythm. However, each is best heard at the lower sternal border and each increases in intensity during inspiration due to augmented right ventricular filling.
Severe tricuspid stenosis is associated with peripheral edema, ascites, and marked hepatic congestion, often resulting in congestive hepatomegaly with cirrhosis, jaundice, malnutrition, and splenomegaly. Tricuspid regurgitation is most often functional and secondary to marked dilation of the right ventricle and tricuspid annulus.
As with tricuspid stenosis, the symptoms of tricuspid regurgitation are the consequence of systolic venous congestion, including ascites, peripheral edema, hepatomegaly, pulsations of the liver, and positive hepatojugular reflux (enhanced jugular venous pulse with liver compression). However, gross jaundice and cirrhosis do not generally occur with tricuspid regurgitation.
A patient with mitral stenosis has a decrease in their dyspnea and pulmonary congestion with an increase in their peripheral edema and hepatomegaly. What valvular pathology may have occurred?
Tricuspid stenosis rarely occurs as an isolated lesion. It is most commonly associated with mitral stenosis, and sometimes with combined mitral and aortic stenosis. Since mitral stenosis generally precedes tricuspid stenosis, most patients present initially with symptoms of pulmonary congestion. Amelioration of dyspnea and pulmonary congestion in a patient with mitral stenosis suggests the development of severe tricuspid stenosis.
Which cation is the major intracellular cation and which is the major extracellular cation?
Potassium is the major intracelluar cation while Na+ is the major extracellular cation. A 70 kg human has about 4,000 mEq of K+ of which only 60 to 70 mEq (<2%) are extracellular. A serum potassium of 3.0 reflects at least a 300 mEq loss of total body K+, as intracellular K+ moves into the extracellular space to replace ongoing K+ losses. Persistent hypokalemia leads to conservation of K+ by the kidneys and preferential excretion of H+ ion in the urine; a metabolic alkalosis results. Normal K+ losses in the urine are between 40 and 60 mEq/day.
What electrolyte deficiency may be most important in increasing the risk of digitalis cardiotoxicity?
Hypomagnesemia may be more important than hypokalemia in increasing the risk of digitalis cardiotoxicity.
Hypomagnesemia is probably the most common electrolyte abnormality found in patients hospitalized in an Intensive Care Unit (ICU). Mg++ depletion is associated with other “hypos”: hypokalemia, hypophosphatemia, hyponatremia and hypocalcemia, which are all frequently associated with the use of diuretics. The lack of magnesium in intravenous fluids and the use of aminoglycosides and diuretics (which enhance renal losses of Mg++) both contribute to hypomagnesemia. Fifty percent of body Mg++ is stored in bone and < 1% is present in plasma. Serum levels are, therefore, unreliable in the assessment of Mg++ deficiency. Low serum Mg++ is known to potentiate the cardiotoxicity of digitalis by interfering with the magnesium-dependent membrane pump that allows calcium to move into muscle fibers.
Normal arterial oxygen content?
Normal cardiac index?
Normal oxygen delivery (i.e., cardiac output times oxygen content in blood) is?
The normal arterial oxygen content (O2 bound to Hgb plus O2 dissolved in plasma: CaO2) is the product of the hemoglobin concentration (15 gm/dL) times the percent saturation (100%) times the oxygen binding capacity of hemoglobin (1.36 cc O2/gm Hgb).
When the hemoglobin concentration and body temperature are normal, the contribution to oxygen content by dissolved oxygen in the plasma is negligible.
- Normal arterial oxygen content is ~20 cc/dL.
- Normal cardiac index is 30 dL/min/m2 or 3 L/min/m2 (range 2.6-4.2)
- Normal oxygen delivery is approximately 600 cc/min/m2.
How does a right to left intracardiac shunt affect thermodilution monitoring of cardiac output?
Accurate measurement of the cardiac output using thermodilution catheters depends on control of multiple variables, and it is reliable only in patients who do not have certain underlying cardiac anomalies.
For example, patients with right-to-left intracardiac shunts have loss of the indicator injectate into the left side of the circulation. Because the indicator solution never passes the thermistor, the computed cardiac output value is falsely high.
How does tricuspid valve regurgitation affect thermodilution monitoring of cardiac output?
Similar to the falsely high cardiac outputs obtained in patients with right to left intracardiac shunts - loss of the indicator injectate that never passes the thermistor.
How do the volume and temperature of the injectate influence the accuracy of the CO measurements in thermodilution?
What about distal migration of the catheter?
Falsely high cardiac output values result from using injectate that is warmer than the reference temperature, and from using less (not more) than the standard volume of injectate. In these situations, the thermistor detects less of a temperature drop and interprets this as higher flow (i.e. greater cardiac output).
Distal migration of the catheter or thermistor against the pulmonary artery wall will result in faster warming of the thermistor than is really indicated by flow of blood past the catheter tip and hence inappropriately increased cardiac output measurements.
A patient is suspected of having HIT. They are not bleeding, but a provider asks if they should give a platelet transfusion. What is your response?
Platelet transfusion should generally be avoided as bleeding is rare and platelet transfusion has been reported to precipitate thrombotic events.
Retrospective studies suggest the frequency of heparin-induced thrombocytopenia (HIT) to be 3% and of HIT with thrombosis to be 1% in patients who receive heparin for five days or more. This incidence is higher in patients following cardiopulmonary bypass. It appears that bovine and porcine heparins are equally likely to induce the development of IgG antibodies to complexes of heparin and platelet factor 4. Platelet activation releases procoagulant microparticles and local endothelial events generate thrombin. Thrombin generation helps to explain the strong association between HIT and thrombosis. In its severe form, this immune-mediated adverse drug reaction is associated with thrombosis that may result in limb amputations, stroke, graft occlusion, pulmonary embolism, phlegmasia cerulea dolens, and death. Venous thrombosis is strongly associated with HIT and is more common than arterial thrombosis.
Warfarin-induced venous limb gangrene, a devastating venous thrombotic syndrome, is related to what deficiency?
How is it relevant to the management of HIT?
Acquired protein C deficiency
Also linked with HIT - If HIT is diagnosed, consider reversal of warfarin using vitamin K.
Discuss the medical management, specifically anti-thrombotics and anti-platelet management in the treatment of HIT.
Remember that HIT is a hypercoagulable state.
UFH should be stopped.
Warfarin should be reversed with vit K.
Aspirin may be indicated to limit platelet-related thrombosis.
Danaparoid can be considered to reduce thrombin generation.
Lepirudin and argatroban can be used inhibit thrombin directly assuming an anticoagulant indication.
Theoretically, platelet ADP blockers may help (ticlopidine, clopidogrel).
Platelet transfusion should generally be avoided as bleeding is rare and platelet transfusion has been reported to precipitate thrombotic events.
Myocardial hypertrophy (without failure) in chronic volume overload is causally associated with what changes to the following:
* wall stress
* wall thickness
* diastolic volume
* sarcomere number and morphology
In chronic volume overload, such as occurs with AVR, ventricular dilatation can increase systolic wall stress via the LaPlace relationship. Wall stress is proportional to ventricular pressure and ventricular size, but inversely proportional to ventricular wall thickness. Hypertrophy, stimulated by the increased wall stress, increases wall thickness, returns the r/h ratio and wall stress to normal, reduces diastolic volumes and augments ventricular pumping function. Hypertrophy increases the number of sarcomeres in parallel and in series, and thus maintains nearly normal sarcomere morphology.
As such, hypertrophy in volume overload appears to be a physiologic adaptive mechanism that normalizes pumping function and maintains myocardial performance. In the late stage of volume overload, hypertrophy can no longer compensate for the increased work load; contractility then falls and myocardial failure ensues. It is important to recognize, however, that hypertrophy and myocardial failure are separate processes with opposite functional effects.
How does impaired liver function affect lactate levels?
Thiamine deficiency?
Nitroprusside use?
Anaeroic metabolism?
Lactate levels increase with all of these states?
Lactic acid is the end product of anaerobic metabolism and is produced by the conversion of pyruvate to lactic acid. Blood levels will increase when anaerobic metabolism occurs. Normally the liver clears lactate from the blood and impaired liver function results in increased (not decreased) blood lactic acid concentrations. Although tissue ischemia may increase blood lactate, blood flow to ischemic tissue is variable and variable amounts of lactate are washed out into the general circulation. Thus, blood lactic acid concentration is an insensitive marker of tissue ischemia. The normal homeostasis of pyruvate is altered by thiamine deficiency and cyanide (from breakdown) nitroprusside, both of which increase conversion of pyruvate to lactate.
Blood component transfusion therapy may be appropriate for a patient with diffuse (nonsurgical) bleeding following coronary artery bypass grafting at what level of the following labs:
* prothrombin/partial thromboplastin time (What level past control?)
* platelet
* serum fibrinogen
* bleeding time
* activated clotting time
And what will you treat with?
- Fresh frozen plasma is administered when the prothrombin time and partial thromboplastin time exceed l.5 times control
- Plt transfusions may be indicated w/ counts at 100,000/µL in the setting of diffuse bleeding.
- Cryoprecipate therapy is indicated if hypofibrinogenemia < l00 mg/dL
- If a qualitative platelet abnormality is demonstrated by a prolonged bleeding time (twice normal) postoperatively, then platelet transfusion is indicated
- ACT >l50 seconds following CPB indicates circulating heparin not bound to protamine. Additional protamine is required for heparin neutralization (not component therapy).
Blood component transfusions should not be given prophylactically or in the absence of clinically significant bleeding, irrespective of laboratory values.
In general, what can cause PACs.
An anatomically dispersed but integrated system of extranodal atrial pacemakers is thought to exist with site-specific differential sensitivity to both adrenergic and cholinergic stimuli. States associated with altered sympathetic tone such as that following a myocardial infarction or following an operation may activate activity of different pacemakers within this system leading to premature atrial contractions (PACs).
What are some of the major characteristics of PACs on EKG?
1) premature occurrence of a P wave; 2) altered P wave morphology; 3) normal or increased P-R interval.
At the left ventricular level, what measurement is most closely related to preload at the cellular level?
End-diastolic volume (LVIEDV).
All pressure measurements, such as PCWP, are only estimates of true preload, which is end-diastolic fiber or sarcomere length.
What is compliance and how does it relate to the left ventricle?
Compliance is an intrinsic property of the left ventricle which determines the relation between end-diastolic volume (LVEDV) and end-diastolic pressure (LVEDP).
How does positive pressure ventilation affect end-diastolic volume of the left ventricle and ventricular compliance?
Positive pressure ventilation decreases LVEDV and compliance by increasing volume of the right ventricle, which pushes the interventricular septum to the left.
A 60-year-old woman in the first few hours following an uneventful mitral valve replacement has the following hemodynamic parameters: Systolic pressure 80 mmHg Heart rate 110 / min Pulmonary artery pressure 25/16 mmHg Cardiac index 2.7 L/(minm2) Systemic vascular resistance 500 dynesec/cm2.
Which pharmacologic agent is most likely to provide an optimal response ?
Phenylephrine.
Although the underlying cardiac pathology is not specified, left ventricular function and reserve are probably adequate since preload is not elevated. Cardiac index is satisfactory and systemic vascular resistance is low. The ideal drug for this patient would increase systemic resistance without increasing heart rate or decreasing contractility. Dobutamine is a positive inotrope that increases both contractility and heart rate. Its mild beta-2 effect reduces vascular resistance slightly. While its use in this scenario might increase the systemic pressure somewhat, it will do so at the expense of increased myocardial oxygen demand. Since the patient has no evidence of inadequate myocardial contractility, the use of this positive inotrope will provide little benefit and may adversely impact the cardiac supply/demand ratio. Epinephrine’s strong beta-1 effects will increase cardiac output by increasing contractility and heart rate. At moderate and high doses its alpha agonist effects increase systemic vascular resistance. Clearly the increased vascular resistance would benefit this patient, but epinephrine’s mixed effects will worsen tachycardia and compromise the cardiac supply/demand ratio. Milrinone, a phosphodiesterase inhibitor, reduces systemic resistance while providing a modest inotropic effect. It is contraindicated in this hypotensive patient because of an already low systemic vascular resistance. Norepinephrine would increase systemic vascular resistance, heart rate and myocardial contractility because of its strong alpha and beta adrenergic effects. In this scenario, its alpha effect would be welcome, but added myocardial oxygen consumption,aggravation of tachycardia and potential ectopy are not desired. Phenylephrine is a pure alpha agonist that will increase systemic vascular resistance. It has no direct cardiac effects and is a valuable drug when hypotension results solely from inappropriate vasodilation. The acute effects of its peripheral activity cannot be known, and other organs can be compromised by vasoconstriction. Caution is appropriate regarding increasing cardiac afterload, as left ventricular work is increased and cardiac output may fall. The need for support with alpha adrenergic agents should be somewhat unsettling for the surgeon. Continuous aggressive monitoring is mandatory and prolonged treatment with phenylephrine or metaraminol (Aramine) should be avoided.
Is stress ulcer ppx required for all cardiac surgery pts (every patient, every time)?
No.
After cardiopulmonary bypass, stress ulceration and upper GI bleeding occur at rates of 0.45% in patients without prophylaxis and 0.35% with prophylaxis. However, a definite clinical benefit has not been shown and a randomized trial in cardiac surgery has not been completed. Established risk factors include valve replacement, aortic cross-clamping, bypass time, reoperation, inflammatory states (e.g., endocarditis) and non-pulsatile flow during bypass. Enteral nutrition reduces the risk of stress ulceration, probably by maintaining gut mucosal integrity. Routine or empiric therapy is not indicated in patients unless ulceration is documented. More general studies on critically ill patients indicate a high risk for ulcers and GI bleeding, and routine stress ulcer prophylaxis is strongly indicated.
Proton pump inhibitors are at least as effective as histamine-2 antagonists at raising pH, but they are not better at reducing stress ulceration in clinical trials. In fact, all agents approved for reducing peptic ulceration are effective in critically ill patients as long as they are dosed appropriately. Several of the identified risk factors for the development of nosocomial pneumonia are similar to those for stress ulceration. Curiously, though, meta-analysis suggests that nosocomial pneumonia is the main complication of ulcer prophylaxis treatment in the ICU. Anti-acid therapy promotes gastric colonization with pathogenic bacteria, and aspiration of these bacteria can cause pneumonia.
In cardiac surgery patients, what risk factors create the highest risk for stress ulcers?
How can it be decreased?
Although there is some disagreement in the literature as to which patients are most likely to benefit from stress ulcer prophylaxis, factors that define highest risk include mechanical ventilation more than 48 hours, severe sepsis, and renal failure.
Other established risk factors include valve replacement, aortic cross-clamping, bypass time, reoperation, inflammatory states (e.g., endocarditis) and non-pulsatile flow during bypass.
Enteral nutrition reduces the risk of stress ulceration, probably by maintaining gut mucosal integrity.
Yesterday, a 59-year-old woman underwent left upper lobectomy for lung cancer. Today her hematocrit is 18%, but no packed red blood cells have been given because of her religious beliefs. She appears to be doing well and you plan to wean mechanical ventilation. Cardiac index is currently 5.0 L/(min*m2), oxygen saturation is 98% and inspired oxygen concentration is 40%.
Which of the following parameters is expected to be significantly altered?
Lactate
Na
pH
Mixed venous oxygen saturation (SvO2)
SvO2.
Decreased oxygen delivery due to anemia is compensated by several mechanisms including increased cardiac output, easier hemoglobin “downloading” due to changes in 2-3DPG levels, and an increase in the oxygen extraction ratio. Of the parameters mentioned, a decrease in the mixed venous oxygen saturation would be expected since this reflects increased oxygen extraction. Provided the patient is adequately compensated, significant anemia can be well tolerated without tissue acidosis (increased lactate) and without electrolyte abnormalities or respiratory decompensation. The optimal threshold “triggers” for transfusion remain controversial.
What is the O2 consumption equation?
O2 consumption = cardiac output * hgb (gm/dl) * 1.34 * (arterial O2 sat - mixed venous O2 sat).
When O2 consumption is constant and arterial blood is highly saturated, only changes in what two parameters can change mixed venous oxygen saturation?
cardiac output or hemoglobin concentration
If hemoglobin concentration is constant, how are cardiac output and mixed venous O2 sat related?
They are directly related. Changes in SVO2 can be used as a rough estimate of changes in cardiac output assuming the patient’s oxygen consumption isn’t changing, or they are not bleeding.
What increases the risk for aminoglycoside related renal failure?
How is it managed?
Underlying renal disease, volume depletion (though it seems to be independent of CO).
Recovery is the rule once the drug is withdrawn, but elevations in Cr may persists for as long as 10 days.
There is no specific therapy, so prevention with euvolemia and early detection with a urinalysis is best management. Furosemide will not reverse this condition (often attempted).
LMWH affects what?
What effect does protamine have on enoxaparin?
Inhibits IIa and Xa.
Protamine reverses the anti-IIa effect, but only partially the anti-Xa effect (60-80%).
Where does the blood flow to the AV node usually come from?
What happens with ischemia to this region?
The RCA usually supplies the PDA (ie is dominant), and therefore supplies the AV node.
In left dominant patients, the circumflex artery supplies the PDA.
Ischemia may cause transient or permanent complete heart block.
What is the preferred metabolic substrate for oxidative metabolism of the heart?
Long chain fatty acids.
After passive transfer from the plasma to the cytosol, fatty acids must first be activated to fatty acetyl-coenzyme A subsequent to further metabolism. Although some activated fatty acid is esterified to triglyceride, the majority serves as substrate for oxidative phosphorylation. Carnitine, a water-soluble, naturally occurring amino acid, is the requisite carrier for transport of these fatty acids from the cytosol across the mitochondrial membrane for beta oxidation. Ischemic depletion of carnitine results in the toxic accumulation of esterified fatty acid intermediates. These metabolites inhibit a variety of critical intracellular enzymes involved with regulation of cell volume, maintenance of ionic gradients, and nucleotide transfer. Fatty acid metabolites are also deleterious because they activate phospholipases and have intrinsic detergent properties that nonselectively alter subcellular membranes. Coenzyme Q plays an important role in the regulation of mitochondrial oxidative metabolism by serving as a carrier of electrons moving between the flavoproteins and cytochromes thus enhancing the flow of electrons through the mitochondrial electron transport chain. Creatine phosphate is the major transport molecule for energy transfer between the mitochondria and the cytoplasm. It receives its energy from ATP and donates its energy to ADP via a reversible reaction mediated by the enzyme creatine phosphokinase. The amino acid glutamate is an intermediary in the Krebs cycle, which after exogenous supplementation can accumulate in the cytosol . After transamination and the malate-aspartate shuttle, it is made available for mitochondrial ATP production by an oxygen-independent pathway.
A 65 year old man with normal preoperative left ventricular function has just returned to the intensive care unit following coronary artery bypass grafting. His intraoperative course was unremarkable. His initial hemodynamic and laboratory data includes:
Pulse: 75 beats per minute
PA pressure: 35/17 torr
Hemoglobin: 11 gm/dL
PCWP: 13 torr
Blood pressure: 130/84 torr
Cardiac index: 1.7 L/min*m2
SVR index: 4100 dynes sec cm -5/m2.
The most appropriate initial treatment of this patient is?
Nitroprusside.
Nitroglycerin is a peripheral venodilator and not as effective at reducing systemic arterial resistance.
The patient has a high SVR as well as HTN with a low CI. Afterload is hurting the output and must be reduced. This will reduce his myocardial oxygen consumption by decreasing wall stress in addition to increasing CI. Rewarming may help if temp is low as hypothermia can increase SVR. Pain control is also nevessary.
Volume will not help as much with an adequate PCWP.
What is the formula for oxygen delivery?
DO2 = (cardiac output) x (O2 content)
O2 content = 1.39 x Hgb x O2 saturation + (0.0031 x PaO2)
How do you treat decreasing mixed venous return in an intubated patient with a normal O2 sat?
What do you tell the resident who wants to increase the FiO2?
Treatment of decreasing mixed venous oxygen saturation must focus on increasing venous return and/or decreasing airway pressure. Crystalloid, albumin or blood transfusion may be appropriate depending on the patient’s hemoglobin level. Decreasing the tidal volume and respiratory rate will decrease airway pressure.
In the absence of hypoxia, increasing the inspired oxygen concentration will not significantly increase hemoglobin saturation or oxygen delivery. The mixed venous oxygen saturation will not be effected, and high FiO2 can contribute to oxygen toxicity.
Which of the agent provides chemical cardioplegic protection by cell membrane hyperpolarization?
ATP-sensitive potassium channel openers induce hyperpolarization by reducing the action potential duration.
Angiotensin converting enzyme inhibitors are established drug therapy for the treatment of depressed left ventricular function following myocardial infarction. The protective effect of these agents is mediated through?
afterload reduction and favorable ventricular remodeling
How do hyperkalemic cardioplegic solutions work?
With K+ concentration between 12-25 mM, they depolarize the membrane potential to -50 mV from a resting potential of -80 mV. At this depolarized potential, the fast Na+ channels are inactivated resulting in diastolic arrest.
Coronary bypass grafting has been very successfully performed utilizing hypothermia with fibrillatory arrest (rather than cardioplegia). What are some important aspects of this technique?
A number of surgeons have very successfully used hypothermia with fibrillatory arrest as their primary system of myocardial protection during coronary artery bypass. If this technique is utilized, attention to detail is necessary.
Since the heart continues to be perfused, myocardial cooling necessarily means systemic cooling. Ordinarily, systemic temperatures are reduced to 20-25 C, and the heart is allowed to fibrillate as the body is cooled. Induced electrical fibrillation of the heart is not necessary.
Active venting is always employed.
Such active venting poses a threat if air is introduced due to the development of negative intracavitary pressure. This air is difficult to remove at the end of the operation - several practitioners of this technique monitor the pressure in the LV w/ a goal of > 5 mmHg.
This technique cannot be used if AI prevents adequate decompression.
A third critical principle of this technique is maintenance of adequate coronary perfusion pressure at 80 mmHg by systemic infusion of alpha adrenergic agents.
What do studies show about the preoperative use of ASA before CABG, particular in regards to their effects on bleeding and transfusion requirement?
Of 21 studies identified on this subject, there were 6 randomized controlled trials (RCTs) that were viewed as Level A evidence. All RCTs except one found that preoperative aspirin results in either increased blood loss (measured by drainage from mediastinal tubes), increased transfusion rates, or increased frequency of re-exploration. Because of the consistent finding of aspirin-associated increased blood loss in the highest quality studies, consensus panels agree that patients who receive aspirin before operation are at increased risk for above normal postoperative bleeding and blood transfusion after CABG.
Other factos: preop plavix, vWF, preoperative anemia (especially those w/ low preop blood volume, including many women).
Autotransfused shed blood is “red cells suspended in serum”. What happens to the different blood components in this blood?
The blood is defibrinated; platelet counts are not normal but are usually between 30,000-60,000/mm3.
The hematocrit will vary with the hematocrit of the patient, ranging between 19% and 30%.
Factor VIII and XI levels are somewhat diminished but not depleted to values that would affect intrinsic coagulation.
Fibrinogen levels are very low.
Fibrinopeptide A and other peptides, generated when fibrin is lysed by plasmin or released when thrombin cleaves fibrinogen, are elevated.
Heart rate, afterload, inotropy.
A beating, vented (and bypassed) heart still requires 3.0-4.0 ml/min/100 gm heart.
Profound topical hypothermia (i.e., 12C), however, decreases oxygen needs another 50% compared to normothermia.
Decreasing temperature to 25C reduces MVO2 by 20%.
The potassium arrested heart even at normothermia only consumes 1.0-1.3 ml/min/100 gm left ventricle. This modality alone decreases MVO2 65-80% compared to the empty-beating state.
Reoperation for coronary disease is indicated for a 78-year-old man. What is the most sensitive surveillance modality to assess for atherosclerotic disease of the ascending aorta?
Epi-aortic ultrasound scanning.
TEE imaging of the distal ascending aorta and arch is poor and these are typical sites for aortic crossclamping and cannulation
What is the most important factor in defining stroke risk for patients who require CPB?
Severe atherosclerotic disease
A patient arrives in the intensive care unit still intubated immediately following aortic and mitral valve replacements surgery, with temporary atrial and ventricular pacing wires present. The mean blood pressure is 63 mmHg. The patient is on 8 μg/min of norepinephrine. Blood gases show pH 7.34, pO2 132 torr, pCO2 35 torr. The serum lactate is 7 mg/dL, and urine output for the past hour is 25 mL. The patient’s ECG is shown.
What is the diagnosis/assessment of this patient?
What is the immediate next step?
Left bundle branch block (LBBB) and 2:1 A-V block with a ventricular rate < 50/min.
This is causing a low index, as evidenced by his lactate level.
Use the pacing wires. DDD if there’s no good sinus atrial rhythm, otherwise AAI is ideal.
Three days after aortic valve replacement surgery, a patient is comfortable on nasal cannula oxygen and sitting in a chair. His mean arterial pressure is 76 mmHg; he is afebrile, alert, and oriented. His urine output is 50 mL/hr. Temporary pacing wires were placed at the time of surgery due to bradycardia on initial separation from cardiopulmonary bypass. He currently is connected to the a temporary pacemaker with the following settings: mode: VVI, output: 20mA, sensitivity 6mV, rate 48/min. The bedside nurse calls a code when, without warning the patient slumps over in conjunction with the rhythm strip shown. A single rapid external shock recovers his vital signs and consciousness.
What happened?
The best next step in management is to?
R-on-T phenomenon.
Disconnect the temporary pacemaker. Should bradycardia become symptomatic the sensitivity setting on the temporary pacemaker should be decreased (e.g., change from 6maA to 1mA), which should enhance the device’s identification of native QRS complexes and inhibit pacing.
R-on-T phenomenon is one in which perturbations to the heart’s electrical activity during the repolarization (T wave on ECG) can produce ventricular fibrillation. This condition can occur whenever an electrical impulse stimulates the heart during the T wave. Outside the hospital setting, electrical stimulation can occur from high voltage contact. Mechanical trauma to the myocardium can elicit an electrical response and, when timed in concert with the T wave, can produce ventricular fibrillation. In the postoperative setting, temporary pacing has been associated with iatrogenic ventricular tachyarrhythmias due to the R-on-T phenomenon.
Modern, microprocessor controlled temporary pacemakers can be programmed to minimize the chances of R-on-T. In VVI mode the pacemaker monitors electrical activity inhibits delivery of pacing spikes based on a sensitivity setting. The sensitivity is a value in millivolts that will inhibit the device from firing. A high sensitivity number setting means a very large electrical signal (strong QRS signal) is needed to alert the device of intrinsic myocardial activity, and to avoid R-on-T. As sensitivity approaches infinity, the device no longer functions in VVI mode. Since it can no longer sense any physiological electrical energy from the heart, it functions as VOO.
The tracing shows 2 QRS complexes not sensed by the pacemaker, evidenced by pacing spikes (arrows) delivered on the T-wave. This paced-R-on-nativeT induced ventricular fibrillation. The patient was alert and awake when this incident occurred. The native R-R interval indicates an intrinsic rate of about 48, so the initial response after defibrillation should be to disconnect the temporary pacemaker.
A 67-year-old underwent AVR/MVR for rheumatic valvular heart disease. Preoperative PA systolic pressure was 72. She is now in the ICU on postoperative day one with the following hemodynamic parameters:
HR 90, BP 110/60, CVP 12, PAP 45/20 on epinephrine 0.05 micrograms/(kg x min) with a CI of 2.3.
Her chest radiograph is shown. The patient was just now noted to have coughed up about 20 mL of bright red blood.
What happened?
What do you do?
Pulmonary artery branch rupture by a PA catheter is a rare event. The incidence of this complication is much less than 1/1000 cases, but it is an emergency associated with a 50% mortality. A pulmonary artery branch can be ruptured by balloon inflation by perforation by the catheter by the tip. In either case, however, the catheter tip has been advanced too far into the pulmonary parenchyma (as shown in the figure). Because of the high morbidity and mortality associated with this complication, after floating a PA catheter many cardiac programs prohibit any subsequent inflation of the balloon to determine the wedge pressure, except in unusual circumstances. The PA diastolic pressure is not a substitute for PA wedge pressure, but it can be used as a measure of LV preload, and trends provide good insight into the LV volume status.
Immediate recognition of catheter-induced PA rupture is essential to avoid overwhelming hemoptysis and hypoxia. Optimal immediate treatment can differ depending on the resources that can be brought to bear. In the ICU good choices include positioning with the “good” lung up, reversal of any anticoagulation, determining the site with bronchoscopy, and protecting the unaffected lung (placing a double lumen endotracheal tube or an occluding intrabronchial catheter). Pulmonary arteriography and embolization is highly effective and is recommended if bleeding does not stop promptly.
Maintaining a clear airway to the uninvolved lung is the primary immediate goal, and lung resection should be considered a last resort. Suture of a ruptured PA is rarely feasible in the acute setting, but a late-appearing pseudoaneurysm should be repaired.
