16: Critical Care Flashcards

Question

Where in the body does blood have the lowest venous oxygen saturation?

Answer 1

Coronary sinus [30% oxygen saturation in the coronary sinus.]

Answer 2

Alpha 1-adrenegic: Vasoconstriction [UpToDate: Potent, direct-acting alpha-adrenergic agonist with virtually no beta-adrenergic activity; produces systemic arterial vasoconstriction. Such **increases in systemic vascular resistance** result in dose dependent increases in systolic and diastolic blood pressure and **reductions in heart rate and cardiac output** especially in patients with heart failure.]

Answer 3

* Cardiogenic shock (after CABG or MI) * In patients with refractory angina awaiting revascularization [UpToDate: Consequent to the improvement in hemodynamic parameters described above, the intraaortic balloon pump counterpulsation (IABP) may be an effective temporary therapeutic option in patients with significant hemodynamic compromise resulting from myocardial ischemia. However, some patients with hemodynamic instability may require other percutaneous support due to IABP failure or as initial therapy. For example, an axial flow pump or a percutaneous left atrial-to-femoral arterial ventricular assist device may be appropriate for patients with low output states or shock when an IABP is deemed unlikely to provide adequate support. IABP is used in a variety of clinical conditions: 1. **Cardiogenic shock** (left ventricular failure or mechanical complications of an acute myocardial infarction) 2. Intractable angina 3. Low cardiac output after cardiopulmonary bypass 4. Adjunctive therapy in high risk or complicated angioplasty 5. Prophylaxis in patients with severe left main coronary arterial stenosis in whom surgery is pending 6. Intractable myocardial ischemia awaiting further therapy 7. Refractory heart failure as a bridge to further therapy 8. Intractable ventricular arrhythmias as a bridge to further therapy **Intraaortic balloon pumping reduces electrocardiographic ST-segment abnormalities in patients with acute coronary syndromes, and is effective in the treatment of angina unresponsive to medical therapy that cannot be treated promptly with percutaneous coronary intervention (PCI) or coronary artery bypass graft surgery (CABG). However, the availability of effective medical therapy and prompt revascularization has all but eliminated this indication**. Rarely, patients with surgical disease and persistent ischemia do require IABP support pending surgery.]

Answer 4

Unresponsive [Causes cardiovascular collapse.]

Answer 5

* Pulmonary Artery Pressure (PAP) = **25/10 (+/-5)** * Pulmonary Capillary Wedge Pressure (PCWP) = **11 (+/-4)** [UpToDate: Normal pulmonary artery (PA) systolic pressures range from **15 to 25 mmHg**, while PA diastolic pressures range from **8 to 15 mmHg**. The mean PA pressure (mPAp) is typically 16 mmHg (10 to 22 mmHg). The mean PA pressure can be elevated (eg, mPAp, \>22 mmHg) by acute conditions (eg, venous thromboembolism or hypoxemic-induced pulmonary vasoconstriction), by acute-on-chronic conditions (eg, hypoxemic-induced vasoconstriction in a patient with underlying chronic cardiopulmonary disease), or by chronic conditions (eg, pulmonary hypertension [PH]). Although PH is defined as a mPAp ≥25 mmHg, many of the etiologies associated with PH will also result in mild elevations of the PA pressure. The pulmonary artery occlusion pressure (PAOP; pulmonary capillary wedge pressure [PCWP] or pulmonary artery wedge pressure [PAWP]) estimates the left atrial pressure. It is best measured with the patient in the supine position, at the end of expiration with the tip of the catheter in zone 3 of the lung. Ideally, the value is measured at least three times and the mean is calculated. The PAOP tracing is obtained by inflating the balloon at the distal tip of the catheter. The balloon obstructs blood flow through a branch of the pulmonary artery. This creates a static column of blood between the catheter tip and the left atrium. Pressure at both ends of the column equilibrates, after which the pressure at the distal end of the catheter is equal to the pressure of the left atrium. Thus, PAOP is a reflection of left atrial pressure. Normal wedge pressures vary from **6 to 15 mmHg**, with a mean of 9 mmHg. Importantly, the PAOP usually estimates the left ventricular end-diastolic pressure (ie, left ventricular preload) if there is no obstruction to flow between the left atrium and left ventricle and the compliance of the left ventricle is normal. Importantly, it does not directly measure the left ventricular end-diastolic volume, capillary hydrostatic pressure, or transmural pressures. Thus, the PAOP may not reliably indicate left ventricular preload when compliance of the left ventricle is abnormal (eg, large myocardial infarction or in cardiac tamponade).]

Answer 6

* FEV1: Decreases * Vital capacity: Decreases * Functional residual capacity: Increases

Answer 7

* Cardiac output (L/min) = **4-8 L/min** * Cardiac Index (L/min) = **2.5-4 L/min** **[**UpToDate: The pulmonary artery catheter (PAC) measures the cardiac output (CO) via either the indicator thermodilution method or the Fick method. The preferred expression of CO is the cardiac index [CI], which is calculated by dividing the CO by the body surface area. Normal hemodynamic measures for CI are 2.8 to 4.2 L/min/m². The causes of a low cardiac output include systolic and diastolic heart failure, but also include severe forms of mitral valve regurgitation, hypovolemia, pulmonary hypertension, and right ventricular failure. Distinguishing these pathologies from one another depends upon presenting clinical and echocardiographic features and well as specific patterns of physiologic variables seen on the PAC.]

Answer 8

VO₂ = CO x (CaO₂ - CvO₂) [CaO₂ is arterial O₂ content. CvO₂ is venous O₂ content.]

Answer 9

* Pulmonary hypertension * Aortic regurgitation * Mitral stenosis * Mitral regurgitation * High PEEP * Poor LV compliance [Wedge pressure measurements should be taken at end-expiration (for both ventilated and nonventilated patients.]

Answer 10

The iliofemoral region

Answer 11

Consider open or percutaneous suction catheter embolectomy if patient is in shock despite massive pressors and inotropes [UpToDate: In patients with a high clinical suspicion for PE who are hemodynamically unstable and who have a definitive diagnosis by portable perfusion scanning or a presumptive diagnosis of PE by bedside echocardiography (because definitive diagnostic testing is unsafe or not feasible), **we suggest systemic thrombolytic therapy rather than empiric anticoagulation or no therapy** (Grade 2C). If bedside testing is delayed or unavailable, the use of thrombolytic therapy as a life-saving measure should be individualized; if not used, the patient should receive empiric anticoagulation. For patients who are hemodynamically unstable and the clinical suspicion is low or moderate, we suggest empiric anticoagulation similar to that suggested for patients who are hemodynamically stable; empiric thrombolysis is not justified in this population.]

Answer 12

* Enzyme: Xanthine oxidase * Most important mediator: Polymorphonucleocytes [Xanthine oxidase is also involved in the metabolism of purines and breakdown to uric acid.]

Answer 13

Dexamethasone

Answer 14

* Kidneys = 25% * Brain = 15% * Heart = 5%

Answer 15

Increased myocardial contractility and pulmonary vasodilation [Milrinone is a **phosphodiesterase inhibitor** which increases cAMP, resulting in increased calcium flux and **increased myocardial contractility**. It also causes vascular smooth muscle relaxation and **pulmonary vasodilation**.] [UpToDate: A selective phosphodiesterase inhibitor in cardiac and vascular tissue, resulting in **vasodilation and inotropic effects** with little chronotropic activity.]

Answer 16

Automatic increase in contractility secondary to increased heart rate

Answer 17

Zone 3 (lower lung) [UpToDate: The tip of the catheter should ideally be positioned in zone 3 (ie, below the level of the left atrium), such that PAOP will be overestimated if placed in zone 1 or 2. The lungs can be divided into three physiologic zones of blood flow. These zones are based upon the alveolar pressure, mean pulmonary artery pressure, and pulmonary capillary pressure: * Zone 1 is the least dependent zone. In this zone, the mean alveolar pressure exceeds the mean arterial pressure, which exceeds the mean pulmonary capillary pressure (PA\>Pa\>Pc). * Zone 2 is the middle zone. In this zone, the mean arterial pressure exceeds the mean alveolar pressure, which exceeds the mean pulmonary capillary pressure (Pa\>PA\>Pc). * Zone 3 is the most dependent zone. In this zone, the mean arterial pressure exceeds the mean pulmonary capillary pressure, which exceeds the alveolar pressure (Pa\>Pc\>PA). Correct placement only occurs in approximately 30% of catheter insertions. Indicators that the catheter has been placed into a zone other than zone 3 include an abnormal position on the lateral chest radiograph (rarely performed in the intensive care unit), marked respiratory variation in the PAOP tracing, and an increase in the PAOP due to positive end-expiratory pressure that exceeds 50% of the amount of applied positive end-expiratory pressure.]

Answer 18

Motor neurons [Can lead to failure to wean from ventilation.] [UpToDate: The second neuromuscular condition that is commonly acquired in the intensive care unit (ICU) is critical illness polyneuropathy (CIP). This disorder was first recognized clinically in the late 1970s and 1980s. Association with sepsis — Critical illness polyneuropathy appears to be a common complication of severe sepsis and is thought to represent a neurologic manifestation of the systemic inflammatory response syndrome (SIRS). There is some correlation with elevations in blood glucose and reductions in serum albumin. The mechanism of axonal injury in CIP is unknown. However, speculation focuses on injury to the microcirculation of distal nerves, causing ischemia and axonal degeneration. During the early stages of sepsis, electrical inexcitability due to sodium channel inactivation may be present in otherwise intact nerves. The association of sepsis with CIP is illustrated by a prospective report that assessed electrophysiologic and clinical data from 43 patients an average of 28 days after the onset of sepsis and multiorgan failure. An axonal polyneuropathy was present in 30 patients (70%), 15 of whom also had clinical evidence of generalized muscle dysfunction, characterized by limb muscle weakness, reduced or absent deep tendon reflexes, and/or delayed weaning from mechanical ventilation. Three severely affected patients were unable to move any of their extremities, failed to improve, and ultimately died. Many patients with severe sepsis who develop neuromuscular weakness in the ICU have a combination of CIM and CIP. In survivors of CIP with mild or moderate nerve injury, recovery of muscle strength generally occurs over weeks to months. However, electrodiagnostic testing may demonstrate residual nerve dysfunction several years after initial presentation. Patients with severe CIP may remain quadriplegic.]

Answer 19

Heparin, Coumadin [UpToDate: For patients with suspected PE who are hemodynamically stable or hemodynamically unstable and successfully resuscitated, the administration of empiric anticoagulation depends upon the risk of bleeding, the clinical suspicion for PE, and the expected timing of diagnostic tests: * For patients with a low risk of bleeding and a high clinical suspicion for PE, we suggest empiric anticoagulation rather than waiting until definitive diagnostic tests are completed (Grade 2C). We use a similar approach in those with a moderate or low clinical suspicion for PE in whom the diagnostic evaluation is expected to take longer than four hours and 24 hours, respectively. * We do not anticoagulate patients with absolute contraindications to anticoagulant therapy or those with an unacceptably high risk of bleeding (Grade 1C). * For patients with a moderate risk of bleeding, empiric anticoagulant therapy may be administered on a case-by-case basis according to the assessed risk-benefit ratio.]

Answer 20

* Pneumonia is most common * Sepsis * Multi-trauma * Severe burns * Pancreatitis * Aspiration * DIC

Answer 21

Impaired diastolic filling of the right atrium

Answer 22

Pre-renal renal failure

Answer 23

1. Decreased pressure sensed by the juxtoglomerular apparatus in the kidney 2. Increased sodium concentration sensed by the macula densa in early distal tubule [Beta-adrenergic stimulation and hyperkalemia also cause release.] [UpToDate: Factors that regulate renin secretion are related to the classical actions of angiotensin II: increased sodium and water reabsorption; and systemic vasoconstriction. Short-term feedback of renin secretion is mediated via angiotensin II; angiotensin II binds to its receptor to inhibit renin gene expression. Long-term feedback of renin secretion is mediated by the physiologic cycle of angiotensin II; angiotensin II increases blood pressure and sodium retention, which then inhibits renin release. The changes in extracellular fluid volume that govern renin release are primarily sensed at three sites: * Baroreceptors (or stretch receptors) in the wall of the afferent arteriole * Cardiac and arterial baroreceptors, which regulate sympathetic neural activity and the level of circulating catecholamines, both of which enhance renin secretion via the beta-1-adrenergic receptors * The cells of the macula densa in the early distal tubule, which appear to be stimulated by a reduction in chloride delivery, particularly in the chloride concentration in the fluid delivered to this site In normal subjects, the major determinant of renin secretion is sodium intake: a high intake expands the extracellular fluid volume and decreases renin release, whereas a low sodium intake (or sodium and water losses from any site) leads to a reduction in extracellular fluid volume and stimulation of renin secretion. Acute increases in renin secretion, such as those occurring with hypovolemia, primarily reflect the release of preformed renin from intracellular secretory granules. Chronic, persistent stimuli to renin release lead to increased synthesis of new prorenin and renin. Increases in renin secretion produce increases in angiotensin II and aldosterone production, sodium reabsorption, and expansion of the extracellular fluid volume. By contrast, decreases in renin secretion produce decreases in angiotensin II and aldosterone production, sodium reabsorption, and reduction of the extracellular fluid volume. Intrarenal formation of angiotensin II probably plays at least a contributory role in the sodium retention induced by renin, as illustrated by the rise in messenger RNA for both renin and angiotensin substrate in the renal cortex following a low-sodium diet.]

Answer 24

* Total lung capacity (TLC): Lung volume after maximal inspiration (TLC=FVC+RV) * Forced vital capacity (FVC): Maximal exhalation after maximal inhalation * Residual volume (RV): Lung volume after maximal expiration (20% of TLC) * Tidal volume (TV): Volume of air with normal inspiration and expiration * Functional residual capacity (FRC): Lung volume after normal exhalation (FRC=ERV+RV) * Expiratory reserve volume (ERV): Volume of air that can be forcefully expired after normal expiration * Inspiratory capacity: Maximum air breathed in from functional residual capacity * FEV₁: Forced expiratory volume in 1 second (after maximal inhalation) * Minute ventilation: MV = TV x RR

Answer 25

* Total lung capacity (TLC): Increased * Residual volume (RV): Increased * Forced vital capacity (FVC): Normal or decreased * Forced expiratory volume (FEV1): Decreased

Answer 26

* Increasing PEEP or FiO₂ increases oxygenation * Increasing rate or volume decreases CO₂

Answer 27

Head down and roll to patient's left [This keeps air in the right ventricle and right atrium. Then aspirate air out with central line or PA catheter to RA/RV) [UpToDate: A patient with venous air embolization should be immediately placed into the **left lateral decubitus position (Durant’s maneuver), Trendelenburg position, or left lateral decubitus head down position**. These positions place the right ventricular outflow tract inferior to the right ventricular cavity, causing the air to migrate superiorly into a position within the right ventricle from which air is less likely to embolize. The potential benefit of appropriate positioning was suggested by an animal experiment in which 40% of animals in the left lateral decubitus position survived the venous injection of a lethal amount of air (the experiment did not assess the left lateral decubitus head down or Trendelenburg position). In contrast, a patient with arterial air embolism should be placed in the supine position. The reason that the optimal position differs for arterial and venous air embolism is that arterial blood flow is more forceful than venous blood flow and air bubbles are propelled forward by the arterial blood flow even if the patient is in a head down position. Since the head down positions have the potential to exacerbate the cerebral edema that is typically induced by cerebral air embolism, a flat supine position is also favored for this reason.]

Answer 28

Superior segment of the right lower lobe [pH \< 2.5 and volume \> 0.4 cc/kg is associated with increased degree of damage.] [UpToDate: The pathophysiology of acid pneumonitis has been studied extensively in experimental animals using intratracheal installation of acid. These animal models require an inoculum that has a **pH of ≤2.5** and that is **relatively large (usually 1 to 4 mL/kg)**. This would translate to an inoculum of at least 25 mL of gastric acid in adult humans. It is probable that smaller volumes produce a more subtle process that either escapes clinical detection or causes a less fulminant form of pneumonitis. The clinical observation that patients with esophageal or gastric reflux experience frequent bouts of recurrent pneumonitis, often accompanied by pulmonary fibrosis, supports this concept. The pathologic changes in the preceding animal models of acid pneumonitis evolve rapidly. Within three minutes, there is atelectasis, peribronchial hemorrhage, pulmonary edema, and degeneration of bronchial epithelial cells. By four hours, the alveolar spaces are filled with polymorphonuclear leukocytes and fibrin. Hyaline membranes are seen within 48 hours. The lung at this time is also grossly edematous and hemorrhagic with alveolar consolidation. All of the findings described above have also been noted on autopsy of patients with fatal aspiration pneumonia. The presumed mechanism is the release of proinflammatory cytokines, especially tumor necrosis factor (TNF)-alpha and interleukin (IL)-8.]

Answer 29

1. Unresponsive to pain 2. Absent cold caloric oculovestibular reflexes 3. Absent oculocephalic reflex (patient doesn't track) 4. No spontaneous respirations 5. No corneal reflex 6. No gag reflex 7. Fixed and dilated pupils 8. Positive apnea test [None of the following can be present: * Temperature \<32oC * Blood pressure \<90 mmHg * Drugs (IE phenobarbital, pentobarbital, ETOH) * Metabolic derangements (hyperglycemia, uremia) * Desaturation with apnea test]

Answer 30

Loss of sympathetic tone usually associated with spine or head injury [Usually presents with decreased heart rate and blood pressure, and warm skin.]

Answer 31

* 1x: Cortisone, Hydrocortisone * 5x: Prednisone, Prednisolone, Methylprednisolone * 30x: Dexamethasone

Answer 32

* Low dose: Beta 1&2-adrenergic (increased contractility and vasodilation) * High dose: Alpha 1&2-adrenergic (vasoconstriction) [At low doses, epinephrine can cause decreased blood pressure. At high doses, it can cause increases in ectopic cardiac pacer activity and myocardial O₂ demand.] [UpToDate: Stimulates alpha-, beta1-, and beta2-adrenergic receptors resulting in **relaxation of smooth muscle of the bronchial tree**, cardiac stimulation (**increasing myocardial oxygen consumption**), and dilation of skeletal muscle vasculature; **small doses can cause vasodilation via beta2-vascular receptors**; large doses may produce constriction of skeletal and vascular smooth muscle.]

Answer 33

Vascular smooth muscle constriction [Alpha 1 receptors also promote gluconeogenesis and glycogenolysis.]

Answer 34

Efferent limb [UpToDate: The glomerular filtration rate (GFR) is equal to the sum of the filtration rates in all of the functioning nephrons; thus, the GFR gives a rough measure of the number of functioning nephrons. The filtering units of the kidney, the glomeruli, filter approximately 180 liters per day (125 mL/min) of plasma. The normal value for GFR depends upon age, sex, and body size, and is approximately 130 and 120 mL/min/1.73 m2 for men and women, respectively, with considerable variation even among normal individuals.]

Answer 35

* Resistance against the ventricle contracting (SVR) = **Afterload** * Determined by Left ventricular end-diastolic volume, contractility, and afterload = **Stroke volume** * Stroke volume/left ventricular end-diastolic volume = **Ejection fraction** * Determined by preload and distensibility of the ventricle = **End-diastolic volume** * Determined by contractility and afterload = **End-systolic volume**

Answer 36

1. {CVP and PCWP **-**} {CO **-**} {SVR **+**}: Hemorrhagic 2. {CVP and PCWP **-**} {CO **+**} {SVR **-**}: Septic 3. {CVP and PCWP **+**} {CO **-**} {SVR **+**}: Cardiogenic 4. {CVP and PCWP **-**} {CO **-**} {SVR **-**}: Neurogenic or adrenal insufficiency

Answer 37

Nipride (Nitroprusside) [Treatment for cyanide toxicity is amyl nitrite, then sodium nitrite.]

Answer 38

1. Temperature \>38^oC or \<36^oC 2. Tacchycardia (\>90 bpm) 3. Tacchypnea (\>20/min or PaCO₂ \<32) 4. White blood cell count \>12,000/uL or \<4,000/uL

Answer 39

Renal and splanchnic smooth muscle relaxation

Answer 40

* NSAIDs: They inhibit prostaglandin synthesis resulting in renal arteriole vasoconstriction * Aminoglycosides: Direct tubular injury * Myoglobin: Direct tubular injury (Tx: Alkalinization of urine) * Contrast dyes: Direct tubular injury (Tx: Pre-hydration, bicarb, N-acetylcysteine)

Answer 41

* 75% +/- 5% * Increases with sepsis, cirrhosis, cyanide toxicity, hyperbaric O2, hypothermia, paralysis, coma, sedation * Decreases with decreased O2 saturation and malignant hyperthermia

Answer 42

After 3rd postoperative day [Frequently preceded by a lucid interval. Need to rule out metabolic (hypoglycemia, DKA, hypoxia, hypercarbia, electrolyte imbalances) and organic (MI, CVA) causes.]

Answer 43

* Nail polish * Dark skin * Low-flow states * Ambient light * Anemia * Vital dyes

Answer 44

Beta 1-adrenergic: Increased contractility mostly, tachycardia with higher doses [UpToDate: Dobutamine (initial dose 0.5 to 1 mcg/kg/minute but frequently 2.5 mcg/kg/minute when cardiac decompensation is severe) is the most commonly used inotropic agent in patients who have cardiogenic shock. Dobutamine is often administered together with norepinephrine to offset the fall in peripheral vascular resistance that occurs when low doses of dobutamine are used.]

Answer 45

* Prorenin/Renin: **Juxtoglomerular cells of kidney** * Angiotensinogen: **Mainly synthesized by the liver** * Angiotensinogen conversion to Angiotensin I: **Rate limiting step catalyzed by circulating renin** * Angiotensin I conversion to Angiotensin II: **Angiotensin converting enzyme (ACE) produced by vascular endothelial cells in the lung** * Release of Aldosterone in response to Angiotensin II: **Zona glomerulosa in adrenal cortex** **[**UpToDate: The classical (historical) view of the renin-angiotensin system (RAS) pathway begins with renin cleaving its substrate, angiotensinogen (AGT), to produce the inactive peptide, angiotensin I, which is then converted to angiotensin II by endothelial angiotensin-converting enzyme (ACE). ACE activation of angiotensin II occurs most extensively in the lung. Angiotensin II mediates vasoconstriction as well as aldosterone release from the adrenal gland, resulting in sodium retention and increased blood pressure. However, it is widely recognized that this classical view of the endocrine RAS pathway represents an incomplete description of the system. Instead of one simple circulating RAS, it is recognized that there are also several tissue (local) renin-angiotensin systems that function independently of each other and of the circulating RAS. In particular, angiotensin II generation at the tissue level by these local systems appears to have physiologic effects that are as important as circulating angiotensin II and, under some circumstances, more important than circulating angiotensin II. Thus, the RAS includes local systems with autocrine (cell-to-same cell) and paracrine (cell-to-different cell) effects in addition to the classical circulating RAS with endocrine effects. Physiology of the RAS is proving far more complex than a simple circulating pathway controlling blood volume and blood pressure. In these local systems, activation of angiotensin II results in harmful effects and target-organ damage that extend beyond vascular and renal hemodynamics to direct tissue actions, including tissue remodeling, endothelial dysfunction, and fibrosis. A more detailed review appears below. A teleological view holds that activation of the RAS was a critical adaptation for survival of mammals that migrated from sea to land, in defense against life-threatening circumstances like salt and water deprivation, diarrhea, or hemorrhage. While protective in its purpose, activation of the system in many patients today is maladaptive and leads to disease, with heart failure being a classic example. Sodium retention, coupled with hyperaldosteronism, results in vascular remodeling of the heart and disease progression. Blockade of the RAS has represented a groundbreaking development in the prevention and treatment of heart failure, chronic kidney disease, myocardial infarction, and hypertension. There are a number of steps at which the RAS can be interrupted. Beta-adrenergic blocking agents reduce renin release. ACE inhibitors block the conversion of angiotensin I to angiotensin II downstream from the renin step, and angiotensin receptor blockers (ARBs) interfere with the interaction of the angiotensin II with its receptor. A newer class of antihypertensive drugs, renin inhibitors, interfere with the first step in the cascade, which is the interaction of renin with its substrate, angiotensinogen. Whether or not to block the RAS is no longer the appropriate question in the clinical scenarios of diabetic nephropathy, chronic kidney disease, and heart failure. Efforts are dedicated to answering how best to optimize blockade. Discoveries of new peptides, enzymes, receptors, and cell-signaling targets of the system are changing our understanding of physiology and providing potential new therapeutic targets.]

Answer 46

1. Fluid resuscitation to temporize situation 2. Need pericardial window or pericardiocentesis [UpToDate: Definitive treatment of cardiac tamponade is achieved by removal of the pericardial fluid. While an occasional patient with few or no clinical signs of hemodynamic compromise may be observed with serial physical examinations and echocardiograms, most patients with cardiac tamponade will require early drainage of the pericardial effusion. * In patients with a documented pericardial effusion and clinical evidence of hemodynamic compromise (ie, tachycardia and hypotension producing a picture of cardiogenic shock) consistent with cardiac tamponade, urgent drainage of the pericardial effusion should be performed. Drainage of the effusion can be performed percutaneously using catheter drainage or surgically. * In patients with a documented large pericardial effusion who are hemodynamically stable without evidence of cardiac tamponade, and in whom sampling the fluid is not needed for diagnostic purposes, we suggest initial observation with serial physical examinations and echocardiograms rather than urgent drainage of the pericardial effusion (Grade 2C). Following either percutaneous or surgical drainage of a pericardial effusion in a patient with cardiac tamponade, the patient should be monitored with continuous telemetry and frequent vital signs for at least 24 to 48 hours. Subsequent monitoring with two-dimensional and Doppler echocardiography prior to discharge from the hospital is warranted to confirm adequate fluid removal and to detect possible recurrent fluid accumulation. Intravenous volume repletion and/or inotropic support may prove temporarily beneficial in patients with cardiac tamponade, but these therapies should be considered as temporizing measures until therapeutic drainage of the pericardial effusion can be performed.]

Answer 47

* Becks triad: 1. Hypotension 2. Jugular venous distention 3. Muffled heart sounds * Indicates pericardial tamponade [Mechanism of hypotension is decreased ventricular filling due to fluid in the pericardial sac around the heart.]

Answer 48

Automatic increase in contractility secondary to increased afterload

Answer 49

* Vasoconstriction * Increased heart rate * Increased heart contractility * Glycogenolysis * Gluconeogenesis * Inhibition of renin release [UpToDate: The classical systemic effects of angiotensin II include: * Vasoconstriction – Angiotensin II produces arteriolar vasoconstriction, which increases systemic vascular resistance and, therefore, systemic blood pressure. * Reabsorption of sodium and water – Angiotensin II stimulates sodium reabsorption directly in the proximal tubule, and indirectly in the cortical collecting tubule by inducing secretion of aldosterone by the adrenal cortex. Both of these actions tend to reverse the hypotension or hypovolemia that is usually responsible for the stimulation of renin secretion. In addition to influencing systemic hemodynamics, angiotensin II has an important role in the regulation of glomerular filtration rate (GFR) and renal blood flow. Angiotensin II produces vasoconstriction of the efferent and afferent glomerular arterioles as well as the interlobular artery. The net effect is a reduction in renal blood flow (due to the increase in renal vascular resistance) and an elevation in the hydraulic pressure in the glomerular capillary, which tends to maintain the GFR when the RAS is activated by a fall in systemic pressure. Beyond these effects, however, angiotensin II has a host of important and mostly deleterious actions, as examples: * Angiotensin II acts as an inflammatory mediator through a variety of mechanisms, including intercellular and vascular adhesion molecules (ICAM and VCAM), reactive oxygen species, nuclear factor-kB, and superoxide, exerting a proinflammatory effect on leukocytes, endothelial cells, and vascular smooth-muscle cells. * Angiotensin II also provides a mitogenic stimulus for vascular smooth-muscle cells and promotes cellular proliferation, which could contribute to atherogenesis, and may also contribute to insulin resistance. The effects of angiotensin II are mediated by binding to two specific angiotensin II receptors: the angiotensin II type 1 receptor (AT1R) and the angiotensin II type 2 receptor (AT2R). The vast majority of its actions, including the classical effects and many deleterious effects including fibrosis and inflammation, are mediated by the AT1R. AT2Rs are more sparsely expressed but can be upregulated in response to injury; effects of angiotensin II binding to the AT2R generally counteract its classical actions, producing vasodilation and natriuresis and possibly protecting against hypertension target-organ damage.]

Answer 50

120-150 beats/min [At rates higher than that the cardiac output begins to drop because of decreased diastolic filling time.]

Answer 51

* Decreased cardiac output * Pulmonary embolism * Pulmonary hypertension * Acute respiratory distress syndrome (ARDS) * Excessive PEEP [Can lead to high CO2 buildup (hypercapnia).]

Answer 52

* Carboxyhemoglobin: Falsely increased O₂ saturation (Tx is 100% O₂, hyperbaric oxygen therapy is rarely necessary) * Methemoglobin: O₂ saturation reads at ~85% (Tx is methylene blue)

Answer 53

* Central Venous Pressure (CVP) = **7 (+/-2)** * Systemic Vascular Resistance (SVR) = **800-1,400**

Answer 54

1. Hypoxemia 2. Neurologic abnormalities 3. Petechial rash [UpToDate: Pulmonary manifestations are the most common presenting features of fat embolus syndrome (FES). Hypoxemia, dyspnea, and tachypnea are the most frequent early findings. In one series, hypoxemia was present in 96% of cases. A syndrome indistinguishable from acute respiratory distress syndrome (ARDS) may develop. Approximately one-half of patients with FES caused by long bone fractures develop severe hypoxemia and require mechanical ventilation. Neurologic abnormalities are also common and typically manifest after respiratory abnormalities, although rare case reports suggest neurological symptoms can occur in isolation. Neurologic manifestations range from the development of an acute confusional state and altered level of consciousness to seizures and focal deficits. One study reported that mental status changes occurred in 59% of patients with FES. The characteristic red-brown petechial rash may be the last component of the triad to develop and occurs in only 20% to 50% (on average 1/3) of cases. It is found most often on the nondependent regions of the body including the head, neck, anterior thorax, axillae, and sub-conjunctiva.]

Answer 55

Decreased ventricular filling due to fluid in the pericardial sac around the heart.

Answer 56

Promotes reabsorption of water at the distal convoluted tubule by upregulating the Na/K ATPase on the membrane (More Na re-absorbed and K secreted) [UpToDate: Aldosterone binds to the mineralocorticoid receptor in various tissues, inducing pleiotropic effects. Its main action is in the kidney, where it increases the expression of epithelial sodium channels in the distal tubule, resulting in sodium and water reabsorption and potassium secretion. These renal actions contribute to extracellular fluid volume expansion, increased blood pressure, decreased serum potassium, and, when aldosterone is produced in excess, the primary aldosteronism. The hypokalemia that marks this syndrome results from aldosterone increasing potassium excretion in urine, feces, sweat, and saliva.]

Answer 57

* Fluid overload * Elevated potassium * Metabolic acidosis * Uremic coagulopathy * Poisoning [UpToDate: Accepted urgent indications for RRT in patients with AKI generally include: * Refractory fluid overload * Hyperkalemia (plasma potassium concentration \>6.5 mEq/L) or rapidly rising potassium levels * Signs of uremia, such as pericarditis, encephalopathy, or an otherwise unexplained decline in mental status * Severe metabolic acidosis (pH \<7.1) * Certain alcohol and drug intoxications The likelihood of requiring renal replacement therapy (RRT) is increased in patients with underlying chronic kidney disease (CKD) in proportion to the degree of reduction in glomerular filtration rate (GFR) at baseline. This was illustrated in a study that compared the prehospitalization estimated GFR (eGFR; from the most recent serum creatinine) in 1746 hospitalized patients who developed dialysis-requiring AKI with that of 600,820 hospitalized patients who did not.]

Answer 58

Early gram-negative sepsis: {Insulin -} {Glucose +} (impaired utilization) Late gram-negative sepsis: {Insulin +} {Glucose +} (insulin resistance) [Hyperglycemia often occurs just before patient becomes clinically septic. Early sepsis triad includes hyperventilation, confusion, and hypotension.]

Answer 59

Swan-Ganz catheter [ECHO does not measure PVR.]

Answer 60

Polymorphonucleocytes (PMNs) [Increased proteinaceous material leads to increased A-a gradient, and increased pulmonary shunt.] [UpToDate: Acute respiratory distress syndrome (ARDS) is a consequence of an alveolar injury producing diffuse alveolar damage. The injury causes release of pro-inflammatory cytokines such as tumor necrosis factor, interleukin (IL)-1, IL-6, and IL-8. These cytokines recruit neutrophils to the lungs, where they become activated and release toxic mediators (eg, reactive oxygen species and proteases) that damage the capillary endothelium and alveolar epithelium. Damage to the capillary endothelium allows protein to escape from the vascular space. The oncotic gradient that favors resorption of fluid is lost and fluid pours into the interstitium, overwhelming the lymphatics. The ability to upregulate alveolar fluid clearance may also be lost. Increase in interstitial fluid, combined with damage to the alveolar epithelium, causes the air spaces to fill with bloody, proteinaceous edema fluid and debris from degenerating cells. In addition, functional surfactant is lost, resulting in alveolar collapse. Lung injury has numerous consequences including impairment of gas exchange, decreased lung compliance, and increased pulmonary arterial pressure. Impaired gas exchange – Impaired gas exchange in ARDS is primarily due to ventilation-perfusion mismatching: physiologic shunting causes hypoxemia, while increased physiologic dead space impairs carbon dioxide elimination. A high minute volume is generally needed to maintain a normal arterial carbon dioxide tension (PaCO2), although hypercapnia is uncommon. Decreased lung compliance – Decreased pulmonary compliance is one of the hallmarks of ARDS. It is a consequence of the stiffness of poorly or nonaerated lung, rather than the pressure-volume characteristics of residual functioning lung units. Even small tidal volumes can exceed the lung's inspiratory capacity and cause a dramatic rise in airway pressures. Pulmonary hypertension – Pulmonary hypertension (PH) occurs in up to 25% of patients with ARDS who undergo mechanical ventilation. Causes include hypoxic vasoconstriction, vascular compression by positive airway pressure, parenchymal destruction, airway collapse, hypercarbia, and pulmonary vasoconstrictors. The clinical importance of PH in most patients with ARDS is uncertain. PH severe enough to induce cor pulmonale is rare, but it is associated with an increased risk of death.]

Answer 61

Normal O₂ delivery-to-consumption ratio = **5:1** [CO increases to keep this ratio constant. O₂ consumption is usually supply independent and does not usually change until low levels of delivery are reached.]

Answer 62

Predominately venodilation with decreased myocardial wall tension from decreased preload; moderate coronary vasodilation [UpToDate: Nitroglycerin forms free radical nitric oxide. In smooth muscle, nitric oxide activates guanylate cyclase which increases guanosine 3’5’ monophosphate (cGMP) leading to dephosphorylation of myosin light chains and smooth muscle relaxation. Produces a vasodilator effect on the peripheral veins and arteries with more prominent effects on the veins. Primarily reduces cardiac oxygen demand by decreasing preload (left ventricular end-diastolic pressure); may modestly reduce afterload; dilates coronary arteries and improves collateral flow to ischemic regions. For use in rectal fissures, intra-anal administration results in decreased sphincter tone and intra-anal pressure.]

Answer 63

* Low dose: Beta 1-adrenergic (Increased contractility) * High dose: Alpha 1&2-adrenergic (vasoconstriction) [Potent splanchnic vasoconstrictor] [UpToDate: Stimulates beta1-adrenergic receptors and alpha-adrenergic receptors causing increased contractility and heart rate as well as vasoconstriction, thereby increasing systemic blood pressure and coronary blood flow; clinically, alpha effects (vasoconstriction) are greater than beta effects (inotropic and chronotropic effects).]

Answer 64

The tip of catheter is placed just distal to the left subclavian (1-2 cm below the top of the arch) [UpToDate: The catheter is inserted in most cases through a common femoral artery and advanced under fluoroscopic guidance such that the distal end is positioned in the proximal descending aorta, usually about one centimeter distal to the origin of the left subclavian artery. Alternative insertion sites, such as the right subclavian artery, have been reported.]

Answer 65

* Pulmonary: Need for mechanical ventilation or PaO₂:FiO₂ ratio \<300 mmHg for 24 hours * Cardiovascular: Need for inotropic drugs or cardiac index \<2.5 L/min/m² * Kidney: Creatinine \>2 times baseline on 2 consecutive days or need for dialysis * Liver: Bilirubin \>3 mg/dL on 2 consecutive days or PT \>1.5 control * Nutrition: 10% reduction in lean body mass or albumin \<2.0 or total lymphocyte count \<1 * CNS: Glascow coma scale score \<10 without sedation * Coagulation: Platelet count \<50 or fibrinogen \<100 or need for factor replacement * Host defenses: WBC \<1,000/uL or invasive infection including bacteremia

Answer 66

* Right subclavian vein = **45 cm** * Right internal jugular vein = **50 cm** * Left subclavian vein = **55cm** * Left internal jugular vein = **60 cm**

Answer 67

1. Temperature \<32^oC 2. Blood pressure \<90 mmHg 3. Drugs (IE phenobarbital, pentobarbital, ETOH) 4. Metabolic derangements (hyperglycemia, uremia) 5. Desaturation with apnea test

Answer 68

Intraoperative hypotension [70% of nephrons need to be damaged before renal dysfunction occurs.]

Answer 69

* Thiamine * Folate * B12 * Mg * K * Benzodiazepines (Ativan) prn

Answer 70

Increased diastolic pressure

Answer 71

1. Patient is pre-oxygenated 2. A catheter delivering O₂ at 8 L/min is placed at the carina through the ET-tube and CO₂ should be normal before the start of the test 3. The patient is disconnected from the ventilator for 10 minutes 4. A CO₂ \>60 mmHg or increase in CO₂ by 20 mmHg at the end of the test is a positive test for apnea 5. A positive test meets brain death criteria [If blood pressure drops below 90 mmHg, the patient desaturates below 85% on pulse oximetry, or spontaneous breathing occurs, the test is terminated (negative for apnea). The patient is then placed back on the ventilator and brain death cannot be declared. Of note, **deep tendon reflexes can still be present with brain death**.] [UpToDate: Visual observation is the standard method for detecting respiratory movement. Eight to ten minutes with no observable respiratory effort is a standard observation period. PaCO2 is measured just prior to reconnection to the ventilator to confirm that the target level (\>60 mmHg or 20 mmHg greater than baseline values) was achieved.]

Answer 72

Parenchymal renal failure

Answer 73

* Right atrium filling: Decreased * Cardiac output: Decreased * Renal blood flow: Decreased * Urine output: Decreased * Pulmonary vascular resistance: Increased

Answer 74

* Increased CO2 * Decreased pH * Increased temperature * Increased ATP production * Increased 2,3-DPG production [Opposite of above causes a left shift (increased O₂ binding.]

Answer 75

* Negative inspiratory force (NIF): \>20 * FiO₂: _\<_40% * PEEP: 5 * Pressure support: 5 * Respiratory rate: \<24/min * Heart rate: \<120/min * PO₂: \>60 mmHg * PCO₂: \<50 mmHg * pH: 7.35-7.45 * Saturations: \>93% [Also off pressors, following commands, can protect airway.]

Answer 76

Arterial vasodilation [Cyanide toxicity at doses \> 3 ug/kg/min for 72 hours. This can be monitored by checking thiocyanate levels and signs of metabolic acidosis.] [UpToDate: Causes peripheral vasodilation by direct action on venous and arteriolar smooth muscle, thus reducing peripheral resistance; will increase cardiac output by decreasing afterload; reduces aortal and left ventricular impedance.]

Answer 77

1. Renin: Kidney 2. Epinephrine: Adrenal gland 3. Norepinephrine: Adrenal gland 4. Antidiuretic hormone (ADH): Pituitary 5. Adrenocorticotropin hormone (ACTH): Pituitary

Answer 78

Chemical pneumonitis from aspiration of gastric secretions [Most frequent site is superior segment of the right lower lobe (RLL)] [UpToDate: The term chemical pneumonitis refers to the aspiration of substances that are toxic to the lower airways, independent of bacterial infection. The prototype and best studied clinical example is chemical pneumonitis associated with the aspiration of gastric acid first described by Mendelson in 1946 and sometimes referred to as Mendelson's syndrome. The original series included 61 obstetrical patients who aspirated gastric contents during ether anesthesia. Respiratory distress and cyanosis rapidly followed, usually within two hours of a witnessed aspiration. Chest radiographs showed infiltrates that were usually located in one or both lower lobes. Despite the initial severity of the illness, all 61 patients had a rapid clinical recovery within 24 to 36 hours, with radiographic resolution within four to seven days without the use of antimicrobial therapy. Subsequent studies have shown that this form of aspiration pneumonia commonly follows a more fulminant course that may result in the acute respiratory distress syndrome (ARDS). In patients with aspiration pneumonia resulting in ARDS, blood gas studies usually show that the partial pressure of oxygen is reduced, accompanied by a normal or low partial pressure of CO2 with respiratory alkalosis. Factors that contribute to hypoxemia include pulmonary edema, reduced surfactant activity, reflex airway closure, alveolar hemorrhage, and hyaline membrane formation. Pulmonary function tests show decreased compliance, abnormal ventilation-perfusion, and reduced diffusing capacity. The major explanation for the difference in the clinical course of chemical pneumonitis since the initial report of the entity by Mendelson in 1946 is differences in the type of patients who develop this complication. Mendelson described healthy, young obstetrical patients, whereas the subjects of subsequent reports were often older, debilitated, or burdened with defined comorbid conditions.]

Answer 79

10-15 mmHg [UpToDate: The alveolar to arterial (A-a) oxygen gradient is a common measure of oxygenation ("A" denotes alveolar and "a" denotes arterial oxygenation). It is the difference between the amount of the oxygen in the alveoli (ie, the alveolar oxygen tension [PAO2]) and the amount of oxygen dissolved in the plasma (PaO2): * A-a oxygen gradient = PAO2 - PaO2 PaO2 is measured by arterial blood gas, while PAO2 is calculated using the alveolar gas equation: * PAO2 = (FiO2 x [Patm - PH2O]) - (PaCO2 ÷ R) where FiO2 is the fraction of inspired oxygen (0.21 at room air), Patm is the atmospheric pressure (760 mmHg at sea level), PH2O is the partial pressure of water (47 mmHg at 37ºC), PaCO2 is the arterial carbon dioxide tension, and R is the respiratory quotient. The respiratory quotient is approximately 0.8 at steady state, but varies according to the relative utilization of carbohydrate, protein, and fat. The A-a gradient calculated using this alveolar gas equation may deviate from the true gradient by up to 10 mmHg. This reflects the equation's simplification from the more rigorous full calculation and the imprecision of several independent variables (eg, FiO2 and R). The normal A-a gradient varies with age and can be estimated from the following equation, assuming the patient is breathing room air: * A-a gradient = 2.5 + 0.21 x age in years The A-a gradient increases with higher FiO2. When a patient receives a high FiO2, both PAO2 and PaO2 increase. However, the PAO2 increases disproportionately, causing the A-a gradient to increase. In one series, the A-a gradient in men breathing air and 100% oxygen varied from 8 to 82 mmHg in patients younger than 40 years of age and from 3 to 120 mmHg in patients older than 40 years of age. Proper determinations of the A-a gradient requires exact measurement of FiO2 such as when patients are breathing room air or are receiving mechanical ventilation. The FiO2 of patients receiving supplemental oxygen by nasal cannula or mask can be estimated and the A-a gradient approximated but large variations may exist and the A-a gradient may substantially vary from the predicted. The use of a 100% non-rebreathing mask reasonably approximates actual delivery of 100% oxygen and can be used to measure shunt.]

Answer 80

* Inflates on T wave (diastole) * Deflates on P wave (systole) [UpToDate: Inflation and deflation of the balloon has two major consequences: 1. Blood is displaced to the proximal aorta by inflation during diastole. 2. Aortic volume (and thus afterload) is reduced during systole through a vacuum effect created by rapid balloon deflation.]

Answer 81

* Total lung capacity (TLC): Decreased * Residual volume (RV): Decreased * Forced vital capacity (FVC): Decreased * Forced expiratory volume (FEV₁): Normal or Increased

Answer 82

The level of the bronchioles (150mL usually)

Answer 83

1. Increase PEEP which will tamponade the pulmonary artery bleed 2. Mainstem intubate the non-affected side 3. Can attempt to place a Fogarty balloon down mainstem on affected side 4. May need thoracotomy and lobectomy

Answer 84

* Previous pneumonectomy * Left bundle branch block

Answer 85

Supine position [UpToDate: A patient with venous air embolization should be immediately placed into the left lateral decubitus position (Durant’s maneuver), Trendelenburg position, or left lateral decubitus head down position. These positions place the right ventricular outflow tract inferior to the right ventricular cavity, causing the air to migrate superiorly into a position within the right ventricle from which air is less likely to embolize. The potential benefit of appropriate positioning was suggested by an animal experiment in which 40% of animals in the left lateral decubitus position survived the venous injection of a lethal amount of air (the experiment did not assess the left lateral decubitus head down or Trendelenburg position). In contrast, **a patient with arterial air embolism should be placed in the supine position**. The reason that the optimal position differs for arterial and venous air embolism is that arterial blood flow is more forceful than venous blood flow and air bubbles are propelled forward by the arterial blood flow even if the patient is in a head down position. Since the head down positions have the potential to exacerbate the cerebral edema that is typically induced by cerebral air embolism, a flat supine position is also favored for this reason.]

Answer 86

Aortic regurgitation [UpToDate: The following conditions are contraindications to intraaortic balloon pump insertion: * **Significant (more than mild) aortic regurgitation since the degree of aortic regurgitation will be increased by counterpulsation** * Aortic dissection or clinically significant aortic aneurysm * Uncontrolled sepsis * Uncontrolled bleeding disorder * Severe peripheral artery disease that cannot be pretreated with stenting. Insertion can be carried out in patients with aorto-bifemoral bypass grafts.]

Answer 87

O₂ delivery = CO x arterial O₂ content (CaO₂) x 10