3 Critical Care

Emily S. Wu Meredith L. Birsner

INTRODUCTION

Intensive care unit (ICU) admission is indicated for patients requiring intensive monitoring and physiologic support for organ failure.

CARDIOVASCULAR CRITICAL CARE

Cardiovascular function in critical care can be assessed with invasive hemodynamic monitoring that provides information on the cardiac performance, fluid status, tissue perfusion, and arterial pressure.

• Intra-arterial lines, most commonly placed in the radial or femoral artery, are used to accurately and continuously assess arterial blood pressure and facilitate blood gas analysis. These lines are vital when monitoring and titrating vasoactive medications for hemodynamically unstable patients.

• A pulmonary artery (PA) catheter (Swan-Ganz PA catheter) can be used to measure or calculate hemodynamic parameters. It is placed via the subclavian or internal jugular vein (preferred) and has two lumens. The proximal lumen is

P.34 positioned in the superior vena cava or right atrium, whereas the other opens at the tip of the catheter and contains a balloon that can be “floated” through the right atrium and ventricle into the PA. Indications include distinguishing cardiogenic from other causes of pulmonary edema; managing perioperative fluids in high-risk patients with severe cardiac, pulmonary, or renal disease; guiding fluid resuscitation in patients with shock, renal failure, or unexplained acidosis; and calculating oxygen consumption and intrapulmonary shunt fraction in patients with acute respiratory failure. Despite its potential usage, clinical trials have demonstrated limited patient benefit.

• Central venous pressure (CVP) is recorded from the proximal lumen of the catheter and reflects right atrial pressure (RAP). A normal value is 1 to 6 mm Hg. When there is no obstruction between the right atrium and ventricle, CVP = RAP = right ventricular end-diastolic pressure. It exhibits a complex waveform that can be affected by various pathologic processes and is most often interpreted as a proxy for fluid status and therefore used to guide fluid management. However, CVP can be misleading and vary based on patient position, changes in thoracic pressure (from respiration or ventilation settings), and cardiac disease.

• Pulmonary capillary wedge pressure (PCWP) is recorded with the PA catheter balloon inflated and wedged in a branch of the PA. A normal value is 6 to 12 mm Hg. When there is no obstruction between the left atrium and ventricle, PCWP = left atrial pressure = left ventricular end-diastolic pressure. As with CVP, PCWP values can be misleading. Left ventricular end-diastolic pressure reflects left ventricular preload only with normal ventricular compliance, which often is not the case in critically ill patients.

• Cardiac index (CI) is cardiac output (stroke volume ? heart rate)ZBSA A normal value is 2.4 to 4 L/m². Cardiac output is measured with a PA catheter using a thermodilution technique. A thermistor located near the end of the PA catheter tip detects the flow of a cold fluid injected via the proximal port to calculate blood flow rate (equivalent to cardiac output).

• SvO² is the oxygen saturation in pulmonary arterial blood and measures overall oxygen extraction from the blood. A decrease in this variable implies decreased oxygen delivery or increased oxygen use. A normal value is 70% to 75%.

Heart Failure

Heart failure is classified by right-sided versus left-sided and diastolic versus systolic failure. Systolic heart failure occurs due to impaired ventricular contraction. Diastolic heart failure is a disorder of ventricular relaxation and therefore inadequate filling. The two can be distinguished by the end-diastolic volume, which increases in systolic heart failure and decreases in diastolic heart failure. Although ejection fraction is decreased in systolic heart failure, it is often maintained in diastolic heart failure.

• Common etiologies of heart failure include cardiac ischemia, hypertensive heart disease, cardiac arrhythmias, pulmonary embolism, and cardiomyopathy.

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• In acute decompensated heart failure, patients most commonly exhibit dyspnea, orthopnea, tachypnea, tachycardia, and anxiety. Decreased peripheral perfusion, pulmonary crackles, wheezing, elevated jugular venous pressure, and peripheral edema may be noted on physical exam.

• The workup for heart failure should include ECG, cardiac enzymes, echocardiography, and chest radiography. Although there is no consensus on the role of brain natriuretic peptide (BNP) and diagnosing and monitoring heart failure in the ICU setting, it can be useful because of its high negative predictive value. In severe cases, invasive hemodynamic monitoring may be used to manage treatment.

• In addition to correcting any precipitating factors such as hypertension, myocardial ischemia, and cardiac arrhythmias, treatment should be aimed at improving symptoms, optimizing volume status, and restoring oxygenation. After the patient recovers from the acute phase, chronic heart failure therapy should be optimized.

• In the presence of hypoxia, patients should receive supplemental oxygen and be positioned upright.

• If there is evidence of fluid overload, loop diuretics should be administered while monitoring daily weights, strict intake and output, and electrolytes.

• Afterload reduction with intravenous (IV) vasodilators such as nitroglycerin, nitroprusside, or nesiritide can be considered in patients with left-sided systolic heart failure without hypotension. If these patients exhibit hypotension, inotropes such as milrinone or dobutamine are more appropriate.

• In general, inotropes and diuretics are considered counterproductive in diastolic heart failure. Rather, vasodilators are more frequently employed.

Acute Coronary Syndrome

Acute coronary syndrome (ACS) is composed of unstable angina and myocardial infarction with and without associated ST segment elevation (non-ST segment elevation myocardial infarction [NSTEMI] and ST-segment elevation myocardial infarction [STEMI]). Factors that cause coronary artery obstruction including thrombus formation or vasospasm lead to myocardial ischemia, hypoxia, and acidosis. Diagnosis is based on patient symptoms, ECG findings, and cardiac biomarker values.

• Patients with suspected myocardial ischemia should be treated with oxygen, sublingual nitroglycerin, and chewable aspirin (162 to 325 mg) as soon as possible. Opiates should be administered for pain and to reduce anxiety, which in turn may help reduce myocardial demand.

• Patients with STEMI symptom onset within the last 12 hours should receive immediate reperfusion therapy.

• Depending on risk factors and eligibility criteria, primary percutaneous coronary intervention (PCI), rather than fibrinolytic therapy, is recommended.

• Patients undergoing reperfusion therapy should receive a loading dose of a thienopyridine such as clopidogrel as early as possible. Anticoagulation, with unfractionated heparin or other agents depending on the type of reperfusion therapy to be

performed, should also be administered.

• Depending on the situation, other medications such as beta-blocker and angiotensin-converting enzyme (ACE) inhibitors should be administered within 24 hours of an STEMI.

• In the absence of contraindications, patients with unstable angina and NSTEMI should be treated with aspirin, a second antiplatelet agent such as clopidogrel,

P.36 beta-blockade, anticoagulant therapy, and a glycoprotein IIb/IIIa inhibitor until a revascularization decision is made.

• If a patient experiences cardiac arrest, code team activation, early and proficient provision of cardiopulmonary resuscitation, and early defibrillation for ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT) should occur immediately.

Cardiac Arrhythmias

• Tachycardia is defined as a heart rate >100 beats per minute (bpm). In pregnancy, a higher threshold, typically 120 bpm, is used. Tachycardias can be classified by the site of origin and regularity of rhythm. Typically, tachycardias that originate above the atrioventricular (AV) node are narrow complex, whereas those that originate below the AV node are wide complex. Patients with rate-related cardiovascular compromise should proceed to immediate synchronized cardioversion per advanced cardiac life support protocol; adenosine can be considered in patients with narrow complex regular tachycardia with monomorphic QRS complexes.

• Narrow complex, regular rhythm tachycardias include sinus tachycardia, atrial flutter, and AV nodal reentry tachycardia (AVNRT). The atrial rate with atrial flutter is typically 250 to 350 bpm, most often with a 2:1 ventricular conduction ratio. T reatment is similar to that in atrial fibrillation, as described in the following text. Acute episodes of AVNRT can be terminated with vagal maneuvers, adenosine, or calcium channel blockers.

• Narrow complex, irregular rhythm tachycardias include atrial fibrillation, multifocal atrial tachycardia (MAT), and atrial flutter with variable AV block. Medical management for atrial fibrillation involves rate control and prevention of thromboembolic events.

• Wide complex, regular rhythm tachycardias include monomorphic VT or supraventricular tachycardia with aberrancy. Preferred treatment for stable patients with likely VT are elective cardioversion or antiarrhythmics.

• Wide complex, irregular rhythm tachycardias include VF, polymorphic VT, and atrial fibrillation with aberrancy.

• Bradycardia is defined as a heart rate ACLS, advanced cardiac life support; cGMP, cyclic guanosine monophosphate. Adapted from Marino PL. The ICU Book, 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2007.

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• Hypercapnic respiratory failure is characterized by increased arterial partial pressure of carbon dioxide (Pa_CO2) >46 mm Hg and pH 80 cm H₂O but varies with age and sex.

ξ If the PI_max is normal, drug-induced central hypoventilation should be considered.

ξ If the PI_max is low, neuromuscular cause of hypoventilation should be considered.

ξ If the A-a gradient is increased with hypoxemia, measure the mixed venous oxygen pressure (Pv_O2) to assess for ventilation-perfusion (V∕Q) abnormalities. Pv_O2 is ideally measured from pulmonary arterial blood using a PA catheter, but superior vena caval blood can be used. Normal values from the PA are 35 to 45 mm Hg.

ξ If the Pv₀₂ is normal, consider a V/Q abnormality.

• V/Q >1 indicates increased dead space ventilation and occurs with PE, congestive heart failure, emphysema, and alveolar overdistension from positive pressure ventilation.

• V/Q gases, a minimum flow rate of 5 L/min is required. The maximum flow rate of 10 L/min provides an FiO₂ of 60%.

• Face masks with bags have an oxygen reservoir of 600 to 1,000 mL. There are two types of reservoir mask devices:

ξ A partial rebreather has a maximum FiO₂ of 70% to 80%. It “captures” initial exhaled air containing a higher proportion of O₂ from the upper airway (anatomic dead space) in the reservoir bag and releases the terminal exhaled air containing more CO₂. The reservoir bag maintains a high O₂ content.

ξ A nonrebreather has a maximum FiO₂ of 100%. It requires a tight seal during use and can be used to administer nebulizer treatments but does not allow easy oral feeding. The reservoir bag maintains 100% O₂ content.

• High-flow oxygen masks deliver a constant FiO₂ at a flow rate that exceeds the peak inspiratory rate, preventing the variability seen with low flow systems. They may be useful in patients with chronic hypercapnia who require a constant FiO₂ to avoid increased CO₂ retention. The maximum FiO₂ is 50%.

• Noninvasive positive pressure ventilation (NIPPV) can be a useful alternative to invasive (i.e., endotracheal or tracheostomy) intubation. It has been used to successfully manage obstructive sleep apnea in general medical patients but is also appropriate for critical care patients with moderate respiratory compromise due to mild neuromuscular weakness, congestive heart failure/cardiogenic pulmonary edema, and decompensated COPD.

ξ A cooperative patient with no risk for emergent intubation and moderate dyspnea, tachypnea, increased work of breathing, hypercapnia, or hypoxemia can be considered for NIPPV.

ξ Contraindications include cardiac or respiratory arrest or severe cardiopulmonary compromise, coma, status epilepticus, potential airway obstruction, patient inability to protect her airway, and emergent conditions.

ξ NIPPV can be supplied via mouthpiece, nasal pillows, face mask, or helmet; the device must fit properly to avoid air leaks. FiO₂ is titrated to the necessary minimum and the backup rate, pressure support, and PEEP are adjusted to maintain an appropriate TV (5 to 7 mL/kg/breath).

ξ Complications with NIPPV include facial or nasal pressure sores, gastric distension, aspiration, and inspissated uncleared secretions.

• Mechanical ventilation should be instituted for patients who cannot be adequately managed with the aforementioned systems, are in respiratory distress, or are at risk for cardiopulmonary collapse. Indicators for endotracheal intubation include tachypnea >35 breaths/min, Pa_O2 46 mm Hg with pH person can generate NIF of -80 cm H₂O.

ξ Rapid shallow breathing index (RSBI or Tobin index) should be of the underlying condition. Symptomatic hypocalcemia or ionized calcium 10.5 mg/dL or ionized serum calcium >1.3 mmol/L. In 90% of cases, the underlying cause is hyperparathyroidism or malignancy; severe hypercalcemia (i.e., total calcium >14 mg/dL or ionized calcium >3.5 mmol/L) is associated with neoplasm. Other causes include thyrotoxicosis, thiazide diuretics, and lithium treatment. The most common mechanism of hypercalcemia in gynecologic oncology patients is increased osteoclastic bone resorption without direct bone metastases.

• Clinical findings are nonspecific but can include gastrointestinal (GI) (e.g., nausea, constipation, ileus, abdominal pain, pancreatitis), cardiovascular (e.g., hypovolemia, hypotension, hypertension, shortened QT interval), renal (e.g., polyuria, nephrolithiasis), and neurologic (e.g., lethargy, confusion, coma) abnormalities. Symptoms are usually present when total serum calcium exceeds 12 mg/dL.

• Acute management aims to increase excretion and storage of calcium.

• Hydration with isotonic saline promotes renal natriuresis and thereby increases calcium excretion.

• Diuresis with furosemide (40 to 80 mg IV every 2 hours) with a goal of 100 to 200 mL urine output per hour further promotes urinary calcium excretion. Urine output, stimulated by hydration or pharmacologic diuresis, should be replaced with isotonic saline to prevent hypovolemia.

• Calcitonin (salmon calcitonin 4 U/kg subcutaneously or intramuscularly every 12 hours) rapidly inhibits bone resorption and may decrease serum calcium levels, although the effect is not profound.

• Hydrocortisone (200 mg IV daily divided into three doses) inhibits some lymphoid neoplastic growth, decreasing bone calcium release.

• Pamidronate disodium (90 mg IV over 2 hours) or zoledronate are effective for severe hypercalcemia, with peak effect in 2 to 4 days.

• Dialysis is appropriate for patients with severe renal failure.

Acid-Base Disorders

Evaluation of acid-base disorders requires arterial blood gas interpretation. A stepwise approach for basic analysis is outlined here.

• Step 1: Determine the primary disorder. Assess the pH and Pa_CO2. If either the pH or Pa_CO2 is abnormal, a disorder is present.

• If the pH is 44 and a metabolic acidosis is present if the HCO₃ 7.44, the patient is alkalemic. A respiratory alkalosis is present if the Pa_CO2 26.

ξ A mixed disorder is present if either the pH or the Pa_CO2 is normal. Compensatory responses never completely correct the primary acid-base disturbance, so equal and opposite processes are occurring.

• Step 2: Determine the expected compensatory response. See Table 3-4.

• In metabolic disorders, if the measured Pa_CO2 is higher than expected, there is a superimposed respiratory acidosis. If the measured Pa_CO2 is lower than expected, there is a superimposed respiratory alkalosis.

• In respiratory disorders, if the change in pH is more than 0.008 times the change in P_co2, then a superimposed metabolic disorder is present.

• Step 3: Calculate the anion gap. The anion gap = Na⁺ - [Cl^- + HCO₃^J. For every 1 g/dL reduction of albumin from 4 g/dL, add another 2.5 to the anion gap. The normal range is 10 to 14 mEq/L. If an anion gap is present, the patient has an anion gap metabolic acidosis, regardless of what other disturbances are present.

• Causes of normal anion gap acidosis (mnemonic USEDCAR) include Urinary diversion (ureterosigmoidostomy), Saline administration (in the face of renal dysfunction), Endocrine disorder (Addison disease, primary hyperparathyroidism), DiarrheaZDrugs (spironolactone, triamterene, amiloride, amphotericin), Carbonic anhydrase inhibitors (acetazolamide, methazolamide, topiramate), Ammonium chloride/hyperAlimentation, and Renal tubular acidosis.

• Causes of increased anion gap acidosis (mnemonic MUDPILES) include Methanol, Uremia, Diabetes (ketoacidosis)/Drugs (metformin), Paraldehyde, Isoniazid/Infection/Ischemia, Lactic acidosis, Ethylene glycol, Salicylates/Starvation.

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• Step 4: If there is an anion gap, calculate the delta gap. The delta gap = (25 - HCO₃) - (anion gap - 12). If this is >5, there is a coexisting nonanion gap metabolic acidosis.

• Step 5: Calculate the osmolar gap in patients with unexplained anion gap metabolic acidosis. Osmolar gap = measured OsM - calculated OsM. Calculated OsM = 2 ? Na + glucose/18 + blood urea nitrogen [BUN]/2.8.

• Increased osmolar gap is seen in ingestion of ethylene glycol, alcohol, methanol, isopropyl alcohol, mannitol, sorbitol, and paraldehyde.

• Treatment is based on the severity and diagnosis. Typically it is only necessary to treat the underlying cause(s). In patients with profound disturbances (i.e., pH suggested by elevated urine specific gravity, decreased fractional excretion of sodium (FEN_a) of 20, and urine sodium 2%, fractional excretion of urea >50%, urine sodium >40 mmol/L, urine osmolarity 50% reduction in GFR. Cl_Cr is calculated by the formula:

• Management of acute oliguria should optimize central hemodynamics and increase glomerulotubular flow. Precipitating factors should be identified and corrected. Nephrotoxic agents should be minimized and all medications renally dosed. Electrolytes should be monitored and repleted.

• If there is evidence for volume depletion, a fluid challenge should first be administered and volume infused until cardiac output is restored. In patients with invasive hemodynamic monitoring, base the management on cardiac filling pressures (CVP and PCWP), cardiac output (using CI), and blood pressure (BP).

• There is no evidence that low “renal dose” dopamine or furosemide treatments are beneficial. Dopamine may increase risk for bowel ischemia.

• Low-dose dopamine (5 mg/kg/min) has traditionally been used to improve inotropy in oliguric renal failure. However, recent studies have shown that dopamine has little benefit in these situations and may increase risk for bowel ischemia.

• Similarly, loop diuretics are often used to treat oliguric renal failure, but multiple studies have suggested that not only is there no benefit, but their use may cause harm to critically ill patients. If loop diuretics are used, it should be as a continuous infusion. Rarely, a “Lasix-dependent” patient is encountered who requires diuretic to maintain adequate urine output. This is very uncommon, however, and most postoperative patients with oliguria are simply hypovolemic. Volume status and cardiac output should be optimized before proceeding with pharmacologic management.

• Special attention should be given to urine output in postoperative gynecologic oncology patients who have had malignant ascites removed. The fluid tends to reaccumulate in the abdominal cavity quickly after drainage and may

require massive ongoing fluid replacement.

• Patients who fail conservative management of AKI may require renal replacement therapy. Indications include volume overload, uremia, hyperkalemia, severe acidosis, and rapidly increasing serum creatinine.

HEMATOLOGIC CRITICAL CARE

Anemia

• Anemia is defined as a hemoglobin level of less than 12 g/dL in women and 14 g/dL in men. Levels of 7 g/dL, or even lower, are typically well tolerated in patients without cardiovascular disease.

• The decision to transfuse depends on the clinical situation and should balance the potential risks of a blood transfusion with patient symptoms, comorbidities, and risk of further bleeding. A landmark study that compared a conservative transfusion threshold (early recognition, elimination/debridement of infectious source if identified, antibiotics, and ICU supportive care with fluids, oxygen, and vasopressors if needed. Mortality ranges from 5% to 60% depending on the bacterial strain and severity of illness.

• Beta-lactam agents, including penicillin G, are effective against GAS, whereas STSS requires vancomycin, nafcillin, or oxacillin.

• Clindamycin is given for its inhibitory action on protein synthesis including toxin suppression.

• In patients who do not show rapid clinical response, immunoglobulins may be administered to neutralize superantigens and potentially shorten the disease course.

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NEUROLOGIC CRITICAL CARE

• In addition to patient comfort, sedation and pain control in the ICU can serve to minimize stress-mediated activation of neuroendocrine pathways and increase in sympathetic tone. Presence of pain, anxiety, and delirium should be evaluated in an acutely agitated patient.

• The most commonly used medications for sedation are haloperidol, opioid analgesics, midazolam, propofol, diazepam, and lorazepam. Midazolam and diazepam are most appropriate for rapid sedation of acutely agitated patients but should be used with caution in elderly patients. Propofol is most useful when the ability to rapidly awaken a patient is needed; however, if greater than 2 days of infusion are administered, triglyceride levels should be monitored.

• To minimize prolonged sedative effects, systematic tapering or daily interruptions in sedative doses is recommended. Sedation goals should be established and regularly reviewed for each patient.

• There exist several scales to assess a patient's level of sedation, including the sedation-analgesia scale (SAS), Richmond Agitation Sedation Scale (RASS), Vancouver Interaction and Calmness Scale (VICS), Motor Activity Assessment Scale (MAAS), and the Ramsay Scale for Scoring Sedation. These scales are subjective, but RASS, MAAS, and VICS have been validated for critically ill patients.

• Delirium is an acute, transient, fluctuating state of confusion characterized by impairment in maintaining attention. Recent studies have suggested an association between presence of delirium and risk of dying. Delirium can be hypoactive (decreased physical and mental activity, inattention), hyperactive (combativeness, agitation), or mixed.

• The mnemonic DELIRIUM can be used to remember risk factors: drugs, electrolyte abnormalities, lack of drugs (withdrawal), infection, reduced sensory input, intracranial problems, urinary retention and fecal impaction, and myocardial problems.

• Tools to assess delirium include the Confusion Assessment Method for the ICU (CAM-ICU), the Intensive Care Delirium Screening Checklist (ICDSC), and the Neelon and Champagne (NEECHAM) Confusion Scale.

• Treatment should include identifying and treating the underlying cause. Concurrent strategies include reorienting patients, restoring normal sleep-wake cycles, removing medications that exacerbate delirium, providing hearing aids/glasses, and removing invasive devices whenever possible. If pharmacologic therapy is used, benzodiazepines should be avoided in favor of antipsychotics such as haloperidol (2 to 5 mg every 6 to 12 hours).

SPECIAL OBSTETRIC CONSIDERATIONS IN CRITICAL CARE

Hypertension, hemorrhage, sepsis, and cardiopulmonary conditions account for the majority of intensive care admissions in the antepartum and postpartum period. Physiologic alterations in pregnancy can continue into the postpartum period and are important to account for when interpreting critical care data.

• Profound hemodynamic alterations occur during pregnancy, including a 40% to 50% increase in blood volume, 30% to 50% increase in cardiac output, decrease in systemic vascular resistance, and increase in heart rate. Little data exists to determine the use of invasive hemodynamic monitoring in obstetric patients.

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• Athough the need for cardiopulmonary resuscitation is rare, left lateral uterine displacement is essential to maximizing

cardiac output generated during chest compressions.

• In addition to etiologies typically seen outside of pregnancy, chorioamnionitis, pyelonephritis, tocolytic therapy, and preeclampsia should be considered when an obstetric patient presents with ARDS. In this condition, pregnancy-induced respiratory alkalosis may be exacerbated by hyperventilation. Otherwise, management with supportive care and lung protective ventilation is similar to that for nonobstetric patients.

• Colloid osmotic pressure is decreased by up to 20% in pregnancy, thereby increasing the risk of developing cardiogenic and noncardiogenic pulmonary edema, especially in women with underlying cardiac conditions. Careful fluid management in these patients is paramount.

• In critically ill obstetric patients, the decision to move toward delivery should be evaluated as a patient's clinical course evolves. If a condition is exacerbated by pregnancy and is refractory to all conservative interventions, delivery can be considered. The risks of prematurity should be carefully balanced with the risks to the mother of maintaining her pregnancy.

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