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. Indications for intensive care include hemodynamic instability, single- or multisystem organ failure, active or potential requirement for ventilator support or vasoactive medications, severe medical illness, and postoperative care after major surgery.
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
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. The hemodynamic parameters that can be measured with a PA catheter are central venous pressure, pulmonary capillary wedge pressure, cardiac index, right ventricular end-diastolic volume, right ventricular stroke work index, stroke volume index, left ventricular stroke work index (LVSWI), systemic vascular resistance index, pulmonary vascular resistance index, arterial oxygen delivery (DO2), mixed venous oxygen saturation (SvO2), and oxygen extraction ratio (O2ER). A parameter that is expressed relative to body surface area (BSA) is called an index.
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)/BSA. 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.
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. Noninvasive positive pressure ventilation (NIPPV) should be considered in patients with severe dyspnea and pulmonary edema.
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,
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. Treatment 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. Rhythm control with chemical or electrical cardioversion is generally a second-line treatment. In patients with atrial fibrillation with rapid ventricular response, IV beta-blockers and nondihydropyridine calcium channel blockers (e.g., diltiazem) are the drugs of choice.
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 <60 bpm. Common causes include electrolyte abnormalities, increased vagal tone, myocardial ischemia, myocarditis, cardiomyopathy, and medications. Initial therapy for persistent bradyarrhythmia in an unstable patient is atropine. If this fails, transcutaneous pacing, dopamine, or epinephrine can be attempted.
Hypotension and Shock
Shock is a clinical syndrome in which decreased perfusion causes cellular injury due to inadequate delivery of oxygen. This triggers an inflammatory cascade that leads to symptoms of vital organ dysfunction, including tachycardia, hypotension, oliguria, and altered mentation. In patients with gynecologic malignancy, common postoperative causes include hemorrhage, pulmonary embolism, myocardial infarction, and sepsis.
No absolute criteria for hypotension define shock, but systolic blood pressure (SBP) <90 mm Hg or a decrease of >40 mm Hg from baseline deserves further evaluation.
TABLE 3-1 Hemodynamic Profiles for Critical Care Diagnosis
PCWP or CVP
CO
SVR
SvO2
Hypovolemic
↓
↓
↑
↓
Cardiogenic
↑
↓
↑
↓
Obstructive
Tamponade
↑
↓
↑
↓
Pulmonary embolus
nl or ↓
↓
↑
↓
Distributive
Early septic shock
↑↓
↑
↓
↑
Late septic shock
↑↓
↓
↑
↑↓
Neurogenic shock
↓
↓
↓
↓
↑, increased; ↓, decreased; ↑↓, either decreased or increased; nl, normal; PCWP, pulmonary capillary wedge pressure; CVP, central venous pressure; CO, cardiac output; SVR, systemic vascular resistance; SvO2, mixed venous oxygen saturation.
The Weil-Shubin classification scheme defines four categories of shock: hypovolemic, cardiogenic, obstructive, and distributive. See Table 3-1 for a comparison of hemodynamic parameters in various shock states. Because a patient may exhibit multiple types of shock, strict classification can be difficult.
Management starts with determining and correcting the etiology of the underlying disease process. Ensuring sufficient perfusion and adequate oxygenation is the primary goal.
Hypovolemic shock is due to intravascular fluid loss (e.g., bleeding, nasogastric [NG] suction, diarrhea). Hemorrhagic shock is a type of hypovolemic shock classified by the volume of blood loss and physiologic response (Table 3-2). Expedient volume resuscitation is required when blood loss exceeds 30% to 40%. The mainstay of treatment in hypovolemic shock is volume replacement.
It is important to replace blood products in patients with significant bleeding or anemia. Patient core temperature should be closely monitored during massive transfusion. Hematologic critical care is further addressed later in this chapter.
TABLE 3-2 Classification of Hemorrhage by Extent of Blood Loss
Parameter
Class I
Class II
Class III
Class IV
Blood loss (mL)
750
750-1,500
1,500-2,000
>2,000
Blood volume lost (%)
<15
15-30
30-40
>40
Pulse rate (beats/min)
<100
>100
>120
>140
Supine blood pressure
Normal
Normal
Decreased
Decreased
Urine output (mL/hr)
>30
20-30
5-15
<5
Mental status
Anxious
Agitated
Confused
Lethargic
From Gutierrez G, Reines HD, Wulf-Guterrez ME. Clinical review: hemorrhagic shock. Crit Care 2004;8:373-381.
Crystalloid is typically available on any unit, inexpensive, and carries less risk than colloid administration, therefore making it a common first choice for volume resuscitation. Ringer lactate is less acidic than normal saline and can ameliorate the hyperchloremic metabolic acidosis that results from large volume saline infusion, although there is no important physiologic difference in the degree of resuscitation provided by Ringer versus normal saline.
Colloid therapy is more costly but may provide better short-term volume expansion, although it has not been shown to confer a survival benefit. Albumin 5% is generally considered safe in ICU patients; however, hetastarch has been shown to increase the risk of renal failure and death in ICU patients and should therefore be avoided.
Vasoactive pharmacotherapy may be required along with fluid resuscitation. Intensive care and possibly invasive monitoring are required. Norepinephrine is often employed in the treatment of severe hypotensive shock (Table 3-3).
Cardiogenic shock occurs with decreased myocardial contractility and function. Common etiologies include myocardial infarction, congestive heart failure, cardiac arrhythmias, and valvular disease.
Treatment is targeted at improving myocardial function. For example, inotropes may be used to improve contractility, and vasopressor agents may be used to increase aortic diastolic pressure in order to improve myocardial perfusion. Where these fail, a mechanical assist device such as an intra-aortic balloon pump should be considered.
Fluid administration in patients with cardiogenic shock should be approached with caution.
Obstructive shock occurs secondary to mechanical obstruction of blood flow (e.g., cardiac tamponade, tension pneumothorax, massive pulmonary embolism [PE], prosthetic valve thrombosis) rather than primary cardiac disease.
Distributive shock results from loss of peripheral vascular tone resulting in relative hypovolemia. It encompasses a wide range of conditions including septic shock, other systemic inflammatory response syndrome (SIRS) responses (e.g., trauma, surgery, pancreatitis, hepatic failure), anaphylaxis, neurogenic shock (e.g., spinal cord injury), acute adrenal insufficiency, and toxic shock syndrome.
The initial approach to treatment is similar in hypovolemic shock. The goal is to restore and maintain adequate intravascular volume and add vasoactive agents as needed.
In addition, adjunctive agents should be added depending on etiology. Epinephrine should be administered in anaphylaxis. Corticosteroids should be provided in acute adrenal insufficiency. Underlying conditions should be addressed.
Sepsis and toxic shock syndrome are discussed later in this chapter.
RESPIRATORY CRITICAL CARE
Respiratory support is frequently required for critical care patients.
Hypoxic respiratory failure is characterized by decreased arterial partial pressure of oxygen (PaO2) <60 mm Hg and/or arterial oxygen saturation (SaO2) <90% and is typically associated with tachypnea and hypocapnia. Initially, the SaO2 may be normal or elevated from baseline.
The differential diagnosis includes drug-induced hypoventilation, acute neuromuscular dysfunction, PE, heart failure, chronic obstructive pulmonary disease (COPD), pulmonary edema, pneumonia, atelectasis, and acute respiratory distress syndrome.
TABLE 3-3 Selected Vasoactive Agents in Critical Care
Drug
Main Effects
Dose
Mechanism
Use
Warnings
Dobutamine
Increased inotropy and systemic vasodilation
3-15 µg/kg/min
Potent β1 agonist, weak β2 agonist
Primarily for decompensated heart failure
Adverse effects include tachycardia, ventricular ectopy. Contraindicated with hypertrophic cardiomyopathy.
Dopamine
Low-dose: renal and splanchnic vasodilation and natriuresis; medium dose: increased inotropy and systemic vasodilation; high dose: systemic vasoconstriction
1-3 µg/kg/min; or 3-10 µg/kg/min; or >10 µg/kg/min
Dose-dependent agonist for dopamine receptors (low), β-adrenergic receptors (medium), and peripheral α-adrenergic receptors (high)
May be useful for cardiogenic or hypotensive shock where both cardiac stimulation and peripheral vasoconstriction are needed
Low-dose dopamine is not appropriate for acute renal failure. Adverse effects include tachyarrhythmia, ischemic limb necrosis, increased intraocular pressure, and delayed gastric emptying.
Epinephrine
Dose-dependent increase in cardiac output, increased systemic vascular resistance, relaxation of bronchial smooth muscle
0.3-0.5 µg IM; 2-8 µg/min infusion
β-Adrenergic receptor agonist (low dose) and α agonist (high dose)
Drug of choice for anaphylaxis. Used in ACLS protocols for cardiac arrest. Nebulized racemic epimer used for laryngospasm and severe asthma exacerbation.
Contraindicated with narrow angle glaucoma, ischemic cardiac disease. Local infiltration can cause tissue necrosis.
Norepinephrine
Dose-dependent increase in systemic vascular resistance
0.2-5 µg/kg/min
α-Adrenergic receptor agonist and cardiac β agonist
Preferred vasopressor for septic shock or refractory hypotension
Extreme vasoconstriction can exacerbate endorgan damage. Extravasation can produce local tissue necrosis.
Nitroglycerin
Low-dose: venodilation; high-dose: arteriodilation
1-50 µg/min; or >50 mg/min
Metabolized in endothelial cells to produce nitric oxide (NO) that stimulates cGMP production, causing smooth muscle relaxation. Dose-dependent vasodilator.
Used for unstable angina and to augment cardiac output in decompensated heart failure.
Rapid onset and metabolism. Tolerance develops quickly. Contraindicated for patients taking phosphodiesterase inhibitors.
Nitroprusside
Systemic vasodilation
0.3-2 µg/kg/min
Releases NO in bloodstream; similar mechanism to nitroglycerin.
Used for rapid control of severe hypertension and for decompensated heart failure.
Risk for accumulation of cyanide metabolite
IM, intramuscular; ACLS, advanced cardiac life support; cGMP, cyclic guanosine monophosphate. Adapted from Marino PL. The ICU Book, 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins, 2007.
Hypercapnic respiratory failure is characterized by increased arterial partial pressure of carbon dioxide (PaCO2) >46 mm Hg and pH <7.35 and is associated with hypoventilation. SaO2 may be normal.
The differential diagnosis includes infection, seizures, overfeeding, shock, chronic neuromuscular disorder, electrolyte abnormalities, cardiac surgery, obesity, and drug-induced respiratory depression. Consider hypercapnia as a cause of hypertension in somnolent, tachycardic postoperative patients who may be overmedicated, and avoid administering additional narcotics.
A stepwise evaluation of respiratory failure (i.e., hypoxemia or hypercapnia) begins with an arterial blood gas and calculation of the alveolar-arteriolar (A-a) oxygen gradient.
The A-a gradient = FiO2 (Patmosphere − PH2O) − PaCO2/RQ − PaO2. It is the difference in the partial pressure of oxygen between the alveolus and the arterial blood. FiO2 is the fraction of inspired oxygen and RQ is the respiratory quotient. A patient at sea level breathing room air (FiO2 = 21%) would therefore have an A-a gradient of 148 − 1.2 (PaCO2) − PaO2. The expected A-a gradient can be estimated using the formula: age/4 + 4. Supplemental oxygen increases the normal gradient by 5 to 7 mm Hg for every 10% increase in FiO2.
If the A-a gradient is normal/unchanged, the culprit is hypoventilation. To distinguish central hypoventilation versus a neuromuscular disorder, maximum inspiratory effort (PImax) is evaluated. PImax is measured by having the patient inspire maximally against a closed valve. For most adults, PImax should be >80 cm H2O but varies with age and sex.
If the PImax is normal, drug-induced central hypoventilation should be considered.
If the PImax is low, neuromuscular cause of hypoventilation should be considered.
If the A-a gradient is increased with hypoxemia, measure the mixed venous oxygen pressure (PvO2) to assess for ventilation-perfusion (V/Q) abnormalities. PvO2 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.
If the PvO2 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 <1 indicates intrapulmonary shunt and occurs with asthma, bronchitis, pulmonary edema, pneumonia, and atelectasis. The portion of cardiac output in an intrapulmonary shunt is called the shunt fraction and is normally <10%. Shunt fractions >50% will not improve with oxygen supplementation.
If the PvO2 is low, consider an imbalance in oxygen delivery/uptake (DO2/VO2) such as anemia, low cardiac output, or hypermetabolism.
If the A-a gradient is increased with hypercapnia, measure the rate of CO2 production (VCO2) to assess metabolic versus other disorders. VCO2 is evaluated by a metabolic cart using infrared light to measure CO2 in expired gas. Normal VCO2 is 90 to 130 mL/min/m2.
If the VCO2 is increased, consider overfeeding (especially with carbohydrate load), fever, sepsis, and seizures.
If the VCO2 is normal, consider increased dead space ventilation (see earlier text) and hypoventilation from respiratory weakness (e.g., shock, multisystem organ failure, prolonged neuromuscular blockade, electrolyte imbalances, cardiac surgery) or central hypoventilation (e.g., opiate or benzodiazepine depression, obesity).
Acute Respiratory Distress Syndrome
Acute respiratory distress syndrome (ARDS) is a leading cause of acute respiratory failure, resulting from inflammatory lung injury. The pathophysiology involves activation of diffuse pulmonary inflammation and endothelial damage producing inflammatory alveolar exudates, microvascular thrombosis, pulmonary fibrosis, and high mortality rates exceeding 50% to 60%. Predisposing conditions include sepsis, blood product transfusion, aspiration or chemical pneumonitis, pneumonia, pancreatitis, multiple or long bone fractures, intracranial hypertension, cardiopulmonary bypass, amniotic fluid embolism, and pyelonephritis in pregnancy. Clinically, ARDS is characterized by severe early hypoxemia, normal pulmonary capillary hydrostatic pressures, and diffuse pulmonary infiltrates.
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