Page 396 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

266 PART 3: Cardiovascular Disorders

This chapter emphasizes how critical illness disturbs ventricular func-
• Mahjoub Y, Pila C, Friggeri A, et al. Assessing fluid responsive-
ness in critically ill patients: false-positive pulse pressure variation tion and the systemic factors governing venous return. This does not
diminish the possibility that occult ischemic heart disease (see Chap. 37)
is detected by Doppler echocardiographic evaluation of the right
ventricle. Crit Care Med. 2009;37:2570-2575. might be unmasked by the stress imposed by multisystem organ failure
or its diverse treatments. To avoid redundancy, I refer liberally to other
• Maitland K, Kiguli S, Opoka RO, et al. Mortality after fluid chapters in this book that discuss ischemic heart disease (Chap. 37) and
bolus in African children with severe infection. New Engl J Med. mechanisms for ventricular dysfunction in the context of other diseases
2011;364:2483-2495. (see Chaps. 25, 26, 33, 36, 38, and 64).
• Michard F, Boussat S, Chemla D, et al. Relation between respira-
tory changes in arterial pulse pressure and fluid responsiveness in ASSESSMENT OF CARDIAC DYSFUNCTION
septic patients with acute circulatory failure. Am J Respir Crit Care
Med. 2000;162:134-138. Depressed cardiac pump function may be due to (1) right and/or left ven-
• Monnet X, Rienzo M, Osman D, et al. Passive leg raising predicts tricular dysfunction, (2) external compression (eg, cardiac tamponade),
(3) excessively elevated right or left ventricular afterload, (4) valvular dys-
fluid responsiveness in the critically ill. Crit Care Med. 2006;34:
1402-1407. function, and (5) abnormal heart rate or rhythm. This chapter focus on right
and left ventricular dysfunction because cardiac tamponade is discussed
• Osman D, Ridel C, Ray P, et al. Cardiac filling pressures are not in Chap. 40, pulmonary embolism in Chap. 38, valvular dysfunction in
appropriate to predict hemodynamic response to volume challenge. Chap. 41, and arrhythmias in Chap. 36. Yet in every case one should
Crit Care Med. 2007;35:64-68. consider the role of the pericardium, lungs and other surrounding
• Préau S, Saulnier F, Dewavrin F, Durocher A, Chagnon J-L. Passive structures, right- and left-ventricular afterloads, valvular function, and
leg raising is predictive of fluid responsiveness in spontaneously heart rate and rhythm. For right and left ventricular dysfunction both
breathing patients with severe sepsis or acute pancreatitis. Crit decreased systolic contractility (a shift down and to the right of the end-
Care Med. 2010;38:819-825. systolic pressure-volume relation [ESPVR]) and increased diastolic stiff-
ness (a shift up and to the left of the diastolic pressure-volume relation)
must be considered (Fig. 35-1). How can one determine the presence of
ventricular dysfunction, distinguish between right and left ventricular
REFERENCES dysfunction, and then identify the specific cause?
Complete references available online at www.mhprofessional.com/hall ■ THE CLINICAL EXAMINATION

Left ventricular dysfunction is characterized by high left ventricular fill-
ing pressures in relation to cardiac output. Likewise, right ventricular
1
CHAPTER Ventricular Dysfunction dysfunction is characterized by high right ventricular filling pressures
in relation to cardiac output. Importantly, there is a close interaction
35 in Critical Illness between the left and right ventricles so that, commonly, left and right
ventricular dysfunction coexist. Initially, evaluation of heart rate, mean
Keith R. Walley blood pressure, pulse pressure, urine output, mentation, and peripheral
perfusion provide a clinical estimate of whether or not cardiac output
is decreased (see Table 35-1). Right ventricular filling pressure may be
judged by distention of jugular veins while dependent pitting edema may
KEY POINTS
reflect chronically elevated right ventricular filling pressure. Evidence of
• Cardiac pump dysfunction may be due to ventricular dys- dependent pulmonary crackles on physical examination due to heart
function, compression by surrounding structures (eg, cardiac failure suggests that left ventricular filling pressure is elevated, usually
tamponade), increased afterload, valvular dysfunction, and/or above 20 to 25 mm Hg. However, in chronic congestive heart failure,
abnormal heart rate and rhythm. where pulmonary lymphatic drainage increases, crackles may not be
• Ventricular dysfunction may be due to decreased systolic contrac- present even at filling pressures as high as 30 mm Hg. Interstitial edema
tility and/or increased diastolic stiffness and may involve right clearance lags decreases in left atrial pressure (Pla) by hours, so rapid
and/or left ventricles. decreases in Pla are not accurately reflected by pulmonary auscultation.
• Systemic vascular factors controlling venous return, and their An audible third heart sound suggests an elevated Pla in the presence of
2
a dilated left ventricle.
interaction with cardiac pump function, must be considered in
order to identify and treat causes of inadequate cardiac output. ■ ECHOCARDIOGRAPHIC EXAMINATION
• Myocardial ischemia, relative to demand, is the most common acute Following a clinical examination that suggests ventricular dysfunction, a
reversible contributor to depressed contractility but exogenous tox- screening echocardiographic examination (FOCUS ) generally provides
3
ins and drugs (β-blockers, Ca channel blockers, etc), a myocardial the most useful information in the shortest period of time. This focused
2+
inflammatory response (due to ischemia-reperfusion, sepsis, etc), screening examination in the emergent or ICU setting evaluates relative
hypoxemia, acidosis, ionized hypocalcemia and other electrolyte chamber size and global ventricular function, determines whether a
abnormalities, and hypo- and hyperthermia also contribute. pericardial effusion is present, and assesses volume status ; knowledge
3,4
• Management of acute-on-chronic heart failure progressively that can immediately direct the next diagnostic and therapeutic steps.
includes oxygen; optimizing preload with diuretics, morphine, To separately evaluate systolic and diastolic function or when regional
and nitrates or fluid infusion for hypovolemia; afterload reduc- wall motion abnormalities, valvular dysfunction, pulmonary hyperten-
tion (including positive pressure ventilation); increasing con- sion, and other pathology is suggested by the initial clinical or screening
tractility using catecholamines or phosphodiesterase inhibitors; echocardiographic examinations, a comprehensive echocardiographic
antiarrhythmic drugs and resynchronization using biventricu- examination performed by an expert is the next most readily avail-
lar pacing; intra-aortic balloon counterpulsation, ventricular able and useful step (see Chap. 29). Correct interpretation is crucial.
assist and ECMO devices; and cardiac transplantation. Ejection fraction and related fractional shortening measurements are
sensitive to changes in preload and afterload. Ejection fraction should
5,6

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