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228 PART 3: Cardiovascular Disorders

CHAPTER The Pathophysiology of the considerable volume resuscitation is needed due to nitric oxide–
31 Circulation in Critical Illness mediated venodilation and decreased Pms, positive inotropic
agents such as dobutamine treat the myocardial depression, and
Edward T. Naureckas arterial vasoconstrictors such as norepinephrine may be needed to
˙
Lawrence D. H. Wood maintain BP despite high Qt due to very low SVR.
• In cardiogenic shock, preload reduction (morphine, nitroglycerin,
furosemide) is effected by venodilation and decreased Pms, but
KEY POINTS VR often increases because cardiac function improves to decrease
˙
• Left ventricular (LV) stroke volume (SV) creates arterial pulse pres- Pra; arterial dilating drugs often increase Qt from the injured LV,
˙
sure (PP) by distending conducting vessels during systole, and sys- so BP may even increase despite impaired contractility and Qt
temic vascular resistance (SVR) preserves diastolic pressure (DP) without increasing myocardial O consumption when heart rate
2
by impeding SV from flowing through arterioles during diastole. does not increase.
• This coupling of ventricular and vascular elements allows rapid • Early airway control and continuous mechanical ventilation
clinical separation of hypotensive patients into those with increased decrease oxygen consumption and prevent respiratory acidosis but
˙
SV and cardiac output (Qt) demonstrating bounding pulses with may decrease VR further in hypovolemic patients by raising pleu-
large PP, low DP, and warm digits (low SVR, high Qt hypotension, ral pressure and Pra; in cardiogenic shock, continuous mechanical
˙
˙
or septic shock) from those who demonstrate thready pulses with ventilation and PEEP have less effect on VR and may increase Qt
˙
small PP and cool digits signaling low SV and Qt with increased by decreasing LV afterload.
SVR, as in cardiogenic or hypovolemic shock. • Cardiogenic and low-pressure pulmonary edema are decreased by
˙
• LV pumping function is described by relating LV end-DP as esti- decreasing Ppw, and Qt and oxygen delivery can be maintained at
mated by pulmonary wedge pressure (Ppw) to SV; LV dysfunction low Ppw with vasoactive drugs and blood transfusion; arterial oxy-
˙
is signaled by increased Ppw and decreased SV and may be due to genation can be supported with PEEP without decreasing Qt and
systolic or diastolic dysfunction. oxygen delivery by effecting PEEP and tidal volumes that achieve
• Systolic dysfunction, or decreased contractility, connotes 90% O saturation of an adequate hematocrit on a nontoxic frac-
2
tion of inspired O without profound acidosis.
increased LV end-systolic volume for a given LV end-systolic 2
pressure that is approximately the mean blood pressure (BP);
common causes of acute systolic dysfunction in critical illness
are myocardial ischemia, hypoxia, acidosis, sepsis, intercurrent This chapter reviews several essential concepts of normal cardiovascular
negative inotropic drugs (β or calcium blockers), and acute-on- function as a basis for approaching and correcting disturbed circulation
chronic systolic dysfunction in cardiomyopathies. in critical illness. It begins with a discussion of left ventricular (LV)
• Diastolic dysfunction connotes decreased LV end-diastolic pumping function and an approach to ventricular dysfunction. Then
follows a review of the mechanisms by which the venous return (VR)
volume despite increased Ppw because the heart cannot fill to the heart is controlled by the systemic vessels as a basis for diagnosis
normally; common causes of diastolic dysfunction in critical and treatment of hypoperfusion states. The pulmonary circulation and
illness are pericardial tamponade or constriction, positive end- factors governing lung liquid flux are described through measurements
expiratory pressure (PEEP), or other causes of increased pleural obtained by right heart catheterization to provide an approach to treat-
pressure as in pneumothorax, pleural effusion, or abdominal ing pulmonary edema without compromising adequate peripheral
distention, ventricular interdependence in acute right heart syn- perfusion. Along this discussion pathway, common mechanical interac-
dromes, and chronic LV stiffness as in LV hypertrophy. tions between respiration and circulation are highlighted as a basis for
• Early differentiation between diastolic and systolic dysfunctions understanding the cardiovascular diseases discussed in the following
in critical illness is aided by a questioning approach and dynamic chapters in this section and in the next section on pulmonary disorders
imaging such as echocardiography; this avoids inappropriate and in critical illness.
ineffective therapy for the wrong etiology of LV dysfunction. A primary role of the cardiovascular system is to deliver energy
• Venous return (VR) to the right atrium is controlled by mechanical sources from the gut and liver and oxygen from the lungs to all sys-
characteristics of the systemic vessels (unstressed volume, vascular temic organ systems for their aerobic metabolism; effluent from these
capacitance, vascular volume); together these determine the mean tissues removes the waste products of metabolism and delivers them
systemic pressure (Pms) responsible for driving VR back to the to the lungs, kidney, and liver for excretion. This process is facilitated
right atrium (Pra) through the resistance to VR. by return of the entire circulation through the lungs, where CO is
2
• For a given Pms, VR increases as Pra decreases to define the VR eliminated and O is taken up to arterialize the blood. As depicted
2
curve of the circulation, whereas SV and Qt from the heart increase in Figure 31-1, this central circulation is located within the thoracic
˙
as Pra and preload increase to define the cardiac function curve that cavity; movement of gas between the atmosphere and the alveolar
˙
intersects the VR curve at a unique value of Pra where VR = Qt. space is caused by the respiratory muscles, especially the diaphragm,
• When Q˙t is insufficient, volume infusion, baroreceptors, or depicted as a piston at the floor of the thoracic cavity. Beyond effect-
ing ventilation to permit pulmonary gas exchange, active movement of
metabolic receptors can increase Pms to increase VR and the piston decreases the pleural pressure (Ppl), which approximates the
Pra; this effect is mimicked by venoconstricting drugs such pressure on the outside of extra-alveolar vessels including the right
as norepinephrine or phenylephrine; alternatively, VR can and left hearts (depicted as chambers labeled Pra [right atrial pressure]
be increased by positive inotropic (dobutamine) or after- and Pla [left atrial pressure]); changes in alveolar pressure (Pa) affect
load-reducing (sodium nitroprusside, fenoldopam) drugs that pressures within alveolar vessels. Once the blood leaves the lung and
decrease Pra by enhancing cardiac function. enters the left heart, the ventricular pumping function ejects blood into
• In hypovolemic shock, hemostasis and volume resuscitation are essen- the stiff, high-resistance arterial circulation to perfuse the systemic
tial, whereas arteriolar constricting agents such as norepinephrine capillary beds, where O is consumed and CO is taken up before the
2
2
may be used briefly to provide a window of higher BP; in septic shock, venous blood returns to the right heart through the large-volume, very
compliant, low-resistance venous circuit. 1,2

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