TRIPASS XR تري باس

 

SVI = SV/BSA

30–75 mL/beat/m

2

Systemic vascular resistance (SVR) Measure of impedance applied by

systemic vascular system to systolic

effort of left ventricle; determined by

autonomic nervous system and

condition of vessels. Determinant of

left ventricular afterload.

SVR = [(MAP – CVP)/CO] × 74

800–1,440 dyne·s·cm−

5

Systemic vascular resistance index

(SVRI)

SVR adjusted for body surface area

(BSA

d

).

SVRI = SVR × BSA

1,680–2,580 dyne·s·cm−

5

·m

2

aCVP is essentially synonymous with RAP.

b2–6 mm Hg = 3–6 cm H2O (conversion: 1 mm Hg = 1.34 cm H2O).

cMay optimally ↑ PCWP to 16–18 mm Hg in critically ill patients.

dBSA, body surface area = 1.7 m

2

(average male).

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The diagnosis of shock is based on the findings of impaired tissue perfusion on

examination.

1 These findings may include the following:

Systolic blood pressure (SBP) less than 90 mm Hg, mean arterial pressure

(MAP) less than 65 mm Hg, or at least a 40 mm Hg decrease from baseline

Tachycardia (heart rate [HR] greater than 90 beats/minute)

Tachypnea (respiratory rate [RR] greater than 20 breaths/minute)

Cutaneous vasoconstriction: cold, clammy, blue, mottled skin (although not typical

of distributive shock)

Abnormal mental status (agitation, confusion, stupor, or coma)

Oliguria: urine output less than 0.5 mL/kg/hour

Metabolic acidosis (usually because of an elevated blood lactate level)

Decreased venous oxygen saturation (mixed [SvO2

], central [ScvO2

]) (reflects a

mismatch between oxygen supply [ḊO2

] and demand [ O2

])

Not all these described findings are encountered in every patient with shock, and

considerable variability exists in both the rapidity and the sequence of onset. This

depends on the severity of the initiating event, the underlying mechanism, and the

baseline condition of the patient, including medications that may alter the clinical

presentation. It is important to consider the patient’s medical and pharmacologic

history, while monitoring for subtle clinical changes that may signal impending

deterioration and necessitate immediate intervention.

TREATMENT OVERVIEW

The treatment of patients in shock requires both treatment of the underlying cause of

shock, as well as early, aggressive measures to maintain adequate perfusion to vital

organs. The general measures used are the restoration of volume in hypovolemic

patients, the use of vasopressors or inotropic agents when volume resuscitation is

inadequate to maintain perfusion, and careful monitoring of the hemodynamic status

of the patient. In sepsis, specific hemodynamic goals have been determined.

4

In other

types of shock, specific goals have not been established; however, the principles of

ensuring adequate tissue perfusion are the same.

HEMODYNAMIC MONITORING

Hemodynamic monitoring in critically ill patients is mandatory to properly assess

and manage various shock states. Both noninvasive and invasive monitoring

techniques can be used to measure cardiovascular performance and differentiate the

causes of various conditions that result in hypoperfusion and organ dysfunction. The

values obtained with hemodynamic monitoring should always be used in conjunction

with clinical judgment.

Noninvasive Monitoring

Noninvasive measures are an important part of hemodynamic monitoring. Clinical

examination and vital signs (temperature, HR, blood pressure [BP], RR) provide

valuable information regarding the cardiovascular system and organ perfusion. Other

noninvasive techniques for monitoring the hemodynamic status of patients include

pulse oximetry (for measuring arterial oxygen saturation [SaO2

]) and transthoracic

echocardiography, which can estimate the functional status of the heart and heart

valves. Cardiac telemetry and/or electrocardiogram may help identify a variety of

causes for shock (e.g., arrhythmia, ischemia, pericarditis). Although important,

noninvasive measures have limitations, and certain hemodynamic values important

for the diagnosis and assessment of illness, as well as the patient’s response to

therapy, must be measured invasively at the present time.

Invasive Monitoring

ARTERIAL PRESSURE LINE

The arterial line is a common tool in the ICU. It consists of a small catheter placed

into an artery (usually the radial or femoral artery) under sterile conditions and

attached to a pressure transducer. This allows for continuous measurement of BP and

can be more accurate than a sphygmomanometer in patients with shock, cardiac

arrhythmias, calcified arteries, or high systemic vascular resistance (SVR). It also

provides for easy access for arterial blood gas (ABG) samples to be drawn and

analyzed. Arterial lines should never be used for medication administration.

CENTRAL VENOUS CATHETER

Common in the ICU, the central venous catheter consists of a large-bore catheter

usually inserted into either a subclavian or a jugular vein. It can be used for infusion

of fluid and medications or frequent laboratory studies. When attached to a pressure

transducer, it can be used to measure the central venous pressure (CVP), a reflection

of right atrial pressure and volume status. In patients with sepsis, however,

guidelines call for dynamic rather than static variables (e.g., CVP) to guide fluid

resuscitation.

4 Central venous catheters are preferred to peripheral venous access for

administration of large fluid volumes, blood products, or vasopressors in patients

with shock, but resuscitative efforts should not be delayed if peripheral access is

available. Central venous catheters that can continuously measure the central venous

oxygen saturation (ScvO2

) have been developed and are becoming more common.

These catheters allow for the assessment and monitoring of tissue perfusion and the

response to interventions. Low ScvO2 has been associated with worse outcomes.

5–7

PULMONARY ARTERY CATHETER

The introduction of flow-directed, balloon flotation pulmonary artery (PA) catheters

by Swan and colleagues

8

(Swan–Ganz catheter) in the 1970s represented a major

advance in invasive bedside hemodynamic monitoring. The PA catheter is inserted

via a central venous access and positioned into the PA; this enables clinicians to

assess both right and left intracardiac pressures, determine CO, and obtain mixed

venous blood samples. These capabilities allow one to evaluate volume status and

ventricular performance, derive hemodynamic indices, and determine systemic ḊO2

and O2

. There are several versions of the PA catheter. Some provide additional

lumens for intravenous (IV) infusions, temporary transvenous pacing, and continuous

monitoring of SvO2

.

9 Catheters are available that can measure CO on a continuous

basis. The essential components for hemodynamic monitoring are incorporated in the

standard quadruple-lumen catheter pictured in Figure 17-2. This catheter is

composed of multiple lumens, each terminating at different points along the catheter.

When properly positioned, the proximal port (C) terminates in the right atrium and is

used to measure right atrial pressure, to inject fluid for CO determination, and to

administer IV fluids. The distal port (B), which terminates at the tip of the catheter

(E), is positioned in the PA beyond the pulmonary valve and is used to measure PA

and pulmonary capillary wedge pressure (PCWP; described in the following) and to

obtain mixed venous blood samples. Intermittent inflation of the balloon is

accomplished by inserting 1.5 mL of air into the balloon inflation valve (D). The

thermistor (A) contains a temperature probe and electrical leads that connect to a

computer, which calculates CO by the thermodilution technique.

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Figure 17-2 Pulmonary artery catheter. See text for definitions of A, B, C, D, and E.

Although the PA catheter is confined to the pulmonary vasculature, left ventricular

(LV) pressure can be ascertained from the PCWP. When the balloon is inflated, the

PA catheter becomes lodged or “wedged.” Because forward flow from the right

ventricle ceases beyond the wedged PA segment, a static fluid column exists between

the LV and the PA catheter tip during diastole when the mitral valve is open. If no

pressure gradients are present in the pulmonary vasculature beyond the balloon and if

mitral valve function is normal, the PCWP then equilibrates with all distal pressures

and thus indirectly reflects left ventricular end-diastolic pressure (LVEDP). Based

on the relationship between pressure and volume, the LVEDP is equivalent to the left

ventricular end-diastolic volume, or the left-sided preload. Because PCWP

measurements are not always available, the diastolic pulmonary artery pressure

(DPAP) may provide an estimate of left-sided preload in the absence of pulmonary

hypertension or cardiac tamponade.

The use of PA catheters has potential complications. Arrhythmias, thrombotic

events, infections, and, very rarely, PA rupture have been reported.

9 Several trials

have questioned the routine use of PA catheters. A meta-analysis of 13 randomized,

controlled trials found that use of a PA catheter did not have a significant effect on

mortality, number of days in the ICU or hospital, or cost.

9 An international consensus

conference recommends against the routine placement of the PA catheter in patients

with shock.

1 Despite this, the PA catheter can provide essential diagnostic and

hemodynamic information for specialists to utilize in certain patient populations.

More studies are needed to determine the value of PA catheter data–driven treatment

protocols. Because hypotension alone is not required to define shock, the presence of

inadequate tissue perfusion on physical examination is more important than the

numbers obtained by invasive monitoring.

1 The use of PA catheters has been

decreasing in the ICU as newer and less invasive technologies become available. In

most situations, the PA catheter is reserved for those patients who specifically

require the monitoring of PA pressures and oxygenation parameters, such as patients

with pulmonary hypertension, refractory shock, right ventricular (RV) dysfunction, or

who are post-cardiac surgery.

1,4

OTHER MONITORING TOOLS

New technologies to monitor a patient’s perfusion status are being developed. Endtidal carbon dioxide monitors are used to determine O2 and help guide therapies

designed to improve ḊO2 and O2

. New devices that can measure CO and tissue

perfusion noninvasively (or minimally invasively), such as gastric tonometry,

esophageal Doppler monitoring, thoracic bioimpedance, and others, have been

developed.

10–12 Devices (e.g., PulseCO, PiCCO, LiDCO) that can measure CO by

pulse wave analysis are being increasingly used in ICUs as an alternative to the PA

catheter.

10–12 An international consensus conference does not currently recommend the

newer, less invasive technologies because of lack of validation in patients with

shock.

1

The effective interpretation and management of hemodynamic parameters requires

a thorough understanding of the physiologic determinants of CO and arterial pressure.

Assuming oxygen content of blood is adequate, CO and SVR are the ultimate

determinants of ḊO2

, adequate arterial pressure, and tissue perfusion. As outlined in

Figure 17-1, CO may be quantified as the product of stroke volume (SV) and HR. SV

is determined by preload, afterload, and contractility. Preload is defined as enddiastolic fiber length before contraction and is represented by left ventricular enddiastolic volume (LVEDV). It is approximated by left ventricular end- diastolic

pressure (LVEDP) and pulmonary capillary wedge pressure (PCWP). Right

ventricular preload is reflected by central venous pressure (CVP) or right atrial

pressure (RAP). Afterload is defined as ventricular wall tension developed during

contraction. It is determined by the resistance or impedance the ventricle must

overcome to eject end-diastolic volume. Left and right ventricular afterload are

determined primarily by systemic vascular resistance (SVR) and pulmonary vasular

resistance (PVR), respectively. Contractility describes the inotropic state of the

myocardium and affects the stroke volume (SV) and cardiac output

(CO)independently of preload and afterload. The effects of these factors on

hemodynamic parameters are interrelated and complex and must be assessed

carefully when selecting therapeutic interventions that will produce the desired

response. A review of the determinants of cardiac performance is found in Chapter

14, Heart Failure. Table 17-2 provides definitions of terms and normal hemodynamic

indices.

ETIOLOGIC CLASSIFICATION OF SHOCK AND

COMMON MECHANISMS

The most common clinical conditions associated with the major forms of shock are

reviewed in the subsequent sections and detailed in Table 17-1. Table 17-3

describes the common hemodynamic findings for the various forms of shock.

HYPOVOLEMIC SHOCK

Shock secondary to reduced intravascular volume is referred to as hypovolemic

shock. Whether the primary insult is the external loss of fluid (e.g., blood, plasma, or

free water) or the internal sequestration of these fluids into body cavities (third

spacing), the overall result is reduced venous return or preload (decreased CVP and

PCWP) and decreased CO (Table 17-3). The severity of hypovolemic shock depends

on the amount and rate of intravascular volume loss and each person’s capacity for

compensation. Although responses vary, a healthy person may tolerate an acute loss

of as much as 30% of his or her intravascular volume.

13 Compensatory mechanisms

such as increased HR, myocardial contractility, and SVR are sufficiently effective for

this loss in volume and measurable falls in SBP are not detected. Losses in excess of

40% generally overwhelm compensatory mechanisms, venous return decreases and

the patient’s condition can deteriorate to overt shock with hypotension and signs of

hypoperfusion. If restorative measures are not taken immediately, irreversible shock

and death may result. The most common and dramatic cause of hypovolemic shock is

hemorrhagic shock in which intravascular volume depletion occurs as a result of

bleeding. Trauma is responsible for most cases of acute hemorrhagic shock; other

significant causes are listed in Table 17-1.

Table 17-3

Hemodynamic Findings in Various Shock States

Hypovolemic Cardiogenic Distributive (Septic)

Heart rate ↑ ↑ ↑

Blood pressure

a ↓ ↓ ↓

Cardiac output ↓ ↓ ↑/↓

b

Preload (PCWP) ↓ ↑ ↔/↓

Afterload (SVR) ↑ ↑ ↓

aPatients may be in a state of compensated shock in which blood pressure is normal, but clinical signs of

hypoperfusion are evident.

bCardiac output is increased early in sepsis but can be decreased in late or severe sepsis.

PCWP, pulmonary capillary wedge pressure; SVR, systemic vascular resistance.

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Acute Hemorrhagic Shock

CASE 17-1

QUESTION 1: N.G. is a 64-year-old woman with a history of peptic ulcer disease, who arrives to the

emergency department (ED) complaining of diffuse abdominal pain and bright red blood in her stool over the

past two days. She is confused and oriented only to person. Her skin is pale and cool, with HR 120

beats/minute, SBP 80 mm Hg, and RR 28 breaths/minute. Describe the physiologic changes in N.G. in response

to her gastrointestinal (GI) bleeding. What are the goals of resuscitation in patients with hemorrhagic shock?

N.G. has lost a significant amount of intravascular fluid directly from her GI tract.

She is hypotensive with a compensatory increase in both HR and RR. Her pale, cool

skin indicates shunting of blood from the periphery to maintain perfusion of vital

organs. Based on her clinical presentation, N.G. is in decompensated shock.