Shock

Published on 14/03/2015 by admin

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Last modified 14/03/2015

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4 Shock

Anatomy

Figure 4.1 illustrates the anatomy of the circulatory system.

Pathophysiology of Circulatory Dysfunction

Normal organ function requires adequate perfusion and delivery of oxygen. Oxygen delivery is determined by arterial oxygen content and cardiac output. Arterial oxygen content is a function of hemoglobin concentration and arterial oxygen saturation. Cardiac output is governed by heart rate, contractility, and loading conditions. Any process that adversely affects cardiac output or arterial oxygen saturation can decrease oxygen delivery and result in circulatory dysfunction.

Cardiac output can be affected by the heart rate, arrhythmias, and alterations in ventricular loading. Preload, afterload, and contractility each affect ventricular loading. The Frank-Starling law (Fig. 4.2) states that the principal force governing the strength of ventricular contraction is the length of muscle fibers.1 In a normal heart, muscle fiber length is determined by intravascular volume, often termed preload. As preload increases, myocardial fibers increase in length, which results in increased force of contraction. Increased force of ventricular contraction increases stroke volume and cardiac output. In contrast, depletion of intravascular volume results in muscle fiber shortening, less forceful cardiac contractions, lower stroke volume, and decreased cardiac output.

Increasing ventricular preload improves myocardial contractility only to a point, beyond which myocardial fibers become overstretched. Overstretched fibers can lead to worsening myocardial contractility and, eventually, increased hydrostatic pressure and interstitial edema (e.g., pulmonary edema).

Changes in afterload can also affect ventricular function. For example, severe hypertension impedes ventricular function by reducing cardiac emptying and flow while increasing myocardial workload. Similarly, reducing afterload increases cardiac emptying and flow while decreasing myocardial workload.

Contractility, a measure of ventricular function, is altered by a variety of factors. Medications such as dobutamine can increase the force of contraction for a given preload. In contrast, diseases such as congestive heart failure can reduce contractility and worsen stroke volume and cardiac output.

Circulatory dysfunction can also occur with alterations in regional or microcirculatory blood flow. Disorders that affect arteriolar tone, such as sepsis, cause maldistribution of blood flow between organs and a mismatch of oxygen delivery with demand. Capillary obstruction and endothelial impairment interrupt intraorgan oxygen delivery, thereby potentially resulting in organ failure.

Circulatory dysfunction exists as a spectrum ranging from mild impairment to shock with overt circulatory collapse. Shock is defined as the inability of the circulatory system to provide adequate tissue perfusion, which potentially leads to cellular dysfunction.1 Four categories of shock have been differentiated and defined by the underlying patho-physiology of the circulatory dysfunction: hypovolemic, cardiogenic, distributive, and obstructive (Box 4.1).2 Because each category requires specialized management, every attempt must be made to determine the exact cause of the shock.

Initial Assessment

An initial circulatory assessment should be performed for every ED patient within the first minutes after arrival. This assessment consists of a review of triage vital signs, a focused history, physical examination, and possibly bedside ultrasonography. The goal of the initial circulatory assessment is to detect signs of organ hypoperfusion and identify any immediately life-threatening disorders. Life-threatening disorders requiring rapid diagnosis and treatment include pulmonary embolism, acute myocardial infarction, cardiac tamponade, tension pneumothorax, aortic dissection, and ruptured abdominal aortic aneurysm.

Vital Signs

For nearly all ED patients, circulatory assessment begins with the noninvasive measurement of vital signs. Although blood pressure and heart rate are central to the initial assessment, it is important to note the respiratory rate and oxygen saturation. Any abnormality in the respiratory rate or oxygen saturation may affect arterial oxygen content and impair oxygen delivery. Noninvasive measurement of vital signs correlates poorly with organ perfusion in critically ill patients but serves as an important component of the initial ED assessment of the circulatory system.3

Blood Pressure

Blood pressure, the driving force for organ perfusion, is determined by cardiac output and arterial tone.1 It is important to understand that no blood pressure value is considered normal for every patient. Normal blood pressure values do not always indicate sufficient oxygen delivery. Blood pressure values should be interpreted in the context of the patient’s clinical findings, medical history, and treatment received.

Blood pressure is one of the most common measurements in all of clinical medicine, yet it is often measured incorrectly.4 In the ED, blood pressure is initially obtained during triage with automated blood pressure devices that apply the oscillometric method. These devices can be adversely affected by ambient noise and cuff position. In addition, automated devices typically overestimate true arterial blood pressure in patients with low-flow states. These limitations, combined with activity in the triage environment and patient anxiety, often result in inaccurate measurements of blood pressure. Understandably, triage values can be an unreliable indicator of true blood pressure. Blood pressure measurements should be repeated serially at the bedside in patients demonstrating any evidence of circulatory insufficiency.

The auscultatory method has long been considered the “gold standard” for noninvasive blood pressure measurement. It determines systolic and diastolic pressure on the basis of detection of Korotkoff sounds. The ideal location is the upper part of the arm. The procedure is performed as follows:

Measure blood pressure bilaterally during the initial circulatory examination. A difference of more than 10 mm Hg is significant and may indicate an aortic emergency. Unfortunately, up to 20% of individuals have significant blood pressure differences between their arms.5 Nevertheless, an aortic emergency must be ruled out in any patient with evidence of circulatory insufficiency and blood pressure discrepancies.

Though considered the gold standard, the auscultatory method has several pitfalls. Box 4.2 lists errors commonly made during measurement of blood pressure with the auscultatory method.

Orthostatic Blood Pressure

Depletion of intravascular volume can impair oxygen delivery by decreasing venous return and cardiac output. Symptoms of volume depletion are attributable to reduced cerebral blood flow and include weakness, lightheadedness, unsteadiness, impaired cognition, tremulousness, and syncope. Orthostatic blood pressure measurements can occasionally aid the EP in detecting otherwise unsuspected intravascular volume depletion, but they must be integrated with specific clinical findings. They are not obtained routinely because they have significant limitations.

A positive orthostatic blood pressure response is defined as a reduction in systolic blood pressure of at least 20 mm Hg or a reduction in diastolic blood pressure of at least 10 mm Hg within 3 minutes after standing in a patient with symptoms of volume depletion.7 Orthostatic blood pressure should be measured with the patient in the supine and standing positions. For patients who are unable to stand or who are markedly unsteady, a sitting position may be used. Wait at least 2 minutes before obtaining a standing blood pressure measurement because nearly all patients have a brief orthostatic response immediately on standing. Always measure the heart rate with orthostatic blood pressure. In normal patients, the heart rate increases from 5 to 12 beats/min with standing. Increases greater than 30 beats/min are abnormal and indicate significant volume depletion.

Orthostatic blood pressure measurements have several limitations. Numerous conditions in addition to volume depletion impair the postural hemodynamic response and result in orthostatic hypotension. Most notable are the effects of aging and medications. Up to 30% of elderly patients demonstrate an orthostatic response in the absence of volume depletion.8 Many elderly patients take medications that alter the postural response to changes in position; such medications include antiadrenergics, antidepressants, antihypertensives, neuroleptics, anticholinergics, and antiparkinsonian drugs. In addition, any disorder causing primary or secondary autonomic dysfunction can lead to orthostatic hypotension.

History

A focused history is essential during the initial circulatory assessment. Key elements are a history of the present illness, previous medical history, medication history, family history, and social history. With respect to the history of the present illness, determine the onset and duration of symptoms, the context in which the symptoms developed, any associated symptoms, and any aggravating or alleviating factors. Important associated symptoms include chest pain, dyspnea, palpitations, syncope, and altered mental status. Review the patient’s medical history and direct attention to disorders that may impair cardiac output or arterial oxygen content.

Medications can result in circulatory abnormalities through direct effects or side effects. Two important classes of medications are antiarrhythmic agents and antihypertensive agents. It is crucial to note whether the patient is taking a beta-blocker or calcium channel blocker because both agents can alter the compensatory response to circulatory insufficiency. Always interpret vital signs in the context of the medical history and medication regimen.

Additional key components of the history are the family and social histories. Directly question patients about their family history of sudden death, premature coronary artery disease, venous thromboembolism, and connective tissue disorders (e.g., Marfan syndrome). Similarly, question patients about their use of illicit substances known to have circulatory effects, namely, cocaine.

Physical Examination

Physical examination of the circulatory system begins with the general appearance of the patient. Observe the patient’s positioning, mental status, skin color, and respiratory pattern. Suspect circulatory abnormalities in restless, diaphoretic, delirious, pale, mottled, or tachypneic patients. In addition, note any distinct clinical features implying an underlying medical condition. Table 4.1 lists the characteristic features of disorders that can affect the circulatory system.

Table 4.1 Characteristics of Conditions That Affect the Circulatory System

CONDITION CLINICAL APPEARANCE POTENTIAL CIRCULATORY IMPLICATIONS
Marfan syndrome Arachnodactyly
Arm span greater than height
Longer pubis-to-foot length than pubis-to-head length
Aortic dissection
Osteogenesis imperfecta Blue sclera Aortic dissection
Aortic aneurysm
Aortic valve insufficiency
Mitral valve prolapse
Hyperthyroidism Exophthalmos Congestive heart failure
Hypothyroidism Expressionless face
Periorbital edema
Loss of lateral third of the eyebrows
Dry, sparse hair
Congestive heart failure
Pericardial effusion
Hemochromatosis Bronze pigmentation of skin
Loss of axillary and pubic hair
Cardiomyopathy
Turner syndrome Short stature
Webbed neck
“Shield” chest
Medial deviation of the extended forearm
Aortic coarctation
Aortic insufficiency Bobbing of the head with heartbeat
Systolic flushing of the nail beds

Examine the head and neck for abnormalities suggesting circulatory disease. Facial edema implies impaired venous return resulting from conditions such as superior vena cava thrombosis and constrictive pericarditis. Examination of the jugular venous pulse provides important information about central venous pressure (CVP) and the dynamics of the right side of the heart.9 Place the patient in a 45-degree recumbent position and shine a light tangentially across the neck. The right side is preferred because of its anatomic alignment with the superior vena cava and right atrium. Beginning at the sternal notch, measure the height (in centimeters) of the internal jugular vein pulsations. Pulsations more than 4 cm above the sternal notch are abnormal and a sign of elevated CVP.9 Figure 4.3 illustrates jugular venous distention in a young woman with pericardial effusion.

The cardiopulmonary examination is a quintessential component of circulatory assessment. Observe the rate, depth, and effort of respirations. Tachypnea accompanied by shallow respirations or the use of accessory muscles indicates impending respiratory failure. Auscultate the lungs for asymmetric breath sounds, rhonchi, rales, and wheezing. Recall that any pulmonary process can adversely affect arterial oxygen content and thereby impair oxygen delivery. Auscultate the heart over the right and left upper sternal edges, the lower left sternal edge, and the cardiac apex. Determine the rate and listen for rhythm irregularities, the intensity of heart sounds, murmurs, gallop rhythms, and pericardial rubs. Though difficult with the ambient noise in the ED, attempt to determine whether cardiac murmurs are systolic or diastolic, which can potentially provide valuable information in patients with acute cardiopulmonary dysfunction. Gallop rhythms are low-frequency heart sounds that are heard best with the bell of the stethoscope.

The extremities must be examined as part of the initial circulatory assessment. It is important to observe their color and temperature. Signs of poor perfusion include cold, pale, clammy, mottled skin associated with delayed capillary refill (normal capillary refill is less than 2 seconds). Inspect for symmetric or asymmetric edema and clubbing of the fingers and toes. Finally, palpate the carotid, radial, femoral, dorsalis pedis, and posterior tibial pulses for rate, amplitude, and regularity.