Stages of Shock
Some think of the shock syndrome as a continuum along which the patient struggles to survive. A convenient way to understand the physiologic responses and subsequent clinical signs and symp-toms is to divide the continuum into separate stages: compen-satory, progressive, and irreversible. (Although some authorities identify an initial stage of shock, changes attributed to this stage occur at the cellular level and are generally not detectable clini-cally.) The earlier that medical management and nursing inter-ventions can be initiated along this continuum, the greater the patient’s chance of survival.
In the compensatory stage of shock, the patient’s blood pressure remains within normal limits. Vasoconstriction, increased heart rate, and increased contractility of the heart contribute to main-taining adequate cardiac output. This results from stimulation of the sympathetic nervous system and subsequent release of cate-cholamines (epinephrine and norepinephrine). The patient dis-plays the often-described “fight or flight” response. The body shunts blood from organs such as the skin, kidneys, and gas-trointestinal tract to the brain and heart to ensure adequate blood supply to these vital organs. As a result, the patient’s skin is cold and clammy, bowel sounds are hypoactive, and urine output de-creases in response to the release of aldosterone and ADH.
Despite a normal blood pressure, the patient shows numerous clinical signs indicating inadequate organ perfusion (Chart 15-2). The result of inadequate perfusion is anaerobic metabolism and a buildup of lactic acid, producing metabolic acidosis. The respira-tory rate increases in response to metabolic acidosis. This rapid res-piratory rate facilitates removal of excess carbon dioxide but raises the blood pH and often causes a compensatory respiratory alkalo-sis. The alkalotic state causes mental status changes, such as con-fusion or combativeness, as well as arteriolar dilation. If treatment begins in this stage of shock, the prognosis for the patient is good.
Medical treatment is directed toward identifying the cause of the shock, correcting the underlying disorder so that shock does not progress, and supporting those physiologic processes that thus far have responded successfully to the threat. Because compensation cannot be effectively maintained indefinitely, measures such as fluid replacement and medication therapy must be initiated to maintain an adequate blood pressure and reestablish and main-tain adequate tissue perfusion.
Early intervention along the continuum of shock is the key to im-proving the patient’s prognosis. Therefore, the nurse needs to as-sess systematically those patients at risk for shock to recognize the subtle clinical signs of the compensatory stage before the patient’s blood pressure drops.
In assessing tissue perfusion, the nurse observes for changes in level of consciousness, vital signs (including pulse pressure), urinary output, skin, and laboratory values. In the compensatory stage of shock, serum sodium and blood glucose levels are elevated in re-sponse to the release of aldosterone and catecholamines.
The role of the nurse at the compensatory stage of shock is to monitor the patient’s hemodynamic status and promptly report deviations to the physician, assist in identifying and treating the underlying disorder by continuous in-depth assessment of the pa-tient, administer prescribed fluids and medications, and promote patient safety. Vital signs are key indicators of the patient’s he-modynamic status; however, blood pressure is an indirect method of monitoring tissue hypoxia. Pulse pressure correlates well to stroke volume, the amount of blood ejected from the heart with systole. Pulse pressure is calculated by subtracting the diastolic measurement from the systolic measurement; the difference is the pulse pressure. Normally, the pulse pressure is 30 to 40 mm Hg (Mikhail, 1999). Narrowing or decreased pulse pressure is an earlier indicator of shock than a drop in systolic blood pressure. Decreased or narrowing pulse pressure, an early indication of de-creased stroke volume, is illustrated in the following example:
Systolic blood pressure − diastolic blood pressure = pulse pressure
Elevation in the diastolic blood pressure with release of cate-cholamines and attempts to increase venous return through vaso-constriction is an early compensatory mechanism in response to decreased stroke volume, blood pressure, and overall cardiac output.
Although treatments are prescribed and initiated by the physi-cian, the nurse usually implements them, operates and trou-bleshoots equipment used in treatment, monitors the patient’s status during treatment, and assesses the immediate effects of treatment. Additionally, the nurse assesses the response of the pa-tient and the family to the crisis and to treatment.
While experiencing a major threat to health and well-being and being the focus of attention of many health care providers, the patient often becomes anxious and apprehensive. Providing brief explanations about the diagnostic and treatment procedures, sup-porting the patient during those procedures, and providing in-formation about their outcomes are usually effective in reducing stress and anxiety and thus promoting the patient’s physical and mental well-being.
Another nursing intervention is monitoring potential threats to the patient’s safety, because a high anxiety level and altered men-tal status typically impair a person’s judgment. In this stage, pa-tients who were previously cooperative and followed instructions may now disrupt intravenous lines and catheters and complicate their condition. Therefore, close monitoring is essential.
In the progressive stage of shock, the mechanisms that regulate blood pressure can no longer compensate and the MAP falls below normal limits, with an average systolic blood pressure of less than 90 mm Hg (Abraham et al., 2000).
Although all organ systems suffer from hypoperfusion at this stage, two events perpetuate the shock syndrome. First, the over-worked heart becomes dysfunctional; the body’s inability to meet increased oxygen requirements produces ischemia; and biochem-ical mediators cause myocardial depression (Kumar, Haery & Parrillo, 2000; Price, Anning, Mitchell et al., 1999). This leads to failure of the cardiac pump, even if the underlying cause of the shock is not of cardiac origin. Second, the autoregulatory func-tion of the microcirculation fails in response to numerous bio-chemical mediators released by the cells, resulting in increased capillary permeability, with areas of arteriolar and venous con-striction further compromising cellular perfusion. At this stage, the patient’s prognosis worsens. The relaxation of precapillary sphincters causes fluid to leak from the capillaries, creating inter-stitial edema and return of less fluid to the heart. Even if the underlying cause of the shock is reversed, the breakdown of the circulatory system itself perpetuates the shock state, and a vicious circle ensues.
Chances of survival depend on the patient’s general health before the shock state as well as the amount of time it takes to restore tis-sue perfusion. As shock progresses, organ systems decompensate.
The lungs, which become compromised early in shock, are af-fected at this stage. Subsequent decompensation of the lungs in-creases the likelihood that mechanical ventilation will be needed if shock progresses. Respirations are rapid and shallow. Crackles are heard over the lung fields. Decreased pulmonary blood flow causes arterial oxygen levels to decrease and carbon dioxide levels to increase. Hypoxemia and biochemical mediators cause an in-tense inflammatory response and pulmonary vasoconstriction, perpetuating the pulmonary capillary hypoperfusion and hypox-emia. The hypoperfused alveoli stop producing surfactant andsubsequently collapse. Pulmonary capillaries begin to leak their contents, causing pulmonary edema, diffusion abnormalities (shunting), and additional alveolar collapse. Interstitial inflam-mation and fibrosis are common as the pulmonary damage pro-gresses (Fein & Calalang-Colucci, 2000). This condition is sometimes referred to as acute respiratory distress syndrome (ARDS), acute lung injury (ALI), shock lung, or noncardiogenic pulmonary edema.
A lack of adequate blood supply leads to dysrhythmias and is-chemia. The patient has a rapid heart rate, sometimes exceeding 150 bpm. The patient may complain of chest pain and even suf-fer a myocardial infarction. Cardiac enzyme levels (eg, lactate de-hydrogenase, CPK-MB, and cTn-I) rise. In addition, myocardial depression and ventricular dilation may further impair the heart’s ability to pump enough blood to the tissues to meet oxygen requirements.
As blood flow to the brain becomes impaired, the patient’s men-tal status deteriorates. Changes in mental status occur as a re-sult of decreased cerebral perfusion and hypoxia; the patient may initially exhibit confusion or a subtle change in behavior. Subsequently, lethargy increases and the patient begins to lose consciousness. The pupils dilate and are only sluggishly reactive to light.
When the MAP falls below 80 mm Hg (Guyton & Hall, 2000), the glomerular filtration rate of the kidneys cannot be main-tained, and drastic changes in renal function occur. Acute renal failure (ARF) can develop. ARF is characterized by an increase in blood urea nitrogen (BUN) and serum creatinine levels, fluid and electrolyte shifts, acid–base imbalances, and a loss of the renal-hormonal regulation of blood pressure. Urinary output usually decreases to below 0.5/mL/kg per hour (or below 30 mL per hour) but can be variable depending on the phase of ARF.
Decreased blood flow to the liver impairs the liver cells’ ability to perform metabolic and phagocytic functions. Consequently, the patient is less able to metabolize medications and metabolic waste products, such as ammonia and lactic acid. The patient becomes more susceptible to infection as the liver fails to filter bacteria from the blood. Liver enzymes (aspartate aminotransferase [AST], formerly serum glutamic-oxaloacetic transaminase [SGOT]; alanine aminotransferase [ALT], formerly serum gluta-mate pyruvate transaminase [SGPT]; lactate dehydrogenase) and bilirubin levels are elevated, and the patient appears jaundiced.
Gastrointestinal ischemia can cause stress ulcers in the stomach, placing the patient at risk for gastrointestinal bleeding. In the small intestine, the mucosa can become necrotic and slough off, causing bloody diarrhea. Beyond the local effects of impaired per-fusion, gastrointestinal ischemia leads to bacterial toxin translo-cation, in which bacterial toxins enter the bloodstream through the lymph system. In addition to causing infection, bacterial tox-ins can cause cardiac depression, vasodilation, increased capillary permeability, and an intense inflammatory response with activation of additional biochemical mediators. The net result is inter-ference with healthy cells and their ability to metabolize nutrients (Balk, 2000b; Jindal et al., 2000).
The combination of hypotension, sluggish blood flow, metabolic acidosis, and generalized hypoxemia can interfere with normal hemostatic mechanisms. Disseminated intravascular coagulation (DIC) can occur either as a cause or as a complication of shock. In this condition, widespread clotting and bleeding occur simul-taneously. Bruises (ecchymoses) and bleeding (petechiae) may ap-pear in the skin. Coagulation times (prothrombin time, partial thromboplastin time) are prolonged. Clotting factors and platelets are consumed and require replacement therapy to achieve hemostasis.
Specific medical management in the progressive stage of shock depends on the type of shock and its underlying cause. It is also based on the degree of decompensation in the organ systems. Medical management specific to each type of shock is discussed in later sections. Although there are several differ-ences in medical management by type of shock, some medical in-terventions are common to all types. These include use of appropriate intravenous fluids and medications to restore tissue perfusion by (1) optimizing intravascular volume, (2) supporting the pumping action of the heart, and (3) improving the compe-tence of the vascular system. Other aspects of management may include early enteral nutritional support and use of antacids, histamine-2 blockers, or antipeptic agents to reduce the risk of gastrointestinal ulceration and bleeding.
Nursing care of the patient in the progressive stage of shock re-quires expertise in assessing and understanding shock and the sig-nificance of changes in assessment data. The patient in the progressive stage of shock is often cared for in the intensive care setting to facilitate close monitoring (hemodynamic monitoring, electrocardiographic monitoring, arterial blood gases, serum elec-trolyte levels, physical and mental status changes), rapid and fre-quent administration of various prescribed medications and fluids, and possibly intervention with supportive technologies, such as mechanical ventilation, dialysis, and intra-aortic balloon pump.
Working closely with other members of the health care team, the nurse carefully documents treatments, medications, and flu-ids that are administered by members of the team, recording the time, dosage or volume, and the patient’s response. Additionally, the nurse coordinates both the scheduling of diagnostic proce-dures that may be carried out at the bedside and the flow of health care personnel involved in the patient’s care.
If supportive technologies are used, the nurse helps reduce the risk of related complications and monitors the patient for early signs of complications. Monitoring includes evaluating blood lev-els of medications, observing invasive vascular lines for signs of infection, and checking neurovascular status if arterial lines are inserted, especially in the lower extremities. Simultaneously, the nurse promotes the patient’s safety and comfort by ensuring thatall procedures, including invasive procedures and arterial and ve-nous punctures, are carried out using correct aseptic techniques and that venous and arterial puncture and infusion sites are main-tained with the goal of preventing infection. Positioning and repositioning the patient to promote comfort, prevent pul-monary complications, and maintain skin integrity are integral to caring for the patient in shock.
Efforts are made to minimize the cardiac workload by reducing the patient’s physical activity and fear or anxiety. Promoting rest and comfort is a priority in the patient’s care. To ensure that the patient gets as much uninterrupted rest as possible, the nurse per-forms only essential nursing activities. To conserve the patient’s energy, the nurse protects the patient from temperature extremes (excessive warmth or shivering cold), which can increase the metabolic rate and subsequently the cardiac workload. The pa-tient should not be warmed too quickly, and warming blankets should not be applied because they can cause vasodilation and a subsequent drop in blood pressure.
Because the patient in shock is the object of intense attention by the health care team, the family members may feel neglected; how-ever, they may be reluctant to ask questions or seek information for fear that they will be in the way or will interfere with the at-tention given to the patient. The nurse should make sure that the family is comfortably situated and kept informed about the pa-tient’s status. Often, family members need advice from the health care team to get some rest; they are more likely to take this advice if they feel that the patient is being well cared for and that they will be notified of any significant changes in the patient’s status. A visit from the hospital chaplain may be comforting to the family and provides some attention to the family while the nurse concentrates on the patient.
The irreversible (or refractory) stage of shock represents the point along the shock continuum at which organ damage is so severe that the patient does not respond to treatment and cannot sur-vive. Despite treatment, blood pressure remains low. Complete renal and liver failure, compounded by the release of necrotic tissue toxins, creates an overwhelming metabolic acidosis. Anaer-obic metabolism contributes to a worsening lactic acidosis. Re-serves of ATP are almost totally depleted, and mechanisms for storing new supplies of energy have been destroyed. Multiple organ dysfunction progressing to complete organ failure has oc-curred, and death is imminent. Multiple organ dysfunction can occur as a progression along the shock continuum or as a syn-drome unto itself.
Medical management during the irreversible stage of shock is usually the same as for the progressive stage. Although the pa-tient’s condition may have progressed from the progressive to the irreversible stage, the judgment that the shock is irreversible can be made only retrospectively on the basis of the patient’s failure to respond to treatment. Strategies that may be experimental (ie, investigational medications, such as antibiotic agents and immunomodulation therapy) may be tried to reduce or reverse the severity of shock.
As in the progressive stage of shock, the nurse focuses on carry-ing out prescribed treatments, monitoring the patient, preventing complications, protecting the patient from injury, and providing comfort. Offering brief explanations to the patient about what is happening is essential even if there is no certainty that the patient hears or understands what is being said.
As it becomes obvious that the patient is unlikely to survive, the family needs to be informed about the prognosis and likely outcomes. Opportunities should be provided, throughout the pa-tient’s care, for the family to see, touch, and talk to the patient. A close family friend or spiritual advisor may be of comfort to the family in dealing with the inevitable death of the patient. When-ever possible and appropriate, the family should be approached regarding any living will, advance directive, or other written or verbal wishes the patient may have shared in the event that he or she cannot participate in end-of-life decisions. In some cases, ethics committees may assist the family and health care team in making difficult decisions.
During this stage of shock, families may misinterpret the ac-tions of the health care team. They have been told that nothing has been effective in reversing the shock and that the patient’s sur-vival is very unlikely, yet the health care team continues to work feverishly on the patient. A distraught, grieving family may inter-pret this as a chance for recovery when none exists. As a result, family members may become angry when the patient dies. Con-ferences with all members of the health care team and the family will promote better understanding by the family of the patient’s prognosis and the purpose for the measures being taken. During these conferences, it is essential to explain that the equipment and treatments being provided are for the patient’s comfort and do not suggest that the patient will recover. Families should be encour-aged to express their wishes concerning the use of life-support measures.
Copyright © 2018-2020 BrainKart.com; All Rights Reserved. Developed by Therithal info, Chennai.