SOLUTION: Assessment and Management of Clinical Problems

BOOK Lewis’s Medical-surgical Nursing Ebook: Assessment and Management of Clinical Problems Edwards, Helen ; Buckley, Thomas ; Aitken, Robyn L ; Brown, Diane Elsevier, 2019 BOOK CHAPTER Nursing Management : Shock, systemic inflammatory response syndrome and multiple organ dysfunction syndrome – Lewis’s Medical-Surgical Nursing ANZ Seckel, Maureen A; Lin, Frances; Lewis’s Medical-Surgical Nursing ANZ, Chapter 65, 1825-1849 Cardiogenic shock Cardiogenic shock occurs when either systolic or diastolic dysfunction of the heart’s pumping action results in reduced cardiac output (CO). Causes of cardiogenic shock are listed in Table 65.1 . Mortality rates for patients with cardiogenic shock approach 60%. 3 Decreased filling of the heart results in decreased stroke volume (SV). The heart’s inability to pump the blood forwards is called systolic dysfunction. Systolic dysfunction primarily affects the left ventricle, since systolic pressure is greater on the left side of the heart. When systolic dysfunction affects the right side of the heart, blood flow through the pulmonary circulation is reduced. The most common cause of systolic dysfunction is acute myocardial infarction (MI). Cardiogenic shock is the leading cause of death from acute MI. 4 Causes of diastolic dysfunction are listed in Table 65.1 . Fig. 65.2 (overleaf) describes the pathophysiology of cardiogenic shock. Whether the initiating event is myocardial ischaemia, a structural problem (e.g. valvular disorder, ventricular septal rupture) or an arrhythmia, the physiological responses are similar: the patient experiences impaired tissue perfusion and cellular metabolism. The early clinical presentation of a patient with cardiogenic shock is similar to that of a patient with acute decompensated heart failure (see Ch 33 ). The patient may have tachycardia and hypotension. Pulse pressure may be narrowed due to the heart’s inability to pump blood forward during systole and increased volume during diastole. An increase in systemic vascular resistance (SVR) increases the workload of the heart, thus increasing the myocardial oxygen consumption. The heart’s inability to pump blood forward also results in a low CO (less than 4 L/minute) and low cardiac index (less than 2.5 L/min/m 2 ). On assessment, the patient is tachypnoeic and has crackles on auscultation of breath sounds because of pulmonary congestion. The haemodynamic profile demonstrates an increase in the pulmonary artery wedge pressure (PAWP), stroke volume variation (SVV) and pulmonary vascular resistance. Signs of peripheral hypoperfusion (e.g. cyanosis, pallor, diaphoresis, weak peripheral pulses, cool and clammy skin, delayed capillary refill) are seen. Decreased renal blood flow results in sodium and water retention and decreased urine output. Anxiety, confusion and agitation may develop as cerebral perfusion is impaired. Tables 65.2 and 65.3 (overleaf) describe the laboratory findings and clinical presentation of a patient with cardiogenic shock. Septic shock Sepsis is defined as a systemic inflammatory response to a documented or suspected infection. It is characterised by a dysregulated patient response along with new organ dysfunction related to the infection ( Box 65.1 ). 9 In as many as 10–30% of patients with sepsis, the causative organism is not identified. Sepsis and septic shock have a high incidence worldwide with global mortality rates of 25% or higher. 10 In Australia and New Zealand, the mortality rate for sepsis has been in a downward trend since the year 2000, but was still up to 18.4% in 2012 BOX 65.1 Source: Dellinger RP et al. Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2012. Crit Care Med. 2013;41:580. DIAGNOSTIC CRITERIA FOR SEPSIS Infection, documented or suspected, and some of the following: General variables • Fever (temperature >38.3°C) • Hypothermia (core temperature 90 beats/min • Tachypnoea • Altered mental status • Significant oedema or positive fluid balance (>20 mL/kg over 24 hr) • Hyperglycaemia (blood glucose >8 mmol/L) in the absence of diabetes Inflammatory variables • Leucocytosis (WBC count >12 × 10 9 /L) • Leucopenia (WBC count 10% immature forms • Elevated C-reactive protein • Elevated procalcitonin Haemodynamic variables • Arterial hypotension (SBP 60 sec) • Ileus (absent bowel sounds) • Thrombocytopenia (platelet count 4 mg/dL) Tissue perfusion variables • Hyperlactataemia (>1 mmol/L) • Decreased capillary refill or mottling FiO 2 , fraction of inspired oxygen; INR, international normalised ratio; MAP, mean arterial pressure; PaO 2 , partial pressure of arterial oxygen; PTT, partial thromboplastin time; SBP, systolic blood pressure. Septic shock is a subset of sepsis with an increased mortality risk due to profound circulatory, cellular and metabolic abnormalities. Septic shock is characterised by persistent hypotension despite adequate fluid resuscitation requiring vasopressors, along with inadequate tissue perfusion resulting in tissue hypoxia. 9 The main organisms that cause sepsis are Gram-negative and Gram-positive bacteria; parasites, fungi and viruses can also cause sepsis and septic shock. 9 Fig. 65.5 (overleaf) presents the pathophysiology of septic shock. When a microorganism enters the body, the normal immune or inflammatory responses are triggered. However, in sepsis and septic shock the body’s response to the microorganism is exaggerated. Both pro-inflammatory and anti-inflammatory responses are activated, coagulation increases, and fibrinolysis decreases. 9 Endotoxins from the microorganism cell wall stimulate the release of cytokines, including tumour necrosis factor (TNF), interleukin-1 (IL-1), and other pro-inflammatory mediators that act through secondary mediators such as platelet-activating factor, IL-6 and IL-8. 9 (See Ch 10 for discussion of the inflammatory response.) The release of platelet-activating factor results in the formation of microthrombi and obstruction of the microvasculature. The combined effects of the mediators result in damage to the endothelium, vasodilation, increased capillary permeability, and neutrophil and platelet aggregation and adhesion to the endothelium. Septic shock has three major pathophysiological effects: vasodilation, maldistribution of blood flow and myocardial depression. Patients may be normovolaemic, but because of acute vasodilation, relative hypovolaemia and hypotension occur. In addition, blood flow in the microcirculation is decreased, causing poor oxygen delivery and tissue hypoxia. The combination of TNF and IL-1 is thought to have a role in sepsis-induced myocardial dysfunction. The ejection fraction is decreased for the first few days after the initial insult. Because of a decreased ejection fraction, the ventricles dilate to maintain the SV. The ejection fraction typically improves, and ventricular dilation resolves over 7–10 days. Persistence of a high CO and a low SVR beyond 24 hours is an ominous finding and is often associated with an increased development of hypotension and MODS. Coronary artery perfusion and myocardial oxygen metabolism are not primarily altered in septic shock. In addition to the cardiovascular dysfunction that accompanies sepsis, respiratory failure is common. The patient initially hyperventilates as a compensatory mechanism, resulting in respiratory alkalosis. Once the patient can no longer compensate, respiratory acidosis develops. Respiratory failure develops in 85% of patients with sepsis, and 40% develop acute respiratory distress syndrome (ARDS) (see Ch 66 ). These patients need to be intubated and mechanically ventilated. Other clinical signs of septic shock include alteration in neurological status; decreased urine output; and GI dysfunction, such as GI bleeding and paralytic ileus. Table 65.3 gives the clinical presentation of a patient with septic shock. Stages of Shock In addition to an understanding of the underlying pathogenesis of the type of shock that the patient is experiencing, monitoring and management are guided by knowing where the patient is on the ‘shock continuum’. Shock is categorised into four overlapping stages: (1) initial stage, (2) compensatory stage, (3) progressive stage, and (4) refractory stage. 12 Initial stage The continuum begins with the initial stage of shock that occurs at a cellular level. This stage is usually not clinically apparent. Metabolism changes at the cellular level from aerobic to anaerobic, causing lactic acid buildup. Lactic acid is a waste product that is removed by the liver. However, this process requires oxygen, which is unavailable because of the decrease in tissue perfusion. Compensatory stage In the compensatory stage the body activates neural, hormonal and biochemical compensatory mechanisms in an attempt to overcome the increasing consequences of anaerobic metabolism and to maintain homeostasis. The patient’s clinical presentation begins to reflect the body’s responses to the imbalance in oxygen supply and demand ( Table 65.4 , overleaf). TABLE 65.4 Symptoms of stages of shock * Compensatory stageProgressive stageRefractory stageNeurological systemOriented to person, place, timeRestless, apprehensive, confusedChange in level of consciousness↓ cerebral perfusion pressure↓ cerebral blood flow↓ responsiveness to stimuliDeliriumUnresponsiveAreflexia (loss of reflexes)Pupils non-reactive and dilatedCardiovascular systemSympathetic nervous system response: • Release of adrenaline/noradrenaline (vasoconstriction) • ↑ MVO 2 • ↑ contractility • ↑ HR Coronary artery dilationNarrowed pulse pressure↓ BP↑ capillary permeability → systemic interstitial oedema↓ cardiac output → ↓ BP and ↑ HRMAP