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postoperative medsurg chapter 20 n141

Terms in this set (45)

Cardiovascular Problems


In the immediate postanesthesia period the most common cardiovascular problems include hypotension, hypertension, and dysrhythmias. Patients at greatest risk for alterations in cardiovascular function include those with alterations in respiratory function, those with a history of cardiovascular disease, older adults, the debilitated, and the critically ill.

Hypotension is evidenced by signs of hypoperfusion to the vital organs, especially the brain, heart, and kidneys. Clinical signs of disorientation, loss of consciousness, chest pain, and oliguria reflect hypoperfusion, hypoxemia, and the loss of physiologic compensation. Intervention must be timely to prevent the devastating complications of cardiac ischemia or infarction, cerebral ischemia, renal ischemia, and bowel infarction.

The most common cause of hypotension in the PACU is unreplaced fluid and blood loss, which may lead to hypovolemic shock. Hemorrhage is always a risk of surgery. Marked blood loss is possible when cauterization or sutures fail. Hemorrhage most often occurs internally, requiring assessment for changes in level of consciousness and vital signs. If changes are detected, treatment is directed toward restoring circulating volume. If there is no response to fluid administration, cardiac dysfunction should be considered the cause of hypotension.


Primary cardiac dysfunction, as may occur in myocardial infarction, cardiac tamponade, or PE, results in an acute fall in cardiac output. Secondary myocardial dysfunction occurs as a result of the negatichronotropic (rate of cardiac contraction) and negative inotropic (force of cardiac contraction) effects of drugs, such as β-adrenergic blockers, digoxin, or opioids. Other causes of hypotension include decreased systemic vascular resistance, dysrhythmias, and measurement errors (e.g., taking BP with an incorrectly sized cuff).

Hypertension, a common finding in the PACU, is most frequently the result of sympathetic nervous system stimulation that may be the result of pain, anxiety, bladder distention, or respiratory compromise. Hypertension may also be the result of hypothermia and preexisting hypertension.

dysrhythmias are caused by hypoxemia, hypercapnia, alterations in electrolyte and acid-base status, circulatory instability, and preexisting heart disease. Hypothermia, pain, surgical stress, and many anesthetic agents can also cause dysrhythmias
Fluid retention during postoperative days 1 to 3 can result from the stress response, which serves to maintain both blood volume and BP. Fluid retention is caused by the secretion and release of two hormones by the pituitary—antidiuretic hormone (ADH) and adrenocorticotropic hormone (ACTH)—and activation of the renin-angiotensin-aldosterone system (RAAS). ADH release leads to increased water reabsorption and decreased urine output, increasing blood volume. ACTH stimulates the adrenal cortex to secrete cortisol and, to a lesser degree, aldosterone. Fluid losses resulting from surgery decrease kidney perfusion, stimulating the RAAS and causing marked release of aldosterone (see Chapter 17). Both mechanisms that increase aldosterone lead to significant sodium and fluid retention, thus increasing blood volume.

Fluid overload may occur during this period of fluid retention when IV fluids are administered too rapidly, when chronic (e.g., cardiac, renal) disease exists, or when the patient is an older adult. Fluid deficits from untreated preoperative dehydration, intraoperative blood losses, or slow or inadequate fluid
replacement can lead to decreases in cardiac output and tissue perfusion. Postoperative losses from vomiting, bleeding, wound drainage, or suctioning can also contribute to fluid deficits.

Hypokalemia can be a consequence of urinary and gastrointestinal (GI) tract losses. Low serum potassium levels directly affect the contractility of the heart and may contribute to decreases in cardiac output and tissue perfusion. Potassium replacement, usually 40 mEq/day, should not be given until renal function is assessed. A urine output of at least 0.5 mL/kg/hr is generally considered indicative of adequate renal function.

Cardiovascular status is also affected by the state of tissue perfusion or blood flow. The stress response contributes to an increase in clotting tendencies by increasing platelet production. In addition, general anesthesia causes peripheral vasodilation, which may contribute to damage of the vascular lining.

A venous thromboembolism (VTE) may form in leg veins as a result of inactivity, body position, and pressure, all of which lead to venous stasis and decreased perfusion. VTE is especially common in older adults, obese individuals, immobilized patients, and patients with a history of PE. It is a potentially life-threatening complication because it may lead to PE and infarction. Suspect PE in any patient with tachypnea, dyspnea, and tachycardia, particularly when the patient is already receiving O2 therapy. Other manifestations may include agitation, chest pain, hypotension, hemoptysis, dysrhythmias, and heart failure. Superficial thrombophlebitis is an uncomfortable but less serious complication that may develop in a leg vein as a result of venous stasis or in the arm veins as a result of irritation from IV catheters or solutions. (PE and VTE are discussed inSyncope (fainting) may indicate decreased cardiac output, fluid deficits, or defects in cerebral perfusion. Syncope frequently occurs as a result of postural hypotension when the patient ambulates. It is more common in the older adult or in the patient who has been immobile for long periods. Normally when the patient stands up quickly, the arterial baroreceptors respond to the accompanying fall in BP with sympathetic nervous system stimulation. This produces vasoconstriction and thereby maintains BP. These sympathetic and vasomotor functions may be diminished in the older adult and the immobile or postanesthesia patient
Neurologic and Psychologic Problems-


Postoperatively, emergence delirium, or waking up wild, is the neurologic alteration that causes the most concern.

It is manifested by behaviors such as restlessness, agitation, disorientation, thrashing, and shouting.

This condition may be caused by hypoxia, anesthetic agents, bladder distention, pain, residual neuromuscular blockade, or the presence of an endotracheal tube.

If delirium occurs, first suspect hypoxia.

Delayed emergence may also be a problem postoperatively.

Fortunately, the most common cause of delayed emergence is prolonged drug action, particularly of opioids, sedatives, and inhalation anesthetics, as opposed to neurologic injury.

Normal awakening can be predicted by the ACP based on the drugs used in surgery.

*Two types of postoperative cognitive impairments seen in surgical patients are:

1.postoperative cognitive dysfunction (POCD) and

2.Delirium.

-1. POCD is a decline in the patient's cognitive function (e.g., memory, ability to concentrate) for weeks or months after surgery.

POCD is primarily seen in the older surgical patient.

-Preexisting cognitive impairment, age, duration of anesthesia, intraoperative complications, and postoperative infections are related to the development of POCD.

2.Postoperative delirium is more common in the older patient, but it can occur in patients of any age.

Delirium may be the result of severe postoperative pain, fluid and electrolyte imbalances, hypoxemia, drug effects, sleep deprivation, and sensory deprivation or overload.

- It is characterized by cognitive dysfunction, varying levels of consciousness, altered psychomotor activity, and a disturbed sleep/wake cycle. (Delirium is discussed in Chapter 60.)

Anxiety and depression may also occur in postoperative patients.

- Any patient may experience these responses as part of grieving for lost body parts or functions or for decreased independence during the recovery and rehabilitation process.

Alcohol withdrawal delirium occurs as a result of alcohol withdrawal in a postoperative patient.

It is characterized by restlessness, insomnia and nightmares, irritability, and auditory or visual hallucinations.

Identification and management of alcohol withdrawal delirium are discussed in Chapter 11.