NURSING MANAGEMENT: SHOCK AND MULTISYSTEM FAILURE

GOALS mgmt of Cardiogenic shock

(1) to limit further myocardial damage and preserve the healthy myocardium and (2) to improve the cardiac function by increasing cardiac contractility, decreasing ventricular afterload, or both ...these goals are achieved by increasing oxygen supply to the heart muscle while reducing oxygen demands.

Serial laboratory markers for ventricular dysfunction

(eg, BNP) and cardiac enzyme levels (ie, CK-MB and troponin-I) are measured, serial 12-lead ECGs are obtained, and frequently an echocardiogram is ordered to assess the degree of myocardial damage or dysfunction.

CARDIOGENIC SHOCK

*Seen most often in patients with myocardial infarction (MI). Other causes of cardiogenic shock are related to conditions that stress the myocardium (eg, severe hypoxemia, acidosis, hypoglycemia, and hypocalcemia), as well as in conditions that result in ineffective myocardial function (eg, cardiomyopathies, valvular damage, and arrhythmias).

MEDICAL AND NRSNG mgmt during SHOCK stage

- Optimizing intravascular volume -Supporting the pumping action of the heart -Improving the competence of the vascular system -Supporting the respiratory system -Continual assessment and reassessment of the body's response to shock -Involving the patient and family in care, particularly in end-of-life decisions

Crystalloids vs Colloids

- crystalloids BETTER! (NaCl, D5W, LR, plasma late) pass freely, EXTRAvascular space/interstitial space, cheaper, less AE - colloids (albumin 5%, alkbuked, albumin, albutein, alburx, flexbumin) more money, larger, remain in intravascular space totally, inc onoctic pressure, questionable benefits (however, note, that these do NOT cause more side effects)

In early goal-directed therapy, the nurse knows that which of the following parameters are monitored in evaluating effectiveness of therapy?

--> early goal directed therapy refers to fluid resuscitation guided by the goal of SVO2 greater than 70% and CVP greater than 8.

DEFINITIONS IN SEPSIS

-->Bacteremia: The presence of bacteria in the blood -->Infection: The presence of microorganisms that trigger an inflammatory response -->Systemic inflammatory response syndrome (SIRS): A syndrome resulting from a severe clinical insult that initiates an overwhelming inflammatory response by the body; defined as two or more of the following conditions: -Temperature >38.5°C or <35.0°C -Heart rate of >90 bpm -Respiratory rate of >20 breaths/min or PaCO2 of <32 mm Hg -White blood cell count of >12,000 cells/mL, <4,000 cells/mL, or >10% immature (band) forms ________________________________________________________________________ -->Sepsis: A systemic response to infection; may occur after a burn, surgery, or serious illness and is defined as the presence of SIRS, plus the presence of an infectious source (either by documented culture or by visualizing focal infection) -->Severe sepsis: Defined as sepsis, plus at least one of the following signs of organ hypoperfusion: -Areas of mottled skin -Capillary refill of >3 seconds -Decreased urinary output (<0.5 mg/kg for 1 hour) -Lactate >2 mmol/L -Abrupt change in mental status -Platelet count of less than 100,000 or disseminated intravascular coagulation (DIC) -Acute lung injury or acute respiratory distress syndrome -Cardiac dysfunction -->Septic shock: Shock associated with sepsis; defined as severe sepsis, plus one of the following: -Mean arterial pressure (MAP) of <60 after fluid resuscitation -Need for vasoactive medication in order to maintain MAP of >60

Pre-shock Compensatory stage -->This results from stimulation of the sympathetic nervous system and subsequent release of catecholamines (epinephrine and norepinephrine). Patients display the often-described "fight-or-flight" response.

-->Tachycardia, peripheral vasoconstriction, and anxiety are common. Blood pressure: Near normal Heart rate >100 bpm (d/t vasoconstriction..adequate CO and SVR) Respiratory status >20 breaths/min Skin: Cold, clammy Urinary output: Mildly decreased Mentation: Confusion Acid-base balance: Respiratory alkalosis *blood is shunted to BRAIN and HEART (As a result, the skin is cool and clammy, bowel sounds are hypoactive, and urine output decreases)

Receptors in the sympathetic nervous system are known as alpha-adrenergic and beta-adrenergic receptors. -->Beta-adrenergic receptors are further classified as *Beta-1 and *beta-2 adrenergic receptors.

-->When alpha-adrenergic receptors are stimulated, blood vessels constrict in the cardiorespiratory and GI systems, skin, and kidneys. -->When beta-1 adrenergic receptors are stimulated, heart rate and myocardial contraction increase. -->When beta-2 adrenergic receptors are stimulated, vasodilation occurs in the heart and skeletal muscles, and the bronchioles relax.

END ORGAN DAMAGE (IRREVERSIBLE)

-->despite treatment, BP remains low. Renal and liver failure, compounded by the release of necrotic tissue toxins, creates an overwhelming metabolic acidosis. Anaerobic metabolism contributes to a worsening lactic acidosis. Respiratory system failure prevents adequate oxygenation and ventilation despite mechanical ventilatory support, and the cardiovascular system is ineffective in maintaining an adequate mean arterial pressure (MAP; MAP = [(2 × diastolic pressure + systolic pressure) / 3]) for tissue perfusion.

Cardiogenic shock treatment

-Dobutamine vasopressor = 1st line drug -Dopamine -Tx underlying condition

RECOGNIZING SHOCK IN OLDER PTS

-During hypovolemic states, medications such as beta-blocking agents (metoprolol [Lopressor]) used to treat hypertension may mask tachycardia, a primary compensatory mechanism to increase CO. -The aging immune system may not mount a truly febrile response (temperature >40°C or 104°F), but an increasing trend in body temperature should be addressed. -The heart does not function well in hypoxemic states, and the aging heart may respond to decreased myocardial oxygenation with arrhythmias that may be misinterpreted as a normal part of the aging process. -Changes in mentation may be inappropriately misinterpreted as dementia. Older people with a sudden change in mentation should be aggressively treated for the presence of infection and organ hypoperfusion.

MEDICAL MANAGEMENT ANAPHYLACTIC SHOCK

-Epinephrine, usually given intramuscularly, is given for its vasoconstrictive action as well its effect of reducing bronchospasm. -Diphenhydramine (Benadryl), given intramuscularly or intravenously, is administered to reverse the effects of histamine, thereby reducing capillary permeability. -Nebulized medications, such as albuterol (Proventil), may also be given to reverse histamine-induced bronchospasm.

RISK FACTORS Septic shock

-Immunosuppression (due to malnutrition, alcoholism, malignancy, diabetes mellitus, AIDS) -Extremes of age (<1 and >65 years) -Malnourishment -Chronic illness -Invasive procedures *Nosocomial infections (infections occurring in the hospital) in critically ill patients that may progress to septic shock commonly originate in the lungs and urinary tract, although they can originate anywhere in the body

IV nitroglycerin (Tridil)

-In low doses acts as a venous vasodilator and therefore reduces preload. -At higher doses, nitroglycerin causes arterial vasodilation and therefore reduces afterload as well. These actions, in combination with dobutamine, increase CO while minimizing cardiac workload. In addition, vasodilation enhances blood flow to the myocardium, improving oxygen delivery to the weakened heart muscle.

Cardiogenic shock causes

-Myocardial infarction (MC) -Cardiomyopathy -Valve disorders -Arrhythmia

Medical Management Treatment of neurogenic shock

....involves restoring sympathetic tone, either through the stabilization of a spinal cord injury or, in the instance of spinal anesthesia, by positioning the patient properly. *If hypoglycemia (insulin shock) is the cause, glucose is rapidly administered

MEDICAL MGMT CARDIAC TAMPONADE AND TENSION PNEUMOTHORAX

...a procedure done by a qualified clinician should be performed immediately to relieve the obstruction. If the patient is experiencing obstructive shock, then these procedures are done emergently at the bedside. A chest radiograph is often used to diagnose a pneumothorax, although computed tomography (CT) scans and even ultrasound are more sensitive. A chest tube or needle decompression is the primary procedure to relieve tension pneumothorax Cardiac tamponade is diagnosed similarly, with echocardiography being the most effective. Pericardiocentesis is the treatment for cardiac tamponade and involves inserting a needle into the pericardium to draw off fluid or blood.

In the case of tension pneumothorax or hemothorax

...air or blood has entered the pleural space and caused a restriction in lung expansion. If enough air is trapped, then eventually pressure builds up and compresses the vessels and myocardium. This compression reduces preload and increases afterload, in addition to restricting the expansion of the myocardium during filling. Clinical presentation may include jugular vein distention, crepitus, dyspnea, chest pain, tachycardia and tachypnea, tracheal shifting away from the tension pneumothorax, and decreased breath sounds on the affected side. Tension pneumothorax is common in trauma but can also develop spontaneously or as a complication from a procedure such as central line placement. Patients who are mechanically ventilated are at higher risk of developing a clinically significant pneumothorax due to increased ventilatory pressures.

Causes of Neurogenic shock

...can be caused by spinal cord injury (commonly above the level of T6), spinal anesthesia, or nervous system damage. -It may also result from the depressant action of medications or from lack of glucose (eg, insulin reaction or shock). Neurogenic shock may have a prolonged course (spinal cord injury) or a short one (syncope or fainting). Normally, during states of stress, the sympathetic stimulation causes the BP and heart rate to increase. In neurogenic shock, the sympathetic system is not able to respond to body stressors.

Cardiac tamponade

...results from excessive blood or fluid inside the pericardium, the sac that surrounds the heart. This can result from a traumatic or infectious cause with a resultant restriction on the pumping ability of the heart. Signs and symptoms of cardiac tamponade include narrowing pulse pressure, chest pain, distant or muffled heart sounds, jugular vein distention, hypotension, and tachycardia.

Septic shock treatment

1. requires complex hospital management, including administration of antibiotics. 2. administering high-flow oxygen during transport. 3.Ventilatory support may be necessary to maintain adequate tidal volume. 4.Use blankets to conserve body heat.

Vasoactive Medications

3 Types: 1) Vasopressors 2) Inotropic Agents 3) Vasodilators *Frequent VS's -- q15m* Infusion via a CVL is preferable or 2 large bore IVs

PULMONARY EMBOLISM

A PE is a clot that gets lodged in the pulmonary vasculature and causes ischemia to the capillary beds. If large enough, the embolism interferes significantly with pulmonary blood flow, which causes blood to back up into the right heart. The heart tries to overcome this by pumping against this obstruction, resulting in increased pulmonary artery pressures. Overall, CO is decreased as the patient goes into right-sided heart failure. Clots that have traveled from the lower extremities cause most PEs. Signs and symptoms of PE include pleuritic chest pain, shortness of breath, tachycardia, and hypoxia

hypovolemic shock

A condition in which low blood volume, due to massive internal or external bleeding or extensive loss of body water, results in inadequate perfusion.

distributive shock

A condition that occurs when there is widespread dilation of the small arterioles, small venules, or both.

anaphylactic shock

A severe reaction that occurs when an allergen is introduced to the bloodstream of an allergic individual. Characterized by bronchoconstriction, labored breathing, widespread vasodilation, circulatory shock, and sometimes sudden death.

Relative hypovolemia

A shifting of fluid from the intravascular space to the extravascular space that can result from a loss of intravascular integrity, increased capillary permeability, or a decreased colloidal osmotic pressure.

anaphylactic shock treatment

Airway and oxygenation; Epinephrine IM, 1-2 L crystalloid IV; Diphenhydramine, albuterol, Solumedrol, Singulair

PHARM THERAPY cardiogenic shock A N T I P L T & B E T A - B L O C K E R S

Antiplatelet Agents and Beta Blockers Antiplatelet agents, such as aspirin, should be given in the setting of acute MI. In addition, a beta blocker is used to decrease workload of the heart and preserve cardiac muscle. *The use of these medications in the setting of cardiogenic shock can be complicated since beta blockers will decrease BP.

Antiplatelet Agents and Beta Blockers

Antiplatelet agents, such as aspirin, should be given in the setting of acute MI. In addition, a beta blocker is used to decrease workload of the heart and preserve cardiac muscle. *The use of these medications in the setting of cardiogenic shock can be complicated since beta blockers will decrease BP

hypoxemia in shock

As the hypoxemia progresses, anaerobic metabolism causes the lactic acid level to rise, which results in increased capillary permeability, further decreasing the CO. The cell membrane becomes more permeable, allowing electrolytes and fluids to seep out of and into the cell. The sodium-potassium pump becomes impaired; cell structures, primarily the mitochondria, are damaged; and cell death results.

Fluid replacement in SHOCK

At least two large-gauge IV lines are inserted to establish access for fluid administration. Two IV lines allow simultaneous administration of fluid, medications, and blood component therapy if required. Because the goal of the fluid replacement is to restore intravascular volume, it is necessary to administer fluids that will remain in the intravascular compartment, to avoid fluid shifts from the intravascular compartment into the intracellular or interstitial compartment

Why does third spacing occur?

Basically, third-spacing occurs due to decreased oncotic pressure in the intravascular space. This drop in oncotic pressure means fluid will "leak out" of the intravascular space into the interstitial space (and yes, this can include the interstitial spaces in the brain leading to cerebral edema!

NURSING CARE CARDIAC TAMPONADE AND TENSION PNEUMOTHORAX

Because patients with tension pneumothorax and cardiac tamponade who are experiencing obstructive shock will need an emergent procedure, nurses should focus on facilitating that process. This includes collecting and setting up equipment, communicating effectively with staff, and helping gain consent from the patient and/or family. Careful monitoring of the patient prior to, during, and after the procedure is essential. If a chest tube is placed, then a chest drainage system (eg, Pleuravac) will need to be set up, and connected to suction as ordered. The chest tube setup needs to be monitored to ensure that it is functioning correctly and also to record output. A postprocedure chest radiograph will be ordered, and the results should be followed closely.

SVR (systemic vascular resistance)

Best indicator of left sided afterload 800-1200

Crystalloids vs Colloids

Both volume expanders -Crystalloid- use mineral salts (IV saline) -Colloid- use gelatin, blood

CO

CO is the amount of blood pumped by heart in liters per minute (usual CO is about 4 to 6 L/min but varies greatly depending on the metabolic needs of the body)

Cardiogenic shock PATHO

CO, which is a function of stroke volume and heart rate, is compromised. -->When stroke volume and heart rate decrease or become erratic, BP falls, and systemic tissue perfusion is compromised... urine output decreases, skin becomes cold and clammy, mental status changes, anxiety is obvious, capillary refill is delayed). -->Blood supply for the heart muscle itself is inadequate, resulting in further decreases in CO. ...This can occur rapidly or over a period of days.... *Patients in cardiogenic shock may experience the pain of angina and develop arrhythmias and hemodynamic instability.

What are catecholamines?

Catecholamines include neurotransmitters such as dopamine, epinephrine (adrenaline) and norepinephrine (noradrenaline), which are released during the body's stress response. They are produced in the adrenal glands, the brainstem, and the brain.

DIURETICS

Diuretics such as furosemide (Lasix) may be administered to reduce the workload of the heart by reducing fluid accumulation. Diuretics must be used cautiously since they can lead to hypovolemia. In addition, aggressive diuresis can lead to metabolic alkalosis, often referred to as a contraction alkalosis. The use of diuretics can also lead to electrolyte abnormalities, the most common of which is hypokalemia

DOBUTAMINE vasoactive

Dobutamine (Dobutrex) produces inotropic effects by stimulating myocardial beta receptors, increasing the strength of myocardial activity and improving CO. Myocardial alpha-adrenergic receptors are also stimulated, resulting in decreased pulmonary and systemic vascular resistance (decreased afterload). Dobutamine enhances the strength of cardiac contraction, improving stroke volume ejection and overall CO.

DOPAMINE vasoactive

Dopamine (Intropin) is a sympathomimetic agent. It may be used with dobutamine and nitroglycerin to improve tissue perfusion. Sympathomimetic agents must be used with caution in cardiogenic shock, since they increase myocardial oxygen demand and can worsen failure. Also, in severe metabolic acidosis, which occurs in the later stages of shock, the effectiveness of dopamine is diminished.

SEPTIC SHOCK AND FEVER

Elevated body temperature (hyperthermia) is common with sepsis and raises the patient's metabolic rate and oxygen consumption. Fever is one of the body's natural mechanisms for fighting infections. Therefore, elevated temperatures may not be treated unless they reach dangerous levels (>40°C [104°F]) or unless the patient is uncomfortable. *Efforts may be made to reduce the temperature by administering acetaminophen or applying a hypothermia blanket. During these therapies, the nurse monitors the patient closely for shivering, which increases oxygen consumption. Efforts to increase comfort are important if the patient experiences fever, chills, or shivering.

Distributive shock causes

Excessive vasodilation & altered distribution of blood flow: blood shunted to non-vital organs

RISK FACTORS FOR HYPOVOLEMIC SHOCK *In elderly patients, dehydration is a common cause of hypovolemia.

External: Fluid losses: Trauma Surgery Vomiting Diarrhea Diuresis Diabetes insipidus NPO status Internal: Fluid shifts: Hemorrhage Burns Ascites Peritonitis Dehydration

FLUID REPLACEMENT complications

Fluid replacement complications can occur, often when large volumes are administered rapidly. -monitor the patient closely for cardiovascular overload and edema. The risk of these complications is increased in the elderly and in patients with preexisting cardiac disease. -Hemodynamic pressure, vital signs, ABGs, serum lactate levels, hemoglobin and hematocrit levels, and fluid I & O are among the parameters monitored. -->Temperature should also be monitored closely to ensure that rapid fluid resuscitation does not precipitate hypothermia. IV fluids may need to be warmed during the administration of large volumes.

Cardiogenic shock treatment

Fluids first, then cautious use of vasopressors; If inotropes and vasopressors fail, intra-aortic balloon pump

Neurogenic shock treatment

General treatment & Atropine for bradycardia & stabilize C-spine & methylprednisolone within 8 hours of injury *NO STEROIDS FOR head injury (TBI)

IV nitroglycerin (Tridil) vasoactive

IV nitroglycerin (Tridil) in low doses acts as a venous vasodilator and therefore reduces preload. At higher doses, nitroglycerin causes arterial vasodilation and therefore reduces afterload as well. These actions, in combination with dobutamine, increase CO while minimizing cardiac workload. In addition, vasodilation enhances blood flow to the myocardium, improving oxygen delivery to the weakened heart muscle.

Mechanical Assistive Devices

If CO does not improve despite supplemental oxygen, vasoactive medications, and fluid boluses, mechanical assistive devices can sometimes be used temporarily to improve the heart's ability to pump. Intra-aortic balloon counterpulsation or left and right ventricular assist devices and total temporary artificial hearts are means of providing temporary circulatory assistance

PHARM THERAPY cardiogenic shock Analgesia

If a patient experiences chest pain, an IV analgesic (commonly morphine sulfate) is administered for pain relief. In addition to relieving pain, morphine dilates the blood vessels. This reduces the workload of the heart by both decreasing the cardiac filling pressure (preload) and reducing the pressure against which the heart muscle has to eject blood (afterload).

Analgesia

If a patient experiences chest pain, an IV analgesic (commonly morphine sulfate) is administered for pain relief. In addition to relieving pain, morphine dilates the blood vessels. This reduces the workload of the heart by both decreasing the cardiac filling pressure (preload) and reducing the pressure against which the heart muscle has to eject blood (afterload)

Nursing Role in PRESHOCK

In assessing tissue perfusion, the nurse specifically observes for changes in level of consciousness, vital signs, urinary output, skin, and laboratory values. Constant reassessment is warranted at this stage. Nurses should try to maintain a calm environment both for patient's and family's sake, and also ensure that assessments and interventions are rapid and ongoing.

Medications commonly used to treat cardiogenic shock include dobutamine, dopamine, and nitroglycerin

In cardiogenic shock, the aims of vasoactive medication therapy are to improve cardiac contractility, optimize preload and afterload, reduce myocardial oxygen demand, and stabilize heart rate and rhythm.

NEUROGENIC SHOCK

In neurogenic shock, vasodilation occurs as a result of a loss of balance between parasympathetic and sympathetic stimulation. -->The patient experiences a predominant parasympathetic stimulation that causes vasodilation lasting for an extended period. However, blood volume is adequate, but because the vasculature is dilated, the blood volume is displaced, producing a hypotensive (low BP) state *Thus, this is a situation where blood volume is stable, but the drastic dilatation of the vasculature causes a relative hypovolemia

SHOCK

In stress states such as shock, catecholamines, cortisol, glucagon, and inflammatory cytokines and mediators are released, causing hyperglycemia and insulin resistance in an effort to mobilize glucose for cellular metabolism.

Nursing Management NEUROGENIC SHOCK

In suspected spinal cord injury, neurogenic shock may be prevented by carefully immobilizing the patient to prevent further damage to the spinal cord. The nurse is aware that orthostatic hypotension caused by loss of vasomotor tone below the level of the spinal cord lesion can occur with position changes. Even slightly raising the head of the bed for a new tetraplegic patient can result in a drastic hypotension *Applying elastic compression stockings and elevating the foot of the bed may minimize pooling of blood in the legs. Pooled blood increases the risk for thrombus formation. Therefore, the nurse must check the patient daily for any lower-extremity pain, redness, tenderness, unilateral edema, and warmth of the calves. If the patient complains of pain, and objective assessment of the calf is suspicious, the patient should be evaluated for deep vein thrombosis. Administration of heparin or low-molecular-weight heparin (Lovenox) as prescribed, application of elastic compression stockings, or use of pneumatic compression of the legs may prevent thrombus formation. Passive range of motion of the immobile extremities also helps promote circulation. *A patient who has experienced a spinal cord injury may not report pain caused by internal injuries. Therefore, in the immediate postinjury period, the nurse must monitor the patient closely for signs of internal bleeding that could lead to hypovolemic shock.

OXYGEN

In the early stages of shock, supplemental oxygen is administered by nasal cannula at a sufficient rate to achieve an oxygen saturation exceeding 90%. Monitoring of ABG values and pulse oximetry values helps determine whether the patient requires a more aggressive method of oxygen delivery.

LR

It is important to assess for liver disease when using this solution as the acidosis may worsen when LR is administered to patients with severe liver dysfunction

Dopamine (Intropin) sympathomimetic agent.

It may be used with dobutamine and nitroglycerin to improve tissue perfusion. Sympathomimetic agents must be used with caution in cardiogenic shock, since they increase myocardial oxygen demand and can worsen failure. Also, in severe metabolic acidosis, which occurs in the later stages of shock, the effectiveness of dopamine is diminished.

Anaphylactic shock symptoms

Itching, hives Swelling of lips, tongue, feet, throat and hands Wheezing, shortness of breathe Nausea and vomiting, abdominal cramps, diarrhea Headache Loss of consciousness

distributive shock

Low BP includes Septic (severe infection), Neurogenic (damage to the spinal cord), Anaphylactic (reaction to substance), Psychogenic (feinting)

Septic shock treatment

Manage Airway and correct Hypoxemia; Fluid resuscitation, Vasopressors, Treat infection

Vasoactive Medications

Medications that act on the vessels to either constrict or dilate, resulting in either increased or decreased blood pressure and/or heart rate

Antiarrhythmic Medications

Multiple factors, such as hypoxemia, electrolyte imbalances, and acid-base imbalances, contribute to serious cardiac arrhythmias in all patients with shock --> antiarrhythmic medications are required to stabilize the heart rate.

Antiarrhythmic Medications

Multiple factors, such as hypoxemia, electrolyte imbalances, and acid-base imbalances, contribute to serious cardiac arrhythmias in all patients with shock. In addition, as a compensatory response to decreased CO and BP, the heart rate increases beyond normal limits. This impedes CO further by shortening diastole and thereby decreasing the time for ventricular filling. Consequently, antiarrhythmic medications are required to stabilize the heart rate.

PHARM THERAPY cardiogenic shock Vasoactive Medications

Multiple pharmacologic strategies to restore and maintain adequate CO. In cardiogenic shock, the aims of vasoactive medication therapy are to: improve cardiac contractility, optimize preload and afterload, reduce myocardial oxygen demand, and stabilize heart rate and rhythm. *Medications commonly used to treat cardiogenic shock include dobutamine, dopamine, and nitroglycerin.

Monitor/Assess

Neurologic assessment is essential after the administration of thrombolytic therapy to assess for the potential complication of cerebral hemorrhage associated with the therapy. IV infusions must be observed closely because tissue necrosis and sloughing may occur if vasopressor medications infiltrate the tissues. Urine output, blood urea nitrogen (BUN), and serum creatinine levels are monitored to detect decreased renal function secondary to the effects of cardiogenic shock or its treatment.

FLUID STATUS in CARDIOGENIC SHOCK

Nurses should use caution when administering fluids rapidly, because rapid fluid administration in patients with cardiac failure may result in acute pulmonary edema.

Nutritional Therapy and Glycemic Control

Nutritional supplementation should be initiated within the first 24 to 48 hours after ICU admission Enteral feeding, rather than parental nutrition, is associated with improved outcomes --> glycemic control has been shown to reduce mortality, and nurses should be aggressively targeting a blood sugar level of 140 to 180 mg/dL.

CVP (central venous pressure)

Often, a central venous line is inserted in order to measure central venous pressure. In addition to physical assessment, the central venous pressure (CVP) helps in monitoring the patient's response to fluid resuscitation. A normal CVP is 2 to 8 mm Hg. Several readings are obtained to determine a range, and fluid replacement is continued to achieve a CVP of 8 to 12 mm Hg; higher-than-"normal" CVPs readings are desired since ventricles tend to stiffen during shock

Cardiogenic shock (seen most often in patients with myocardial infarction (MI))

Other causes of cardiogenic shock are related to conditions that stress the myocardium (eg, severe hypoxemia, acidosis, hypoglycemia, and hypocalcemia), as well as in conditions that result in ineffective myocardial function (eg, cardiomyopathies, valvular damage, and arrhythmias).

PHARM THERAPY cardiogenic shock O X Y G E N

Oxygen In the early stages of shock, supplemental oxygen is administered by nasal cannula at a sufficient rate to achieve an oxygen saturation exceeding 90%. *Monitoring of ABG values and pulse oximetry values helps determine whether the patient requires a more aggressive method of oxygen delivery.

W OBSTRUCTIVE SHOCK KEEP IN MIND

Patients who experience obstructive shock are often quite suddenly sick. This affects the entire health care team, as decisions need to be made quickly and the nurse should work hard to maintain a calm environment. Since obstructive shock usually has a sudden onset, families are quite often surprised when given news about massive PE or other causes of obstructive shock. Having other support personnel in place, such as social work or a chaplain, to provide support is a good idea.

RISK FACTORS Anaphylactic shock

Penicillin sensitivity Transfusion reaction Bee sting allergy Latex sensitivity Severe allergy to some foods or medications

Physical assessment NURSING @ SHOCK

Physical assessment focuses on observing the jugular veins for distention and monitoring CVP (normal 2-8... achieve 8-12) -->CVP is typically low in hypovolemic shock; it increases with effective treatment, and is significantly increased with fluid overload and heart failure. -->The nurse must monitor cardiac and respiratory status closely. *Report changes in BP, pulse pressure, heart rate and rhythm, and lung sounds to the provider.

MEDICAL MGMT MODS

Prevention remains the top priority in managing MODS. Elderly patients are at increased risk for MODS because of the lack of physiologic reserve associated with aging and the natural degenerative process, especially immune compromise. Early detection and documentation of initial signs of infection are essential in managing MODS in elderly patients. Subtle changes in mentation and a gradual rise in temperature are early warning signs. Other patients at risk for MODS are those with chronic illness, malnutrition, immunosuppression, or surgical or traumatic wounds. If preventive measures fail, treatment measures to reverse MODS are aimed at (1) controlling the initiating event, (2) promoting adequate organ perfusion, and (3) providing nutritional support.

End-Organ Dysfunction

Requires mechanical or pharmacologic support HR: Erratic or asystole RR: Requires ventilation SKIN: Jaundice Anuric, requires dialysis Unresponsive PROFOUND ACIDOSIS

In septic shock treatment

Specimens of blood, sputum, urine, and wound drainage are collected for culture using aseptic technique. Additional cultures may be obtained from the cerebrospinal fluid (in the case of suspected meningitis) or pleural space (if empyema is suspected). *Any potential routes of infection must be eliminated. IV lines are removed and reinserted at other body sites. If possible, urinary catheters are removed or replaced. Any abscesses are drained, and necrotic areas are débrided. *Vital signs, hemodynamics (CVP, SvO2, SVR, CO), urinary output, mental status, and physical assessment findings must be reported accurately and in a timely fashion

RISK FACTORS Neurogenic shock

Spinal cord injury Spinal anesthesia Depressant action of medications Glucose deficiency

Nursing ALERT SvO2

SvO2 is an abbreviation for venous oxygen saturation. Tissue hypoxia is determined by the SvO2 or the mixed venous oxygen level. It reflects the amount of oxygen in venous blood, therefore the amount of oxygen that has been extracted or used from the body. Normal SvO2 values range from 60% to 80% and indicate adequate tissue perfusion. When the SvO2 drops, it reflects the increased consumption of oxygen and the need for intervention.

SHOCK

Systolic <80 to 90 mm Hg HR: 100 to 150 bpm RR: Rapid, shallow respirations; crackles SKIN: Mottled, petechiae U/O: Severely decreased MENTATION: LETHARGY ACID-BASE: MET ACIDOSIS

Clinical Manifestations and Assessment of NEUROGENIC SHOCK

The clinical characteristics are signs of parasympathetic stimulation. ------->It is characterized by dry, warm skin rather than the cool, moist skin seen in hypovolemic shock <------- Another characteristic is hypotension with bradycardia, rather than the tachycardia that characterizes other forms of shock.

DISTRIBUTIVE SHOCK

The displacement of blood volume causes a relative hypovolemia because not enough blood returns to the heart, which leads to subsequent inadequate tissue perfusion. -->distributive shock can be caused either by a loss of sympathetic tone or by release of biochemical mediators from cells. (leads to vasodilation) Other causes of distributive shock are rare but include toxic shock syndrome, Addisonian crisis, and myxedema coma. --> In all types of distributive shock, massive arterial and venous dilation allows blood to pool peripherally.

During shock stage

The heart and kidneys are among the first organs to show signs of dysfunction. Up until now on the continuum, the myocardium has kept pace by increasing CO, but this can only go on for a limited time. The body's inability to meet increased oxygen requirements produces ischemia, and biochemical mediators cause myocardial depression. This leads to failure of the cardiac pump, even if the underlying cause of the shock is not of cardiac origin. The systemic impact of hypotension, and thus hypoperfusion, on the kidneys results in decreased urine output. A Foley catheter is inserted, and urine output should be measured vigilantly: A urine output of less than 30 mL/hr or 0.5mL/kg/hr is indicative of renal hypoperfusion and/or hypovolemia. In addition, the inflammatory response to injury is activated, and proinflammatory and anti-inflammatory cytokines and mediators are released, which in turn activate the coagulation system in an effort to reestablish homeostasis. At the same time, acidosis impairs all enzymatic functions, including coagulation. A cascade of progressive organ failure resulting from poor tissue perfusion

PATHO of MODS

The inflammation, tissue injury, and other sequelae associated with MODS are thought to be caused by an unregulated host response. MODS may result from any form of shock because of inadequate tissue perfusion. As previously described, in shock, all organ systems suffer damage from a lack of adequate perfusion that can result in organ failure.

SEPTIC SHOCK

The most common type of distributive shock, is caused by widespread, overwhelming infection in combination with a dysregulated host immune response. *Signs of hypermetabolism include increased serum glucose and insulin resistance. *confusion may be the first sign of infection and sepsis in elderly patients.

HF resulting in CARDIOGENIC SHOCK

The nurse assesses for jugular vein distention (JVD), rales, shortness of breath, and S3 gallop.

VASOACTIVE drug A L E R T!

The nurse is vigilant in observing the patient's response to vasoactive agents because of the potential of worsening myocardial ischemia by increasing cardiac work.

Drug Alert

The nurse is vigilant in observing the patient's response to vasoactive agents because of the potential of worsening myocardial ischemia by increasing cardiac work. Vasoactive medications should never be stopped abruptly, because this could cause severe hemodynamic instability, perpetuating the shock state.

NURSING MANAGEMENT ANAPHYLACTIC SHOCK

The nurse must assess all patients for allergies or previous reactions to antigens (eg, medications, blood products, foods, contrast agents, latex) *Allergy to penicillin is one of the most common causes of anaphylactic shock. Patients who have a penicillin allergy may also develop an allergy to similar medications.

VASOACTIVE Nursing considerations

The nurse must monitor vital signs frequently (at least every 15 minutes until stable, or more often if indicated). --Vasoactive medications should be administered through a central venous line, because infiltration and extravasation of some vasoactive medications can cause tissue necrosis and sloughing. --An IV pump must be used to ensure that the medications are delivered safely and accurately. --Often, invasive monitoring using an arterial line is used to titrate medications accurately. *maintain the MAP at >65

Patients who are in shock have special needs, including nutritional needs. What physiological phenomenon underlies these unique nutritional needs?

The release of catecholamines that creates an increase in metabolic rate and caloric requirements (The catecholamines released cause glycogen stores to be depleted, and without additional nutritional support, nutritional needs are met by breaking down lean muscle tissue.)

Early goal-directed therapy

This approach involves using CVP, MAP, urinary output, and SvO2 to guide therapy. The patient's response to treatment are closely monitored, and resuscitation is continued until: >CVP is greater than 8, >MAP is greater than 65 mmHg, >urine output is 0.5 mL/kg/hour or more, and >SvO2 is greater than 70%. *This approach is associated with a decreased mortality and should be considered standard of care in the management of septic shock.

ANAPHYLACTIC SHOCK

This reaction provokes mast cells to release potent vasoactive substances, such as histamine or bradykinin, causing widespread vasodilation, capillary permeability, and potentially catastrophic vascular collapse. An equally important feature of anaphylactic shock is the onset of severe bronchospasm, which causes airway compromise (stridor, wheezing, shortness of breath) and urticaria. *A delayed recurrence of the reaction, without reexposure to the allergen, can sometimes occur. This has been termed a biphasic reaction and most commonly occurs 8 to 10 hours after the first symptoms.

Vasoactive Medications

Used when fluid therapy alone doesn't maintain MAP Support hemodynamic status; stimulate the SNS Give through central line Dosages are usually titrated to patient response High dose = constrict, low dose = dilate

DRUG ALERT with VASOACTIVE meds

Vasoactive medications should never be stopped abruptly, because this could cause severe hemodynamic instability, perpetuating the shock state.

neurogenic shock:

a type of distributive shock state resulting from loss of sympathetic vascular tone causing low blood pressure

MULTIPLE ORGAN DYSFUNCTION SYNDROME

acutely ill patients that requires medical intervention to support continued organ function. It is another phase in the progression of shock states. The actual incidence of MODS is difficult to determine because it develops with acute illnesses that compromise tissue perfusion. It is defined as severe organ dysfunction of at least two organ systems lasting at least 24 to 48 hours in the setting of sepsis, trauma, burns, or severe inflammatory conditions. It is important to note that the definition includes the number of dysfunctional organs and duration. Mortality rates when two organ systems are involved are 40%; and persistent dysfunction (>72 hours) present in three organ systems can result in a mortality risk of 80%.

Distributive shock occurs when:

blood pools in expanded vascular beds and tissue perfusion decreases

Obstructive Shock

caused by a physical obstruction to blood flow, either in the heart or major blood vessels. This causes a decrease in CO and thus a decrease in tissue perfusion. Common causes of obstructive shock include: cardiac tamponade, tension pneumothorax, and pulmonary embolism (PE). Obstructive shock is common in the setting of trauma.

CARDIOGENIC SHOCK prevention

conserving the patient's energy, promptly relieving angina, and administering supplemental oxygen, aspirin, and beta blockers

anaphylactic shock

distributive shock state resulting from a severe allergic reaction producing an overwhelming systemic vasodilation and relative hypovolemia in addition to bronchial spasm

septic shock

distributive shock state resulting from combination of infectious trigger and impaired host response, resulting in decreased tissue perfusion

In the case of CARDIOGENIC SHOCK d/t ischemia

due to ischemia or infarction, the patient may require thrombolytic therapy, angioplasty, coronary artery bypass graft surgery, intra-aortic balloon pump therapy, or some combination of these treatments

GLYCEMIC CONTROL

in critically ill patients, a less aggressive glycemic target of 140 to 180 mg/dL is appropriate

peritonitis

inflammation of the peritoneum (membrane lining the abdominal cavity and surrounding the organs within it)

Dobutamine (Dobutrex) INOTROPIC EFFECTS

inotropic effects by stimulating myocardial beta receptors, increasing the strength of myocardial activity and improving CO. Myocardial alpha-adrenergic receptors are also stimulated, resulting in decreased pulmonary and systemic vascular resistance (decreased afterload). Dobutamine enhances the strength of cardiac contraction, improving stroke volume ejection and overall CO.

insulin when shock

insulin is administered if dehydration is secondary to hyperglycemia, and desmopressin (DDAVP) is administered for diabetes insipidus.

Crystalloids

intravenous electrolyte solutions that move freely between the intravascular compartment and interstitial spaces

Nursing care of a patient with a PE

involves monitoring and initiating ventilatory and hemodynamic support similar to other types of shock. A primary function of the nurse in this situation is to facilitate diagnostic testing and imaging and then instituting treatment in a timely manner. Patients with a PE large enough to cause obstructive shock have a very high mortality and often die within an hour of presentation.

SVR

is the resistance to the flow of blood out from the ventricles. It is helpful to consider SVR to be a vise grip on the aorta. If the vise is tightened, the SVR rises, and it is much harder for the ventricle to pump blood out, whereas if the vise grip is released from the aorta, there is little resistance to the outflow of blood.

MEDICAL MGMT The treatment of PE

is usually aimed toward preventing clot expansion, although, if the patient is experiencing obstructive shock, then other treatment such as thrombolytic drugs or surgical embolectomy may be considered. Depending on the severity of the PE, mechanical ventilation and hemodynamic support may be needed to stabilize the patient. PE is usually diagnosed using a CT angiogram but other imaging and lab tests can be used as well.

Nursing assessment during CARDIOGENIC SHOCK

it is important to monitor the patient for decreased BP after administering morphine or nitroglycerin. Patients receiving thrombolytic therapy must be monitored for bleeding. Arterial and venous puncture sites must be observed for bleeding, and pressure must be applied at the sites if bleeding occurs. Neurologic assessment is essential after the administration of thrombolytic therapy to assess for the potential complication of cerebral hemorrhage associated with the therapy. IV infusions must be observed closely because tissue necrosis and sloughing may occur if vasopressor medications infiltrate the tissues. Urine output, blood urea nitrogen (BUN), and serum creatinine levels are monitored to detect decreased renal function secondary to the effects of cardiogenic shock or its treatment.

Assessing MODS

it is not possible as yet to predict which patients will develop MODS, partly because much of the organ damage occurs at the cellular level and therefore cannot be directly observed or measured. The most common types of organ dysfunction seen with MODS are acute renal failure and acute respiratory distress syndrome. Advanced age, malnutrition, and coexisting diseases appear to increase the risk of MODS in acutely ill patients.

In the case of heart failure resulting in cardiogenic shock, the nurse assesses for:

jugular vein distention (JVD), rales, shortness of breath, S3 gallop.

Distributive shock causes

low SVR - sepsis, anaphylaxis, neurogenic

Distributive Shock aka (circulatory shock) SEPTIC, ANAPHYLACTIC, NEUROGENIC

occurs when the body's ability to adjust vascular tone is impaired, and thus blood volume is abnormally displaced in the vasculature (eg, when blood volume pools in peripheral blood vessels)

systemic inflammatory response syndrome (SIRS)

overwhelming inflammatory response in the absence of known infection causing decreased tissue perfusion

SIRS (systemic inflammatory response syndrome)

presents clinically like sepsis. The only difference between SIRS and sepsis is that there is no identifiable source of infection. SIRS stimulates an overwhelming inflammatory immunologic and hormonal response similar to that seen in septic patients. Any overwhelming insult can stimulate SIRS and may progress to sepsis. Therefore, despite an absence of infection, antibiotic agents may still be administered because of the possibility of unrecognized infection

Obstructive shock treatment

relieve obstruction

Relative hypovolemia

results when fluid volume moves out of the vascular space into extravascular space, such as with sepsis and burns and the different distributive shocks

Septic Shock S/S

rising core temperature, increased WBC, C-reactive protein, chills, hypotension, widened pulse pressure, decreased skin perfusion, decreased urine output, edema, decreased capillary refill, hyperglycemia, decreased bicarbonate, change in mental status

septic shock

sepsis and uncontrollable decreased blood pressure

hypovolemic shock

shock state resulting from decreased intravascular volume due to fluid loss or deficit; causes include hemorrhage and dehydration

distributive shock

shock state resulting from displacement of blood volume creating a relative hypovolemia and inadequate delivery of oxygen to the cells

cardiogenic shock

shock state resulting from impairment or failure of the myocardium

obstructive shock

shock state resulting from the obstruction of the great vessels or heart itself; examples include cardiac tamponade, tension pneumothorax, pulmonary embolism, and abdominal compartment syndrome

Crystalloids

substances in a solution that diffuse through a semipermeable membrane

General interventions for cardiogenic shock include

supplemental oxygen, controlling chest pain, providing selected fluid support, administering vasoactive medications, controlling heart rate with medication or pacemaker, and using a mechanical assist device if needed.

General interventions for cardiogenic shock include:

supplemental oxygen, controlling chest pain, providing selected fluid support, administering vasoactive medications, controlling heart rate with medication or pacemaker, and using a mechanical assist device if needed. *Serial laboratory markers for ventricular dysfunction (eg, BNP) and cardiac enzyme levels (ie, CK-MB and troponin-I) are measured, serial 12-lead ECGs are obtained, and frequently an echocardiogram is ordered to assess the degree of myocardial damage or dysfunction.

SIRS

systemic inflammatory response syndrome (sever bacteremia)

SIRS criteria

temp >38C <36, WBC >12 <4, HR>90, RR>20 (consider infection, need 2/4)

HYPOVOLEMIC SHOCK

the normal intravascular volume is 4 to 6 L. Hypovolemic shock occurs when there is a reduction in intravascular volume by 15% to 25%, which represents a loss of 750 to 1,500 mL of blood in a 70-kg (154-lb) person. *(IVS, inside blood vessels) interstitial space (ISS, surrounding tissues)

In the case of cardiogenic shock due to ischemia or infarction, the patient may require...

thrombolytic therapy, angioplasty, coronary artery bypass graft surgery, intra-aortic balloon pump therapy, or some combination of these treatments

VASOACTIVE MEDS

used to (1) increase the strength of myocardial contractility, (2) regulate the heart rate, (3) reduce myocardial resistance, and (4) initiate vasoconstriction.