Adult Health III Chapter 14

epidemiology hypovolemic shock

- Hypovolemic shock is defined as inadequate intravascular volume producing decreased cardiac output that results when there is a severe loss of blood or fluids due to acute injury or illness. -An acute bleed may be the result of penetrating or blunt trauma or massive GI bleeding. Rapid fluid loss may be due to severe vomiting and diarrhea, excessive urination, or loss of fluids due to burns. -The most common cause of hypovolemia is blood loss.

Contractility

force of the mechanical contraction. Poor contractility decreases stroke volume thus decreasing cardiac output.

What are the 4 stages of shock

four distinct stages of shock: initial, compensatory, progressive, and refractory. Each stage is characterized by specific clinical manifestations, the initiation of compensatory mechanisms, and progressive indications of worsening hypoperfusion.

CO

is the amount of blood ejected by the heart every minute. It is a function of stroke volume and heart rate (HR).

Oxygen delivery (DO2)

mount of oxygen delivered to the tissues. It is assessed through the evaluation of cardiac output and arterial oxygen content. Arterial oxygen content is a combination of hemoglobin levels, the percentage of hemoglobin saturated with oxygen, and the amount of oxygen dissolved in the plasma (the partial pressure of oxygen in arterial blood [PaO2])

refractory stage

refractory stage is marked by prolonged inadequate blood supply to the cells, resulting in cell death and multisystem organ failure. There is a loss of aerobic metabolism, and only extremely inefficient anaerobic metabolism is available. Shock is irreversible at this stage.

Stroke volume

the amount of blood ejected with each ventricular contraction. It is influenced by three variables: preload, afterload, and contractility.

compensatory stage

the compensatory stage is characterized by the initiation of compensatory mechanisms in an effort to maintain adequate volume, cardiac output, and blood flow to the tissues. These mechanisms include neural, endocrine, and chemical compensations. Neural compensation - detection of hypotension by baroreceptors in the carotid sinus and aortic arch that results in the stimulation of the sympathetic nervous system and the release of the catecholamines epinephrine and norepinephrine from the adrenal medulla. -Heart rate and contractility increase, improving cardiac output. -Also in response to this catecholamine release, systemic vasoconstriction occurs, resulting in increased blood pressure and redistribution of blood flow from nonessential organ systems such as the kidneys, GI tract, and skin to vital organs such as the heart and brain. Endocrine Compensation compensation or hormonal mechanisms that exert control over blood pressure include: angiotensin II, epinephrine and norepinephrine, aldosterone and antidiuretic hormone (ADH). -Angiotensin II, created in response to low BP, is an end product of a series of events. -->After a drop in blood pressure, the kidneys respond by releasing the enzyme renin. Renin reacts with angiotensinogen to create angiotensin I. Angiotensin I is then converted in the lungs to angiotensin II via angiotensin converting enzyme. Angiotensin II is a potent vasoconstrictor which increases blood pressure. Angiotensin II also acts on adrenals to release aldosterone. The release of aldosterone promotes sodium and water reabsorption in the kidneys, which increases circulating fluid volume. This is called the renin-angiotensin-aldosterone system (RAAS). -Aldosterone release is also stimulated by the release of adrenocorticotropic hormone in response to low blood pressure from the anterior pituitary, which then stimulates the adrenal cortex to release aldosterone. -Also in an effort to increase circulating volume, antidiuretic hormone is released by the posterior pituitary in response to decreased blood volume. It acts on the kidney to conserve water. -Other compensatory mechanisms include the release of the catecholamines epinephrine and norepinephrine, from the adrenal medulla causing vasoconstriction as part of the fight or flight mechanism in the sympathetic nervous system. - There is also a compensatory mechanism to increase glucose levels for energy. Circulating glucose levels are increased through the release of glucocorticoids from the adrenal cortex in response to decreased blood pressure. Chemical Compensation -produced through the reaction of chemoreceptors in the aorta and carotid arteries that are stimulated by low oxygen levels. Low oxygen levels occur as a result of decreased blood flow through the alveoli. Tachypnea, or hyperventilation, occurs in an effort to increase circulating oxygen levels. - The respiratory alkalosis that results causes a constriction of the carotid arteries. Although tachypnea is effective at improving oxygen levels, cerebral hypoxia and ischemia may result.

Hearts rate

the number of ventricular contractions per minute or heart beats per minute. It can be affected by many variables. Stimulus from the autonomic nervous system or hormones from the adrenal medulla can adjust the HR up or down. Changes in blood pressure sensed by baroreceptors can also affect HR.

Hemodynamic monitoring with shock

-Monitoring of blood pressure, cardiac output, and the variables that affect cardiac output provides valuable insights into the presence, stages, or resolution of shock. -Invasive hemodynamic monitoring is done through an arterial line, and a central venous catheter or pulmonary artery (PA) catheter.

Lab and diagnostics for cardiogenic shock

- 12-lead electrocardiogram (ECG), cardiac enzymes, and a chest radiograph. -The initial diagnostic test should be the 12-lead ECG, conducted to rule out or rule in myocardial infarction as the cause of shock. -Cardiac enzymes will also help confirm the presence or absence of AMI. -The chest radiograph is obtained to rule out other causes of hypotension and shock such as tension pneumothorax or cardiac tamponade. A chest radiograph will also confirm the presence of pulmonary edema.

Anaphylactic Shock patho

- Anaphylaxis, or anaphylactic shock, is a severe and life-threatening systemic hypersensitivity reaction. It is caused by an allergic reaction causing a release of histamine and resulting in widespread venous dilation, increased capillary permeability, and smooth muscle contraction. This results in hypotension, edema, and respiratory distress due to the contraction of the smooth muscle of the airways. Rapidly developing airway compromise and/or circulatory collapse may occur. -Common characteristics consist of sudden onset and rapid progression of symptoms that include airway compromise and circulatory collapse. Airway compromise is caused by airway muscle contraction and throat and/or tongue swelling. Circulatory collapse is caused by widespread vasodilation and capillary leak resulting in decreased venous return resulting in decreased cardiac output. -Common triggers include food such as seafood and medications such as antibiotics.

Physical assessment of shock: CNS

- Changes in central nervous system perfusion may be the initial indication of inadequate DO2 to the tissues. -in addition to low DO2, the respiratory alkalosis that results from tachypnea causes vasoconstriction of the carotid arteries, resulting in decreased cerebral blood flow. -Restlessness, confusion, and irritability are several beginning indicators of poor cerebral perfusion. Without treatment, continued poor perfusion may progress to lethargy and coma.

cardiogenic shock pathophysiology

- Cardiogenic shock is defined as a state of hypoperfusion at the tissue level resulting from severe impairment of ventricular contraction in the presence of adequate vascular volume. As a result of damaged myocardium, there is a marked reduction in contractility, which reduces the ejection fraction (the percentage of blood ejected from the ventricle with each contraction) and cardiac output. The result is increased left and right ventricular filling pressures but decreased cardiac output. -Mixed venous oxygen saturation decreases with increased oxygen extraction at the tissue level because of low cardiac output. The ultimate result is univentricular or biventricular failure, profound hypotension, and pulmonary edema. -The decreased cardiac output leads to stimulation of compensatory mechanisms. In the case of cardiogenic shock, the sympathetic stimulation that increases HR and contractility also increases myocardial workload and myocardial oxygen demand, worsening the ischemia. -Systemic vasoconstriction also increases the workload on an already stressed heart by increasing afterload. -Renin-angiotensin-aldosterone system-induced fluid retention increases filling pressures, which ultimately contributes to the development of pulmonary edema and hypoxemia. -The end result is a vicious cycle of increased cardiac workload and increased myocardial oxygen demand combined with poor perfusion of myocardial tissue (Figure 14.3). This worsens myocardial ischemia, which, if left untreated or unsuccessfully managed, ends in death.

Clinical Manifestation of hypovolemic shock

- Clinical manifestations vary depending on the stage of shock. Initially, the patient may be in a compensated state and have no outward symptoms. Without intervention, clinical manifestations appear because of the stimulation of compensatory mechanisms. Early Stages -blood pressure may remain within normal limits, but the HR is typically increased. -patient may present as restless or confused. -Urine output decreases because of the reabsorption of sodium and water. -skin becomes pale, cool, and clammy. - Pulses are weak with sluggish capillary refill. -Hyperventilation is present, producing a respiratory alkalosis. -Decreased or hypoactive bowel sounds are present because of the shunting of blood to vital organs. -Hyperglycemia is evident because of the initiation of the fight-or-flight response in the initial compensatory phase. Late Stages (more pronounced clinical manifestations) -lethargy -hypotension -metabolic and respiratory acidoses -anuria -cold, cyanotic skin with weak or absent pulses -dysrhythmias. Without effective intervention, the patient enters the refractory stage of shock. -Coma - severe hypotension -ischemic and necrotic cold extremities -renal failure -hepatic failure follow. Hemodynamic parameters -decreased right atrial pressure or central venous pressure and decreased PA wedge pressures, which reflect decreased volume. -Decreased SVO2 is present as a result of decreased cardiac output. -An increased systemic vascular resistance reflects the initiation of compensatory mechanisms

Disseminated intravascular coagulopathy (DIC)

- DIC is a hematological disorder most commonly caused by sepsis. It occurs because of enhanced coagulation that results from the release of procoagulant factors as part of the inflammatory response associated with sepsis. -typically occurs in two stages: a clotting, or thrombotic, stage and a bleeding stage. First Stage: initial thrombotic stage (last hours or several days) -large amounts of thrombin are produced in response to decreased levels of protein C and antithrombin III, resulting in the excessive production of fibrin clots and consumption of clotting factors. -As a result of the excessive coagulation, clots lodge in the microvasculature causing ischemia and necrosis. Patients present with cyanosis and ischemia in the fingers and toes and the tip of the nose -Organ ischemia may also be present. Patients are at risk for thrombophlebitis, PE, and cerebral vascular accident. second stage: initiation of fibrinolysis. -Although impaired in sepsis, the process of fibrinolysis occurs in an attempt to break down and remove the clots. The breakdown of the clot results in increased circulating fibrin degradation products, which are powerful anticoagulants. They impair the activity of thrombin, resulting in a decreased ability to form fibrin clot. -The combination of lack of available clotting factors and the anticoagulant properties of the fibrin degradation products results in excessive bleeding due to the inability to form clots. Disseminated intravascular coagulopathy is characterized by increased levels of fibrin degradation products, increased D-dimer levels (an indicator of clot breakdown), decreased platelets, prolonged prothrombin and activated partial thromboplastin times, and decreased antithrombin III levels. Treatment -volume replacement with crystalloids such as normal saline, blood replacement, and replacement of clotting factors with fresh frozen plasma and platelets. -Identifying and correcting the cause as well as treating other disorders caused by the excessive clotting and bleeding such as hypotension, hypoxemia and respiratory distress, and the metabolic acidosis associated with poor tissue perfusion is essential.

Complications from Sepsis/septic shock

- Disseminated intravascular coagulopathy (DIC) - Multiple organ dysfunction syndrome

General Assessment of shock

- The first challenge is to quickly determine the presence and extent of shock. In some circumstances such as obvious extensive external bleeding, a massive myocardial infarction, or rapid changes after spinal cord injury, shock may be evident quickly. Other times, it may be less obvious, such as bleeding that results in an internal sequestration or collection of blood that may occur with a femur fracture or retroperitoneal hemorrhage (i.e., blood accumulation in the abdominal cavity behind the peritoneum). -the second challenge is monitoring the progression of shock and resuscitation through physical assessment, hemodynamic monitoring, and laboratory analysis. Conventional parameters such as restoration of normal blood pressure are not adequate to gauge the extent of shock or the success of resuscitation strategies. The initiation of compensatory mechanisms in the second stage of shock may temporarily restore homeostasis without fully repaying oxygen debt, allowing continuing hypoperfusion at the tissue level -Physical assessment parameters to assess perfusion at the tissue level such as level of consciousness, urine output, respiratory status, pulse quality, skin color and/or mottling, and temperature are important to monitor. -Hemodynamic monitoring and laboratory analyses of endpoints such as lactate, base deficit, SVO2, and blood gas analysis are also essential parameters to consider when evaluating the extent of shock and success of resuscitation.

cardiogenic shock treatment priorities

- Treatment priorities include stabilizing oxygenation and initiating drug therapy to increase blood pressure and cardiac output. Consideration of emergency revascularization, an attempt to restore blood flow through percutaneous coronary intervention, may be indicated. Intra-aortic balloon pump (IABP) therapy to increase myocardial oxygen supply and decrease myocardial oxygen demand may also be considered. If these treatments are not successful, a ventricular assist device (VAD) may be necessary. Stabilizing oxygen -Airway and breathing assessment -. Intubation and mechanical ventilation are frequently necessary to support ventilation and maximize oxygenation. This may help decrease myocardial workload, increase myocardial oxygen supply, and preserve myocardial tissue. Medications -vasopressors such as dopamine and norepinephrine, should be started to sustain blood pressure and help maintain adequate mean arterial pressure.(Care should be taken when using vasopressors to increase blood pressure because they will also increase systemic vascular resistance, increasing myocardial workload) -Inotropic support, medications such as dobutamine that increase myocardial contractility, should also be initiated to improve cardiac output. -Nitroglycerin may be very carefully added in an attempt to decrease preload and afterload. It decreases preload through venous dilation and decreases afterload through arterial dilation. It will also decrease blood pressure, so it should be used with extreme caution. -Nitroprusside may also be used with extreme caution to decrease afterload. -Diuretics may also be used with caution in an attempt to decrease filling volumes. -Morphine sulfate may also be administered to relieve pain due to a myocardial infarction or act as vasodilator that decreases venous return and preload -Because many classes of medications are used in the treatment of cardiogenic shock, an arterial line is essential for continuous monitoring of blood pressure. Although not clearly beneficial in other forms of shock, a PA line has been shown to be helpful in the complex management of a patient in cardiogenic shock. The evaluation of cardiac output, preload, afterload, systemic vascular resistance, and SVO2 is essential in order to gauge response to treatment. Emergency Revascualrization -Early revascularization through percutaneous coronary intervention has been shown to increase short-term and long-term survival in most patients in cardiogenic shock. -Percutaneous coronary intervention involves balloon angioplasty, or the insertion of a catheter through an artery up into the involved coronary artery and inflation of a balloon to break up the plaque causing the obstruction of flow. Typically, a stent is placed to maintain patency of the vessel. -Intra-aortic balloon pump therapy: (used when drug therapy does not improve cardiac output) The IABP catheter is inserted into the aorta, usually via the femoral artery. Upon placement, the tip of the catheter should lie just below the aortic arch, about 2 cm from the left subclavian artery. The primary goal of IABP therapy is to increase myocardial oxygen supply and decrease myocardial oxygen demand. There is a balloon at the tip of the catheter. It is timed to inflate at the start of diastole and deflate just before systole. When the balloon inflates, blood is displaced toward the coronary arteries and also into the systemic circulation, improving coronary and systemic perfusion. Deflating the balloon decreases afterload, thus decreasing the workload of the left ventricle -VAD: may be necessary if other treatments have not been successful. A VAD is a surgically inserted mechanical pump that assists the pumping of the left ventricle and decreases the workload of the heart. The pump works by displacing blood from the left ventricle into a receptor within the pump. The pump then works to eject blood into the aorta.

Sepsis/Septic Shock Epidemiology

- Typically, these patients have underlying comorbidities and are 65 years of age or older. -Infection with gram-positive organisms is more commonly associated with the progression of sepsis than infection with gram-negative organisms. -The incidence of sepsis is increasing= attributed to innovations and changes in health care and our aging population. (The use of invasive procedures and monitoring devices is much more common. This increases the patient's risk of infection. The use of chemotherapy and immunosuppressive drugs is increasing, making patients more vulnerable to infection) - A huge factor is the increase in antimicrobial resistance to antibiotics. -Sepsis and septic shock are two clinical conditions on a continuum that starts with infection and ends with septic shock. -In worst case, disseminated intravascular coagulopathy (DIC), a hematological disorder associated with enhanced coagulation, and multiple organ dysfunction syndrome (MODS) may result. -Sepsis is defined as life threatening organ dysfunction caused by a deregulated host response to infection. Septic shock occurs when circulatory and metabolic abnormalities are profound, greatly increasing mortality.

Medical management for sepsis/septic shock: bundles of care

- bundles of care to help simplify the very complex treatment needed by patients in severe sepsis. They may vary hospital by hospital, but the basic elements should be adhered to in order to optimize treatment. These bundles include activities that need to be completed within 3 hours and within 6 hours -SEE TABLE 14.7

Neurogenic shock patho

- caused by disruption of the sympathetic nervous system typically as a result of spinal cord injury or regional spinal anesthesia, or an injury to the brain -It is very uncommon in patients with lower spinal cord injuries. The sympathetic nervous system disruption causes several problems 1. vascular tone is significantly decreased, hampering vasoconstriction and leaving vessels relaxed and dilated. 2.Vascular volume is increased in the peripheral vessels, but venous return to the right heart is decreased, resulting in decreased cardiac output. This is termed relative hypovolemia. This problem is made worse by the heart's inability to compensate through tachycardia. 3.unopposed parasympathetic activity may result in profound bradycardia. As with other types of shock, the decreased cardiac output of neurogenic shock causes systemic hypoperfusion, resulting in anaerobic metabolism and metabolic acidosis. These patients are especially susceptible to orthostatic hypotension.

Sepsis/septic shock Clinical manifestation

- clinical manifestations of septic shock reflect the poor vascular tone and vasodilation that results in increased vascular capacity and blood pooling in the venous system. There is adequate blood volume but a state of relative hypovolemia exists because of decreased venous return to the right heart. Septic shock is typically divided into early and late stages Early stages of septic shock, sometimes termed hyper-dynamic or warm sepsis, reflect the initial inflammatory response. - tachycardia with bounding pulses and warm flushed skin and is febrile. -Blood pressure may be normal as a result of initial compensatory responses. -Initial signs of decreased organ perfusion may be present, such as confusion and decreased urine output. -Hemodynamic parameters indicate increased cardiac output that occurs as long as there is adequate fluid resuscitation. Filling pressures, right atrial pressure, and PAOP remain low. Systemic vascular resistance is low because of profound systemic vasodilation. Mixed venous oxygen levels are temporarily increased due to the increase in cardiac output. Late stages of septic shock, also referred to as hypodynamic or cold shock -cool, pale skin, weak and thready pulses, and hypothermia. -Tachycardia persists, but blood pressure remains low. -Further signs of end-organ hypoperfusion, such as lethargy or coma and anuria, may be present. -Hemodynamic parameters indicate decreased cardiac output with variable filling pressures depending on fluid resuscitation. Systemic vascular resistance may remain low but may increase as vasoconstriction occurs with compensation and drug therapy. Mixed venous oxygen levels decrease, reflecting overall inadequate DO2 to the tissues. Ultimately mixed venous oxygen levels may increase because of the maldistribution of blood flow in the microcirculation, resulting in decreased oxygen extraction at the tissue level.

Anaphylactic Shock Treatment priorities

- immediately removing the trigger if possible.(If the trigger is the administration of antibiotics or blood, the infusion should be stopped immediately. If the trigger is a bee sting, the stinger should be removed.) -->Sometimes the trigger is unknown or has been ingested, so removal is not possible. -Maneuvers to induce vomiting are not recommended. - Definitive treatment should not be delayed. -As in any emergency situation, maximizing oxygenation through the initiation of oxygen via a 100% non-rebreather mask is the first priority. -Circulatory support via administration of IV fluid is essential. Treatment with IV epinephrine is the first-line therapy. Intravenous vasopressin has been found to be an effective alternative in refractory anaphylactic shock (see Table 14.5). -Other medications utilized to treat anaphylaxis include antihistamines, corticosteroids, and inhaled bronchodilators.

Lab analysis of shock

- laboratory studies provides valuable information regarding the presence, severity, or resolution of shock. -Several very important indicators include ABG analysis, SVO2,or ScvO2, base deficit, and lactate level. -Arterial blood gas analysis provides information on oxygenation, ventilation, and the presence of acidosis or alkalosis (metabolic or respiratory), which provides insight into the adequacy of treatment. Results will vary on the basis of early or late shock. -hyperventilation in early shock produces a respiratory alkalosis -In later stages of shock, a metabolic acidosis will be present. The presence of hypoxemia, or decreased PaO2, indicates the development of respiratory complications such as adult respiratory distress syndrome (ARDS) -Evaluation of VO2 via SVO2 or ScvO2 is also an extremely valuable parameter to consider when evaluating sufficiency of DO2 or oxygen debt. As stated earlier, when that value falls below normal it means the tissues are extracting more oxygen than normal. That results from a decreased DO2 and gives us information on oxygen debt -An elevated lactate level indicates increased anaerobic metabolism due to tissue hypoperfusion. It can be used as an overall assessment of the state of shock and as an evaluation of the resuscitative effort. -->Base deficit, a value obtained with an ABG analysis, also provides an indication of the level of acidosis. It is defined as the amount of base required to achieve a pH of 7.4. A higher level of base required to achieve a normal pH (a negative base deficit) is consistent with acidosis. Base deficit is a sensitive indicator of the level of severity and potential for complications of shock. -Hemoglobin and hematocrit, part of the equation of arterial oxygen content, provide information about oxygen-carrying capacity and are valuable for determining the effectiveness of DO2. -Electrolytes, renal studies, liver studies, and glucose level are all valuable indicators of the state of shock. Unfortunately, by the time they are elevated, shock has progressed to later stages.

hypovolemic shock nursing management

Assessment and Analysis The clinical manifestations of hypovolemic shock are related to the decrease in cardiac output and impaired blood flow to all vital organs. The manifestations vary depending on the stage of shock. Without adequate treatment, the results are hypotension; tachycardia with weak pulses; tachypnea; cold, cyanotic, and mottled skin; decreased or absent urine output; severely decreased level of consciousness; and severely decreased or absent bowel sounds. Continuing decompensation results in multiple organ system failures as evidenced by increased renal studies such as blood urea nitrogen (BUN) and creatinine and increased liver function tests. The refractory stage is evidenced by coma, severe hypotension, bradycardia, and acute respiratory failure due to profound cellular hypoxia. Hemodynamic parameters also vary according to the stage of shock. If a PA catheter is in place, decreased cardiac output will be noted beginning in the initial stage of shock. The compensatory stage is notable for an increase in systemic vascular resistance due to the sympathetic nervous system response. Right atrial pressure and PAOP are decreased. Although initial compensation maintains a normal blood pressure, hypotension eventually results. Nursing Interventions ■ Assessments • Neurological statusA decreased level of consciousness occurs as a result of decreased cardiac output and carotid vasoconstriction that occurs as a result of tachypnea and respiratory alkalosis. • Vital signsBlood pressure may remain normal initially because of stimulation of compensatory mechanisms. Tachycardia will be present as one of the compensatory mechanisms. Hypotension and bradycardia signal the end of effective compensation. • Hemodynamic readingsDecreased cardiac output occurs as a result of decreased filling pressures, as evidenced by decreased right atrial pressure and decreased PAOP. Increased systemic vascular resistance is evident as the sympathetic nervous system is stimulated, resulting in vasoconstriction to increase blood pressure and cardiac output. • Urine outputDecreased urine output occurs as a result of decreased cardiac output and stimulation of compensatory mechanisms that increase reabsorption of sodium and water. • Skin color and temperatureCold and clammy skin may be a sign of decreasing peripheral perfusion and progressing shock. Laboratory Tests • ABGsInitial ABGs may reflect a respiratory alkalosis due to tachypnea. Later stages of shock reveal a metabolic acidosis due to anaerobic metabolism. • SVO2Decreased SVO2 is an indicator of inadequate oxygen delivery. • Hemoglobin and hematocritHemoglobin and hematocrit values may be decreased if the cause of hypovolemic shock is bleeding. • Metabolic profileRenal failure and liver failure, as evidenced by increased BUN and creatinine levels and liver function test results, may become evident as a result of decreased organ perfusion. • Lactate/base deficitIncreased lactate level and negative base deficit are evidence of poor perfusion at the cellular level. Decreasing lactate level is an endpoint demonstrating adequate resuscitation. ■ Actions • Apply a 100% non-rebreather maskMaximizing oxygenation is the number one priority. • Anticipate and prepare for intubationIntubation and mechanical ventilation may be required to improve oxygenation. • Insert two large-bore IVs for fluid administrationLarge-bore IVs facilitate the rapid infusion of fluid necessary to reverse hypovolemic shock. • Administer fluid replacement as prescribed: • Normal saline • Lactated Ringer's solution • Hypertonic saline • Blood products Fluid replacement is the foundation of treatment in hypovolemic shock. ■ Teaching • Instruct patient and family on the cause of hypovolemiaDepending on the cause of hypovolemia, patient and family understanding may help prevent a repeat occurrence. • Allow family members visitation during hospital treatment; provide frequent updates on condition and treatmentFamily visitation and information can help to decrease a patient's and family's anxiety. Evaluating Care Outcomes Rapid intervention with adequate oxygenation and fluid resuscitation may result in the restoration of hemodynamic stability. Careful monitoring of endpoints such as blood pressure, filling pressures, SVO2, level of consciousness, urine output, lactate level, and base deficit will help determine the adequacy of fluid resuscitation.

Hemodynamic monitoring with shock: pulmonary artery (PA) catheter

- pulmonary artery (PA) catheter is a flexible, balloon-tipped, catheter that is guided through the right side of the heart and into the pulmonary artery. Pulmonary artery catheter monitoring allows us to obtain detailed information about cardiac output and the variables that affect it: preload, afterload, and contractility. -PA catheter has four lumens: proximal, distal, thermistor, and inflation, each of which leads to a specific port. (I) The proximal port, located approximately 30 cm from the tip of the catheter, is used to monitor right atrial pressure or central venous pressure; a reflection of right heart preload. It is also the port used to inject the solution to obtain a thermodilution cardiac output. (2) distal lumen port is located at the tip of the PA catheter. Through this port, you can monitor systolic, diastolic, mean PA pressures, and the pulmonary artery wedge pressure, also referred to as pulmonary artery occlusive pressure (PAOP). The PAOP is obtained when the balloon located at the end of the inflation lumen is inflated with 1.5 mL of air. Specifically the PAOP reflects left heart preload or the amount of blood in the left ventricle at the end of diastole, also referred to as left ventricular end-diastolic pressure. (Figure 14.2). The balloon floats into a wedge position in the PA, which occludes that branch of the PA obscuring data from the right heart. In this position, the values obtained reflect pressures proximal to the balloon or left heart pressures. The distal lumen port can also be used for drawing SVO2 samples. The SVO2 obtained through a PA line provides information on oxygen extraction throughout the entire body. (3) thermistor port: temperature sensor- , built into the tip of the PA catheter. It continuously measures the ambient blood temperature around it. To obtain a cardiac output, a small bolus of cooler saline is briskly injected into the PA catheter through the proximal port. As a result of the injection of cooler fluid, the temperature of the blood flowing by the sensor changes. The time it takes for the cold injectate to pass the sensor is measured in liters of blood pumped per minute. This is called the "thermodilution" method of obtaining cardiac output. PA can assess -Afterload, also known as systemic vascular resistance, is a calculated value obtained using mean arterial and mean right atrial pressure divided by cardiac output. -Pulmonary vascular resistance, the afterload of the right heart, is obtained by substituting PA pressures into that calculation. -Contractility is another value calculated through measurements obtained via the PA catheter. It is inferred by evaluating the right and left ventricular stroke work indexes, or calculations of work done by the heart with each contraction.

Oxygen consumption (VO2)

- reflects the amount of oxygen extracted from the blood at the tissue level. -It can be measured through evaluation of a blood sample, a mixed venous oxygen saturation (SVO2). The SVO2 level reflects the amount of oxygenated blood returned to the right heart. -Normal Svo2 values are between 60% and 75%. -When that value falls below normal it means the tissues are extracting more oxygen than normal. That results from a decreased DO2 which may be a decrease in oxygen content, hemoglobin, or cardiac output. It may also reflect an inability to increase delivery in response to stressors such as pain or fever. -Oxygen debt is the difference between normal VO2 and VO2 during the low DO2 state. The longer there is an imbalance between cellular oxygen supply and demand, the larger the oxygen debt becomes. This resulting oxygen debt must be repaid in order to maintain cellular function.

Physical assessment of shock: Respiratory system

- respiratory system also provides insight as to the presence and progression of shock. -Early stages of shock are characterized by increased respirations done in an effort to increase oxygenation and decrease carbon dioxide (CO2) levels due to the metabolic acidosis. -Oxygenation can be measured through pulse oximetry, but poor peripheral circulation may cause inaccurate readings. -Arterial blood gases (ABGs) may be necessary for more accurate assessment.

Medical Management Obtructive shock

- stabilize oxygenation: Airway and breathign assessment--> Intubation and mechanical ventilation are frequently necessary to support ventilation and maximize oxygenation. Improving or enhancing oxygenation may help decrease myocardial workload, increase myocardial oxygen supply, and help preserve myocardial tissue. -Vasoactive drugs may be utilized to help maintain blood pressure in the short term, but early definitive treatment of the cause of obstructive shock is necessary for survival. -Cardiac tamponade: blood or fluid in the pericardial sac must be removed or drained as quickly as possible. This is a medical emergency. If the fluid is not promptly removed, death may ensue quickly. Removing the fluid or blood can be done through a procedure called pericardiocentesis. This procedure uses a large-bore needle inserted into the pericardial sac, guided by ultrasonography or echocardiography when possible, to remove the fluid. A pericardial window, a procedure to remove part of the pericardium to relieve pressure, may also be performed. After removal of the blood or fluid, it is essential to identify and treat the source of the problem. If the cause is left unknown and untreated, the cardiac tamponade may reoccur. -If the cause of shock is impaired ventricular emptying due to PE= the definitive treatment is to remove the clot through the use of thrombolytic therapy; if thrombolytics are contraindicated or unsuccessful, suction thrombectomy may be indicated. Thrombolytics are medications capable of dissolving a clot. They are infused via a catheter directly into the clot. Suction thrombectomy is performed by inserting a catheter and guiding it toward the clot. The clot is essentially sucked through the catheter. Another option is a mechanical device at the tip of the catheter such as a rotating head that may be used to break up the clot. Infrequently, surgery (a pulmonary embolectomy) is required to remove the clot if other methods are unsuccessful. Depending on the cause of the PE, long-term anticoagulation therapy may be indicated to decrease the likelihood of a recurrent event.

Anaphylactic Shock clinical manifestation

-Airway compromise include shortness of breath, tachypnea, wheezing, stridor, cyanosis, and confusion due to hypoxia. Untreated, this will lead to respiratory arrest. - s/s circulatory problems are tachycardia; hypotension; cool, pale, clammy skin; and weak pulses. -As in neurogenic shock, these patients are particularly vulnerable to orthostatic hypotension. -sudden onset and rapid progression of skin or mucosal changes. These changes include flushing, urticaria (an itchy, red, raised rash), and angioedema, which is similar to the swelling of urticaria only deeper. It is edema of the subcutaneous or submucosal tissues, usually occurring around the eyes and mouth. -Hemodynamic changes include hypotension, tachycardia, decreased cardiac output, decreased filling pressures, and decreased systemic vascular resistance.

Distributive Shock epidemiolgy

-Distributive shock is the result of disease states that cause poor vascular tone and vasodilation resulting in increased vascular capacity and venous pooling. Even though blood volume is adequate, a state of relative hypovolemia exists because of decreased venous return to the right heart. -Sepsis is the most common cause of widespread vasodilation and distributive shock. -Anaphylaxis, another cause of distributive shock, is caused by the release of histamine, which results in vasodilation, decreased venous return, and hypotension. -The least common form of distributive shock is neurogenic shock which is due to a loss of vasomotor tone. There is a loss of stimulation from the sympathetic nervous system resulting in vessel walls relaxing and dilating. Venous return is decreased, and the patient is hypotensive with a decreased cardiac output. Neurogenic shock can be caused by an injury to the brain, general or spinal anesthesia, or spinal cord injury. The term "spinal shock" is used when neurogenic shock is caused by an injury to the spinal cord. When the spinal cord is damaged, there is a loss of autonomic and motor reflexes below the level of the injury.

Hypoveolemic shock

-Hypovolemic shock results when there is a rapid fluid loss resulting in inadequate circulating volume. -Most commonly, hypovolemic shock is secondary to blood loss from penetrating or blunt trauma or severe gastrointestinal (GI) bleeds. -penetrating trauma include gunshot wounds and knife injuries. -Blunt trauma include blood loss into the abdomen due to damage to the liver, trauma to the thoracic cavity resulting in a ruptured aorta, or long bone or femur fractures. -Excessive fluid loss may be caused by severe vomiting or diarrhea. -Extensive burns can also cause severe loss of fluids, resulting in hypovolemic shock.

Sepsis/septic shock Nursing Management

Assessment and Analysis Unlike other forms of shock, the early clinical manifestations of septic shock are related to the initial increase in cardiac output which occurs due to the tachycardia and decreased SVR associated with sepsis. The patient presents as warm and flushed with bounding pulses. Later manifestations reflect the prolonged poor tissue perfusion. Hypotension, tachycardia, and tachypnea are present. Systemically, the patient has a decreased level of consciousness and weak pulses with cold, cyanotic, and mottled skin. Urine output and bowel sounds are decreased or absent. Without successful intervention, the clinical manifestations of enhanced coagulation such as necrotic tissue in the extremities begin to appear. In later stages, excessive bleeding from any puncture wounds, IV sites, or wounds begins. Nursing Interventions ■ Assessments • Neurological status Decreased level of consciousness occurs a result of decreased cardiac output. • Vital signs Hypotension is present because of vasodilation, producing relative hypovolemia and decreased venous return. Tachycardia will be present as one of the compensatory mechanisms. Initially, the patient will be febrile as an adaptive response. In later stages, the patient will be hypothermic, potentially signaling the body's inability to continue the adaptive response. • Hemodynamic readings Initially, cardiac output is increased; however, as sepsis progresses, cardiac output decreases as a result of continued decreases in filling pressures such as right atrial and pulmonary artery occlusion pressures. Initially systemic vascular resistance is decreased as a result of widespread vasodilation. Later it may increase due to compensation and vasopressor therapy • Urine output Decreased urine output occurs as a result of decreased cardiac output. • Skin color and temperature Initially, the patient's skin is flushed and warm because of increased cardiac output. Later, the skin becomes cold and clammy, signaling the progression of shock. Tissue necrosis in the extremities may indicate the enhanced coagulation of DIC. • Bleeding Excessive bleeding from wounds and puncture sites may be present because of consumption of clotting factors in DIC. Laboratory testing. • ABGs Initial ABGs may reflect a respiratory alkalosis due to tachypnea. Hypercapnia and hypoxia are present as respiratory failure worsens. Later stages of shock reveal a metabolic acidosis due to anaerobic metabolism. • SVO2, ScvO2 Decreased SVO2 and ScvO2 are typically indicators of inadequate oxygen delivery. In later sepsis, values may be elevated because of maldistribution of blood flow and are not indicative of recovery. • Metabolic profile Renal failure and liver failure, as evidenced by increased BUN and creatinine levels and liver function test results, may become evident as a result of decreased organ perfusion. • Lactate/base deficit Increased lactate level and negative base deficit are evidence of poor perfusion at the cellular level. Normalizing levels are an endpoint demonstrating adequate resuscitation. Sustained abnormal levels are indicators of increased risk of mortality. ■ Actions • Meticulous hand washing and aseptic technique with all procedures Hand washing and aseptic techniques are basic interventions to help prevent and control infection. • Administer oxygen as ordered Maximizing oxygenation is essential. • Anticipate and prepare for intubation Intubation and mechanical ventilation may be required to improve oxygenation or if respiratory failure ensues. • Mouth care every 4 hours and when needed Oral care is effective at reducing the occurrence of ventilator-associated pneumonia. • Obtain two blood cultures from two different sites: urine, sputum, and wound cultures Cultures are obtained to identify the offending organism. • Administer antibiotics as ordered after cultures are obtained Antibiotics are the first-line treatment in an attempt to control the infection. • Administer fluid replacement as ordered Aggressive fluid replacement is the initial treatment to restore filling volumes and blood pressure in septic shock. • Administer vasoactive drips such as norepinephrine or dopamine as ordered Vasoactive drips may be necessary to restore vascular tone if fluid replacement therapy is not effective at increasing blood pressure and cardiac output. ■ Teaching • Instruct patient and family on the cause of sepsis and the importance of meticulous hand washing Patient and family understanding of factors important in preventing, minimizing, and controlling infection are essential in the treatment. • Allow family member visitation during hospital treatment Family visitation can help decrease a patient's and family's anxiety. Evaluating Care Outcomes Rapid recognition of the presence of sepsis is essential in preventing progression along the continuum. Swift intervention with antibiotics and fluids is essential in maintaining cardiac output. Vasoactive support may be necessary if fluid replacement is not effective at maintaining blood pressure. Hemodynamic monitoring and frequent laboratory assessments are necessary to monitor the effectiveness of treatment. Supportive care such as mouth care, frequent turning, nutrition, and DVT prophylaxis are essential to prevent complications. Timely, aggressive medical care combined with meticulous monitoring and supportive care help ensure recovery. Successful treatment is demonstrated by satisfactory blood pressure level and cardiac output and adequate tissue perfusion.

Medical management sepsis/septic shock

-Prevention- hand washing, meticulous aseptic technique for invasive procedures, and elimination of invasive therapies when possible. Aggressive mouth care in ventilated patients may help prevent ventilator-associated pneumonia. -Frequent assessment of vital signs, hemodynamic parameters as indicated, and cultures and laboratory analyses including white blood cell count and differential are essential. Utilizing SVO2 or ScvO2 to evaluate effectiveness of therapy should be done with caution. Either may be elevated in the presence of tissue hypoxia because of the maldistribution of blood flow that occurs in sepsis. -prompt recognition and treatment are essential in halting the progression of sepsis along the continuum. Identification of the offending microorganism and prompt treatment with antibiotics have been shown to decrease mortality in sepsis -blood culture before abx prescribed -fluid resuscitation -Steroid replacement therapy -bundles of care

Hypovolemic shock Medical Management

-Resuscitation priorities in hypovolemic shock include maximizing oxygenation, initiating fluid resuscitation, and identifying and treating the underlying cause. -Maximizing oxygenation is essential in the treatment of the patient in shock. Assessing and stabilizing the patient's airway is the immediate first priority. High-flow oxygen via a 100% non-rebreather mask may be utilized if the patient is able to adequately maintain and protect his or her airway. If spontaneous respiratory effort is inadequate, intubation and positive-pressure mechanical ventilation should be considered. (Positive-pressure mechanical ventilation should be used with caution because the associated increased intrathoracic pressures decrease cardiac output further, exacerbating poor DO2 to the tissues.) -Treatment with isotonic crystalloid fluids such as normal saline solution or lactated Ringer's solution is the mainstay of initial resuscitation. Blood product replacement is necessary in the case of acute blood loss. Utilizing fresh frozen plasma and platelets as well as red blood cells is beneficial when replacing lost blood. The use of hypertonic solutions such as 7.5% saline that pull fluid from the cellular and interstitial spaces may be indicated in some circumstances. It is important to continue resuscitation until the oxygen debt accumulated when cardiac output was low has been repaid. This is evidenced by endpoints such as stabilization of blood pressure, cardiac output within normal limits, adequate filling volumes, adequate urine output, and lowering of lactate to within normal limits. -Identifying and controlling further loss of blood or fluid is an obvious priority in this patient. If bleeding or fluid loss is not immediately apparent, diagnostic studies may be necessary to determine the cause of shock. Computed tomography scans may be necessary to determine if blunt trauma has caused thoracic or abdominal bleeding.

cardiogenic shock epidemiology

-Risk factors for cardiogenic shock include any disorder that results in the acute deterioration of myocardial mechanical contraction. -Most commonly, cardiogenic shock results when more than 40% of the myocardium is damaged because of AMI. -Other risk factors include end-stage congestive heart failure, cardiomyopathy, hypertension, diabetes, multiple vessel coronary artery disease, and acute vascular disease

Shock

-The tissues of the body require a continuous supply of oxygen in order to maintain cellular functioning. -Shock is a life-threatening syndrome that occurs when the circulatory system is unable to supply adequate amounts of oxygen to the tissues to meet basic metabolic requirements. This creates a state of tissue hypoxia which is an imbalance of cellular oxygen supply and demand. -Without immediate treatment to reverse this imbalance, organ system failure and death may result.

Preload

-amount of blood in the ventricles at the end of diastole. It is a reflection of a patient's fluid volume status. -The values obtained to measure preload are sometimes referred to as filling pressures. -An increase in preload may result in an increase in cardiac output. -decrease in preload may decrease cardiac output.

Obstructive shock Clinical Manifestations

-clinical manifestations are the result of decreased cardiac output and impaired peripheral perfusion: a decreased level of consciousness, decreased urine output, poor pulses, pale cool skin, and decreased bowel sounds. -Chest pain, nausea and vomiting, and shortness of breath are also common findings. -Muffled heart sounds may be apparent with cardiac tamponade. -Signs of right heart failure, such as jugular vein distention, may be noted with increased right heart afterload or impaired filling. -Hemodynamic parameters obtained through a PA catheter indicate variable right atrial pressure and PAOP depending on the problem, imparied filling or impaired emptying. Systemic vascular resistance is high, and cardiac output is very low. Mixed venous oxygen saturation is decreased

Hemodynamic monitoring with shock: arterial line

-critically ill patient in shock benefits from the placement of an arterial line. Blood pressure is continually displayed, and it provides easy access to blood for analysis, especially ABG samples. As mentioned previously, oxygenation is sometimes better measured through ABGs because of peripheral shunting and inaccurate pulse oximetry readings.

Medical management for sepsis/septic shock: Fluid replacement therapy

-essential to restore hemodynamic stability, maximize DO2, and begin repaying oxygen debt. -crystalloid solution such as normal saline is commonly used to maintain filling pressures, as measured through right atrial pressure or PAOP. -aggressive resuscitation in early sepsis (i.e., within the first 6 hours) has been shown to decrease mortality. -If fluid resuscitation is not successful at restoring blood pressure, initiation of vasopressors such as dopamine or norepinephrine to maintain a mean arterial pressure greater than 65 mm Hg may become necessary -suggested that the use of norepinephrine as the first line vasopressor.

Physical assessment of shock: GI system

-indicates poor perfusion through sluggish, hypoactive bowel sounds that reflect a slowing of intestinal activity. Nausea and vomiting may also be present. -The GI system is particularly vulnerable to poor perfusion and ischemia. -Cell damage in the GI tract allows translocation of intestinal bacteria to the systemic circulation, increasing the risk of sepsis. -Some have suggested that hypoperfusion in the GI system may initiate systemic inflammatory response syndrome (SIRS), which, if not resolved, it may be the precursor to multiple organ dysfunction syndromes (MODS).

Medical management for sepsis/septic shock: Steroid replacement therapy

-is controversial -Adrenal insufficiency is a common feature of sepsis, but the use of high-dose steroids has been shown to have no benefit; their use has not been shown to decrease mortality in sepsis. Studies have been inconclusive as to the benefits of low-dose steroids in septic shock. -The surviving sepsis guidelines recommend low-dose steroids if the patient has not been responsive to fluid and vasopressor therapy.

Hemodynamic monitoring with shock: Central Venous Catheter

-long catheter threaded through the superior vena cava with the distal port resting in the superior vena cava or right atrium. -this allows central venous pressure (CVP) monitoring. This value indicates mean right atrial pressure or CVP pressure and is used as an estimate of volume returning to the right heart or right heart preload. -A decreased CVP reading may be indicative of a low volume state such as hypovolemic shock or peripheral vasodilatation that occurs as a result of distributive shock. -An elevated CVP may indicate increased volume that may occur with cardiogenic shock. -This line may also be used as a port to draw a blood sample to evaluate VO2, central venous oxygen saturation (ScvO2), if a PA line is not in place. Unlike the sample drawn through the PA line, the ScvO2 provides information primarily on oxygen extraction in the brain and upper body --> not reflective of whole body but correlation has been found between SVO2 and ScvO2 for monitoring and treatment purposes.

Progressive stage

-progressive stage is marked by the failure of compensatory mechanisms to maintain adequate blood pressure and circulating fluid volumes. -There is extensive shunting of blood to vital organs, which results in decreased blood flow to the periphery. -Without effective treatment, profound hypoperfusion occurs, resulting in worsening metabolic acidosis, electrolyte imbalances due to the failure of the sodium potassium pump, and respiratory acidosis.

Physical assessment of shock: renal system

-renal system provides a clear indication of poor perfusion if urine output decreases. -Oliguria is a common finding in early shock because of decreased perfusion of the renal tubules, which stimulates the initiation of the renin-angiotensin-aldosterone system. -later stages of shock will present with anuria, increased creatinine level, and other signs of acute renal failure.

cardiogenic shock clinical manifestation

-requently present with clinical symptoms similar to those of AMI, such as chest pain, diaphoresis, nausea, and vomiting. The decreased cardiac output and resulting compensatory mechanisms cause a decreased level of consciousness, decreased urine output, poor pulses, pale cool skin, and decreased bowel sounds. -Shortness of breath, crackles on auscultation, and decreased saturation of arterial blood with oxygen (SpO2) are evident as a result of pulmonary edema. -Decreased cardiac output greatly impairs tissue perfusion, leading to anaerobic metabolism that produces lactic acid, as evidenced by increased lactate levels. Arterial blood gases reveal a metabolic acidosis. -As shock progresses, clinical manifestations become more pronounced. Profound hypotension and bradycardia develop. Organ systems begin to fail. Laboratory analysis reveals increases in creatinine and liver enzymes, demonstrating renal and liver failure. Coma, cyanotic, mottled skin, absent bowel sounds, and anuria are present. -Hemodynamic parameters obtained through a PA catheter include increased right atrial pressure and PAOP. Systemic vascular resistance is high, and cardiac output is very low. Mixed venous oxygen saturation is decreased.

Inital stages

-shock is marked by hypoxia due to decreased DO2 to the cells. -Clinical manifestations are subtle or subclinical, but cellular damage may be occurring. -Invasive hemodynamic monitoring would note decreased cardiac output. Without identification and treatment at this stage, shock will progress to the next level.

Treatment priorities in neurogenic shock

-treatment focus is on providing cardiovascular support while attempting to resolve the primary cause of shock. -Cardiovascular support is done through cautious fluid resuscitation and the use of vasoactive IV medications such as dopamine, epinephrine, norepinephrine, or phenylephrine (see Tables 14.5 and 14.6). -If necessary, bradycardia is treated with atropine. -Repeated episodes of bradycardia may require transcutaneous or transvenous pacing. -Ventilatory support through intubation and mechanical ventilation may be required.

Clinical manifestation Neurogenic shock

-warm, dry skin and a flushed appearance due to systemic vasodilation. -Hemodynamic parameters include decreased cardiac output, decreased right and left filling volumes, and decreased systemic vascular resistance.

Obstructive shock patho

1. Obstructive shock is caused by a mechanical barrier to ventricular filling or ventricular emptying (increased afterload) causing decreased cardiac output. As in cardiogenic shock, symptoms are independent of fluid volume status. 2. The mechanical obstruction to the pumping action of the heart results in decreased cardiac output and poor perfusion at the tissue level. The specific pathophysiology varies depending on the cause of shock. For instance, a PE, typically the result of mobilization of clot material to the lungs from a deep vein thrombosis (DVT), may result in obstructive shock. This is a result of extreme increases in right heart afterload due to an obstruction to blood flow into the lungs because of a clot or embolus in the PA. 3. Alveoli are ventilated but not perfused producing an extreme ventilation perfusion mismatch. Obstructive shock caused by cardiac tamponade is the result of excessive pressure on the heart muscle that occurs as fluid fills the pericardial sac. This may be the result of trauma to the cardiac muscle that results in bleeding and blood in the pericardial sac or a large, uncontrolled pericardial effusion. As the fluid accumulates around the heart, less blood enters the ventricles with each successive diastole, impairing ventricular filling.

Nursing Management cardiogenic shock

Assessment and Analysis As in hypovolemic shock, the clinical manifestations of cardiogenic shock are related to a decrease in cardiac output and impaired tissue perfusion. Hypotension, tachycardia, and tachypnea are present. Systemically, the patient has a decreased level of consciousness and weak pulses with cold, cyanotic, and mottled skin. Urine output and bowel sounds are decreased or absent. Without successful intervention, profound hypotension, bradycardia, and hypoxia result. Nursing Interventions ■ Assessments • Neurological status Decreased level of consciousness occurs as a result of decreased cardiac output. • Vital signs Hypotension and tachycardia are present because of decreased cardiac output. Respiratory rate increases in an effort to increase tissue oxygenation and remove CO2 to compensate for metabolic acidosis. • Hemodynamic parameters Both right and left preloads are increased because of impaired pumping ability of the heart, but cardiac output is low. As a result of compensation for low cardiac output, vasoconstriction occurs, increasing systemic vascular resistance. • Urine output Decreased urine output occurs as a result of decreased cardiac output and stimulation of compensatory mechanisms that increase reabsorption of sodium and water. • Skin color and temperature Cold and clammy skin may be a sign of progressing shock. Laboratory Tests • ABGs Initial ABGs may reflect a respiratory alkalosis due to tachypnea. Later stages of shock reveal a metabolic acidosis due to anaerobic metabolism. • Svo2 Decreased SVO2 is an indicator of inadequate DO2. • Metabolic profile Renal failure and liver failure as evidenced by increased BUN and creatinine levels and liver function test results may become evident because of decreased organ perfusion. • Lactate/base deficit Increased lactate level and negative base deficit are evidence of poor perfusion at the cellular level. Decreasing lactate levels are an endpoint demonstrating adequate resuscitation. ■ Actions • Apply a 100% non-rebreather oxygen mask Maximizing oxygenation is essential. • Prepare for intubation and mechanical ventilation Intubation and mechanical ventilation are frequently necessary with patients in cardiogenic shock in an effort to decrease VO2 and increase oxygen availability. • Administer fluids as prescribed Fluids may be utilized cautiously to increase cardiac output if filling pressures are low and there are no signs of pulmonary edema. • Administer medications as ordered: • Vasoactive drugs such as norepinephrine or dopamine Vasoactive drugs produce vasoconstriction, increasing blood pressure. • Inotropic medications such as dobutamine Inotropic medications increase contractility and cardiac output • Diuretics Diuretics may be very cautiously utilized to decrease vascular volume if filling pressures are extremely elevated. • Morphine sulfate Morphine will relieve pain, which can help to decrease myocardial VO2. It will also decrease venous return through vasodilation. • Restrict activity Restricting activity will decrease cardiac workload and VO2. ■ Teaching • Instruct patient and family about the importance of rest periods. Increased activity or stress levels cause increased myocardial VO2 and can worsen the progression of shock. • Teach patient and family about the causes of cardiogenic shock and myocardial infarction. Early recognition and treatment of myocardial infarction will help avoid a complication of cardiogenic shock. Evaluating Care Outcomes -Rapid recognition of the presence of cardiogenic shock is essential in effective treatment. Swift intervention with inotropic and vasoactive support helps maintain adequate cardiac output and blood pressure to ensure sufficient oxygen supply to the tissues. Careful monitoring of clinical manifestations and hemodynamic status helps evaluate therapeutic interventions. -Successful treatment is demonstrated by a satisfactory blood pressure level and cardiac output and adequate tissue perfusion.

Nursing Management of obstructive shock

Assessment and Analysis As in other forms of shock, the clinical manifestations of obstructive shock are related to a decrease in cardiac output and impaired tissue perfusion. Hypotension, tachycardia, and tachypnea are present. The patient has a decreased level of consciousness and weak pulses with cold, cyanotic, and mottled skin. In addition, the patient may present with muffled heart sounds due to the presence of excessive fluid in the pericardial sac or signs of right heart failure due to elevated right heart afterload. As shock progresses, urine output and bowel sounds may become decreased or absent; typically, without definitive treatment of the cause, death occurs rapidly. Nursing Interventions ■ Assessments • Neurological status Anxiety and restlessness may occur initially but will progress toward a decreased level of consciousness as a result of decreased cardiac output. • Vital signs Hypotension and tachycardia are present because of decreased cardiac output. Respiratory rate increases in an effort to increase tissue oxygenation and remove CO2 to compensate for metabolic acidosis. • Hemodynamic parameters Both right and left afterloads may be increased as a result of mechanical resistance to ventricular emptying; filling pressures are variable depending on the cause; elevated with impaired emptying, decreased with impaired filling. Increased oxygen consumption is evidenced through a decreased SVO2. Cardiac output is low. • Urine output Decreased urine output occurs as a result of decreased cardiac output and stimulation of compensatory mechanisms that increase reabsorption of sodium and water. • Skin color and temperature Cold and clammy skin is present as a result of poor peripheral perfusion. Laboratory Tests • ABGs Initial ABGs may reflect a respiratory alkalosis due to tachypnea. • SVO2 Decreased SVO2 is an indicator of inadequate oxygen delivery. ■ Actions • Apply a 100% non-rebreather oxygen mask Maximizing oxygenation is essential. • Prepare for intubation and mechanical ventilation Intubation and mechanical ventilation are frequently necessary with patients in obstructive shock in an effort to decrease VO2 and increase oxygen availability. • Administer medications as ordered: • Vasoactive medications such as norepinephrine and dopamine Vasoactive medications produce vasoconstriction, increasing blood pressure and allowing the patient to stabilize until definitive treatment is implemented. • Anticoagulation via heparin administration if the cause of obstructive shock is PE Anticoagulation is used to decrease the formation of new clots and prevent the existing clot from increasing in size while the body is naturally dissolving it. • Thrombolytic therapy if the cause of obstructive shock is PE Thrombolytics are given to dissolve the clot. • Prepare for definitive treatment of the cause, for example: • If cardiac tamponade: • Pericardiocentesis Pericardiocentesis is a procedure to drain fluid or blood from the pericardial sac, relieving pressure and allowing the ventricles to fill normally. • Prepare for emergency transport to the operating room for a pericardial window procedure A pericardial window procedure will ease the pressure on the heart muscle, allowing the ventricles to fill. • If PE: • Suction thrombolectomy Suction thrombolectomy is done to remove the obstruction to ventricular emptying. ■ Teaching • Teach patient and family about the causes of PE: avoid prolonged periods of inactivity, walk every hour, drink plenty of fluids Mobilization helps reduce the likelihood of PE formation by decreasing the formation of a DVT, typically the initial source of the PE. Dehydration may increase the tendency to clot. • Anticoagulation teaching: • Regular follow-up laboratory testing - international normalized ratio Determine effective dosing of anticoagulants • Use electric razors, soft toothbrushes, no flossing Avoid potential causes of bleeding • Limit foods high in vitamin K, such as green leafy vegetables These foods interfere with the efficacy of anticoagulants. Evaluating Care Outcomes Rapid recognition of the presence of obstructive shock is essential in effective treatment. Swift intervention with inotropic and vasoactive support helps maintain blood pressure, but definitive treatment of the cause is required to promote survival. Careful monitoring of clinical manifestations and hemodynamic status help evaluate therapeutic interventions. Successful treatment is demonstrated by satisfactory blood pressure, cardiac output and adequate tissue perfusion.

Physical assessment of shock: cardiovascular system

Blood pressure -is a valuable indicator of fluid status and cardiac output. A decreased blood pressure level can be indicative of a problem. I n shock, blood pressure decreases because of inadequate venous return to the heart, vasodilation, or decreased contractility of the heart muscle. It is important to remember that a return to baseline blood pressure level does not mean the resolution of the problem, but prolonged hypotension does indicate the continued presence of shock. -A common finding indicative of the compensatory stage of shock is a narrow pulse pressure, which results from compensatory vasoconstriction causing an increase in diastolic pressure with only a slight increase in systolic pressure. Heart Rate -Tachycardia is a typical finding due to stimulation of the sympathetic nervous system as a way to increase cardiac output. -If shock is not resolved but is allowed to progress into later stages, the HR may slow. -Skin color, temperature, quality of pulses, and capillary refill indicate perfusion in the extremities. -Because of shunting of the blood to vital organs, the skin and periphery become cool, pale, mottled, or cyanotic with thready pulses and sluggish capillary refill.

Cardiogenic shock

Cardiogenic shock is characterized as inadequate pumping ability of the heart muscle, most typically the result of an acute myocardial infarction (AMI). Independent of fluid volume status, the inadequate pumping of the heart results in decreased cardiac output and poor perfusion at the tissue level.

Distributive shock

Distributive shock is the result of disease states such as sepsis, anaphylaxis, or neurogenic or spinal shock that cause poor vascular tone and vasodilation, resulting in increased vascular capacity and venous pooling. In this form of shock, blood volume is adequate, but a state of relative hypovolemia exists because of venous pooling and decreased venous return to the right heart.

hypovolemic shock patho

I. Acute loss of circulating fluid volume results in decreased venous return to the right heart and decreased stroke volume and cardiac output, resulting in decreased perfusion at the tissue level. 2.decreased intravascular volume results in the initiation of several compensatory mechanisms 3. initial response is the stimulation of the sympathetic nervous system, which increases the HR in an attempt to increase cardiac output. The sympathetic nervous system also stimulates the release of epinephrine and norepinephrine from the adrenal medulla, improving contractility and inducing systemic vasoconstriction. Blood pressure and cardiac output are increased. Blood flow is redirected from nonessential organs to vital organs such as the heart and brain. 4.endocrine system, through the RASS and the release of antidiuretic hormone from the posterior pituitary, increases sodium and water reabsorption in the renal tubules, effectively increasing venous return to the right heart. The renin-angiotensin-aldosterone system, as a result of the end product angiotensin II, also produces a potent systemic vasoconstriction that increases blood pressure and venous return.

sepsis/septic shock clinical manifestation

Infection 1. invasion of a pathogen initiates a series of complex responses by the host's immune system. 2The initial, immediate response is activation of the innate immune response. This response is nonspecific to any antigen. It involves the mobilization of macrophages and neutrophils to the area, the activation of pro-inflammatory cytokines or signaling molecules, activation of complement proteins; proteins that immobilize and breakdown pathogens, and the activation of the coagulation system. 3Activated coagulation produces a fibrin mesh to help localize the invading organism as well as activates bradykinin which dilates vessels and increases capillary permeability. 4. Local blood vessels dilate increasing circulation to the involved area which allows an influx of immune cells causing local redness, warmth and edema. This is done in an effort to kill the invading organism and keep the response localized Sepsis 1. Sepsis occurs when the inflammatory response is no longer localized. The response becomes amplified and uncontrolled 2. normal deactivation process which decreases the production of pro-inflammatory cytokines as well as produces anti-inflammatory cytokines is impaired. The excessive release of proinflammatory cytokines results in damage to the endothelial cells lining the blood vessels, producing vasodilation, decreased vasomotor tone, and increased capillary permeability. 3. sepsis and septic shock result when proinflammatory cytokines overpower anti-inflammatory cytokines, resulting in overwhelming and excessive systemic inflammation, massive peripheral vasodilation and increased capillary permeability. --> Other forces that contribute to widespread inflammation are substances produced by the invading organisms. Endotoxins released by gram-negative bacteria and exotoxins produced by gram-positive bacteria add to the pro-inflammatory effect. 4. A part of the excessive inflammation is activated and enhanced coagulation resulting in widespread fibrin deposition and excessive clotting throughout the vascular system. It also results in decreased fibrinolysis (breakdown of clots). This occurs due to decreased levels of activated protein C and antithrombin III seen in septic patients. The primary role of protein C is to modulate the production of thrombin and promote fibrinolysis. Antithrombin III deactivates thrombin. The role of thrombin in the coagulation cascade is to modulate the conversion of fibrinogen to fibrin clots. Decreased levels of both protein C and antithrombin III lead to enhanced formation of thrombin, resulting in clot formation as well as impaired fibrinolysis, which ultimately results in impaired blood flow due to microvascular clots and organ dysfunction.

Normal CO

Normal cardiac output is 4 to 6 L/min. Typically, cardiac output is indexed, meaning it is calculated on the basis of the patient's body surface area.

Anaphylactic Shock Nursing Management

Nursing Management Assessment and Analysis Anaphylactic shock is characterized by a sudden and severe hypersensitivity reaction causing a release of histamine that results in widespread vasodilation and decreased venous return. This results in respiratory distress, circulatory collapse, and skin reactions. Airway compromise is manifested by wheezing, stridor, and shortness of breath. Skin reactions include itching, a raised red rash, and severe swelling, specifically around the eyes. Hemodynamically, the patient is hypotensive and tachycardic with decreased filling pressures and decreased cardiac output. Nursing Interventions ■ Assessments • Vital signs/hemodynamic parametersHypotension and decreased filling pressures are present because of widespread vasodilation, resulting in decreased venous return and cardiac output. Tachycardia results as a compensatory mechanism. Systemic vascular resistance remains low because of the vasodilation. • Respiratory assessmentShortness of breath, wheezing, and decreased oxygenation may be present because of airway smooth muscle contraction and edema of the throat and/or tongue. • Skin assessmentUrticaria and angioedema are indicators of an allergic reaction. Pale, cool, clammy skin is an indicator of poor peripheral perfusion related to decreased cardiac output. ■ Actions • Remove trigger immediatelyIf possible, remove the trigger. If not possible, do not delay definitive treatment; the hallmark of anaphylaxis is sudden onset and rapid progression of symptoms. • Apply oxygen via a 100% non-rebreather maskMaximizing oxygenation is the first priority in order to increase DO2 to the tissues. • Insert an IV and administer IV fluid as orderedInfusion of IV fluids helps increase and maintain vascular volume. • Administer medications as ordered: • IV epinephrineEpinephrine is a vasoactive drug that reverses peripheral vasodilation. • AntihistaminesAntihistamines may help counter histamine-mediated vasodilation and bronchoconstriction. • CorticosteroidsThe anti-inflammatory action of steroids may help shorten the anaphylactic reaction. • Inhaled bronchodilatorsBronchodilators help relieve bronchoconstriction, relieving respiratory distress. ■ Teaching • Teaching related to the cause of anaphylaxisUnderstanding the cause of the anaphylactic response is essential in avoiding repeat occurrence. • Administration of epinephrine via an EpiPenTypically, allergic reactions occur in the home or away from the hospital. Patients or family members must know how to use the EpiPen as a first-line treatment in an allergic reaction to avoid anaphylactic shock if possible. Evaluating Care Outcomes As with other forms of shock, prompt recognition and treatment of anaphylactic shock is essential. Without a rapid response, airway compromise can quickly lead to death. Successful treatment is demonstrated by the resolution of skin reactions, itching, swelling, and most importantly, airway compromise, as evidenced by resolution of wheezing and shortness of breath.

Nusing management Neurogenic shock

Nursing Management Assessment and Analysis The clinical manifestations of neurogenic shock are slightly different from the manifestations of other forms of shock. Similar to other forms of distributive shock, the patient has decreased cardiac output as a result of decreased vascular tone and reduced venous return; however, because of the disruption in the sympathetic nervous system, the patient may be bradycardic rather than tachycardic. The patient may appear pink and flushed as a result of vascular vasodilation. Nursing Interventions ■ Assessments • Vital signs Hypotension and bradycardia may be present because of disruption of sympathetic nervous system activity. • Hemodynamic parameters Cardiac output, right atrial pressure, and PAOP, are low related to decreased venous return to the right heart secondary to systemic vasodilation. Systemic vascular resistance is low secondary to systemic vasodilation. • Respiratory rate and SpO2 Respiratory rate may be low because of the injury causing neurogenic shock, such as cervical spinal cord injury. This may cause a decrease in oxygenation. ■ Actions • Administer IV fluid as ordered Cautious fluid resuscitation is provided to increase vascular volume, which matches the increase in size of the vascular space due to massive dilation. • Administer IV medications as ordered: • Vasoactive drips Administration of vasoactive drips aids in increasing vasomotor tone and systemic vascular resistance. • Atropine Atropine is used for the treatment of bradycardia to block the action of the vagus nerve in the parasympathetic nervous system, increasing the HR. • Prepare for transcutaneous pacing or transvenous pacing Pacing may be necessary to treat recurrent episodes of bradycardia. • Raise the head of the patient's bed slowly Because of loss of systemic vasomotor tone, patients in neurogenic shock are particularly vulnerable to orthostatic hypotension. • Apply venous thromboembolism prophylaxis, such as sequential compression devices or medication such as heparin Patients in neurogenic shock are at high risk for venous thromboembolism, particularly in cases where the etiology of neurogenic shock is spinal cord injury. ■ Teaching • If the cause of neurogenic shock is spinal cord injury, teaching related to the anticipated impact on the patient's immediate and future health-care issues is vital. Psychosocial support from social workers, clergy, or a professional requested by the family is also essential in the care of the patient. A spinal cord injury has profound long-term health-care and life implications. Understanding of treatment and outcomes is essential to maximize recovery. Evaluating Care Outcomes As with other forms of shock, prompt recognition and treatment of neurogenic shock is essential. Adding to the urgency is the patient's inability to compensate for the decreased cardiac output with tachycardia because of the disruption of the sympathetic nervous system. Pacing to maintain a normal HR may be required while the patient is treated and stabilized. A stabilized blood pressure, HR within normal limits, and adequate cardiac output are signs of a successful intervention.

Obstructive shock

Obstructive shock is caused by a mechanical barrier to ventricular filling or ventricular emptying (increased afterload), causing decreased cardiac output. Examples of disorders resulting in impaired filling include cardiac tamponade and tension pneumothorax. example of a disorder resulting in increased afterload is severe valvular disease.

Afterload

Refers to the resistance to flow that the ventricle must overcome to eject its contents. Increasing afterload may make it harder for the heart to eject blood into the systemic circulation

Obstructive Shock epidemiology

Risk factors for obstructive shock include -extracardiac disorders that impair ventricular filling or emptying. -disorders resulting in impaired filling include cardiac tamponade and tension pneumothorax -Impaired emptying is also referred to as increased right or left afterload. An example of a disorder resulting in increased right afterload is acute pulmonary embolism (PE).

Multiple organ dysfunction syndrome

complication that occurs as a result of the excessive inflammation associated with severe injury or sepsis. The cause of MODS is multifaceted. Several factors lead to decreased DO2 to the organ systems, causing impaired tissue perfusion. • apoptosis is accelerated in sepsis. • Widespread damage to the vascular endothelium, that occurs as a result of inflammation and causes the increased capillary permeability and vasodilation of sepsis, continues as a result of the excessive production of inflammatory mediators. • microvascular dysfunction that causes maldistribution of blood flow in the capillary beds continues, resulting in uneven flow to different organ systems. • Enhanced coagulation leads to clots in the microcirculation, mechanically obstructing flow. Additionally: • The accelerated production of glucose as initial compensation eventually becomes harmful. This hypermetabolism causes increased cellular oxygen demand. • Direct toxicity of mitochondrial cells that occurs with excessive inflammation affects the ability to use oxygen even when present. -Eventually, poor DO2 coupled with increased oxygen demand and poor oxygen utilization results in profoundly impaired cellular functioning, metabolic acidosis, and organ failure. -The initial organ system to become symptomatic is typically the lungs, with the development of acute respiratory distress syndrome (ARDS). Sequential failure is frequently the renal system, the hepatic system, then the GI system. -The focus of medical management of MODS is supportive in the form of controlling infection, maximizing oxygenation, and restoring and maintaining intravascular volume. - Antibiotics are given as appropriate. Fluid is administered to maintain intravascular volume. -Blood products are administered as necessary to maintain adequate hemoglobin levels. -Mechanical ventilation is usually necessary to protect the airway and support oxygenation.