P/P SHOCK

anaphylactic shock

A type of distributive shock that results from widespread systemic allergic reaction to an antigen Anaphylactic response-increased vascular permeability, bronchoconstriction, increased mucous production, increased inflammatory mediators causes - insect stings, medication reaction, food allergy rapid onset, dyspnea (tight throat, bronchospasm, laryngeal edema), feelings of apprehension, tingling and swelling in mouth, face, throat, and tongue, itching, decreased BP, tachycardia, loss of consciousness GOALS 1. treat or remove the cause 2. prevent cardiovascular instability (manage BP) 3. promote optimal tissue perfusion AIRWAY SUPPORT: O2, keep airway patent, ventilator Medications: IV EPINEPHRINE, Antihistamines, Corticosteroids

pharmacotherapy

Adrenergic agonists activate the sympathetic nervous system to produce fight-or-flight symptoms Two receptor types= Alpha/Beta Nonselective adrenergic agonists activate both alpha and beta receptors and are used to treat bronchospasm, cardiac arrest, and hypotension Alpha-adrenergic agonists are used to elevate blood pressure (phenylephrine) Used to treat hypotension associated with shock Intense vasoconstrictive Act in CNS to decrease sympathetic activity Contraindications/precautions- Severe HTN Beta-adrenergic agonists are used to treat asthma, shock, heart failure, and other cardiac disorders. B1-Most significant receptor site in cardiac muscle Activation results in fight-or-flightIncreased HR, increasing strength of myocardial contraction B2-Most important receptor site is in lungs. Relaxation of bronchial smooth muscle Epinephrine and isoproterenol also effective bronchodilators alpha agonist affect more BP while beta impact cardiac output more. Sometimes you need both and that would be when have non-selective (ie Epinephrine) Epinephrine, NE, dopamine for shock or anaphylaxis when blood pressure, heart rate need to be quickly restored to normal levels. Epinephrine has both α-adrenergic and β-adrenergic properties and has a greater affinity for alpha- and beta-receptors than norepinephrine. Its use is associated with a higher rate of cardiac dysrhythmias Norepinephrine (Levophed)vasoconstriction that results in an increase in blood pressureNorepinephrine is considered the vasopressor of choice for treatment of septic shockNorepinephrine acts primarily as an α-adrenergic agonist, causing vasoconstriction that results in an increase in blood pressure. It also has β-adrenergic properties, which causes an increase in cardiac output and heart rate. short duration of action, which allows for rapid adjustment of dosing in response to changes in a patient's hemodynamic status Phenylephrine: Prevents or reverses acute hypotension in critical care/shock pure α-adrenergic agent that causes vasoconstriction and impairment of tissue blood flow throughout the body Dobutamine (Dobutrex)Short-term treatment of certain types of shock Nonselective beta-adrenergic agonist Isoproterenol-Nonselective beta-adrenergic agonistCardiogenic or bacteremic shockactivator of both beta1- and beta2-adrenergic receptors throughout bodySerious dysrhythmias All of these meds are potent, have a rapid onset and the effects of the meds stop quickly after the infusion stops so need to keep an eye on the amount left in the bottle.Onset is 1-2 minutes...lasts for 1-2 minutes after the infusion is terminated!!Adjust the dose per MD orders (based on CV status of client)Assess and Document lung sounds, VS, hemodynamic parameters per policy, mental status changes, skin temp, color of nail bedsRecord and monitor urine output (as all of these tell if the med is working to increase perfusion)MUST have Continuous cardiac monitoring

types of shock

Cardiogenic shock is caused by failure of the heart. [blood pump problem] Hypovolemic shock is caused by a large depletion of blood or fluids from the body. Distributive shock involves widespread vasodilation, which causes extensive hypoperfusion of tissues. [blood volume problem] vasogenic/distributive shock - anaphylactic, neurogenic, septic - [blood vessel problem] Anaphylactic shock is triggered by a severe allergic reaction. neurogenic shock occurs because of spinal cord or brain injury. Septic shock results from mechanisms during infectious processes (toxins, chemical mediators) Hypovolemic and cardigenic are focused on decreased cardiac output directly while distributive results in decreased CO due to the decreased peripheral resistance The key in distributive patho is looking at what is causing the vasodilation/lack of SVR (systemic vascular resistance).

risks

In each type of shock it is imperative as the RN that you identify early who might be at risk for shock so that can be monitoring for it as well as taking some actions to prevent it. Examples Hypovolemic shock- surgical, trauma, and burn patients Septic- immunocompromised (burns again), geriatric patients with complicated UTIs Cardiogenic- MI, heart failure Neurogenic- spinal cord injuries

Sepsis

Infection usually begins in one organ system and then spreads into the bloodstream, causing sepsis. Immunosuppressed persons, older adults, and infants are most susceptible to sepsis. At risk patients: AIDS patients, cancer patients, infants, diabetes patients, intubated patients, transplant patients For example, a common cause of sepsis is a urinary tract infection in older adults; this is termed urosepsis. Sepsis is a state in which the immune system is overwhelmed and causes severe multiorgan compromise.Septic shock is a medical emergency and has a high death rate—up to 60% mortality.Microbial exotoxins or endotoxins can stimulate potent vasodilation, causing hypotension. Sepsis can activate the coagulation cascade.The widespread vasodilation, inflammation, and microthrombi can lead to extensive tissue hypoperfusion with ischemia, leading to MODS. The hemodynamic derangements observed in septic shock and SIRS are due to a complicated cascade of inflammatory mediators. Inflammatory mediators are released in response to any of a number of factors, such as: infection, inflammation, or tissue injury. When a microorganism enters the body, the normal immune/inflammatory responses are started. However, in severe sepsis and septic shock, the body's response to the microorganism is exaggerated. Endotoxins from the microorganism cell wall stimulate the release of cytokines, including tumor necrosis factor (TNF), interleukin-1 (IL-1), and other proinflammatory mediators that act through secondary mediators such as platelet activating factor, IL-6, and IL-8.The release of platelet activating factor results in the formation of microthrombi and obstruction of the microvasculature. With Sepsis, at Least One of the Following Manifestations of Inadequate Organ Function or Perfusion Is Typically Included: Alteration in mental state Hypoxemia (arterial oxygen tension lower than 72 mm Hg and overt pulmonary disease not the direct cause of hypoxemia) Elevated plasma lactate level Oliguria (urine output lower than 30 mL or 0.5 mL/kg for at least 1 hour) Elevated blood glucose with difficulty controlling Due to vasodilation and inflammation The patient may appear pink and the skin may be warm despite the onset of shock; called "warm shock." Early septic shock (warm or hyperdynamic) causes reduced diastolic blood, widened pulse pressure, flushed warm extremities, and brisk capillary refill from peripheral vasodilation with a compensatory increase in cardiac output. In late septic shock (cold or hypodynamic), myocardial contractility combines with peripheral vascular paralysis to induce a pressure-dependent reduction in organ perfusion. The result is hypoperfusion of critical organs such as the heart, brain, and liver. Sepsis and shock are medical emergencies Most healthcare facilities will have protocols in place to assess for and treat sepsis. This includes screening for acutely ill, high-risk patients. Prevention: Asepsis, Assessing need for indwelling lines, keep concept of homeostasis in mind (maintain BG between 70 and 120) Appropriate routine microbiologic cultures (including blood) be obtained before starting antimicrobial therapy in patients with suspected sepsis and septic shock if doing so results in no substantial delay in the start of antimicrobials. (Best practice statement). Appropriate routine microbiologic cultures always include at least two sets of blood cultures (aerobic and anaerobic) a protocolized approach to blood glucose management in ICU patients with sepsis, commencing insulin dosing when 2 consecutive blood glucose levels are >180 mg/dL. This approach should target an upper blood glucose level ≤180 mg/dL rather than an upper target blood glucose ≤110 mg/dL. (Strong recommendation; high quality of evidence)It is recommended that blood glucose values be monitored every 1 to 2 hrs until glucose values and insulin infusion rates are stable, then every 4 hrs thereafter in patients receiving insulin infusions. (Best practice statement) Fluid Resuscitation: isotonic IVF Vasopressors: pt is hypotensive!! Inotropic drugs for cardiac contractility From Surviving Sepsis Campaign Guidelines 2016: We recommend norepinephrine as the first choice vasopressor (key is to raise MAP to target)We suggest guiding resuscitation to normalize lactate in patients with elevated lactate levels as a marker of tissue hypoperfusion.

compensatory shock

One of the classic signs of shock is a drop in blood pressure (BP), which occurs because of a decrease in CO and narrowing of pulse pressure.Blood flow to the most essential (vital) organs, the heart and brain, is maintained, while blood flow to the nonvital organs, such as the kidneys, GI tract, skin, and lungs, is diverted or shunted.So there are beginning signs of decreased perfusion. baroreceptors in carotid and aortic bodies activate SNS response to decrease BP - vasoconstriction while blood to vital organs maintained - heart, brain decreased blood to kidneys activates renin-angiotensin system - angiotensin I converted to angiotensin II - vasoconstriction, increased venous return to heart - stimulates release of aldosterone - increased sodium reabsorption stimulates ADH

S/S

MAP= Mean Arterial Pressure; normal is 60-100 MAP decreased Stage 1- Early, Reversible, and Compensatory Early: drop in MAP 10-15mmHg sustained drop seen with fluid loss 1000ml or more the sympathetic nervous system and renin-angiotensin-aldosterone system (RAAS) are triggered; results in an increase in the heart rate and contraction thus increasing cardiac output (fight or flight) as well as Peripheral vasoconstriction ID and treat underlying cause to prevent progression downward End result: Compensatory stage perfusion of tissues, cells and organs are maintained. Stage 2: Intermediate or Progressive sustained decrease in MAP of 20mmHg or more below normal levels See in fluid loss of 1800 to 2500mL Fluid shifts to interstitial space. Anaerobic metabolism begins. Acidosis and hyperkalemia are occurring The lungs, kidneys, gut, pancreas, and liver suffer decreased perfusion. All available blood is conserved for the heart and brain Rapid tx is needed!! Stage 3 -Irreversible (You are too late!!) There is tissue anoxia. Cellular death is occurring.Severe metabolic acidosis is now irreversibleMyocardial and cerebral ischemia occur. The normal intestinal barrier to microbes and their toxins breaks down which releases microbes and their toxins into the general circulation leading to systemic inflammatory response

Distributive shock

Results from wide spread vasodilatation and decreased peripheral resistance. Unlike the other types defined earlier, dis- tributive shock does not present with decreased cardiac output and is commonly referred to as "warm shock, Distributive shock has several causes. Septic shock is the most common form of distributive shock, with considerable mortality. In the United States, this is the leading cause of noncardiac death in intensive care units (ICUs). Other causes of distributive shock include anaphylaxis and neurogenic shock due to brain or spinal cord injury. In distributive shock, the inadequate tissue perfusion is caused by decreased systemic vascular resistance (SVR) and a high cardiac output. The early changes are primarily characterized by the evolution of changes in contractility and dilation of peripheral small vessels and the impact of resuscitation efforts. During distributive shock, patients are at risk for diverse organ system dysfunction that may progress to multiple organ failure (MOF). Mortality from severe sepsis increases markedly with the duration of sepsis and the number of organs failing. In distributive shock due to anaphylaxis, decreased SVR is due primarily to massive histamine release from mast cells after activation by antigen-bound immunoglobulin E (IgE), as well as increased synthesis and release of prostaglandins. Neurogenic shock is due to loss of sympathetic vascular tone from severe injury to nervous system. The blood vessels relax and become dilated, resulting in pooling of the blood in the venous system and an overall decrease in blood pressure. Neurogenic shock can be a complication of injury to the brain or spinal cord.

neurogenic shock

The underlying cause of neurogenic shock is widespread vasodilation that reduces venous return to the heart>> decreased venous return reduces the volume of blood that can be pumped out of the ventricles >> low blood volume causes widespread hypotension. Can occur in response to spinal cord injury or spinal anesthesiaResults in massive vasodilation without compensation due to the loss of SNS vasoconstrictor tone, leading to pooling of blood in vessels, tissue hypoperfusion, ultimately impaired cellular metabolism There are involuntary muscles within blood vessel walls that maintain the squeeze so that the volume within the vessels stays constant even if the body changes position against gravity. Think of when you get up out of bed in the morning. If your blood vessels didn't squeeze a little tighter, gravity would make the blood flow to your feet, the lowest part of your body, away from your brain, and you might pass out. The squeeze is maintained by signals from nerves in the sympathetic trunk, a long bundle of fibers running from the skull to the tailbone alongside the vertebral column.In brain or spinal injury, the sympathetic trunk stops working and blood vessels dilate and result in blood pooling away from the heart. Since there isn't enough blood returning to the heart, the heart has a hard time pumping blood around the body. This situation looks like hypovolemic shock, since effectively there isn't enough fluid going into the heart but because there isn't enough sympathetic tone or adrenaline release, the heart rate does not show a compensatory increase to increase cardiac output. decreased BP, decreased HR, decreased Temp Essentially blood pools in the venous and capillary beds.Causes massive vasodilatation in the venous vasculature >> decreasing venous return to heart >> decreasing cardiac output.Neurogenic is the rarest form of shock! Blood Pressure-Hypotension HR- Bradycardia (early sign); Tachy (late) Skin: Warm, dry skin (early); pale and cool (late) LOC: Mental status anxious and restless and progresses to lethargy and comatose. Renal: Urine- Oliguria Other: Flaccid paralysis if etiology is spinal cord injury, hypothermia Treatment includes fluids and medications to increase the tone in the blood vessel walls.Careful fluid replacement with BP goal = increase afterload

hypovolemic shock

There needs to be enough red blood cells and water in the blood for the heart to push the fluids around within the blood vessels. When the body gets dehydrated, there may be enough red blood cells, but the total volume of fluid is decreased, and pressure within the system falls. Hypovolemic (hypo=low + volemic=volume) shock due to water loss can be the endpoint of many illnesses, but the common element is the lack of fluid within the body. Typical greater then 15% of volume lost Cause is any loss of fluid from the body, and the larger the amount the more likely the body cannot compensate. IE vomiting and diarrhea (esp in young/old), ascites (remember shift of volume from vascular space), severe burns. Hypovolemic Shock>>> Low Coronary Artery Perfusion>>>MI severe FVD s/s anxiety, blue lips and finger nails, chest pain, rapid HR, shallow breathing, low urine output KEY IS Early Recognition- Do not rely on BP! Goal is to Increase preload, more for the heart to distribute How will you evaluate treatment Restore circulating volume—CO, BP, arterial pressure, central venous pressure Tissue perfusion—Urine output, skin color, mental status, etc. Correction of cause—No bleeding, no vomiting, no diarrhea Treatment can be giving fluids but at some point need to identify the cause and manage that too. So managing perfusion (BP) while treating the cause

cardiogenic shock

When the heart loses its ability to pump blood to the rest of the body, blood pressure falls. Although there may be enough red blood cells and oxygen, they can't get to the cells that need them. The heart is a muscle itself and needs blood supply to work. When a heart attack occurs, the blood supply to part of the heart is lost, and that can stun and irritate the heart muscle so that it isn't able to beat with an appropriate squeeze to push blood to the rest of the body. This decreases stroke volume, and cardiac output falls. Treatment includes trying to restore blood supply and the use of medications to support blood pressure. In more dire circumstances, machines can be used to assist the heart to support blood pressure. causes: right ventricular infarct, endocarditis of mitral valve, pulmonary embolism, ventricular tachycardia, left ventricular damage, MI, myocarditis The hypoperfusion is compounded by the fact that most cardiogenic shock due to left ventricular failure is accompanied by pulmonary edema (remember if not pumping out will back up into the lungs), which dramatically reduces the ability of oxygen and carbon dioxide to diffuse across the alveoli-capillary membrane. Also, since left ventricular failure is often caused by an AMI (acute myocardial infarction) be aware that your patient experiencing cardiogenic shock, may also be having an A MI So will be seeing signs of shock- no perfusion to the body or heart itself (not feeding coronary arteries) but also of fluid overload in the heart. Hypotension Rapid, thready pulse Distention of hands and neck veins Increased, labored respirations, crackles Pulmonary edema Skin pale, cyanotic, cold, moist Restlessness, anxious, lethargy to coma Oliguria to anuria Edema, hemodynamic changes, dysrhythmias Hemodynamic monitoring will allow for continuous measurement of the blood pressure. An arterial line will be inserted. The patients Pulmonary artery pressures will also be measured to monitor overall cardiac function cardiac output.IMPORTANT TO REMEMBER Cautious fluid administration is necessary to reduce the risk of overload and pulmonary edema (this is why it is important to know your cause/risk factors). Pulmonary capillary wedge pressure (PCWP) provides an indirect estimate of left atrial pressure (LAP). [increased] The central venous pressure (CVP) is the pressure measured in the central veins close to the heart. It indicates mean right atrial pressure and is frequently used as an estimate of right ventricular preload. The CVP does not measure blood volume directly, although it is often used to estimate this [increased] treatment is aimed at airway and cardiac support. Early assessment & treatment!!! Treatments: Treat Reversible Causes Protect ischemic myocardium- decrease workload of heart (give O2, decrease afterload); remember afterload will make heart work harder. Improve tissue perfusion- maximize CO goal is to increase cardiac output and reduce afterload This is why we act fast in suspected MI - to limit/reduce myocardial damage Although the patient may present in a state of shock, treatment should also consist of treating the underlying cause (AMI, CHF) which if managed effectively, can relieve the hypoperfusion. Have to OPTIMIZE PUMP FUNCTION: Aggressive airway management: Mechanical Ventilation Judicious fluid management (dont overload heart that is why have hemodynamic monitoring) Vasoactive agents (dobutamine Dopamine) Morphine as needed (Decreases preload, anxiety) Cautious use of diuretics in CHF (do need some volume to perfuse- this is shock state not just "normal" CHF) Vasodilators as needed for afterload reduction Short acting beta blocker, for refractory tachycardia goal MAP >65

progressive stage

distinguishing features of decrease cellular perfusion and altered capillary permeability leakage of protein into interstitial space increased systemic interstitial edema The cardiovascular system is profoundly affected in the progressive stage of shock. CO begins to fall, resulting in a decrease in BP and coronary artery, cerebral, and peripheral perfusion. So now the s/s are much more pronounced and systemic.

refractory stage

exacerbation of anaerobic metabolism accumulation of lactic acid increased capillary permeability profound hypotension and hypoxemia tachycardia worsens failure of one organ system affects others recovery unlikely In the final stage of shock, the refractory stage, decreased perfusion from peripheral vasoconstriction and decreased CO exacerbate anaerobic metabolism. Increased capillary permeability allows fluid and plasma proteins to leave the vascular space and move to the interstitial space. Blood pools in the capillary beds.Loss of intravascular volume worsens hypotension and tachycardia and decreases coronary blood flow. Decreased coronary blood flow leads to worsening myocardial depression and a further decline in CO.Now nothing is being perfused.

MODS

if shock is not treated early multiple organ dysfunction syndrome is a clinical syndrome characterized by progressive and potentially reversible dysfunction in two or more organs or organ systems that is induced by a variety of acute insults, commonly sepsis. It is the leading cause of death in the ICU. SHOCK > SIRS > MODS Stage 1: The patient has increased volume requirements and mild respiratory alkalosis, which is accompanied by oliguria, hyperglycemia, and increased insulin requirements. Stage 2: The patient is tachypneic, hypocapnic, and hypoxemic. There is moderate liver dysfunction and possible hematologic abnormalities. Stage 3: The patient develops shock with azotemia and acid-base disturbances. There are significant coagulation abnormalities. Stage 4: The patient is vasopressor dependent and oliguric or anuric. Ischemic colitis and lactic acidosis follow. cardiovascular dysfunction lung dysfunction GI dysfunction liver dysfunction CNS dysfunction renal dysfunction skin dysfunction

shock

shock is not a disease but a consequence of a condition. Patients can experience more than one type simultaneously.Shock is the body's last attempt to compensate to maintain function and homeostasis. Shock is the inability of the heart and lungs to satisfy the metabolic and oxygen requirements of the peripheral tissues. Commonly, shock occurs when blood pressure (BP) falls below a systolic measurement of 90 mm Hg or drops 40 mm Hg below the patient's normal BP. Shock is considered a clinical syndrome. Shock is a condition in which the cardiovascular system fails to perfuse tissues adequately. An impaired cardiac pump, circulatory system, and/or volume can lead to compromised blood flow to tissues Regardless of its cause shock there are effects on the body's organ system you can expect, results from shunting of blood to heart and brain. In (stage 1 )compensated and mild (stage 2) the body is working to correct the imbalance so dont always see signs of dysfunction but trying to correct versus later states those systems are now no longer working. Shock = inadequate tissue perfusion Types of shock: hypovolemic, cardiogenic, distributive =septic, neurogenic, anaphylactic Signs of shock: altered MS, tachycardia, hypotension, tachypnea, low UOP (decreased perfusion) Always start with ABCs Resuscitation begins with fluid (exception - cardiogenic shock)

SIRS

systemic inflammatory response syndrome mediator excess: cytokines (tumor necrosis factor, interleukins), oxygen free radicals, etc widespread endothelial injury and dysfunction vasodilation and increased capillary permeability tissue edema neutrophil entrapment in microcirculation