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Shock notes

by: Brenna Notetaker

Shock notes Nurs 4020

Brenna Notetaker
GPA 3.4

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med surg nursing shock notes
Mrs. Swift
Class Notes
med surg, shock
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This 13 page Class Notes was uploaded by Brenna Notetaker on Monday February 8, 2016. The Class Notes belongs to Nurs 4020 at East Carolina University taught by Mrs. Swift in Fall 2015. Since its upload, it has received 12 views.

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Date Created: 02/08/16
Shock 09/11/2015 ▯ Decreased tissue perfusion, imbalance of supply of oxygen and the demand of the body ▯ Stages of shock  initial stage o usually not clinically apparent (body has been able to deal with the balance of supply of oxygen and nutrients) o metabolism changes from aerobic to anaerobic – causes a build up of lactic acid (body normally removes it in liver and blood)  compensatory stage o Body tried to compensate for build up of lactic acid o attempt to overcome consequences of anaerobic metabolism to maintain homeostasis o drop of blood pressure (classic sign of shock, occurs because of decreased cardiac output)– activated baroreceptors in carotid and aortic -> activation of renin-angiotensin system to increase BP and increase CO o Vasoconstriction and retention of sodium and water (trying to get cardiac output back up) o becomes clinically apparent o metabolic changes- lactic acid buildup causes palpitation, headache, altered mental status, muscle weakness, respiratory rate increase in response to metabolic acidosis (trying to blow off extra CO2 to get pH back to normal) o GI- decrease blood flow to GI tract, decrease motility, decreased bowel sounds, paralytic ileus (due to decreased blood flow to GI tract) o skin- cool or clammy; sepsis causes warm and flush skin o SNS- activation of SNS increase oxygen and nutrients that heart needs (hard on heart) o outcome  if perfusion deficit corrected, patient recovers  if deficit not corrected, patient enters progressive stage  progressive stage o begins when compensatory mechanisms fail o aggressive interventions needed to prevent multiple organ dysfunction syndrome (2+ organ systems failing) o complications  respiratory- first system to show dysfunction, rapid and shallow breathing, altered capillary permeability all over body (antisarca- diffuse profound edema), fluid leaks out and can cause pulmonary edema (crackles), hypoxia, alveoli stop producing surfactant (collapse)  CV- HR increases, stroke volume decrease, decreased cardiac output (increased HR, hypotension, decreased peripheral perfusion (slow capillary refill, pulses), ischemia of distal extremities (especially hands and feet) can lead to infarction, mottling, dysrhythmias (due to myocardial dysfunction))  neuro- confusion, loss of consciousness, coma if loss of blood flow occurs  renal- tubular ischemia (acute renal failure), urinary output low, electrolytes, BUN, creatinine, decreases excretion of medications (medication accumulation), kidneys cannot excrete lactic acid passing through and will worsen metabolic acidosis  hepatic- liver breaks down lactic acid, blood sugars (gluconeogenesis in liver), liver failing to filter bacteria (higher risk for infection), liver enzymes elevated  GI- ischemia, stress ulcers (lead to GI bleed), necrosis of small intestines, assess for bloody diarrhea, decreased ability to absorb nutrients from food, increased risk for DIC  irreversible/refractory stage o continued anaerobic metabolism o increased capillary permeability- marked edema (palpable or around organs) (fluid shift)- intravascular system decreases which can make shock worse o accumulation of lactic acid o more edema (internal and external) o cerebral ischemia is expected o profound hypotension, profound hypoxia, tachycardia, organ systems start to fail o recovery is unlikely o General care  oxygen- to increase oxygen supply and decrease body demand, cluster care to preserve oxygen  fluids- blood administration to increase hemoglobin, hemoglobin may look normal at first/slightly low (shift of fluid causes it to decrease, administration of fluid=hemodiluted=low Hcg and Hct); for septic, hypovolemic, and anaphylactic shock fluids are very important  2 large bore IVs  isotonic fluids (NS)- if liver is failing, LR cannot be broken down in the liver -> buildup of more lactate  too much fluids too fast -> fluid overload S/S (especially if they have HF components)  hypothermia may occur  albumin since it is a large molecule and cant cross capillary membrane  medications  to increase blood pressure (Levofed, dopamine, fenylephrine)- vasopressors  inotropic to help heart beat more effectively with larger output  vasodilators (nitroglycerine) to increase oxygen to heart muscle  nutrition  decrease mortality of shock  enteral nutrition within the first 24 hours if the gut is still functioning  parenteral is second choice  large weight gains attributed to large amounts of fluid (1kg=1L fluid) o assessment  tissue perfusion- capillary refill, peripheral pulses, urine output, VS (BP), may need invasive monitoring (CVP, A- line), LOC (especially cerebral tissue perfusion), skin color (cool and mottled= poor tissue perfusion) and temperature  history- events leading up to episode of shock, onset and duration of symptoms, treatments tried prior to hospitalization  allergies- anaphylaxis is a type of shock ▯ Classifications: types of shock (causes are different, body response is the same)  Cardiogenic (pump shock) o ability of heart to contract and pump blood to body is impaired o decreases oxygen and nutrients to tissues o causes: MI (most common, especially LV impairment), cardiomyopathy, severe hypertension, pericardial tampenade (pressure on heart effects ability to pump effectively), ventricular hypertrophy, dysrhythmias, disorders of the valves (Table 67-1 in book) o even with treatment, mortality rates are 50-85% o presentation  cardiovascular- high HR, hypertension, decreased capillary refill (due to decreased CO)  respiratory- tachypnea, pulmonary congestion, Swanz- Ganz catheter for pulmonary artery wedge pressure to get L atrial pressure, difficulty breathing  renal- increased water and sodium retention from renal blood flow is decreased -> urine output decreases  Skin- cold, clammy, pallor, cyanosis o medical management  correct underlying cause (If MI -> restore blood flow with cardiac cath, if valve problem -> fix valve, ect)  initiate first line treatment (oxygen), treat pain (from myocardial ischemia), hemodynamic monitoring, A-line started, pulmonary artery catheter inserted, central line inserted (for CVP)  labs- BNP (elevated), troponin and cardiac markers (elevated), BUN (elevated), EKG to assess myocardial damage, ST segment elevation may be present, chest x- ray, pulmonary infiltrates  fluid resuscitation is not as vital, fluids must be given very carefully  medications  dobutamine (inotropic)- increases CO, increased stroke volume, increases oxygen demand of heart (bad effect) -> chest pain  nitroglycerine (vasodilator)- dilates venous and arterial systems, improves oxygen delivery to myocardial delivery, watch for hypertension  dopamine- improves contractility of heart, increases heart rate, higher doses can cause vasoconstriction (increase systemic vascular resistance -> makes heart work harder to pump), may cause chest pain and ST segment elevation  norepinephrine (Levofed), vasopressin (vasoconstrictors)- increases cardiac workload, increases afterload, decreases perfusion to kidneys, lungs, GI tract, skin, decreases capillary refill, cold peripheral extremities  epinephrine- increases oxygen demands of heart  antiarrhythmic- Lopressor, amiodarone, Verapamil, Cardizem (diltiazem)… good for dysrhythmia that caused cardiogenic shock  circulatory assist devices (help the heart pump, not long term)  intra-aortic balloon pump  ventricular assist device  nursing management  prevention- ID at risk patients early (chest pain, heart attack, dysrhythmias, valve problems), conserve oxygen level, get supplemental oxygen, relieve angina, plan to treat patient  monitor hemodynamic status- a-lines, CVP, maintain equipment, document, report  enhance safety and comfort, reduce anxiety (increase oxygen to tissues)  monitor respiratory and renal status  position with head up (unless BP is high)  hypovolemic (low blood flow) o most common type of shock o decreased intravascular volume o absolute hypovolemia- GI loss (vomiting, diarrhea), hemorrhage, dialysis (fistula drainage), diabetes insipidus (excessive urine output), hyperglycemia (DKA), diuresis (too many diuretics) o relative hypovolemia- right amount of fluid is there but fluids moves into extravascular space, caused by fluid shift from burns or 3 spacing, internal bleeding, massive vasodilation, sepsis (increased capillary permeability) o response to acute volume loss depends on (ability to respond well)  extent of injury or insult  age: older patients  general state of health : healthy patient can compensate for 15% of blood volume, SNS occurs if >15% o presentation (all the same as others)  cardiac: decreased CO, decreased stroke volume, capillary refill slow, BP down, increased HR  pulmonary: initially respiratory rate increases, as it goes on respiratory rate decreases  renal: decreased  skin: cold, clammy, pallor  neuro: decreased mental status, anxiety, confusion, agitation, LOC  GI: decreased blood flow to GI tract, decreased bowel sounds o medical management  treat underlying cause  fluid and blood replacement (NS)  hemodynamic monitoring: BP (redistribution of fluids -> HOB flat and raise legs), HR, A-line, CVP  redistribution of fluids  labs: Hbg, Hct, lactate (going to be high from accumulation), urine specific gravity will be high (more concentrated), electrolyte abnormalities  pharmacology o nursing management  prevention  administer blood and fluid safely: monitor for adverse reactions, monitor for fluid volume overload  other: oxygen as needed, safety, comfort  distribution or circulatory o neurogenic  hemodynamic phenomenon when someone suffers injury (neurologic) -> loss of balance of sympathetic and parasympathetic nervous system  parasympathetic nervous system becomes dominant system -> vasodilation and bradycardia -> same effects as hypovolemic (insufficient tissue perfusion- like in all types of shock)  predisposing factors: number one cause is spinal injury, spinal anesthesia, disease of spinal cord, vasomotor center depression (caused by opioids, Benzodiazepines)  overstimulation (shock between PSNS and SNS) can last up to 6 weeks  presentation  same as other shock  decreased BP, bradycardia (because of PSNS stimulation), pulmonary dysfunction (more likely if higher on spinal cord-cervical), bladder dysfunction (from spinal cord injury), decreased urine output, initially skin is warm and flushed (vasodilation), at risk for hypothermia as heat disperses, body takes on temperature of room around them eventually, flaccid paralysis below level of spinal cord injury, loss of reflexes, bowel dysfunction  medical management  restore SNS function  fluids and medications  if caused by opioids -> give narcan  administer vasopressors to decrease vasodilation  administer atropine to increase HR  solumedrol to decrease spread of spinal cord damage  nursing management  positioning- elevate HOB at least 30 degrees after spinal or epidural anesthesia (to prevent spead of anesthesia up spinal cord)  immobilization the spinal cord after injury or suspected injury  cardiovascular support- anti-embolism stockings to prevent pooling in legs, elevate lower extremities, assess for DVT (most likely will be on heparin for prevention) passive ROM to promote circulation, monitor for internal injury which can lead to hypovolemic shock (ex: car accident)  neurologic support  neurogenic shock vs spinal shock  NOT the same thing  spinal shock is transient and may occur with neurogenic shock  Spinal shock is neurological activity below the level of an injury  Spinal shock is normally short term/temporary  Neurogenic shock is talking about what’s happening to the circulatory system  in spinal shock, patients experience the absence of all neurologic activity below the level of injury o anaphylactic  severe allergic reaction and a capillary leak caused by histamine  vasodilation and capillary permeability -> decreased CO -> decreased blood flow to organs  rapid hypotension  neurologic compromise (lack of blood flow)  respiratory distress (due to laryngeal edema or bronchospasm)  circulatory failure (from vasodilation and capillary leak)- leads to cardiac arrest  can occur after any exposure to allergen (topical, parenteral, inhalation, ingestion)– parenteral reactions are worse  pg 1635 table 67-3: presentation of shock  presentation  cardiovascular: 3 spacing, chest pain  pulmonary- SOB, edema of larynx and epiglottis, wheezing, stridor (listen to throat, its upper airway), runny nose  renal- may be incontinent  skin- flushing, pleuritis, angioedema (swelling of mouth and tongue- occludes airway, can be so bad they cant close mouth)  neurological- anxiety, confusion, feelings of impending doom, LOC changes  GI- swelling of lips and tongue, abdominal cramping/pain, nausea, vomiting, diarrhea  hemodynamics- decreased BP, increased HR, decreased CO, low CVP readings  respiratory and circulatory failure are the major risks  medical management  remove causative agent (first thing)  fluids: aggressive fluid replacement needs because of vasodilation and capillary permeability  medications: epinephrine IV (causes vasoconstriction and bronchodilation, apposes histamine), antihistamines (Benadryl IV to reverse effects of histamine, albuterol- bronchospasm), IV steroids (to help with hypotension if it persists after fluid replacement)  support cardiovascular and respiratory function: due to swelling… be prepared to give CPR, assess airway to see if they need to be intubated  nursing management  prevention- verify allergies, medical alert bracelet, observe for reactions if giving anything new, patent IV access so you can give fluids and medications  latex is the most severe and immediate reaction  medications  fluids o septic/SIRS  SIRS- systemic inflammatory response syndrome  usually the cause is not found o sepsis (most common type of distributive shock and is the most common cause of death in the ICU for non coronary patients) - systemic inflammatory response to infection  any type of bacteria or fungus can cause it o severe sepsis- sepsis plus organ dysfunction (mortality rate is almost 50%) o septic shock- sepsis plus hypotension plus tissue hypoxia even though you have normalized the fluid state  microorganisms invades body -> immune response -> poor tissue perfusion, increase cap permeability -> tissues and organs don’t get oxygen and nutrients  release of cytokines from immune response from infection that can active coagulation system -> greater risk for clots  presentation  cardiovascular- increase HR, bounding pulses, normal BP at first and will respond to fluids, but will decrease later and will not respond to fluids  pulmonary- low oxygen level, respiratory failure, ARDS, pulmonary hypertension (crackles), need ventilator support  renal- urine output decreases, renal failure  skin- warm and flushed at first from infection, then cool and mottled as it progresses and CO decreases  neurological- altered mental status, agitation, LOC decreases (maybe to point of coma), fever at first and then hypothermic as it progresses (body is overwhelmed)  GI- N/V, diarrhea, decreased bowel sounds (paralytic ileus)  hypermetabolism- increased serum glucose, cells to not respond as well to insulin (insulin resistance), greater risk of mortality if they become hypoglycemic (higher target blood glucose for sepsis to prevent hypoglycemia, to protect brain)  nursing management  cultures before starting antibiotics (start with broad spectrum until cultures come back)  aggressive fluid replacement is needed (NS so liver doesn’t have to break it down)  Xigris- given to patients with organ dysfunction to decrease body response to control events during shock, prevents coagulation to prevent clots (thromboembolic events); used as last resort  nutritional- if their nutrition is impaired they will be less likely to recover, give tube feedings over parenteral because gut absorbs it better and the risk for infection is lower (vascular infection)  be aware of risks to all patients (aseptic technique, monitor at risk sites to infection– IV, central lines, pressure ulcers)  collaborate with health team to ID site of infection  fever treatment- fever is the body’s way to kill bacteria, some hospitals wont treat temperature until it is very high  administer IV fluids and medications- antibiotics are very important and depend on causative agent  monitor kidneys and liver- acute liver or kidney failure, medications may be damaging liver and kidneys further, kidney and liver function tests, WBC count (increased from infection), in severe septic shock WBC and temp will be low, platelets may be low (cant give DVT prophylaxis), check coagulation studies (high PT and PTT from low platelet counts)  hemodynamic status  assess fluid status- rehydrate but do not fluid overload, strict I&O, daily weights  nutritional status- albumin to assess nutritional status because it assess protein, if we give IV albumin it keeps volume in the intravascular space because albumin molecules are big and will stay in the intravascular space  obstructive o decrease CO occurs because physical obstruction in the heart o physical obstruction to blood flow (returning to the heart or leaving the heart) o not due to heart structure problem o causes  tension pneumothorax  PE especially if it lodges in an artery and occludes it  superior vena cava syndrome- pressure that prevents blood from coming back to the heart, common with burns with abdominal compartment syndrome  thrombus of right ventricle that prevents blood to go to lungs o presentation  cardiovascular- low BP, CO decreased, JVD especially if its due to a clot, may lead to cardiac arrest, afterload is increased  pulmonary- increase respiratory rate especially with PE, shortness of breath, as it progresses the RR may go down  renal- decrease urine output  skin- cool, clammy skin from decrease CO  neurological- decreased cerebral perfusion, LOC changes, confusion, anxiety  GI- decreased or absent bowel sounds (ileus)  hemodynamic parameter- CVP may be high because blood is trying to get into heart and cant, same as with other shock o medical management  early recognition and treatment is primary strategy  superior vena cava syndrome- remove tumor, decompressive laparotomy with abdominal compartment syndrome ▯ MODS (multiple organ dysfunction syndrome)  Complication of any form of shock  organs are compromised and begin to fail  must have at least 2 organ system that are affected  usually the CNS is last to fail, heart and lungs are usually first  caused by decreased perfusion  most commonly seen with septic shock when it has progressed  advanced age, malnutrition, preexisting medical conditions  presentation o pulmonary- respiratory failure, trouble breathing, intubated and mechanically ventilated o metabolic- hypermetabolic state (increased insulin resistance), hyperglycemia, lactic acidosis o hepatic- liver function tests high o renal- BUN and creatinine high, creatinine clearance low, GFR low o hematologic- immunocompromised, aseptic technique is very important (any introduction to new pathogen is likely deadly) o cardiovascular- risk for clotting goes down, risk for bleeding goes up, all medication stop working, arrhythmias, pauses (on monitor) o neurological- decreased mental status, coma  medical management o prevention o early detection- subtle mental changes o control initiating event o chronic illness, malnourishes, surgical or trauma wounds, immunosuppressed are more likely to get to this point o promote adequate tissue perfusion o provide nutritional support  nursing management o same as septic shock o support and monitor organ perfusion o support family and keep them informed ▯ nursing diagnosis  ineffective tissue perfusion (NUMBER ONE): goal is to restore perfusion and prevent long term damage from hypo perfusion  anxiety (impending doom) nursing implementation  identify patients at risk  prevent it if able- monitor fluid balance (vomiting, bleeding, diarrhea), hand washing, aseptic technique, know kinds and causes of shock  neurological status- assess often and track subtle changes  cardiovascular- capillary refill, peripheral pulses, vitals  respiratory status- lung sounds, increased work of breathing, pulse ox decrease  renal- monitor urine output and kidney function tests  skin- temperature, pallor, flushing, cyanosis  GI- bowel sounds, ileus, bleeding  infection prevention- especially if patient cant do it themselves, oral care, general hygiene  musculoskeletal- passive ROM  psychological care- patient may have fear or anxiety, important to address it because it may aggravate respiratory or cardiac status ▯ ▯


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