7577788
Descripción
Fichas por Kristi Breese, actualizado hace más de 1 año
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Creado por Kristi Breese
hace casi 8 años
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| Pregunta | Respuesta |
| Shock | -A syndrome characterized by decreased tissue perfusion and impaired cellular metabolism. -Results in an imbalance between the supply and demand for O2 and nutrients. |
| Etiology/Patho of Systemic Inflammatory Response Syndrome | Response to a variety of insults (sepsis, ischemia, infarction & injury) |
| Clinical manifestations of SIRS | Depends on the organ. It is a generalized inflammation in organs remote from the site of initial insult. |
| SIRS is Manifested by 2 or more of the following: | -T>38 C (100.4 F) or < 36 C (96.8 F) -HR > 90 bpm -RR > 20 or PCO2 < 32 mm Hg -WBC > 12,000, or < 4,000 or > 10% bands |
| What do we need to maintain BP & perfusion? | -Adequate cardiac pump -Adequate vasculature or circulatory system -Sufficient blood volume |
| 4 categories of shock | 1. Cardiogenic 2. Hypovolemic (absolute or relative) 3. Distributive (neurogenic, anaphylactic, septic) 4. Obstructive |
| Types of cardiogenic shock | -Compromised CO r/t systolic or diastolic dysfunction -Dysrhythmias -Structural factors |
| Symptoms of cardiogenic shock | -Early presentation similar to decompensated HF. -↑ HR, SVR, pulmonary pressures -↓ B/P, CO (< 4L/min), urine output - +/- CP, Tachypnea, crackles, cyanosis, diaphoretic, poor cap refill, weak pulses, anxiety, confusion. |
| Outcomes of cardiogenic shock | Mortality rate of 60% despite aggressive Rx |
| Causes of cardiogenic shock | -Acute MI – most common cause of systolic dysfunction -Trauma -Cardiomyopathy -Brady or Tachydysrhythmias -Severe valve stenosis or regurgitation |
| Collaborative care of cardiogenic shock | -Restore blood flow to the heart by balancing supply and demand of oxygen. -Cardiac Cath with angioplasty or stent -Thrombolytic Therapy -Medications (oxygen, nitrates, inotropes, β blockers, anti-dysrhythmics) -IABP or VAD -Serial assessments and monitoring |
| As cardiogenic shock progresses.. | -Hypovolemia is generally not an issue -What kind of pressors? -Consider Nitroglycerine or nitroprusside drips – how will these help? Works on decreasing the afterload |
| IABP | -30 mL balloon sits in aorta -Inflates during diastole -Deflates during systole |
| LVAD | -Often used in patients awaiting heart transplantation -Pulls blood from the apex of the LV and sends out to ascending aorta |
| Systolic BP less than 90 and MAP less than 60 | Your patient is in shock |
| Hypovolemic shock | Defined as a loss of intravascular fluid volume |
| Symptoms of hypovolemic shock | -↓ B/P, CVP, preload, SV, UO, cap refill -↑ HR, SVR -Pallor, tachypnea, anxiety, confusion, agitation |
| Outcomes of hypovolemic shock | -Will attempt to compensate -Depends on severity of volume depletion and time frame. (how much and how fast is volume lost!) |
| Absolute hypovolemia | -External loss of whole blood (hemorrhage from trauma, surgery, GI, bleeding) -Loss of other body fluids: vomiting, diarrhea, diuresis (excessive), DI & DKA |
| Relative hypovolemia | -Pooling of blood or fluids (bowel obstruction) -Fluid shifts (burns, ascites) -Internal bleeding (fracture of long bones, ruptured spleen, lac liver, hemothorax, pancreatitis) -Massive vasodilation |
| Hypovolemic Shock Interventions | -ABCs -Stabilize airway -Supplemental O2 -2 large bore IVs -Fluid resuscitation (isotonic crystalloids, colloids - blood & blood components) -Diagnostics (imaging & labs) -Definitive tx to stop hemorrhage or prevent fluid loss (ex: surgery) |
| Anaphylactic shock | Defined as an acute life-threatening hypersensitivity reaction to a sensitizing substance (e.g. drug, chemical, vaccine, blood, food, venom). |
| Symptoms of anaphylactic shock | -↓B/P, ↑ HR, massively decreased SVR -Flushing, angioedema, itching, anxiety, dizziness, chest pain, incontinence, swelling of the lips and tongue, laryngospasm, wheezing, stridor, respiratory compromise |
| Outcomes of anaphylactic shock | Depends on how quickly treatment begins |
| Collaborative care of anaphylactic shock | -Prevention -Epinephrine -Benadryl -Patent Airway -Bronchodilators -Fluids -Steroids -H2 Blockers |
| How will we know when our patient with anaphylactic shock is improving? | -Increase BP -Improved breathing -Decreased HR -Less anxiety |
| Sepsis | The systemic inflammatory response to infection. Manifestations are the same criteria for SIRS in the presence of infection. |
| Septic shock | Sepsis induced hypotension and hypoperfusion despite adequate fluid resuscitation |
| Severe sepsis | Sepsis associated with organ dysfunction, septic shock. May include acidosis, oliguria, altered LOC |
| Septic shock defined | Sepsis is the human body’s systemic inflammatory and coagulopathic response to suspected or confirmed infection. It is a life-threatening illness that often progresses to a severe form manifested by multiple organ failure and death. This can occur even after the primary infection or primary insult has been treated successfully. |
| Outcomes of septic shock | -Mortality rates 28% - 50% despite aggressive Rx. Greater with Gram negative (–) organism. -Sepsis is the leading cause of death in non-coronary adult ICUs in the US. -Sepsis is the 6th leading cause of death overall. -Studies show that more than 750,000 Americans develop severe sepsis each year, at a rate of more than 2,000 new cases each day. -Sepsis is the most common cause of shock we will encounter as nurses. |
| Who's at risk for septic shock? | -Those older than 65 years old -Neonates -Immunocompromised patients -Individuals who have undergone invasive procedures -Individuals with specific types & sites of infections -Prior antibiotic therapy -Critically ill patients -Genetic predisposition (esp polymorphism of TNF-2) |
| What infections put us most at risk for septic shock? | -The lung, the abdomen & the urinary tract -Skin infections, IV & central catheters |
| How will we know when our interventions are successful in hypovolemic shock? | -Increase BP -Decrease HR -Improvement of cap refill -Increase of UO -Improvement in mental status -Improvement in skins |
| Early sepsis | -Usually + temperature -Hyperventilation, tachypnea -Respiratory alkalosis -Decreasing UO -Warm, flushed, moist skins, including ext -Increased cardiac output -Altered LOC |
| Late sepsis | -Myocardial dysfunction -Decreased EF -Respiratory failure, ARDS -Decreased UO -Delayed CFT -GI Bleed, paralytic ileus -Cool and mottled – remember cold shock is dead shock! |
| Collaborative care of septic shock | -Airway management -Fluids – usually crystalloids (NS) -Vasopressors – levophed (norepi), vasopressin, neosynephrine (or all 3!) -Antibiotics -Hemodynamic monitoring -Daily Labs -Nutritional therapy |
| Collaborative care of septic shock (cont) | -No Single Dx Study – individualize! -H & P very important (URI, Surgery, Chest pain, Trauma). -Labs, Labs, Labs! Cultures! -Lactate levels -12-Lead EKG -Hemodynamic monitoring (including CO). -Pulse Oximetry – but where to monitor?? |
| Obstructive shock | Develops when a physical obstruction impeding the filling or outflow of blood flow occurs -> resulting in a decrease in CO. |
| Causes of obstructive shock | Cardiac tamponade, tension pneumothorax, abdominal compartment syndrome, massive pulmonary embolism. |
| Stages of shock | -Compensatory stage -Progressive stage -Refractory stage |
| Compensatory stage of shock | -Body activates neural, hormonal, and biochemical compensatory mechanisms to overcome consequences of anaerobic metabolism. -Drop in blood pressure with an immediate response by carotid and aortic baroreceptors to activate SNS – increased HR and vasoconstriction is the most common response. |
| Manifestations of the compensatory stage | -Oriented x 3, but restless, apprehensive -Shunting of blood to heart and brain -Increase in myocardial contractility and HR -Normal or slightly decreased BP -Decreased blood flow to lungs -Decrease GI blood supply -Decreased renal blood flow (renin, aldosterone and ADH up) |
| Progressive stage of septic shock | -This stage begins as the compensatory mechanisms fail. -Aggressive interventions are necessary to prevent MODS. -Continued ↓ in cellular perfusion → cap permeability. -Anasarca develops. -Lungs usually first to show critical dysfunction. -Cardiovascular collapse – decrease in coronary and peripheral perfusion. -Metabolic acidosis -Renal failure. -GI Dysfunction cont. (GIB) -Increase liver enzymes, altered drug and waste metabolism -DIC (Disseminated intravascular coagulation). |
| Spotting DIC in lab results | |
| The paradox of DIC | -Both a bleeding and thrombotic disorder -ALWAYS a complication of another disorder – usually massive trauma, sepsis, an OB emergency, or metastatic cancer. -Underlying condition triggers proinflammatory cytokines which activates the clotting cascade causing microclots to form within the capillaries. |
| DIC | -We begin to see widespread microvascular coagulation. All the systemic clotting factors are being used up at microvascular level. Liver and bone marrow can’t keep up. No clotting factors left for periphery~~Bleeding everywhere! -Decreased H/H, platelet count and fibrinogen levels -D-dimer up, PT/INR up, Fibrin split (or degradation) products up |
| Nursing Interventions in DIC | -ABCs and ongoing assessment, INO -Administer volume NS, packed cells -Clotting products as needed include FFP, cryoprecipitate, platelets -Pressor infusions if continues hypotensive AFTER fluids -In some cases, heparin may be given -Coags every four hours – compare with baseline -Avoid needle sticks, interventions if possible |
| Refractory stage of shock | -During this final stage of shock: ↓perfusion from peripheral vasoconstriction & ↓ C.O. exacerbate anaerobic metabolism -->Low BP -Lactic acid leads to cap permeability and loss of vascular fluid -->Edema -Profound hypotension and hypoxemia. -Continued organ failure. -Body is in overwhelmed! -Hypothermia can occur Remember: COLD SHOCK IS DEAD SHOCK!! |
| Nursing management of shock | -Adequate tissue perfusion -Restoration of normal or baseline VS -Return/recovery of organ function & avoidance of complications from prolonged hypoperfusion. -Verify patient’s wishes |
| Multiple organ dysfunction syndrome (MODS) | -The failure of 2 or more organ systems in a acutely ill patient such that homeostasis cannot be maintained without interventions. Direct result of SIRS combined with co-morbid infection -Clinical manifestations depends on the organ |
| So what do we do? (MODS) | -Prevent! Any way we can!! -Identify early! Know your patient! Establish a baseline so you can identify subtle changes in status! -Assess, re-assess, re-assess! -Careful administration of medications -Collaborate with healthcare team -Don’t forget skin and nutrition concerns! |
| Normal Lab Values - BMP Na+ K+ Ca++ Cl- BUN Cr Glu | Na+ 135-145 K+ 3.5-5.0 Ca++ 8.5-10 Cl- 95-107 BUN 7-20 Cr 0.5-1.2 Glu 65-110 |
| Normal Lab Values - CBC WBC RBC Hgb Hct Platelet | WBC 4-11 RBC 3.5-6 Hgb 11.5-17.6 Hct 35-49 Platelet 150-400 |
| Normal Lab Values - ABGs pH PaCO2 PaO2 HC03 SaO2 Base Excess (BE) | ph 7.35-7.45 PaCO2 35-45 Pa02 80-100 (60) HCO3 22-26 SaO2 >90 BE +/-2 |
| Normal Lab Values - Liver Fx Tests Protein Albumin Bilirubin ALT AST Ammonia | Protein 6-8.4 Albumin 3.5-5.5 Bilirubin 0.3-1 ALT 10-35 AST <35 Ammonia 15-45 |
| Normal Lab Values - Coag Studies PTT PT INR | PTT 25-35 sec PT 11-15 sec INR 0.9-1.2 (2-3 for therapeutic) |
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