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Cc 9 shock 2
Critical Care (408)
Loma Linda University
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Shock Compensatory Stage inadequate systemic O delivery activate autonomic responses to maintain systemic O delivery sympathetic nervous system norepinephrine, epinephrine, dopamine, cortisol release causes vasoconstriction, ↑HR, ↑contractility CO renin-angiotensin axis Na+ & H2O conservation & vasoconstriction ↑ BV & BP
homeostatic mechanisms kick in. body still able to maintain CO, BP, and tissue perfusion
Progressive Stage cellular responses to ↓ systemic O2 delivery ATP depletion ion pump dysfunction cellular edema hydrolysis of cellular membranes & cellular death endothelial inflammation & disruption inability of O2 delivery = demand result lactic acidosis ( metabolic acidosis) CV insufficiency ↑ metabolic demands ( acidosis) body can’t keep up. not enough O2 to cells switch from aerobic to anaerobic metabolism. acidosis, vasodilation, inflammatory mediators, SIRS. every system affected. cells start to die
Refractory Stage progression of physiologic effects as shock ensues cardiac depression respiratory distress renal failure DIC result: end organ failure death
unresponsive to treatment & irreversible. organs start to die MODS. death d/t ineffective tissue perfusion and circulatory system unable to meet body’s demands
inadequate oxygen delivery to meet metabolic needs global tissue hypoperfusion & metabolic acidosis metabolic acidosis = accumulation of lactic acid Initial Stage of Shock CO ↓ reason varies by type of shock tissue perfusion threatened Approach to the Patient in Shock – ABCs cardiorespiratory monitor pulse oximetry supplemental oxygen IV access ABG, labs foley catheter vital signs including temperature
Diagnosis physical exam v/s mental status skin color temperature pulses hemodynamics infectious source labs CBC chemistry lactate coagulation studies cultures ABG
Estimate BP by Pulse
if you palpate a pulse, SBP is at least that number
carotid: 60 radial: 70 femoral: 80 pedal: 90
Goals of Treatment (ABCDE) Airway control WOB respiratory muscles consume a significant amount of O mechanical vent & sedation decreases WOB & improves survival optimize Circulation maintain adequate O2 Delivery achieve End points of resuscitation
Treatment – Maintain O Delivery ↓ O2 demand provide analgesia & anxiolytics (anti- anxiety) to relax muscles and avoid shivering maintain arterial O saturation/conte nt give supplemental oxygen Hgb >10 g/dL serial lactate levels or central venous oxygen saturation (ScvO2) to assess tissue oxygen extraction ScvO2 – from central line
Treatment – End Points of Resuscitation goal of resuscitation: maximize survival & minimize morbidity use objective hemodynamic & physiologic values to guide therapy goal directed approach UOP > 0. mL/kg/hr CVP: 8- mmHg if intubated MAP: 65 – 90 mmHg central venous oxygen concentration (ScvO2) > 70%
Hypovolemic Shock Cardiogenic Shock inadequate intravascular fluid volume most common type of shock loss of circulating volume (decreased preload) decreased SV & decreased CO inadequate cellular O2 supply & ineffective tissue perfusion ↑HR | ↓BP | ↓CO | ↑SVR | ↓CVP | ↓PAOP
SBP < 90
mmHg CI < 2 L/ m/m PAOP > 8mmHg
ischemia loss of left ventricle function lose 40% of LV clinical shock ensues ↓CO lactic acidosis & hypoxia ↓stroke volume (SV) tachycardia as compensation ischemia & infarction worsens heart can’t pump blood forward ↑HR | ↓BP | ↓CO | ↑SVR | ↑CVP | ↑PAOP Non-Hemorrhagic vomiting diarrhea dehydration bowel obstruction pancreatitis burns neglect environmental
Hemorrhagic GI bleed trauma massive hemoptysis coughing up blood abdominal aortic aneurysm (AAA) rupture ectopic pregnancy post-partum bleeding
Etiology – Causes of Cardiogenic Shock acute MI sepsis myocarditis myocardial contusion aortic or mitral stenosis acute aortic insufficiency
Signs/Symptoms cool, mottled skin tachypnea hypotension altered mental status narrowed pulse pressure crackles (rales) murmur
Evaluation/Diagnostic Labs CBC ABG/lactate electrolytes BUN, creatinine coagulation studies blood type & cross match As indicated X-ray: CXR, pelvic x-ray CT: abd/pelvis, chest GI endoscopy bronchoscopy vascular radiology
Nursing Actions ABCs establish 2 large bore IVs or central line crystalloids normal saline or LRs > 3L packed RBCs (PRBCs) O negative or cross matched control any bleeding if hemorrhagic arrange definitive treatment
Diagnostic Tests EKG chest x-ray (CXR) CBC chemistry (chem 10) cardiac enzymes coagulation studies
Treatment Goals treat underlying cause enhance effectiveness of heart pump improve tissue perfusion Nursing Actions revascularization procedure for MI patients medications inotrope diuretic antidysrhythmic maintain airway/oxygenation intra-aortic balloon pump (IABP) Anaphylactic Shock Neurogenic Shock Septic Shock Anaphylaxis severe systemic hypersensitivity reaction multisystem involvement IgE mediated Anaphylactoid Reaction indistinguishable from anaphylaxis do not require a sensitizing exposure not IgE mediated
loss or suppression of sympathetic tone least common type of shock most common cause: spinal cord injury (SCI) higher cord injuries > likelihood of shock can be caused by anything that disrupts SNS ↓HR | ↓BP | ↓CO | ↓SVR | ↓CVP | ↓PAOP
Sepsis > SIRS criteria (systemic inflammatory response syn) temp >38C or <36C (>100 or <96) HR > RR > presumed existence of infection blood pressure can be normal
asthma previous anaphylaxis
Reoccurrenc e rates 40-60% insect sting 20-40% radiocontrast agents 10-20% penicillin
Common Causes antibiotics (drugs) insects food
flushing urticaria (hives/rashes) Next throat fullness anxiety chest tightness shortness of breath lightheadednes s Finally altered mental status (ALOC) respiratory distress circulatory collapse
treat hypothermia coagulation studies liver function test (LFT), lipase, UA ABG, VBG (venous blood gas?), lactate blood culture x2, urine & sputum culture chest x ray (CXR) foley catheter Treatment Goals control infection reverse pathophysiologic responses promote cardiovascular, pulmonary, metabolic support Nursing Actions sepsis bundle – 3- & 6-hour bundles check lactate level initial bolus of 30mL/kg for HypoTN or lactate > maintain tissue/organ perfusion w/ fluids, vasopressors, positive inotropes achieve CVP 8-12mmHg monitor ScVO2 – maintain >70% packed RBCs or dobutamine mechanical ventilation for oxygenation low volume low PEEP sedation antibiotics pan culture before antibiotics! panculture: blood culture x2, sputum, urinanalysis, wound, intravascular catheters low dose corticosteroids only for pts who are hypotensive after fluids & vasopressors aggressive glucose control maintain <150mg/dL IV infusion if necessary nutritional support high caloric needs d/t hypermetabolic state enteral (tube) preferred over parenteral (TPN)
Septic Shock - Nurse Driven Sepsis Protocol early identification & treatment of sepsis Procalcitonin (PCT) used to determine systemic bacterial infections normal PCT < 0 PCT > associated w/ systemic infections procalcitonin markedly elevated (up to 5000x) w/in 2-4hrs in severe forms of systemic inflammation or bacterial infections level persists until recovery
Diagnostics clinical diagnosis airway compromise hypotension involvement in cutaneous (skin), respiratory, or GI systems drug, food, insect exposure labs have no role Treatment ABCs angioedema & respiratory compromise require immediate intubation IV, cardiac monitor, pulse oximetry IV fluid supplemental oxygen epinephrine important in treatment vasopressor & beta2 response causes bronchodilation second line med treatment corticosteroid H1 & H2 blockers
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neurogen ic septic ↑
Cc 9 shock 2
Course: Critical Care (408)
University: Loma Linda University
