T10: Shock Flashcards
shock
characterized by decrease tissue perfusion and impaired cellular metabolism; imbalance in supply/demand for O2 and nutrients
early signs of shock
NORMAL BP, INCREASED HR, NORMAL skin color, COOL/MOIST skin temperature, anxious, INCREASE RR with INCREASED depth
late signs of shock
LOW BP (lower than 90mmHg systolic), INCREASED HR weak and thready, PALE skin, COLD skin temperature, coma, INCREASED RR with shallow breaths
hypovolemic shock
shock state caused by internal or external blood or fluid loss
Absolute hypovolemia
complete loss of intravascular fluid volume
o Ex: hemorrhage, Gi loss (vomiting, diarrhea), diabetes insipidus, hyperglycemia, diuresis
Relative hypovolemia
termed “third spacing” results when fluid moves out of the vascular space into the extravascular space (fluid is still in the body)
o Ex: leaking of fluid like in burns
clinical manifestations of hypovolemic shock
o Anxiety
o Dry mucous membranes, tenting
o Tachypnea
o Increased in CO, heart rate
o Decrease in stroke volume, PAWP, UO
o If volume loss is >30%, decompensation blood volume needs replacing
diagnostics for hypovolemic shock
o Serial measurements of hemoglobin and hematocrit levels, electrolytes, lactate, blood gases, central venous oxygenation (SvO2), and hourly urine outputs.
o DAILY WEIGHTS
o I&Os
interventions for hypovolemic shock
o Management focuses on stopping loss of fluid and restoring the circulating volume
o Fluid resuscitation
how is fluid resuscitation calculated
a 3:1 rule (3 mL of isotonic crystalloid for every 1 mL of estimated blood loss)
cardiogenic shock
decreased filling of the heart will result in decreased stroke volume, systolic dysfunction is the hearts inability to pump the blood forward; ULTIMATELY COMPROMISED CO due to the hearts inability to maintain CO needed to meet body needs
clinical manifestation of of cardiogenic shock
o Tachycardia
o Hypotension
o Narrowed pulse pressure
o ↑ Myocardial O2 consumption
o Pallor and cool, clammy skin
o Decreased cap refill
o Anxiety, confusion, agitation
o ↑ pulmonary artery wedge pressure
o Decreased renal perfusion and UO
goal for cardiogenic shock
to restore blood flow to myocardium by restoring balance between O2 supply and demand
interventions for cardiogenic shock
o Angioplasty with stenting, Emergency revascularization, Valve replacement
o Hemodynamic monitoring
o Drug therapy
o Circulatory assist devices-Decrease SVR and left ventricular workload
drug therapy for cardiogenic shock
- Nitrates to dilate coronary arteries
- Diuretics to reduce preload
- Vasodilators to reduce afterload
- β-adrenergic blockers to reduce HR
types of distributive shock
neurogenic, anaphylactic, septic
neurogenic shock
occurs most commonly in clients with injuries of spinal cord T5 OR ABOVE. Massive a VASODILATION leading to pooling in vessels, tissue hypoperfusion, and ultimately impaired cellular metabolism
clinical manifestations of neurogenic shock
- HYPOTENSION AND BRADYCARDIA
- Inability to regulate body temperature (resulting in heat loss)
- Dry skin
- Poikilothermia: taking on temperature of the environment
interventions for neurogenic shock
- In spinal cord injury: spinal stability
· Spinal precautions, cervical stabilization with a collar - Treatment of hypotension and bradycardia with vasopressors and atropine
- Monitor for hypothermia
anaphylactic shock
acute, life-threatening hypersensitivity (allergic) reaction causing massive vasodilation, release of vasoactive mediators and increased capillary permeability
clinical manifestations of anaphylactic shock
- Anxiety, confusion, dizziness
- Sense of impending doom
- Chest pain
- Incontinence
- Swelling of lips and tongue, angioedema
- Wheezing, stridor due to laryngeal edema
- Flushing, pruritus, urticaria
- Respiratory distress and circulatory failure
intervention for anaphylactic shock
- First strategy is PREVENTION
- Epinephrine IM is first drug of choice
- Diphenhydramine, ranitidine given as adjunctive therapies to block the ongoing release of histamine from the allergic reaction.
- Maintain a patent airway
- Aggressive fluid replacement as hypotension results from leakage of fluid out of the intravascular space int o the interstitial space
· Usually crystalloids - IV corticosteroids if significant hypotension persists after 1-2 hours of aggressive therapy
septic shock
presence of sepsis with hypotension despite fluid resuscitation, presence of inadequate tissue perfusion resulting in hypoxia
sepsis
systemic inflammatory response to a suspected infection causes damage to its own tissues
severe sepsis
sepsis + organ dysfunction
clinical manifestations of septic shock
- ↑ Coagulation and inflammation
- ↓ Fibrinolysis
· Formation of microthrombi
· Obstruction of microvasculature - Hyperdynamic state: increased CO and decreased SVR
· Vasodilation
· Maldistribution of blood flow
· Myocardial dysfunction (Decreased ejection fraction, Ventricular dilation)
-Tachypnea/hyperventilation
- Results in respiratory alkalosis
- ↓ Urine output
- Altered neurologic status
- GI dysfunction, GI bleeding, paralytic ileus
intervention for septic shock: fluids
Fluid replacement to restore perfusion (usually 30-50mL/kg is done wit isotonic crystalloids, albumin may be added)
intervention for septic shock: drugs
- vasopressors may be added
· Drug of choice is norepinephrine - Exogenous vasopressin for patients refractory to vasopressor therapy
IV corticosteroids - Antibiotics
If the patient remains hypotensive after initial volume resuscitation with minimally 30 ml/kg…
vasopressors may be added
intervention for septic shock: glucose levels
keep Glucose levels <180 mg/dL
intervention for septic shock: stress ulcers
prophylaxis with proton pump inhibitors (e.g., pantoprazole [Protonix])
intervention for septic shock: DVTs
prophylaxis (e.g., heparin, enoxaparin [Lovenox])
obstructive shock
physical obstructed blood flow with decreased CO
Causes of obstructive shock
Restricted diastolic filling of right ventricle from compression, superior vena cava syndrome or abdominal compartment syndrome, cardiac tamponade, tension pneumothorax, pulmonary embolism
clinical manifestations of obstructive shock
o Decreased CO, increased afterload
o JVD
o Pulsus paradoxus
interventions for obstructive shock
o Primary strategy is early recognition and treatment to relieve obstruction
- Mechanical decompression (for pericardial tamponade, tension pneumothorax, and hemopneumothorax may be done by needle or tube insertion)
- Thrombolytic therapy (for pulmonary embolism)
- Radiation, debulking, or removal of mass
- Decompressive laparotomy (for abdominal compartment syndrome or for patients with high intraabdominal pressure)
nursing management for shock: focused assessment of tissue perfusion
o Vital signs, peripheral pulses, level of consciousness, capillary refill, skin (e.g., temperature, color, moisture), urine output
what position should not be used for hypotention
o Do not treat hypotension with Trendelenberg position
- Lessens resp effectiveness, Increased ICP
Urine output of ___ may indicate inadequate perfusion of the kidneys.
<0.5 mL/kg/hr
nursing management for shock: personal hygiene status
o Perform bathing, nursing measures carefully
o Turn every 1 to 2 hours
o Passive/active range of motion
Stages of Shock: Initial
not usually clinically apparent;
o Metabolism changes at cellular level from aerobic to anaerobic
- Lactic acid builds up and must be removed by the liver
- Process requires O2, but unavailable due to decreased tissue perfusion
Stages of Shock: Compensatory
decreased CO triggers neural, hormonal, & chemical mechanisms to restore tissue perfusion
- impaired GI motility and compensation fro changes in tissue perfusion
o Cool clammy skin, except for septic patient who is warm and flushed
o ↓ Blood to kidneys activates renin-angiotensin system
Stages of Shock: Progressive
compensatory mechanisms begin to fail, organ perfusion decreased
Stages of Shock: Progressive (neuro)
o Mental status changes (this is an important finding in this stage)
Stages of Shock: Progressive anasarca
diffuse profound edema
- Fluid leakage from vascular space affects solid organs and peripheral tissues
- ↓ Blood flow to pulmonary capillaries
Stages of Shock: Progressive (sustained hypoperfusion)
- Weak peripheral pulses
- Ischemia of distal extremities
Stages of Shock: Progressive (cardiac)
o Myocardial dysfunction results in
- Dysrhythmias
- Myocardial ischemia-Possible myocardial infarction
- End result: complete deterioration of cardiovascular system
labs for cardiac
electrolytes, ECG, O2 sat, ck-mb, troponin, BNP
Stages of Shock: Progressive (respiratory)
o With further increases in capillary permeability, the fluid moves TO THE ALVEOLI, with resultant alveolar edema and a decrease in surfactant production.
- Pulmonary edema-Bronchoconstriction-↓ Functional capacity
- Edema-Decreased surfactant-Worsening V/Q mismatch
Stages of Shock: Progressive (respiratory clinical manifestations)
tachypnea, crackles, and increased work of breathing
labs for respiratory
CXR, O2 sat, ABG’s, VQ scan
Stages of Shock: Progressive (renal)
o prolonged hypoperfusion is renal tubular ischemia
- May result in acute kidney injury (which can be worsened by nephrotoxic drugs)
- Decreased urine output
- Elevated BUN and serum creatinine
- Metabolic acidosis (occurs from the kidneys inability to excrete acid and reabsorb bicarbonate)
Stages of Shock: Progressive (liver)
o fails to metabolize drugs and waste
- Jaundice (results from accumulation of bilirubin)
- Elevated enzymes (ALT, AST, GGT)
- Loss of immune function
- Risk for DIC and significant bleeding
Stages of Shock: Refractory
multiple organ system failure d/t failure of compensation leading to gross vasodilation
most people at this point the pt is multisystem organ failure leading to death
(ominous outcome as failure of liver, lungs, and kidneys will result in accumulation of waste products such as lactate, urea, ammonia, and carbon dioxide.)
interprofessional care for shock: O2
INCREASE oxygen and ventilation supply
o Optimize CO with fluid replacement or drugs
o Increase hemoglobin by transfusion
o Increase arterial oxygen with supplemental oxygen and mechanical ventilation
interprofessional care for shock: volume expansion
o NEED one or two large-bore IV catheters (14-16 gauge), intraosseous access device, or central venous catheter
o Isotonic crystalloids (e.g., normal saline, lactated Ringers) and colloids (e.g., albumin)
fluid responsiveness is determined by
Vital signs (automatic BP cuff of arterial catheter), cerebral and abdominal pressures, capillary refill, skin temperature, urine output
Two major complications of large volumes
-Hypothermia
-Coagulopathy
if Persistent hypotension after adequate fluids
Vasopressor may be added
· norepinephrine [Levophed], dopamine [Intropin]) and/or an inotrope like dobutamine [Dobutrex]
fluid resuscitation
-Warm crystalloid and colloid solutions
-Replace clotting factors (because packed RBCs do not contain clotting factors)
Goal of drug therapy – correct low tissue perfusion
- Vasopressor drugs (e.g., norepinephrine)
- Achieve/maintain MAP >60 to 65 mm Hg
- Reserved for patients unresponsive to fluid resuscitation
- Continuously monitor end-organ perfusion
Start enteral nutrition within
first 24 hours
Start trophic feeding at
slow drip of small amounts of enteral nutrition (10mL/hr)
