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:explode:Shock :explode: (COLLABORATIVE CARE (Primary goal of drug therapy…
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Shock
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Stages
Non-Progressive / Compensatory
Clinically Apparant Compensatory Mechanisms
Neural
Hormonal
Biochemical
To Overcome Anaerobic consequences and Maintain Homeostasis
MAP decreases by 10-15 mm Hg
Tissue Hypoxia in Nonvital Organs
Acidosis and Hyperkalemia
To prevent progression: stop conditions that started shock and intervene supportively
Carotid/Aortic baroreceptors
Activate SNS d/t decreased BP
Vasoconstriction while maintain blood to Vital Organs
Decrease blood flow
To kidneys
RAAS activated
Increased Venous return to heart
To skin
Cool and clammy - Except Septic (warm and flushed)
Impaired GI motility
Risk for Paryltic Ileus
Perfusion Deficit
Corrected --> Recovery w/ no Residual Sequelae
Not Corrected --> Enter Progressive Stage
Progressive
liver fails to metabolize
jaundice, increase enzymes, loss of immune function, risk for DIC and significant bleeding
hypoperfusion of kidneys
acute kidney injury
pt. will need dialysis
GI system
ulcers, bleeding, risk of translocation of bacteria, decreased ability to absorb nutrients
decreased CO2
decreased peripheral perfusion, hypotension, weak peripheral pulses, ischemia of distal extremities
Initial
Metabolism: Aerobic --> Anaerobic
Lactic Acid accumulates and must be removed by blood; broken down by liver
Requires O2
MAP decreased by <10 mm Hg
HR and RR increased/slight increase in Diastolic BP
Increased HR = Adaptive responses of Vascular Constriction
Usually not clinically apparent
Irreversible/Refractory
Accumulation of lactic acid
Manifestations
rapid loss of consciousness
non palpable pulse
cold, dusky extremities
slow, shallow respirations
Profound hypotension
unmeasurable oxygen saturation
Recovery is unlikely
hypoxemia
tachycardia worsens
failure to one organ system affects others
increased capillary permeability
Exacerbation of anaerobic metabolism
Widespread abnormal cellular metabolism; Imbalance in O2/nutrient Supply/Demand
Oxygenation and tissue perfusion needs not met; Can be caused by any problem impairing O2 delivery;
Syndrome:
decreased tissue perfusion
impaired cellular metabolism
"whole-body" response
Classifications
Distributive
Blood volume distributed to interstitial tissues where it cannot circulate or deliver oxygen;
Cause
loss of sympathetic tone, blood vessel dilation, pooling of blood in venous and capillary beds or capillary leak
Neurogenic
Can occur in response to
spinal anesthesia
; Results in
massive vasodilation
, leading to
pooling of blood in vessels
Clinical Manifestations
Hypotension, Bradycardia, Temperature dysregulation (heat loss), Dry Skin,
Poikilothermia
(taking on temperature of environment)
Hemodynamic phenomenon; Can occur
within 30 mins of spinal cord injury at T5
vertebra or above;
Can last up to 6 weeks
COLLABORATIVE CARE
In spinal cord injury = spinal stability; Treatment of the
hypotension and bradycardia with vasopressors and atropine
; Fluids used cautiously as hypotension generally is not related to fluid loss;
Monitor for hypothermia
Chemical
Sepsis
Clinical Manifestations
Increase coagulation and inflammation, Decreased fibrinolysis (Formation of miclothormbi & Obstruction of microvasculature) Hyperdynamic state: Increased CO and decreased SVR
Physical Clinical Manifestations
Tachypnea/Hyperventilation, Temperature dysregulation, Decreased urine output, Altered neurologic status, GI dysfunction, Respiratory failure is common
3 Major pathophysiologic effects
Vasodilation, Maldistribution of blood flow, Myocardial depression (decreased ejection fraction & ventricular dilation)
Systemic inflammatory response to documented or suspected infection; Severe sepsis = sepsis & organ dysfunction; Presence of sepsis with hypotension despite fluid resuscitation; Presence of inadequate tissue perfusion resulting in hypoxia
COLLABORATIVE CARE
Fluid Replacement to restore perfusion (hemodynamic monitoring) Vasopressor drug therapy, Vasopressin for patient refractory to vasopressor therapy; IV corticosteroids for patients who require vasopressor therapy, despite fluid resuscitation, to maintain adequate BP; Antibiotics after cultures are obtained (Blood, wound exudate, urine, stool, sputum) Broad-spectrum antibiotics are given first ; More specific antibiotics are then given based on the organism identified; Glucose levels <180 mg/dL; Stress ulcer prophylaxis with H2 receptor blockers; DVT prophylaxis with low dose unfractionated heparin or lo molecular weight heparin
Capillary leak Syndrome
Anaphylaxis
Clinical Manifestations
Anxiety, confusion, dizziness, Sense of impending doom, Chest pain, Incontinence, Swelling of the lips & tongue, Angioedema, Wheezing, Stridor, Flushing, Pruritus, Urticaria, Respiratory distress and Circulatory failure
Hypersensitivity reaction; Massive vasodilation ,Release of vasoactive mediators, Increased capillary permeability
COLLABORATIVE CARE
Epinephrine & Diphenhydramine; Maintain a patent airway (nebulized bronchodilators, Aerosolized epinephrine, Endotracheal intubation or crycothyroidotomy may be necessary; Aggressive fluid replacement; IV corticosteroids if significant hypotension persists after 1-2 hours of aggressive therapy
Hypovolemic
Relative hypovolemia
Results when fluid volume moves out of the vascular space into extravascular space (Intracavitary space)
Third Spacing
Response to acute volume loss depends on
extent of injury, age, general state of health
Absolute Hypovolemia
loss of intravascular fluid volume
Hemorrhage, GI loss (vomiting, diarrhea), Fistula drainage, Diabetes insipid, Hyperglycemia, Diuresis
Clinical Manifestations
Anxiety, Tachypnea, Increase in CO & HR; Decrease in stroke volume, PAWP, urinary output; If loss >30% blood volume is replaced
COLLABORATIVE CARE
Management focuses on stopping loss of fluid and restoring the circulating volume;
Fluid replacement is calculated using a 3:1 rule
Obstructive
Develops when physical obstruction to blood flow occurs with decreased CO (from restriction to diastolic filling of the right ventricle due to compression & Abdominal compartment syndrome)
Impaired ability of normal heart muscle to pump effectively; Conditions outside heart prevent either adequate filling of heart or adequate contraction of healthy heart muscle;
Pericarditis most common cause
; Cardiac tamponade
Patient will experience:
Decreased CO, Increased after load, Variable left ventricular filling pressure.
Rapid assessment and immediate treatment
COLLABORATIVE CARE
Early recognition and treatment; Mechanical decompression; Radiation or removal of mass; Decompressive laparotomy
Cardiogenic
Early Manifestations
Tachycardia, Hypotension, Narrowed pulse pressure; Increased myocardial O2 consumption
Physical assessment
Tachypnea, Pulmonary congestion, Pallor and cool clammy skin, Decreased capillary refill time; Anxiety, confusion, agitation.
Increase in pulmonary artery wedge pressure & Decreased renal perfusion and UO
Precipitating Causes
MI; Cardiomyopathy; Blunt cardiac injury; Severe systemic or pulmonary hypertension; Cardiac tamponade; Myocardial depression from metabolic problems
Systolic or diastolic dysfunction; compromised CO; Actual heart muscle is unhealthy and pumping is directly impaired; myocardial infarction is the most common cause
COLLABORATIVE CARE
Restore blood flow to the myocardium by restoring the balance between O2 supply and demand; Thrombolytic therapy; Angioplasty with stunting; Emergency revascularization; Valve replacement; Hemodynamic monitoring ; Drug therapy (Diuretics to reduce preload) Circulatory assist devices (intraaortic balloon pump, ventricular assist device)
Diagnostic studies
Thorough history and physical examination; No single study to determine shock (Blood studies
Elevation of lactate
Base deficit, 12 lead ECG, Chest X-ray, Hemodynamic monitoring)
COLLABORATIVE CARE
Primary goal of drug therapy
Correction of decreased tissue perfusion;
Vasopressor drugs
(Norepinephrine)
Achieve/maintain MAP >60 to 65 mmHg; Reserved for patients unresponsive to fluid resuscitation; Continuously monitor end-organ perfusion
Oxygen and Ventilation
Increase supply, Optimize CO with fluid replacement or drugs, Increased hemoglobin by transfusion, Increase arterial oxygen with supplemental oxygen and mechanical ventilation
Primary goal of drug therapy
Correction of decreased tissue perfusion
Vasodilatory therapy (Nitroglycerin & Nitroprusside)
Achieve/Maintain MAP> 65 mmHg
Ensure patent airway
&
Maximize oxygen delivery
Volume expansion
If the patient does not respond to 2-3 L of crystalloids, blood administration and central venous monitoring may be instituted
Complications of fluid resuscitation
Hypothermia & Coagulopathy
Successful management
Identification of patients at risk; Thorough patient history, physical exam and clinical findings to establish diagnosis; Interventions to control or eliminate the cause of decreased perfusion; Protection of target and distal organs from dysfunction; Provision of multisystem support care
Cornerstone of therapy for septic, hypovolemic & anaphylactic
Shock = Volume expansion (Isotonic crystalloids (Normal Saline) for initial resuscitation of shock
Nutrition
vital to decreasing morbidity from shock; Initiate internal nutrition within the first 24 hours; Initiate parenteral nutrition if central nutrition contraindicated or fails to meet at least 80% of caloric requirements; Monitor protein, nitrogen balance, BUN, glucose, electrolytes
Nursing Assessment
ABC, Focused assessment of tissue perfusion (Vital signs, Peripheral pulses LOC, Capillary refill, Skin (temp, color, moisture), Urine output, Brief history (Events leading to shock & onset and duration of symptoms), Health history (Medications, Allergies, Vaccinations)