LO1 TO LO3 Flashcards
describe compensatory stage of shock:
-BP
-HR
-RR status
-Acid base imbalance
-Skin
-Urine output
-mentation
-normal bp
-over 100 bpm (vasoconstriction)- release of catecholamines
-greater than 20
-rr alkalosis
-cool and clammy (blood shunted to organs)
-decrease urine output (ADH) and hypoactive bowels
-confused, anxious
describe progressive stage of shock:
-BP
-HR
-RR status
-Acid base imbalance
-Skin
-Urine output
-mentation
-systolic is less than 80-90, MAP is less than 65 Hg (requires fluid resuscitation) to restore
-above 150 bpm
-rapid shallow respirations (holding co2), crackles
-metabolic acidosis
-mottled, petechiae
-0.5 mL/kg/hr (less than 30 mL/hr) THINK OF KIDNEYS NOT WORKING
-lethargy
describe irreverable stage of shock:
-BP
-HR
-RR status
-Acid base imbalance
-Skin
-Urine output
-mentation
-requires mechanical or pharm support
-hr is erratic
-rr status: need intubation or mechanical ventilation
-profound acidosis
-jaundice (LIVER ENZYMES ELEVATED)inter
-anuric, need dialysis
-unconscious
how to calculate MAP
2 diastolic plus systolic divided by 3
what is an early sign of shock
narrowing of pulse pressure (normal between 30-40) this is because the body is trying to vasocontrict ; late is wide (septic shock-wide is early)
nursing interventions for compensatory stage
-assess for BP drop
-get MAP
-start IV
-adminster fluids
medical management for compensatory
treating cause
nursing intervention for progressive stage of shock
-early intervention
-hemodynamic monitoring thru map, caprefill, hr, bp
-check serum electrolytes
-change in mental status
-blood gasses
-prevent complications: hob 30 degrees, for aspiration, oral care, good IV, prevent infection
-providing rest
medical management for progressive
fluids, optimizing intravascular volume, supporting pump of heart, improving incompetence of vasculature
when administering cryalloids for a pt in shock what should u assess
for overload of fluids
what are 3 classes of meds given for shock
-ionotropic (improve cardiac output) ex. dopamine and adrenaline
-vasodialtors (reduce preload and afterload which decreases o2 demands for heart)
- vassopressor (increase bp with vasoconstriction)
what side of the heart pumps blood to the body
left
Briefly describe the compensatory mechanisms of shock.
the response of the primary and secondary regulatory mechanisms . Activation of homeostatic response, increased sympathetic response (increase HR, BP, contractility), increased respiratory rate to increase 02 saturation and delivery, activation of renin-angiotensin (increases reabsorption of sodium and water), increased catecholamines and cortisol to increase glucose for metabolism.
How do this body system react to shock
renal system
Renal system - Increased release of aldosterone and ADH. This increases reabsorption of sodium and water from the intravascular compartment. This response is triggered by the drop in blood pressure. Urine output drops to less than 30 mL/hr.
How do this body system react to shock
cardiovascular system
Cardiovascular system - When blood pressure drops due to low volume, epinephrine and norepinephrine are released by adrenal medulla. These increase the heart rate and cause vasoconstriction, thus, BP will increase. Eventually, compensatory mechanisms fail and BP drops. Pulse quality becomes weak and thready. Decrease in cardiac output.
How do this body system react to shock
nervous system
Become anxious and restless; then confused to lethargic, and eventually non-responsive.
How do this body system react to shock
respiratory system
Respiratory system - Increase in respiratory rate in an attempt to get oxygen to the cells. Decrease in oxygen saturation.
Explain the hemodynamics of shock and treatment:
ABGs
Lactate level
Electrolytes/fluid volume
ABG’s – initially, the patient will be in respiratory acidosis due to CO2 retention. As the lactate levels increase, the patient will present with metabolic acidosis. After massive blood transfusion, patients can convert to metabolic alkalosis because of the conversion of citrate to bicarbonate in the liver.
Lactate level – lactate levels increase as oxygen is not available to the cells. Cells then use anaerobic metabolism which creates lactic acidosis.
Electrolytes/fluid volume
With blood transfusion, hyperkalemia will result from the destruction of stored red blood cells in the transfused unit. Hyperkalemia is at a greater risk for patients in metabolic acidosis as well as renal failure.
Hypocalcemia – excess citrate may combine with ionized calcium in the blood causing a decrease in available ionized calcium in the blood. Temporary problem where a calcium replacement is only given to those patients who are symptomatic.
Patient experiences hypovolemia then volume overload and CHF can become complications of treatment with blood transfusion and large volumes of IV fluid. Caution with patients who have a compromised cardiovascular system. Use of packed RBC’s instead of whole blood is preferred. IV Lasix may be administered between units of blood to remove excess fluid to prevent cardiac overload.
describe cardiogenic shock
poor pump — decrease in pre and afterload = decrease in stroke volume and in HR THUS HEART CANT EJECT BLOOD IN SYSTOLE —- POOLING OF BLOOD INTO LUNGS
3 types of distributive shock
anaphylactic
septic
neurogenic
true or false. fluid bolus should be given rapidly for cardiogenic shock.
false. never give a rapid bolus of fluids with cardiac failure because it may result in acute pulmonary edema
describe distributive shock
massive venous and arterial vasodialation= pooling of peripheral blood
risk factors for neurogenic shock
depressant meds
spinal injury
spinal anesthesia
risk factors for septic shock
immunocompromised
greater than 65
malnourished
chronic illness
invasive procedure
emergent surgeries
in neurogenic shock what type of activation happens
parasympathetic causes vascular smooth muscle to dialate= pooling of blood
what is diff abt neurogenic shock and how it presents
pt presents with warm and dry skin and is bradycardia and hypotensive instead of tachy
what type of spine injury puts pts at risk for neurogenic shock
above T5
what can you see in SIRS (initial infection)
elevated temp more than 38 or less than 36
hr is greater than 90
rr rate is greater than 20 per min
white blood cells greater than 12 000
describe patho of sepsis
immune response, cytokines produce inflammatory response, – increased capillary permeability which leads to a leaky capillaries= vasodialtion= poor tissue perfusion
rue or False: The parasympathetic nervous system loses the ability to stimulate nerve impulses in patients who are experiencing neurogenic shock. This leads to hemodynamic changes.
FALSE….the statement should say: The sympathetic (NOT parasympathetic) nervous system loses the ability to stimulate nerve impulses in patients who are experiencing neurogenic shock. This leads to hemodynamic changes.
A 42-year-old male patient is admitted with a spinal cord injury. The patient is experiencing severe hypotension and bradycardia. The patient is diagnosed with neurogenic shock. Why is hypotension occurring in this patient with neurogenic shock?
The sympathetic nervous system (which is a division of the autonomic nervous system) is unable to stimulate the nerves that regulate the diameter of the blood vessels (there’s a loss of vasomotor tone). So, now the vessels are relaxed and this causes massive vasodilation. Systemic vascular resistance will decrease and hypotension will occur.
signs of septic shock
-high temp above 38
-increased wbcs
-rr over 20
-altered mental status
-hr above 90
-dyuria
-abdominal pain and distention
-sob
neck stiffness wound discharge
describe recognition stage of immune response
antigen is present— lymph notes increase release of lymphocytes and macrophages process antigens thru phagocytosis
describe proliferation stage of immune response
lymphocytes send message for T to become killer T and B release antibodies (lymph nodes enlarge)
describe response stage of immune response
either cell mediated thru T by connecting to invader antigen or humoral thru B
physical barriers
skin, mucous membranes, respiratory tract, cilia
mechanical barriers
hand washing, vomitting, urination (sloughing off and replacement of dead skin cells also removes adherant bacteria)
biochemical barriers
mucus, perspiration, ear wax , tears (biochemical secretions that trap microgorganism and kill them)
triggers for seizures
Specific time of day or night
Sleep deprivation – overtired, not sleeping well, not getting enough sleep, disrupted sleep
Illness (both with and without fever)
Flashing bright lights or patterns
Alcohol - including heavy alcohol use or alcohol withdrawl
Drug use - Use of cocaine and other recreational drugs such as Ecstasy
Stress
Menstrual cycle or other hormonal changes
Not eating well, long times without eating, dehydration, not enough fluids, low blood sugar, vitamins, and mineral deficiencies
Specific foods, excess caffeine or other products that may aggravate seizures
Use of certain medication
does co2 cause vasodialation or vasoconstriction
vasodialaor= worsening icp
describe diabetes insipidus
decreased ADH from compression of pituitary gland= polyuria and polydipsia
-increased urine osmolality
COMPLICATION OF ICP INCREASE
hypernatremia
describe syndrome of inappropriate diuretic hormone (SIADH)
increased ADH= becomes overloaded, urine output diminishes, serum sodium dilute so hyponatremia
-increased urine osmolality
-EXTRACELLULAR FLUID
describe cerebral salt wasting syndrome (CSW)
hyponatremia from hypovolemia nad loss of extracellular water because of sodium transport abnormality
