Shock Flashcards
BP regulation and Kidneys
Kidney regulate BP by
releasing renin which converts angiotensin I to II (this acts as a vasoconstrictor)
This leads to the release of aldosterone
which promotes Na and H20 retention
Hypernatremia then
stimulates release of ADH
which causes further retention of H20 to raise blood volume and Bp
This process can take hours to many days
Nursing actions: Fluid bolus, blood transfusion to help the body regulate.
Compensatory Stage
Compensatory Stage: Subtle Changes/Trending down/Decreased from baseline
- BP remains normal or on lower end, increased HR (increasing contractility), increased RR
PaCO2 < 32 (respiratory alkalosis), SNS release epinephrine and norepinephrine to cause
vasoconstriction. Body shunts to protect vital organs causing cool, pale skin. (Renin tells
kidneys to slow down production causing decreased urine output, altered LOC.
- Narrowing pulse pressure: SBP (number in-between) DBP: 90/70 - 120/80. First sign
Progressive Stage
Things start to fail
- SBP < 90, MAP < 65, HR >150, RR rapid/shallow, PaCO2 >45 (metabolic acidosis/lactic acid
building up, skin mottled/petechiae, urine output decreased < 30mL/hr, lethargy, MODs
(kidney failure/dialysis
Irreversible Stage
- Sedation medications d/t tubes and to conserve energy. Severe organ damage past the point
of survival, BP HPTN, Renal/Liver failure (anuria/jaundice), respiratory failure, cardiac
dysfunction (erratic), worsening metabolic acidosis r/t lactic acidosis, multiple organ failure.
Comfort measures. Discuss with family about advance directives and possible palliative care
Hypovolemic shock
Hypovolemic shock risk factors:
Trauma
Surgery
Vomiting
Diarrhea
Diuresis
Diabetes insipidus
Hemorrhage
Burns
Ascites
Peritonitis
Dehydration
Necrotizing pancreatitis
hypovolemic shock
care management
Place client in modified trendelenburg
- Replace fluid! Number one concern. IV Access
with at least 2 sites. (IO: � or CVAD: Central Line).
- Reverse dehydration (N/V/diarrhea, hyperglycemia)
(antiemetics, antidiarrheal, insulin, Desmopressin:
given for D.I.: given to decrease urination)
- Monitor for s/s hypervolemic complications with
frequent assessment. � , JVD, breathing, peripheral
edema, warm fluids to prevent hypothermia.
- Fluid Replacement:
Crystalloids: Given for dehydration. NS & LR. Widely available and inexpensive. First
line.
- Advantage: LR: Lactate ion helps buffer metabolic acidosis by converting lactate in NaBi.
- DisAd: Requires large volume of infusion. NS can cause hypernatremia, hypokalemia,
BOTH can: pulmonary edema, and abdominal compartment syndrome (ACS).
II. Colloids: volumizing shampoo Patient who has CHF
- Albumin: Rapidly expands plasma volume. Expensive, requires human donors, limited
supply. Can cause HF.
III. Blood Products:
- Plasma, packed RBCs, and platelets. Rapidly replaces volume lost due to hemorrhage.
Disadvantage: Cross match (transfusion reaction
cardiogenic shock
-Impaired ability for heart contract and pump blood.. which can
cause inadequate O2 for heart and tissues.
-Coronary (common): Affects actual coronary arteries! MI/
Anterior Wall MI at greater risk d/t left ventricle damage
secondary to LAD artery. (widow maker)
-Non-Coronary: Affects inside the heart. Stress to heart muscle
(hypoglycemia, hypocalcemia < 2.1, severe hypoxemia),
cardiomyopathy, cardiac tamponade
cardiogenic shock treatment
Treatment: Treat underlying cause. Treatment priorities for
patients in cardiogenic shock are focused upon ensuring adequate
oxygenation, pain control, and maintaining hemodynamic
stability.
-Two types of medications may be given in combination: inotropic
agents and vasodilators.
- Medications:
-Dobutamine: Vasopressor to increase strength of myocardial
activity and improving cardiac output. Decreases after load,
allowing heart to rest.
-Nitroglycerin: Used with coronary blockage to get more oxygen
to the myocardium. Used with dobutamine. Venous vasodilator. High doses can cause too
much arterial dilation.
- Dopamine: Improves tissue perfusion when used with other 2. Increases HR/vasoconstriction
past therapeutic levels. (BIG PROBLEM
Anaphylactic Shock
Severe allergic reaction to antibodies
-vasodilation and capillary permeability
-Clinical Manifestations: generalized flushing,
diffuse erythema, laryngeal edema (difficulty
breathing), bronchospasm, hypotension,
dysrhythmias
-Treatment: remove causative agent (DC ABT,
etc.), fluid replacement, vasopressors,
diphenhydramine (Benadryl), maintain airway
- If allergic to PCN, can take penicillin derivative
and be monitored closely (stay and observe after
infusion)
-Flush the line and stop infusion immed
Septic Shock
-Most common type of distributive shock
Most common areas of origin:
- Bloodstream (bacteremia), most commonly CVAD’s
- Lungs (pneumonia)
- Urinary tract (urosepsis); most commonly urinary catheters
- Elderly patients at risk
- Early Stages:
- BP will remain WNL or respond to fluid therapy, tachycardia, hyperthermia, fever, warm,
flushed skin with bounding pulses, elevated RR, subtle changes in mentation, decreased
urine
- Progression to septic shock:
- HPTN (not responding to fluids/meds), shunting (skin cool/pale, mottled), tachycardia,
tachypnea, oliguria/anuria, non-responsive. Temp will be normal or below.
- Labs: �
- Lactic acid (lactate): Derived from muscle cells and erythrocytes: common markers for
sepsis >2 (H), >4 (c)
- CRP: Present during a inflammatory response- Procalcitonin: Substance produced in response to bacterial infections/tissue injury. Sepsis
marker that is most studied.
septic Shock treatment
Treatment:
- Fluid replacement to correct tissue hypo-perfusion
- Pharm: Broad spectrum ABT, vasopressors, DVT/PUD prophylaxis
- Nutritional: Should be initiated 24 to 48 hours of admission
- Sepsis Stages:
I. SIRs: Temp >100.4 or < 96.8, HR>90, RR>20,WBC >12K or <4K, PaCO2 <32
II. Sepsis: 2 SIRs + Confirmed/Suspected infection
III. Severe Sepsis: sepsis + signs of end organ damage, HPN SBP<90, Lactate >4
IV. Septic Shock: Severe sepsis with persistence, MODs, HPTN SBP <90, Lactate >4
- Sepsis Bundle:
- Complete within 1 hour of symptoms: Measure lactate level (if >2, remeasure), blood
cultures, administer broad spectrum ABT, administer crystalloid for HPTN or lactate > or =
4) within 30 mins, administer vasopressors d/t HPTN to maintain MAP=65
- Complete within 3 hours of symptoms: Lactate level, Blood cultures, BS ABT, fluid
resuscitation with crystalloid
- Complete ASAP/within 6 hours of symptoms: Vasopressors if fluid did not improve HPTN
to keep MAP 65 or >. If HPTN continues, reassess VS, capillary refill, ScVO2 goal >70%,
bedside cardiovascular ultrasound, passive leg raise, fluid challenge.
- Norepinephrine (Levophed) given is if fluids do not correct HPTN
Neurogenic Shock
Vasodilation occur as a result of a loss of balance between the
parasympathetic (vasodilation) and the sympathetic
stimulation (constriction). PSN wins!
- HPTN/Brady d/t blood being displaced in body (not loosing
blood)
- Causes: Spinal cord injuries or issues
- Treatment: Restore sympathetic tone, position patients to
allow epidural to move around and work, keep HOB > 30
degrees, DVT prophylaxis, monitor for s/sx of hypovolemic
shock.
Multiple Organ Dysfunction Syndrome (MODs):
Falls into Stage II: progressive phase of shock
- Can occur with all forms of shock, however, is most common with sepsis
- Dysfunction and mortality: One organ= 20% mortality, >4 organ dysfunction= 60%
- Lungs: dyspnea, RF
- Liver: Increased bilirubin and liver function tests
- Neuro: Coma
- Renal: Decreased urine output
