Shock Flashcards
meds for shock
VIVA
vasoconstrictors, inotropes, vasodilators, antidysrhythmics
- vasoconstrictors: V PANE: vasopressin, phenylphrine, alpha-range dopamine, norepi, epi
- inotropes: BEN MD: beta-range dopamine, epi, norepi, milrinone, dobutamine
- vasodilators: NN Hy Lol: nitroprusside, NTG, hydralazine, labetalol
- antidysrhythmics: PALED VA Lol: procainamide, amiodarone, lidocarine, esmolol, diltiazem, verapamil, adenosine, labetalol
tx for shock
major focus on improving tissue perfusion (meds), supporting O2 delivery and Hgb levels (give blood if Hgb very low, intubate and MV, give O2), give crystalloid or colloid if intravascular volume depletion, give enteral therapy within 24-48 hrs or TPN if can’t do enteral but should delay it for 7 days, keep glucose in 140-180, identify and correct cause of lactic acidosis, don’t give sodium bicarb for acidosis.
Assess response to therapy, prevent and maintain surveillance for complications, and provide emotional/comfort support.
consequences of shock
- cardiovascular: ventricular failure and microvascular thrombus
- neuro: SNS dysfunction, cardiac/resp depression, thermoregulatory failure, coma
- pulm: ARDS, acute lung failure
- renal: AKI
- hematologic: DIC
- GI: GI tract failure, liver failure, pancreatic failure
causes of hypovolemic shock (internal vs external)
internal causes: hemothorax, 3rd spacing, hemorrhagic pancreatitis, ruptured spleen/liver, dissecting aneurysm, ascites, peripheral edema
external losses: loss of blood, plasma, body fluids (surgery, obstetric delivery, burns, gi loss)
classes/stages of hypovolemic shock
Class I: loss up to 15%, or up to 750 mL
Class II: loss up to 15-30%, or 750-1500 mls
Class III: loss of 30-40%, or 1500-2000 mL
Class IV (severe and usually refractory): loss >40% or loss >2000 mL
how much fluid and what type to give in hypovolemic shock?
can give blood or isotonic crystalloids (NS/LR)
- 3:1 ratio (300 mLs for every 100 mLs of fluid lost)
- hemodynamic monitoring monitors fluid replacement
- fluid challenge
evaluating effectiveness of fluid volume resuscitation
- BP arterial pressure 65-70 (map??)
- CVP 6-8
- UO 0.5 ml/kg/hr
- normal BUN/Cr
- serum lactate returning to normal
S/S of cardiogenic shock (initial vs later)
initial:
- decline in CO
- chest pain
- tachycardia
- ABGs: resp alkalosis and hypoxemia
- pulm edema
later as compensation fails:
- continued increased HR
- chest pain
- dysrhythmias
- deteriorating pulm function, resp distress
- ABGs: resp acidosis, metabolic acidosis, hypoxemia
- renal failure
- decreased LOC from cerebral hypoperfusion
diagnosis of cardiogenic shock
- CI less than 2.2 l/min/m2 in presence of elevated PAOP >15 mm Hg
- echo confirms diagnosis by giving noninvasive estimate of PAOP and EF and clarifies etiology
tx of cardiogenic shock
-mechanical: IABP and VAD
-pharm approach:
diuretics and venous vasodilators to decrease preload, positive inotropes to increase CO, arterial vasodilators to decrease afterload
complications of IABP, LVAD, ECMO
- infection
- bleeding
- thrombocytopenia
- hemolysis
- embolus
- stroke
- device malfunction
- circulatory compromise of a cannulated extremity
- sirs
- sepsis
causes of obstructive shock
- impaired diastolic filling (cardiac tamponade, tension pneumo, constrictive pericarditis, compression of great veins)
- increased right ventricular afterload (PE, severe pulm HTN, increased intrathoracic pressures)
- increased left ventricular afterload (aortic dissection, systemic embolism, aortic stenosis)
s/s of cardiac tamponade
- muffled heart sounds
- hypotension
- pulsus paradoxus (decrease in SBP during inspiration)
s/s of tension pneumo
- decreased breath sounds on affected side
- tracheal shift away from affected side
tx of obstructive shock
- pericardiocentesis
- thoracentesis
- surgical reduction of long bone fx (preventing PE)
- intermittent pneumatic compression devices
- ROM
- prophylactic anticoagulants
hemodynamic changes that occur in distributive types of shock
- decreased BP
- decreased SV
- decreased CO
types of distributive shock
- neurogenic
- anaphylactic
- septic
causes of neuro shock
- sci (most common)
- spinal anesthesia
- nervous system damage
- vasomotor depression
what does the loss of sympathetic tone in neuro shock lead to?
-massive peripheral vasodilation, inhibition of baroreceptor response, and impaired thermoregulation.
The massive vasodilation (arterial and venous) causes decreased SVR and decreased BP and relative hypovolemia with blood pooling in the venous circuit leading to decreased preload.
Loss of baroreceptor response causes bradycardia which worsens CO.
Loss of vasomotor tone results in inability for blood vessels to dilate/constrict for temp maintenance which leads to loss of thermoregulation
s/s of neuro shock
- bradycardia with hypotn
- warm dry flushed skin
- decreased CO/CI
- declining RAP and pAOP (venous vasodilation decreasing preload)
- decreased SVR (arterial vasodilation causing decreased afterload)
- hypothermia (unable to thermoregulate)
tx of neuro shock
- immobilize spine and positioning
- IV fluids carefully, watch for overload
- vasopressors if pt doesnt respond to fluid
- slow rewarming to prevent more vasodilation
how does anaphylactic shock occur
-antigen-antibody response causes cellular breakdown and the release of powerful vasoactive mediators from the mast cells and basophils –> vasodilation causes decreased BP, relative hypovolemia, fluid shifts
s/s of anaphylactic shock
- upper airway: laryngeal edema
- lower airway: bronchial constriction
- excessive mucus production
- angioedema (swelling of eyes, lips, tongue, hands, feet, genitalia)
- tachycardia and hypotension
- skin: itching, pain, pruritis, urticaria
tx of anaphylactic shock
-remove trigger
-establish airway
-meds:
Epi for bronchodilation and vasoconstriction
Histamine blockers like ranitidine and benadryl as secondary agents
Corticosteroids to reduce inflammation
IV fluids to counteract hypotn
