Hypovolemic Shock Flashcards
what is the main artery used to measure BP?
brachial
describe Ohm’s law
pressure = flow x resistance
compare stage 1 HTN, stage 2 and HTN crisis
stage 1: 130-139/80-89
stage 2: >140/>90
crisis: >180/>120
what is the MAP and what eqaution is used to determine this?
MAP= CO x systemic vasc resistance, equation= DBP + (pulse pressure/3)
how do SNS and PNS reg arterial pressure?
Baroreceptors
how does pit gland reg arterial pressure?
vasopressin
how does kidney reg arterial pressure?
renin angiotensin aldosterone system via Na+ reabsorption and water retention
how do adrenal glands reg arterial pressure?
catecholamines, aldosterone and glucocorticoids
how does the heart reg arterial pressure?
ionotropic, chronotropic and atrial natriuretic peptide
What effect does increased baroreceptor activity have on BP?
increased baroreceptor activity increases PNS activity -> reduction in BP
describe baroreceptors
nerve endings that sense artery wall stretch
what is the RAAS and what effect does it have on BP?
Renin angiotensin aldosterone system, increases BP and systemic vasc resistance
which has a faster response and why: baroreceptors or RAAS?
Baroreceptors have a faster response as RAAS is dependent on hormonal changes inducing transcription of denes which can take hours
what effect does angiotensin II have?
vasoconstriction, increase Na+ reabsorption and water retention, stimulates further aldosterone release and activates SNS
describe reasons for vasopressin release
released from post pit in response to: increase in plasma osmolarity, reduction in blood vol, increases angiotensin II = increased BP
how does vasopressin increase BP?
V1:constriction of blood vessels and V2:kidney fluid reabsorption
describe atrial natriuretic peptide and what causes it’s release
ANP is a vasoactive peptide released from the atria in response to a ride in atrial pressure linked to venous pressures = lowering of BP
how does ANP reduce BP?
through vasodilation, inhibition of Na+ reabsorption -> diuretic effect
how does the adrenal gland affect BP?
catecholamines such as epi and nor epi -> increase in HR and vasoconstriction, aldosterone acts with RAAS locally causing vasoconstriction, glucocorticoids cause vasoconstriction
what changes occur to baroreceptors in pregnancy?
increase in sensitivity
what changes occur to RAAS in pregnancy?
enhanced activity
decreased vasc responsiveness to which hormones occurs in preg?
angiotensin II, norepi and vasopressin
what changes occur to ANP in preg?
increase by 40%
list the diff types of shock
hypovolemic, cardiogenic, distributive, obstructive
define haem shock
EBL >500ml within 24 hours of birth
what needs to be considered with EBL
pt prior Hb, total blood vol (100ml/kg)
define APH
any bleeding from genital tract post K24 and prior to birthp
list causes of PPH
tissue, trauma, tone, thrombin, laceration
list risk factors for haem shock
placental disorders, multiple preg, PET, GHTN, prev PPH, asian, obesity, anaemia
list risk factors for haem shock in labour
febrile, IOL, CS, retained tissue, op vaginal delivery, macrosomia, mat age >40, epis
describe stage 1 of hypovolemic shock
pre shock: compensatory mechanisms with increased sym tone-> increased HR, cardiac contractility and peri vasoconstriction, eaerly changes in vitals with loss of 10% BV, mildly elevated BP
describe stage 2 of hypovolemic shock
shock state: BV cont decrease 25-30% of BV -> shock state with drop in SBP, tachy, oliguria, O2 deliv to vital organs inadeq-> lactic acidosis, blood flow redirected to brain and heart = propagates tissue ischemia and worsens lactic acidosis
describe stage 3 of hypovolemic shock
untreated -> haemodynamic compromise, refractory acidosis, reduction in CO = MOF and death, avg time from onset 2hrs
list components of active management third stage
uterotonics and fundal massage
list the components of managing an acute incident
recognition, communication, resus, monitoring, management, theatre
