integrated CV responses: haemorrhage, shock and aging Flashcards
what is circulatory shock? what are its causes? symptoms?
inadequate blood flow throughout body;
haemorrhage/MI/anaphylaxis/sepsis/burns/vomiting
anxiety/weak pulse/clammy skin/reduced urine output
immediate responses to haemorrhage, purpose
maintain BP and CO
- reverse stress relaxation (veins shrink around reduced blood volume-> maintain venous pressure and help venous return
- increased HR and force
- peripheral vasoconstriction
- CNS causes gut and renal vasocontriction
- RAAS activated
response to severe blood loss
decreased blood volume-> decreased stimulation of atrial+ cardiopulmonary stretch receptors -> signal sent to hypothalamus + brainstem->
ADH released-> increased thirst + reabsorption-> blood volume restored
adrenalin released-> vasoconstriction-> increased TPR+CVP-> increased CO+BP
changes in BP vs CO during blood loss with time
BP better protected as its vital for tissue perfusion, when BP <50mmhg-> SNS vasoconstriction-> plateaus for a bit before dropping
CO drops gradually
how long does it take to restore blood volume
3 days
how is blood volume restored
internal transfusion
increased thirst
decreased urine output
renal mechanisms
what happens in internal transfusion
haemodilution (blood cells lost and are not replaced) + liver releases more glucose to blood+ venous pressure falls + vasoconstriction-> net hydrostatic pressure falls-> fluid reabsorption at venous end -> blood volume rises
how do renal mechanisms restore blood volume
decreased bp-> baroreceptors stimulated-> brainstem/hypothalamus stimulated
decreased blood vol-> decreased atrial stretch-> brainstem/hypothalamus stimulated AND decreased ANP-> Increased na+water reabsorption
ADH release
SNS-> RAAS
what happens to proportion of hb after haemorrhage? why
immediately after: normal because RBC and plasma have fallen to same extent
drops over 12-24h because blood volume is restored and RBC hasnt been replaced (haemodilution)
HB recovers slowly after
what happens to ventilation/platelet count/fibrinogen/coagulation time/wbc
ventilation: increase due to decreased blood flow through carotid bodies
platelet: increase (from spleen)
fibrinogen: increase (BUT AFTER 15 MIN ALL CLOTTING FACTORS REDUCED AS THEY HAVE BEEN CONSUMED)
coagulation time: reduced
WBC: increase
line between irreversible shock and reversible shock; what happens in irreversible shock, and non-progressive shock
reversible shock until 1h after haemorrhage in which transfusion is administered
after 1h, therapy will only give temporary respite/ST compensatory mechanisms due to irreversible cardiac damage and failure of compensatory mechanisms
non-progressive shock: blood volume and CO restored in 16-24h
consequences of progressive and refractory shock
decreased BP-> decreased tissue perfusion-> hypoxia + acidosis + toxins + disseminated intravascular coagulation (blood clots form throughout body) -> decreased vascular tone + increased vascular permeability -> loss of fluid to tissues-> BP not restored even with transfusion
multiorgan failure: renal/hepatic/cardiac/sepsis/intestinal
4 cardiovascular effects of aging
- atherosclerosis
- Systolic rises; DP falls
- reduced baroreflex sensitivity
- impaired cardiac performance during exercise
vascular changes in aging
elastic layers become thin and fragmented-> reduced elasticity-> dilation
collagen content rises-> increased stiffness
intimal layer thickens
SNS drive increases, NO release decreases-> increased TPR + decreased blood flow during exercise
overall, systolic pressure rises
cardiac changes in aging, why
maximum attainable HR falls
decreased cardiac contractility
cardiac fibrosis slows cardiac relaxation-> early diastolic filling
decreased sensitivity of b1 receptor
atherosclerosis-> increased afterload-> decreased CO
