Physiology Circulatory Shock Flashcards
4 compensatory mechanism
- Baro R
- Reaborption of fluid into capillary
- falling arterial and capillary hydorstatic P –> Reduces GFR into capillary
- Fall in renal BF and BP trigger increase in renin/angiotesnin activity / vasopressin release, and aldosterone release
Symptoms of shock (7)
Pallor of skin and mucous membranes
Clammy skin
Rapid, weak, thready pulse
Arterial hypotension
Decerased core body temp
Feeble respiration
Restless, apathaic , semi-rational behavior
What is shock
Failutre of cirucaltyr system to maintain cellular perfusion and fucntion
What causes shock
critical impairment of BF to vital organs and tsisues and/or the ainability of tissues to utilize essential nurtrients
Three major types of shock
Hypovolemic shock
Cardiogenic
Septic shock
What is hypovolemic shock
Severe lsos of circualting blodo volue
Threat to ciruulation of tissues by decreasing venous return and CO
Loss of ciruclating blood (hypovolemic shock) may reuslt from
Hemorrage- internal or external bleeding
Loss of vascular volume- burns, trauma, radiation
Loss fo 5-10% blood volume
little or no efect on BF
Reinfusion will result in spontanous recovery of vascular funcitona nd no long-term consequnces
Loss of 15-20% ttoal blodo volume
Significant all in CO
MAP is well maintaine
Blood to soe beds is signifcantly reduce,d but reinfusion will lead to spontaneous recovry
Loss of 25-50%
provoeks severe drop pin venous return, CO and pulse prssure
MAP falls , thouh ti is still maintatined better than CO by baroR /symp function
early signs of circulatory shock appear
Shock state reversed by eary reinfusion of volume and aggressive treatmetn
Loss >30%
pressure falls below mean levels of 50 mmHG
irrerersible shock ensues
Reinfusion of fluid ay not be able to restore normal CV fucntion
Mechanism that help maintain CV ufcntion in the face of decrsed circulating blood
- BaroR reflex (sympathetic NS, tTPR, and Heart rate inccreased)
- Arterial and capillary hydrostatic P favor –> REABSORPTION OF FLUID INTO CAPILLARY
- Reduction in CO –> REDUCES GLOMERULAR FILTRATION AND FAVORS RETENTION OF FLUID IN THE VASCULAR SYSTEM
- Fall in renal BF/BP –> increase in RENIN/AGNTIOTENSIN ACTIVITY, VASOPRESSN RELEASE, AND ALODSTERONE RELEASE
What does BaroR reflex do?
through SNS, total TPR and HR are increased to minimize fall in BP
Inc Symp –> increse ventricular contracility –> preload is limited
INc BaroR -> Increase Arterial Resistance in well-inenrveated vascualr beds (sphlanci, renal, skin) so aretial pressure maintainted in Heart and Brain
Increase venous tone
Reabsorption of fluid into capillary
resulting shift of fluid volume from interstitium to circulation helps maintan vascualr volume
Reduction in CO reduces blood flow and arterial pressure at the kidny\
Decreaseds GF and retention of fluid in vascular system
Reduction in CO reduces BF and arterial pressure at the kidny
Autoregul
Decompensatory changes
With minor hemorrhage, reinfusion restores ciruclating blood volume, BP, and CO.
Reinfusion of blood after a severe or prolonged hemorrhage may fail to restore vascular function
Expt: Hemorrhage produced hypovolemia and hypotension for more than two hours in an experimental animal
After 3 hours, animal reifused into anamimal. Result
Blood volume was rstored and BP and CO improved temporarilty.
With tie, both BP and CO fell, even in teh face of continued expansion of vascular volume
what does it mean if fialture of vasculature to recover from hypovolemia after reinfusion
implies that the underlying mechanisms of vascular control have been altered
in microcirculation, prolonged hyptoension reduces BF through tissue
With prolonged ischemia the endothelial cells swell and paritall occlude the capillaries
Lymphcyte aggregation, tirggered by inflammatory response, may occlude capllaries even further
what are the tissue cahgnes in hypovolemic shock>
- vascular permeability, edema, ischemia
- Faiture of aerobmic metaoblism, membrane transprot, HBO2, transprot, lysosomal rupture –> tissue damage
- Aerobic (glycolysis) metabolism- acidosis
- Systemic Inflammateroy Response Syndrome
Cardiogenic Shock– 3 kinds
- Acute MI
- Massive Valve Failture
- Percardial effusion
Acute MI
infarct invovles 30-35% or more of LV
would dramatically reduce ventricular force and SV
Small infarcts are not liekly to produce cardiogenic shock ,but may produce smaller , more progressive hane resultin gin CHF
Massive Valve Failture
Rutpure (infarction) of chorda tendinae could produce massive, suden mitral regurgitation
Reuce CO suddenly
Pericardial Effusion
Rutpure Coronary BV
COuld produce a heorrhage into space outside of heart and insdie inelastic PERICARDUM
cardiac filling would be mechanically reduced and severel limited
In spite of adequate atrial P, cardiac preload would be reduced and SV limited
Massive Valve Failture
Rutpure (infarction) of chorda tendinae could produce massive, suden mitral regurgitation
Reuce CO suddenly
Pericardial Effusion
Rutpure Coronary BV
COuld produce a heorrhage into space outside of heart and insdie inelastic PERICARDUM
cardiac filling would be mechanically reduced and severel limited
In spite of adequate atrial P, cardiac preload would be reduced and SV limited
Pericardial Effusion
Rutpure Coronary BV
COuld produce a heorrhage into space outside of heart and insdie inelastic PERICARDUM
cardiac filling would be mechanically reduced and severel limited
In spite of adequate atrial P, cardiac preload would be reduced and SV limited
What accompanies Cardiogenic Shock
fall in arterial systolic P below 90 or more than 60 mmgh
Cardiac INdex falls below 2.2 L/min/m2
Is ventricular filling adequate?
Ventricular FillingP is adequate
Venous return is adequate
Pulmonary capillary wedge pressure is greater than 15 mmHG
Features of Cardiogenic Shock
Reduced CO
Reduced arterial P
Reduced Tissue Perfusion, coronary perfusion
Reduced oxygen deliveyr, both coronary and peripheral tissue
SIRS
Vascular Collapse
Features of Septic Shock
1% all hospitals admissions
Mortality between 30-80%
Insult occurs at tissue level
Bacterial or funagl
Septic shock
Vascular Damage (SIRS)
Vascular permiablity, clogging, and coagulation, ischemia
Hemodynamics
REDUCED TPR!!!
incrased CO
increased central venous P
anaeroic metabolism and lactic acidosis
O2 delivery may be adeaquate; tissues can’t utilize it
Principels of Shock Treatment
Improve tissue perfusion
Improve CO
-incrase left atrial P by increasing vascular volume
non-septic shock; above 2.2L/min/m2
Spetic shock; above 4.0L/min/m2
Acidosis
Primary cause: BV, Cardiac support, infection
Treatment
Basic
Improve tissue perfusion!!!
Vasoldiators –> so increase O2 delviary, and tisue perfusion
Tx Acidosis with bicarb drugs
