shock Flashcards
shock :
* An — , — of the cardiovascular system to adequately — the tissues with nutrients and gases
– potentially —
* Can be distinguished based on the nature of the underlying —
– cardiogenic shock : —-
– distributive shock : fall in —
– hypovolaemic shock : loss of —
* This has nothing to do with people being described as “in shock”
acute failure
supply
fatal
problem
pump failure
peripheral resusrance
blood volume
cariogenic shock:
* Decrease in —
– leads to a drop in — and so —
* Any — drop in — could lead to cardiogenic shock
– —
– decreased —
* heart failure / myocardial infarction
– obstruction to —
* stenosis, embolism
– restriction of cardiac —
* cardiac tamponade: fluid/blood in —
cardiac output
pressure and perfusion
acute
cardiac output
arrythmias
contractility
outflow
filling
pericardial sac
Distributive Shock:
* Widespread drop in –
– leads to a drop in — and so —
* Can be — due to the increased —
– — (histamine causes vasodilatation)
– — shock (bacterial toxins cause inflammation)
* Can be —- due to decreased — outflow
– decreased SNS —
– — shock or — blockade
peripheral resistance
pressure and perfusion
vasogenic
vasodilation
anaphylaxis
septic shock
neurogenic
SNS flow
vasoconstriction
spinal shock or autonomic blokade
Hypovolaemic Shock:
* An inadequate — due to – loss
– leads to a drop in — and so —
* Major causes of hypovolaemia are:
– — blood loss due to trauma or surgery
– — leads to loss of plasma volume
– — excessive loss of fluids (e.g. dehydration)
blood volume
fluid
haemorrhage
burns
dehydration
Hypovolaemic & Cardiogenic Shock:
1-
low Blood volume
(Preload reduction) –>
low Right atrial pressure
(ventricular filling) –>
low Right ventricle stroke volume(Starling’s law)—>
low Right ventricle output
low Left atrial pressure
(Preload reduction)–>
low Left ventricle stroke volume —>
low Cardiac output
which leads to low —-
2-
low Left atrial pressure
(Preload reduction) + Left ventricle stroke volume + obstruction to outflow —> low Left ventricular pressure –>
low Cardiac output –> so low —
mean arterial pressure
mean arterial pressure
Distributive Shock
* Total peripheral resistance is maintained by —
– the level of — on the arteries
– Poiseuille’s Law (R = —- )
* Arterial tone is maintained by the — of — and— acting upon the arteries
* Distributive shock promotes — over —
– septic shock; increased — so more —
– neurogenic shock; decreased — activation so less —
arterial tone
constriction
R= nL/r power 4
balance
constrictor and dilators
dilators
consitrotrs
iNOS
dilatation
SNS
less constriction
the NO pathway:
1- —- activation at the — leads to high — in the endothelium which will lead to eNOS that converts L-arginine to L-citruline+ — ( non thrombogenic surface)
2- NO—> GC which converts — to — leading to —- at the —
( however when we do have thrombogenic surface as LPS/cytokines/peptidogylcan we will have INOS leading to NO production
endothelial
lumen
ca+2
NO
GTP —> cGMP
vasodilation
smooth muscle
( this NO pathway is also related to septic shock )
Septic Shock:
* BP is 90/50 mmHg and heart rate is 120 BPM
* Excessive —- leads to a drop in peripheral resistance
– specifically —- pressure
– MAP = CO x TRP
* Activation of the —- and increased —- output
– increased cardiac output
– increased peripheral resistance
vasodilation
diastolic
baroreceptors
sympathetic
baroreceptor reflex and septic shock:
1- when the blood pressure is low we will have — firing of the baroreceptors at the central control ( medulla/hypothalmus)
2- in response — SNS so the force of contraction + venoconstrciton + vasocontrciton + heart rate will —
3- PNS will —
4- in result this will — the cardiac output + blood pressure + peripheral resistance
less
increase
increase
drop
increase
pls check slide 18
Sympathetic Vasoconstriction:
* Widespread vasoconstriction occurs in numerous beds:
– — (cold and clammy)
– — (will reduce —-)
– — tract (see splanchnic circulation)
– —- muscle
* Some tissues are relatively preserved :
– — (has both α1- & β1-ARs, dilation predominates)
– — (few —- so not too much constriction)
* In distributive shock this may be blunted
– either insufficient SNS (—-) or too much NO/dilators (—)
skin
kidney
filteration
gastrointestinal
skeletal muscle
α1-adrenoceptors
neurotic
sepsis
sympathetic venosonstriction :
* Same — mechanism that exists in arteries but in veins
* Physiological advantage:
– raise — pressure
– increase — for —
– increase stroke volume and cardiac output
* Practical problem:
– difficult to — veins for i.v. fluids
Internal Transfusion:
* In normal circumstances, net fluid movement is from — to —
* In shock there is fluid movement from the — into —
* Pre-capillary — in addition to the fall in — pressure leads to a fall in —
* With sudden loss of — of blood volume, ~ – ml fluid moves back into circulation in about 10 min-
- Capillary Dynamics - Shock
* Net filtration pressure = (Pc− Pi)− σ(πc− πi)
α1-adrenoceptor
central venous
preload in right ventricle
cannulate
capillaries –> interstitial spaces
interstitial spaces–> blood vessels
vasoconstriction
artriel blood pressure
capillary bp
20% , 600 ml
PLS check slide 22
Responses to Shock:
* Acute responses to shock quickly raise — to maintain —
– —- mediated changes to blood pressure
* increased heart rate, stroke volume & vasoconstriction
– internal transfusion
* Long term adaptations to shock similar to long-term blood pressure regulation
– blood volume regulation via—- activation promoting — and —
– decreased release of —
- renin-angiostesin system:
1- Angiotensinogen (453 aa) released constinously from the — , renin releases by — activation on —
2- angiotensin I ( 10 aa) is the — precursor will be converted to angiotensin ii ( 8 aa) by —
3- this will cause – and release — which is responsible for —
bp
perfusion
baroreceptor
RAS
salt and water retention
ANP
liver
SNS
kidney
Angiotensin Converting Enzyme (ACE)
vasocontrction
aldosterone
salt and water retention
Thirst & Anti-Diuretic Hormone:
* Both thirst and release of anti-diuretic hormone (ADH) are triggered
by high plasma osmolality
– typically >295 mosmol/kg
* In — blood volume states both mechanisms are triggered independently of —
* ADH is secreted from the — and stimulates —from the kidney
Natriuretic Peptides:
* Atrial natriuretic peptide (ANP) release in response to — blood volume
– as are the other natriuretic peptides
* Promote Na+ and water —
* Regulate —, counterbalance —
* Not an appropriate response to shock but play an important role in normal balance
– should be decreaed
low
plasma osmolaity
posterior pituitary
water reasbprtion
increased
excretion
blood volume
Ras
Shock & Acid Base Balance:
* Shock decreases – and causes tissue —
* Hypoxia causes — and the build up of —
– needed to regenerate the — in glycolysis
– normal plasma lactate 1 mmol/l, in severe shock 9 mmol/l
* The resultant lactic acidosis may:
– depress peripheral — responses to catecholamines
– depress the — (both further exacerbating shock)
– and ultimately cause –
perfusion
hypoxia
anaeorbic metabolism
lactic acid
NAD
peripheral vascular
myocardium
coma
Decompensated shock:
Decompensated shock
* Prolonged or severe drops in pressure can lead to—
– at this point subsequent — therapy may not help
* Prolonged poor perfusion can lead to —
– particularly — and —
* Reduced — outflow and the build up of — metabolites in poorly perfused tissues act to further reduce — blood pressure
* This leads to a —
irreversible shock
replacement therapy
organ failure
liver and kidney
sympathetic
vasodilatory
arterial
downward spiral
decompensated shock :
* The acidosis depresses — , — can no longer maintain adequent blood pressure
– coronary — falls myocardium depressed further
* Decreased SNS activity leads to — failure
* Sluggish flow through microcirculation can lead to small — forming increasing —
– and so —
* Prolonged hypoxia leads to local — and release of —
increased —
– blood volume and pressure — further
Irreversible shock:
* The — stage that does not respond to treatment
* Due to the large amount of — damage, recovery is —
myocardium
reflexes
perfusion
vasomotor
small clots
viscosity
resistance
local inflammation
toxic
capillary permeability
decrease
terminal
cellular
impossible lol
General Treatment for Shock
* —
– pressure is low, expansion of volume is appropriate
* — agents
– increase resistance and increase pressure
– noradrenaline, Ang II
* Inotropes
– increase — and increase cardiac output
– adrenaline, noradrenaline, digoxin
* — (septic shock)
* – (anaphylaxis)
fluids
vasopressors
force of contraction
antibiotic
antihistamines
Replacement Fluids:
* Blood
– particularly appropriate in —
* Crystalloids
– examples: isotonic – and —
– can get a range of combinations of these two
– also more complex solutions that closely resemble —
* Colloids
– — molecules retained within the — walls
– examples: albumin, starch derivatives & dextrans
haemorrhage
saline and dextrose
plasma
large
capillary
Which Replacement Fluid?
* Colloids
– stay in the — space, hold fluid there
– theoretically — volume (1 L for each 1 L lost)
* Saline
– moves — from — to —
– expands — volume
– theoretically— volume (3 L for each 1 L lost)
* in practice it is closer to 1.5– 2 L
* Dextrose/Glucose
– dextrose is taken up by – and take — with it
– expands – - and – volume
– theoretically – volume (9 L for each 1 L lost)
vascular
1:1
freely
vascular –> interstitial space
extraceullar volume
3:1
cells
fluids
intra and extracellular fluids
9:1
Summary:
Summary
* Situations like shock and exercise show the integration of the
cardiovascular system
* With falling pressure the acute and chronic mechanisms for maintain
blood pressure and perfusion are initiated
* These act to maintain perfusion, but in some cases the response may
have a deleterious effect on some tissues
* If not treated quickly damage may be too great
