Shock/Hypotension Flashcards
Arterial pressure dependent on
volume of blood within arterial system
rate of inflow (from LV) vs rate of runoff to veins (blood leaving)
Arterial pressure rises when
inflow is greater than outflow (rapid ejection phase of ventricular systole)
Arterial pressure falls when
inflow is less than outflow (Diastole)
Blood pressure in systemic arteries will be lower than normal when
blood volume in arteries is decreased due to decreased cardiac output or decreased TPR (inc rate of runoff from arteries to veins)
Diastolic pressure
determined by factors that alter rate or time of runoff
1) rate of runoff- how fast blood flows from arterial to vennous system (determined by TPR)
2) runoff time- runoff during diastole; determined by heart rate- dec HR longer time for runoff, diastolic pressure decreased
3) arterial systolic pressure- starting pt from which runoff causes pressure to decrease
Arterial systolic pressure determined by
1) ejection rate- from LV; how quickly blood volume in arteries increase
2) SV- arterial pulse pressure index of SV. volume increases, pulse pressure increases.
3) arterial compliance- chronic decreases in compliance increase systolic pressure
4) arterial diastolic pressure- pressure begins to increase during ejection
pulse pressure in aortic stenosis is
decreased because of rate of ejection is decreased due to high resistance of aortic valve
MAP calculation
MAP= Diastolic + 1/3 Pulse pressure
Pulse pressure= systolic - diastolic pressure
MAP=COxTPR
MAP is the driving pressure for blood flow in systemic circulation
HR controlled by
PARA and SYM on SA node
SYM nerves influence
HR, preload, afterload, inotropic state
SV determined by
preload, afterload, inotropic state
Preload
stretch on myocardial fibers before contraction
-determined by EDV
related to ventricular filling- affected by heart rate (dec hr, inc filling time, EDV greater, inc SV) and rate of venous return (inc vr, inc rate of filling, edv greater, inc sv)
Starling’s law
stroke volume inc when preload is inc due to greater stretch which results in more favorable overlap of thin and thick filaments
afterload
ventricular wall tension during ejection
-resistance that must be overcome to eject blood
pressure at start of ejection (aortic diastolic pressure) or peak pressure (aortic systolic pressure) used as indices of afterload
-changes in TPR affect afterload- inc in TPR slows rate of runoff of blood from arteries to veins- inc arterial diastolic pressure- inc afterload
inc in TPR will
slow rate of runoff from arteries to veins–> inc arterial diastolic pressure –> inc afterload
Inotropic state
represents force of contraction
dep on cytosolic calcium level
more ca- more cross bridges formed- inc contractile force
NE will
enhance calcium entry into myocytes and inc inotropic state
Venoconstriction
decrease venous compliance, increasing venous pressure- increase venous return to the heart- increasing sv on next beat
hypovolemic shock
decreased blood volume resulting in inadequate CO
skin feels cold and clammy because decreased blood flow to skin
low central venous pressure
dec blood volume–> dec venous return–> dec EDV–> dec SV–> dec CO–> dec MAP
distributive shock
generalized systemic vasodilation- dec TPR
warm shock
cardiogenic shock
inadequate cardiac output by diseased or impaired heart
high central venous pressure
skin feels cold and clammy
Blood flow to most systemic organs is reduced in hemorrhagic shock bc
map is reduced and
vascular resistance is increased due to increased sym firing to arterioles via baroreflex
how do brain and heart maintain blood flow during shock
local arteriolar dilation by local vasodilators
in other organs- arterioles constrict due to inc SYN via baroreflex
Increased myocardial O2 consumption when
inc inotropic state (beta1 activation)
inc hr
inc afterload, preload, hypertrophy
ischemia of heart during shock
although vessels are dilated via local vasodilators, there is increased O2 demand because of the sym firing leading to inc inotropic state
pulse during shock
described as weak because loss of blood impairs filling of ventricles (dec preload)
-this will result in reduced SV–> reduced pulse pressure–> weak pulse fet
red SV–> dec C–> dec MAP
baroreceptor reflex in hemorrhagic shock
increased SYM and dec PARA
leads to arteriolar vasoconstriction, inc TPR, inc venous return slightly because blood volume reduced
inc inotropic state and HR but CO is still low due to low bv
also HR will increase- decrease diastolic filling time, decrease EDV–> dec SV
change in intracellular fluid volume caused by hemorrhage or dehydration?
dehydration
- ecf is hypertonic, so blood will leak out of cells and icf volume is decreased
- hypertonic contraction
Distributive- septick shock mechanism
release of inflammatory mediators–> vasodilation via NO in endothelial cells and impaired vascular reactivity–> dec TPR–> dec MAP
What happens to afterload in distributive shock
it is decreased because of decrease in TPR
Increase in SYM firing due to the decrease in MAP will result in inc inotropic state
systemic arteriolar dilation
decreases TPR- lower resistance to flow, higher rate of runoff, lower arterial diastolic pressure
systemic arteriolar constriction
increases TPR- higher resistance to flow–> lower rate of runoff–> inc arterial diastolic pressure (afterload)
venoconstriction
SYM response
decrease venous capacity to hold blood, so more blood will return to the heart
Edema in shock
Leukocyte adherence to post capillary venules results in increased vascular permeability- development of edema
O2 diffusion into cells impaired
Even though there is the presence of NO, which normally inhibits leukocyte adherence, pro inflammatory mediators outweigh NO and adherence occurs
Anaphylactic shock
allergen–> mast cell degranulation–> release of histamine–> arteriolar vasodilation–> dec TPR–> dec MAP
Inc vascular permeability due to histamine causes plasma loss to interstitium (must give antihistamines)
Neurogenic shock
Loss of vascular tone due to inhibition of normal tonic activity of SYM vasoconstrictor nerves
-deep general anesthesia, pain reflexes associated with traumatic injury, transient vasovagal syncope
dec TPR and dec MAP due to generalized arteriolar vasodilation
Cardiac tamponade- cardiogenic shock
pericardial sac surrounding heart gets filled with fluid, impairing filling of heart- dec magnitude on ecg
dec ventricular filling and EDV–> SV dec–> CO dec–> dec MAP
paradoxical pulse
in cardiac tamponade
- greater than normal decline in systolic arterial pressure during inspiration (>10 mmHg)
- inc in venous return to rv during inspiration causes exaggerated reduction in lv volume becauuse it causes the septum to bulge into left ventrical
Physiological splitting of second heart sound
inspiration causes increase in intrathoracic volume, decreasing intrathoracic pressure–> dec right atrial pressure–> increases gradient between peripheral veins and RA–> inc blood flow into right atrium and inc EDV of RVentricle–> inc SV–> inc ejection time–> delayed closure of pulmonic valve
Affect of inspiration on left ventricle
Increase in intrathoracic volume will decrease intrathoracic pressure–> distending pulmonary veins–> dec pressure in pulmonary veins and pooling of blood–> dec return to LA–> dec EDV of LV–> dec SV
Beta 1 receptors activated by
NE from SYM
- SA node: inc HR
- AV node: inc conduction velocity (dec PR interval)
- atrial and ventricular muscle- increase inotropic state
Alpha 1 receptors in
vascular smooth muscle
- arteriolar constriction- inc TPR
- venoconstriction- inc venous return
Beta2 receptors in
skeletal muscle arterioles
- circulating Epi causes vasodilation
- fight or flight response
Irreversible shock
due to prolonged shock and impaired organ blood flow causing local accumulation of vasodilator metabolites (overcome effects of SYM) and lactic acid
- arteriolar vasodilation- low TPR
- cellular injury bc of impaired blood flow- release of toxic factors (myocardial depressant factor)- impaired contractility- dec CO
