Hypotension Flashcards
What are the different forms of shock
Hypovolemic - ack of fluids, skin is cold and clammy since the TPR is low by baroreflex, low central venous pressure
Distributive - septic, anaphylaxis or neurogenic, arterioles have dilated, reducing TPR dramatically, also called low resistance or warm shock
Cardiogenic - impaired pump function like in heart failure, cardiac tamponade and MI, skin feels cold and clammy, high central venous pressure as blood cannot be pumped
Explain the form of contraction in hemorrhage and dehydration
Hemorrhage is isotonic contraction
Dehydration and hypertonic contraction
How is the pulse in hemorrhagic shock
It is weak and thready, since the pulse pressure is low due to the fact that there is low stroke volume
What drops faster? CO or MAP
MAP stays almost same when about 30% of the blood is removed since the baroreflex keeps maintaining the MAP whereas CO reduces much more significantly
How does the curve shift up
Decrease in afterload and increase in inotropic shock due to hemorrhagic shock.
Also notice that the preload is decreasing
What happens to NO levels in distributive shock
Systemic release of inflammatory mediators cause increased expression of iNOS in endothelial cells which cause massive amounts of NO to be released. This causes arterioles dilation.
Also vasoconstrictors are less effective in these people as massive amounts of NO reduces the effectiveness of vasoconstrictors
Explain the process of microvascular inflammation in spetic shock
Cytokines and other inflammatory mediators will cause the TPR to become low, increasing blood flow to the organs and causing edema to develop which will impair O2 transport to the cells of the organs.
Edema develops due to the development of increased permeability in the post capillary venules
What are the examples of neurogenic shock
- Over administration of anethasia
- Vasovagal syncope
- Pain reflex from deep trauma
The one thing common in all of these is that the sympathetic nervous system is far less active than normal, causing vasodilation and a decrease in TPR
Cardiac Tamponade
Trauma that ruptures blood vessels in the pericardial sac or infection in the paricardial sac causes fluid accumulation in the pericardial sac which causes higher pressures to develop in the pericardial sac.
This leads to impaired hear filling during diastole and as a result CO goes down due to decrease in SV
How does this look like in graph, what other 2 examples cause a similar change
Hypertrophy and diastolic heart failure
Paradoxical pulse
In cardiac tamponade, there is a greater than normal decline in the systemic arteriolar pressure during inspiration since more blood goes to the right side of the heart which causes the median septum to push against the left ventricle and there is more reduction in the volume of the left ventricle.
The increasing bulging into the left ventricle also further decrease the stroke volume
How does the EKG change in cardiac tamponade
It dampens the waves, the waves are not that high
Is there increased levels of sympathetic firing in the distributive shock
Yes there are but increased NO minimizes the effect of NE and hence vasoconstrition does not occur
How do you differentiate between hemorrhagic and cardiogenic shock
By assessing the central venous pressure which is high in cardiogenic shock and low in hemorrhagic shock
The hepatojugular relflex can be useful where the person puts pressure on the abdomen which causes distention of the jugulur vein. This marks increae in central venous pressure which is what happens in cardiogenic shock
Compensatory changes in microcirculation in distributive shock
Hydrostatic pressure is low whereas oncotic pressure has remained the same so water will flow from the tissues into the capillaries which will compensate for low TPR to some extent
Can you use L Name in septic shock to inhibit NO production
No since low levels of NO will cause leukocyte adherence to the endothelial cells, worsening the pathogenesis of the septic shock
What is irreversible shock
Massive hemorrhagic shock will cause the hypotensive blood pressure to stay constant for a while and then it will decrease.
Even if blood transfusion is given, it will increase the blood pressure initially but then the pressure will go down and the person will die anyway
How does this happen
Severe hemorrhagic shock has several effects:
- There is accumulation of vasodilators, which are found in organs with high metabolic rate, cells die and these are released in an uncontrolled fashion
- There is lactic acidosis which also contributes to impaired cell function and the blood pressure drops
- Some cells when they die they release toxic factors called MYOCARDIAL DEPRESSANT FACTOR which reduces the heart function and contractility of the heart goes down, this lowers CO.
How is there injury to endothelial cells in blood transfusion after hemorrhagic shock
This is systemic reperfusion injury
- ROS are made during ishemia in the endothelial cells, increased O2 inactivate NO and these ROS then cause injury to the cells
- More leukocytes adhere to the endothelial cells
- There is endothelian 1 formation
- Production of inflammatory mediators increases
