Vascular problems 2 Flashcards
What are the 5 P’s of compartment syndrome?
Pallor Paraesthesia Pulse deficit paralysis Pain (on passive extension of compartment) and perishing cold
Tissue pressure levels in compartment syndrome
Pe > 35mmHg: impaired perfusion due to closure and spasm in pre capillary vessels
Change in compartment volume may be due to?
Haemorrhage
Oedema
Inflammation
Compartment syndrome? Why loss of feeling in patients fingers?
Nerves compressed therefore afferent sensations cant travel along nerve. Also due to ischaemia of nerves
Why does patient still have radial pulse?
Because systolic pressure still enough to overcome increase in tissue pressure. Increase in TP may have just affected the pre capillary BV’s atm, if bleed happens in major artery will lose radial pulse / weaker
How to distinguish between non-cariogenic and cariogenic PE
- History, physical exam and labs:
NC: pulmonary or non pulmonary infection, history of aspirate, high white cell count, BNP <100
C: History of MI, or likely to have MI, low output state, heart sounds, peripheral oedema, JVP distention, BNP >500 - Chest radiograph
NC: normal cardiac silhouette, absence of Kerleys B lines
C: enlarged cardiac silhouette, presence of kerleys B lines - Transthoracic echocardiogram:
C: enlarged cardiac chambers, decreased LV function - Pulmonary artery catheterisation to check occlusion pressure.
If a patient has lost a lot of blood, why might they have a reduced pulse and MAP, have an elevated heart rate and be pale and sweaty
Pulse pressure and MAP low because he’s lost a lot of blood, inc HR to maintain CO. Pale and sweaty to increase sympathetic drive, and redistribution of the blood flow from the periphery inwards. Under haemodynamic stress the receptors that activate stress seem to go off.
HR increase to maintain CO and perfusion pressure
Why is the patients haematocrit reduced and how can we use this information to measure the extent of his blood loss.
When losing blood you’re losing red cells and fluid so ratio of cells the same, but at some point are reabsorbing fluid from tissue intersitium to try and maintain volume which partly explains decrease in haematocrit.
If you catch patient soon after haemorrhage haematocrit unchanged because not enough time for tissue to be reabsorbed from interstitum. The fact that haematocrit is low suggests its has been a couple of hours
Why is the patient unable to maintain BP in the medium term despite replacement of blood he has lost
circulatory shock!
Sustained ischaemia can cause problems in the microcirculation that are not easily reversed
Loss of vascular tone due to
- Inadequate perfusion of BV walls via vasa vasorum
- Imparied adrenergic neurotransmission due to the depletion of noradrenaline in nerve terminals
- Perivascular accumulation of vasodilator metabolites and local release of histamine, serotonin, kinins and prostaglandins
Local accumulation of the autocoids above and toxins may compromise capillary integrity leading to increased capillary permeability
With reduced BF shear rates in the venous circuit reduced, results in stasis and clogging of microcirculation.
Capacity to retain pre capillary smooth muscle activity in pre capillary vessels diminished but post capillary vessel tone maintained. As a result capillary hydrostatic pressure rise relative to the very low levels seen initially as a result of blood loss.
Loss of capillary integrity due to accumulation of cytokines and autocoids leads to leakage of plasma proteins into interstitial space
Treatment?
Try and maintain perfusion pressure by getting them to lie down, legs up. Hopefully eventually effects of sustained ischaemia get reversed.
Compensatory haemorrhage
Initially as blood is removed you get large increase in HR, sympathetic drive to heart doubles, similar to kidney as you draw more blood you get to a point where HR completely falls off and sympathetic nerve activity decreases to 0. then BP starts to fall.
