Hypovolemic shock

'Hypovolemic shock is a sudden disorder of organ and tissue perfusion that leads to organ changes and threatens the patient's life. It originates from a relative or absolute lack of intravascular fluid. It arises from the following causes:

External and internal bleeding (so-called hemorrhagic shock),
Fluid sequestration (ascites, fluidothorax, …),
Large fluid losses (diarrhoea, vomiting, polyuria, burns…).

Pathogenesis

There is a decrease in venous return and thus a decrease in cardiac output and systolic BP.
With losses less than 10% of blood volume - the cardiac index is not reduced or significant arterial hypotension (or only orthostatic hypotension) due to the activation of the sympathoadrenal system - cardiac output is redistributed, absorption of fluid from the interstitium, tachycardia, oliguria (increased secretion ADH).
Loss of more than 20-30% of blood volume - reduction of cardiac output, blood pressure initially kept high enough (due to contraction of precapillary sphincters with hypoperfusion of less important organs - but gradually their function is damaged - e.g., in the lungs only the lung base is perfused with blood, the upper lung lobes represent a dead space that can lead to hypoventilation), later BP drops - tachycardia is joined by hypotension, cold acral parts of the body, oliguria to anuria and acidosis (lactic, possibly even respiratory), with plasma losses and dehydration, and additionally an increase in hematocrit.

Main shock parameters

Depending on the amount of lost blood (systolic blood pressure, pulse, diuresis):

Assessing the severity of shock by blood loss (assessed weight 70 kg, 5 L circulating blood volume) ^[1]
estimated blood loss	BP (mmHg)	heart rate (beats/min)	diuresis	state of consciousness	respiratory rate	liquid to replenish the volume
< 15% (<750ml)	norm	norm	norm	slightly anxious	14−20/min	crystalloids
15−30% (750−1 500 ml)	under 100	>100	oliguria	anxious	20−30/min	crystalloids
30−40% (1 500−2 000 ml)	below 90	>120	anuria	confusion	30−40/min	crystalloids+blood
> 40% (>2 000ml)	under 60	>140	anuria	lethargy	>30/min	crystalloids+blood

Oliguria = below 500 ml/day (20 ml/hour).
Anuria = below 100 ml/day (4 ml/hour).
A perfusion pressure of 90 mmHg is the lowest pressure for normal functioning of most tissues.
A perfusion pressure of 60 mmHg is the lowest pressure for normal brain activity.

A heart rate above 100/min and a systolic pressure below 100 torr is considered the "start of shock".
The shock index', i.e. the ratio between heart rate and systolic blood pressure, is also used for evaluation:
- normal HR / systolic BP = 60 / 120 = 0.5
- start of shock (compensation) 100 / 100 = 1
- severe shock (decompensation) 120 / 60 = 2

Clinical picture

= so-called cold hypotension:

'Clinical picture given by hypovolemia: hypotension, oliguria to anuria, reduced CVP (central venous pressure) (as opposed to cardiogenic shock),
'Clinical picture given by compensatory mechanisms: tachycardia, tachypnea, sweating, pallor of the limbs.

Prognosis

good'
this shock is the only type of shock that can be intervened by replenishing fluids
80% survive

Links

Original text is from WikiSkripta https://www.wikiskripta.eu/w/Hypovolemick%C3%BD_%C5%A1ok

Source

Incomplete citation of web. PASTOR, Jan. [cit. 5/30/2010]. <https://langenbeck.webs.com/>.

References

↑ {{#switch: book |book = Incomplete publication citation. LONGMORE, J. M. (J. Murray). Oxford handbook of clinical medicine. Oxford university press, 2010. 0 s. 8; 978-80-7262-438-6. |collection = Incomplete citation of contribution in proceedings. LONGMORE, J. M. (J. Murray). Oxford handbook of clinical medicine. Oxford university press, 2010. 0 s. 8; {{ #if: 9780199232178 |978-80-7262-438-6} } |article = Incomplete article citation. LONGMORE, J. M. (J. Murray). 2010, year 2010, |web = Incomplete site citation. LONGMORE, J. M. (J. Murray). Oxford university press, ©2010. |cd = Incomplete carrier citation. LONGMORE, J. M. (J. Murray). Oxford university press, ©2010. |db = Incomplete database citation. Oxford university press, ©2010. |corporate_literature = LONGMORE, J. M. (J. Murray). Oxford handbook of clinical medicine. Oxford university press, 2010. 0 s. 8; 978-80-7262-438-6} }

[1] {{#switch: book |book = Incomplete publication citation. LONGMORE, J. M. (J. Murray). Oxford handbook of clinical medicine. Oxford university press, 2010. 0 s. 8; 978-80-7262-438-6. |collection = Incomplete citation of contribution in proceedings. LONGMORE, J. M. (J. Murray). Oxford handbook of clinical medicine. Oxford university press, 2010. 0 s. 8; {{ #if: 9780199232178 |978-80-7262-438-6} } |article = Incomplete article citation. LONGMORE, J. M. (J. Murray). 2010, year 2010, |web = Incomplete site citation. LONGMORE, J. M. (J. Murray). Oxford university press, ©2010. |cd = Incomplete carrier citation. LONGMORE, J. M. (J. Murray). Oxford university press, ©2010. |db = Incomplete database citation. Oxford university press, ©2010. |corporate_literature = LONGMORE, J. M. (J. Murray). Oxford handbook of clinical medicine. Oxford university press, 2010. 0 s. 8; 978-80-7262-438-6} }

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