Decreased pulmonary artery wedge pressure (PCWP)
Introduction
Introduction Patients with hemorrhagic shock can be observed by central manometry to reduce central venous pressure (CVP) and pulmonary wedge pressure (PCWP), decreased cardiac output, decreased venous oxygen saturation (SVO2), and increased systemic vascular resistance. A large number of blood loss caused by shock is called hemorrhagic shock, which is common in bleeding caused by trauma, bleeding from peptic ulcer, rupture of esophageal varices, and bleeding caused by obstetrics and gynecology. Whether or not shock occurs after blood loss depends not only on the amount of blood loss, but also on the rate of blood loss. Shock is often caused by rapid, large (more than 30 to 35% of total blood) blood loss without timely replenishment.
Cause
Cause
Microcirculatory disorders (ischemia, congestion, disseminated intravascular coagulation) cause microcirculation arterial blood perfusion insufficient, important vital organs due to hypoxia and functional and metabolic disorders, is the common law of all types of shock. The changes in microcirculation during shock can be roughly divided into three phases, namely microcirculation ischemic phase, microcirculation hepatic phase and microcirculation coagulation phase.
(1) Microcirculation ischemic period (ischemic hypoxia)
The characteristics of this microcirculation change are:
1 The arterioles, posterior micro-arteries, and anterior capillaries contracted, and the microcirculation perfusion was drastically reduced and the pressure was reduced.
2 venules and venules are less sensitive to catecholamines and less contractile.
3 arteriovenous anastomosis may have different degrees of openness, blood from the arterioles through the arteriovenous anastomosis directly into the venules.
A key change that causes microcirculatory ischemia is the sympathetic nervous-adrenal medullary system that is strongly excited. Different types of shock can cause sympathy through different mechanisms - decreased renal output and decreased arterial blood pressure during adrenal medullary shock and cardiogenic shock. The sympathetic-adrenal medullary system is excited by sinus arch reflex; Endotoxin can directly stimulate sympathetic endotoxic shock - the adrenal medullary system makes it intensely excited.
The total effect of sympathetic excitation, increased catecholamine release on the cardiovascular system is increased peripheral total resistance and increased cardiac output. However, the responses of blood vessels in different organs are quite different. The blood vessels of the skin, abdominal viscera and kidney are dominated by a rich sympathetic vasoconstrictor.
Moreover, receptors have an advantage. Therefore, when sympathetic excitation and catecholamines increase, the small arteries, venules, arterioles and capillary anterior red muscles of these sites contract, and the sympathetic vasoconies are distributed due to the arterioles. The densest, precapillary sphincters are most responsive to catecholamines, so they contract most strongly.
The result is that the pre-capillary resistance is significantly increased, the microcirculation perfusion flow is drastically reduced, and the mean blood pressure of the capillaries is significantly reduced. Only a small amount of blood flows into the venules and venules through the direct pathway and a few true capillaries, and the tissue is severely deficient. Bloody hypoxia.
The sympathetic vasoconstrictor fibers of the cerebral vessels are the least distributed, the alpha receptor density is also low, and the caliber can be unchanged. Although the coronary arteries also have sympathetic innervation, there are also alpha and beta receptors, but sympathetic excitation and catecholamine increase can be enhanced by cardiac activity, and the metabolic level is increased, so that the vasodilator metabolites, especially adenosine, increase and the coronary arteries expand.
Sympathetic excitability and reduced blood volume can also activate the renin-angiotensin-aldosterone system, while angiotensin II has a strong vasoconstrictor effect, including contraction of the coronary arteries.
In addition, increased catecholamines can also stimulate platelets to produce more thromboxane A2 (thromboxane A2, TXA2). TXA2 also has a strong vasoconstrictor effect.
Examine
an examination
Related inspection
Pulmonary ventilation function pulmonary ventilation imaging
In many cases, it is not too difficult to diagnose bleeding. Both medical history and physical signs can reflect the lack of vascular content and the compensatory response of adrenal energy. However, experimental testing is not entirely true. Because in the short time after acute blood loss, body fluid movement is not very obvious, it is difficult to reflect through blood test indicators. If the process of blood loss is slightly longer and the body fluid movement is gradually increased, the blood will be concentrated, which is manifested by increased hemoglobin, increased hematocrit, and increased ratio of urea nitrogen to creatinine. If the process of blood loss is long, the amount of blood loss is large, especially the loss of free water is gradually increased, and serum sodium is also increased. In short, the amount of blood loss in shock should be fully estimated, and it is often estimated that the clinical is insufficient.
When the blood loss is large, causing severe low-volume shock, and it is difficult to grasp the actual and regular changes in the clinical, especially if the rehydration therapy is difficult to show positive effects, it should be considered that the central venous catheter or pulmonary artery can be placed. Catheter for invasive hemodynamic monitoring. Central venous pressure (CVP) and pulmonary wedge pressure (PCWP) were reduced by central manometry, cardiac output was reduced, venous oxygen saturation (SVO2) was reduced, and systemic vascular resistance was increased.
Diagnosis
Differential diagnosis
Insufficient capacity beyond the compensatory function will present a comprehensive symptom of shock. The blood output from the heart is reduced, and although the surrounding blood vessels contract, the blood pressure still drops. Reduced tissue perfusion, promotes anaerobic metabolism, and increases lactic acid and metabolic acidosis. Redistribution of blood flow allows brain and heart supply to be maintained. Further contraction of blood vessels can cause cellular damage. Damage to vascular endothelial cells results in loss of body fluids and proteins, aggravating hypovolemia. Multiple organ failure will eventually occur. The intestinal mucosa is impaired in the defense of antibodies derived from the intestine caused by hemorrhagic shock, and is likely to be an important pathogenesis of pneumonia and other infectious complications. The lethal dose of blood loss has an ability to cross-tolerate the attack on endotoxin. The lethal dose of blood loss can protect against lethal endotoxin challenge.
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