NCLEX Prep

NCLEX QOTD

Answer: Bradycardia & hypotension are the hallmark signs of neurogenic shock. This type of shock falls under the distributive umbrella.

Renin Angiotensin Aldosterone System (RAAS) review

RAAS Review 
It’s critical to understand RAAS for critically ill/traumatically injured shock patients. The RAAS regulates blood pressure and fluid balance in the body. When blood volume or sodium levels in the body are low, or potassium is high, cells in the kidney release the enzyme, renin. Renin converts angiotensinogen, which is produced in the liver, to the hormone angiotensin I. An enzyme known as ACE or angiotensin-converting enzyme found in the lungs metabolizes angiotensin I into angiotensin II. Angiotensin II causes blood vessels to constrict and blood pressure to increase. Angiotensin II stimulates the release of the hormone aldosterone in the adrenal glands, which causes the renal tubules to retain sodium and water and excrete potassium. Together, angiotensin II and aldosterone work to raise blood volume, BP and sodium levels in the blood to restore the balance of sodium, potassium, and fluids in an attempt to normalize the BP in an otherwise “shocky” patient.


Hypovolemic shock occurs due to loss of in total volume of blood, available for circulation. Whether the bleeding is caused by blunt or penetrating trauma, the loss of blood stimulated baroreceptors in the carotid bodies and aortic arch to speed up the HR. HR X SV=CO.



When pts are trying to compensate hypovolemic shock, RAAS (Renin angiotensin aldosterone system) is activated.
The activated RAAS system releases angiotensin II. Angiotensin II causes vasoconstriction of arteries and veins, thereby increasing blood pressure. It also promotes adrenal cortex to secrete aldosterone. Aldosterone in turn stimulates sodium and water retention as well as excretion of potassium from kidneys. The resulting high sodium ions in the serum causes secretion of ADH (antidiuretic hormone). ADH intensifies water reabsorption, resulting in increased blood volume, BP (blood pressure) and CO (cardiac output). This is why we frequently see our hypovolemic trauma patients present with tachycardia and hypotension, depending on which stage of shock they present with. 
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Trauma Triad Of Death

💉🚑🚑💉💉🚑🚑💉💉🚑🚑🚑🚑 The lethal trauma triad of death is one of the things that increases trauma patients morbidity & mortality. By majority, the answer would be hypovolemic shock. Hypovolemia is defined as a state in which there is a decrease in plasma volume within the body. Hypovolemia, if severe enough, produces shock. Shock is defined as inadequate tissue perfusion combined with the inadequate removal of cellular wastes, ultimately producing a defect in oxidative metabolism and therefore a subsequent dysfunction in the way that the body transports, delivers, and utilized oxygen. Hypovolemic shock in trauma patients often stems from acute hemorrhage. •

Hypovolemic shock secondary to hemorrhage produces a lethal triad

of:

1.) acidosis

2.) hypothermia

3.) coagulopathy

Hypovolemic shock produces several defects in physiology. The decreased intravascular fluid volume decreases venous return to the heart, which ultimately reduces preload and stroke volume (SV). The body initially compensates for the decreased SV by increasing the heart rate in order to maintain cardiac output (CO). Eventually CO decreases and subsequently results in decreased end-organ perfusion.

As the body becomes deprived of oxygen, aerobic metabolism shifts to anaerobic metabolism. This shift causes the build up of lactic acid, which ultimately produces metabolic acidosis. The hemorrhage in hypovolemic shock results in extreme activation of prothrombin, which causes an excess of thrombin formation. The excess thrombin causes the conversion of fibrinogen to fibrin. Fibrin activation produces wide-spread clot formation. This process depletes coagulation factors. Overtime, secondary fibrinolysis and coagulopathy results in further bleeding. As the hemorrhage progresses, hypothermia results from excess shunting of blood away from extremities producing a “shocky” looking patient who is clamped down.

The patient usually has delayed cap refill and w/kids an early sign is a gap between central and peripheral pulses. Giving volume such as whole blood or 1:1:1 of PRBC’s/platelets/FFP is what the patient needs in order to achieve homeostasis, maintain normal perfusion and to hopefully achieve a MAP of 65.