Hypovolemic Shock

Shock

• Syndrome marked by decreased tissue perfusion and impaired cellular metabolism
• Oxygen and nutrients are not supplied to cells at the required levels
• Shock is classified as one of the following: cardiogenic, hypovolemic (absolute or relative), distributive, or obstructive

Hypovolemic Shock

• Absolute hypovolemia stems from loss of intravascular fluid volume
• Hemorrhage is a potential cause
• Gastrointestinal losses from vomiting or diarrhea can cause it
• Fistula drainage and diabetes insipidus are potential causes
• Severe dehydration because of hyperglycemia is a cause
• Relative hypovolemia occurs when fluid moves into the extravascular space (intracavitary)
• "Third spacing" describes fluid volume movement out of the vascular space
• Burns, end-stage liver diseases, and ascites all can cause this

Response and Manifestations

• Extent of injury impacts the body's volume loss response
• Age and general health affect volume loss response
• The body compensates for up to 15% fluid loss, possibly with an increased heart rate
• Greater than 30% blood loss usually necessitates replacement
• Manifestations include anxiety and tachypnea
• As the body compensates there is an increase in CO and heart rate, along with low BP
• Stroke volume, PAWP, and urinary output decrease, indicating involved organs
• Irreversible tissue destruction occurs when greater than 30% of blood volume is lost and not replaced

Septic Shock

• Sepsis describes a systemic inflammatory response to a documented or suspected infection
• Severe sepsis becomes complicated by organ dysfunction
• Gram-positive or gram-negative bacteria is the most common cause
• Fungi, parasites, and viruses can also lead to sepsis
• Sepsis leads to hypotension that does not respond to fluid resuscitation
• Hypoxia results because of inadequate tissue perfusion
• Sepsis causes a dysregulated response to infection leading to organ disjunction
• Mortality rate is greater than 25% without treatment

Pathophysiologic Effects of Septic Shock

• The three major effects are vasodilation, maldistribution of blood flow, and myocardial dysfunction
• Decreased ejection fraction and ventricular dilation
• Coagulation increases while fibrinolysis decreases
• Cytokines and secondary mediators are released in response to bacteria
• Platelet-activating factor contributes to microthrombi, which worsens tissue perfusion
• Septic shock is marked by increased coagulation and inflammation, along with decreased fibrinolysis
• Formation of microthrombi and obstruction of the microvasculature
• Hyperdynamic state of increased CO and decreased systemic vascular resistance if not corrected in 24 hours indicates poor prognosis
• Decreased urine output is an indication of perfusion issues
• Tachypnea and hyperventilation results in respiratory alkalosis
• Respiratory failure develops in 85% of patients, and 40% of those develop ARDS (acute respiratory distress syndrome)
• Cerebral perfusion decreases, indicated by altered neurologic status
• Because of decreased tissue perfusion in the gut, GI dysfunction, GI bleeding, and paralytic ileus

Stages of Shock

• Initial
• Compensatory
• Progressive
• Refractory

Initial Stage of Shock

• The stage is usually not apparent clinically, but the patient may feel unwell, have an elevated temperature, and experience slight tachycardia
• Metabolism changes at the cellular level from aerobic to anaerobic, causing lactic acid to build up
• The liver must remove lactic acid, a process that requires oxygen
• In process, decreases in oxygen levels leads to decreased tissue perfusion

Compensatory Stage of Shock

• Compensatory mechanisms are triggered
• Neural, hormonal, and biochemical attempts to overcome anaerobic metabolism consequences and maintain homeostasis
• Lab, ABGs, and assessments changes are present
• Baroreceptors in carotid and aortic bodies activate the SNS response to decreased BP
• Vasoconstriction occurs, with blood diverted to vital organs like the heart and brain
• The kidneys are the first to show signs of compensation, causing a decrease in urine output
• SNS stimulation increases the myocardial O2 demand by increasing HR and contractility, leading to coronary artery vasodilation
• Shunting blood from the lungs to increase physiologic dead space leads to V/Q mismatch, decreased arterial O2 levels, and increased respiration rate/depth
• Impaired GI motility results in slowed peristalsis and risk for paralytic ileus
• Skin is cool and clammy, except in septic patients, who are usually warm and flushed
• Decreased blood to kidneys activates the renin-angiotensin system
• Angiotensin I becomes angiotensin II causing vasoconstriction
• Increased venous return to the heart
• Stimulates the release of aldosterone, increased sodium reabsorption, and release of ADH
• If the cause of shock is corrected, the patient recovers with little or no residual effects
• If cause of shock is not corrected, patient enters progressive stage

Progressive Stage of Shock

• Compensatory mechanisms begin to fail
• Patient is moved to ICU for advanced monitoring and treatment
• Decreased cellular perfusion and altered capillary permeability are features
• Fluid and protein leak into the interstitial space
• Systemic interstitial edema (+3, +4 pitting edema)
• Cardiac output begins to decrease, resulting in a decrease in BP
• Decrease blood pressure causes a decrease in coronary, cerebral, and peripheral perfusion
• Anasarca (diffuse profound edema)
• Fluid leaks into solid organs and peripheral tissues
• Weeping through the skin may be visible
• Shunts blood flow away from pulmonary capillaries
• Sustained hypoperfusion
• Weak peripheral pulses
• Ischemia of distal extremities causes blue or gray fingers or toes
• Myocardial dysfunction results in dysrhythmias, myocardial ischemia, and possible myocardial infarction, ending with complete cardiovascular system deterioration and potential arrest
• Fluid movement from pulmonary vasculature to the interstitium leads to pulmonary edema and bronchoconstriction
• Decreased functional residual capacity
• The patient would present with the beginning of respiratory failure symptoms of tachypnea, tachycardia, and LOC decrease
• Pulmonary system shows the signs of dysfunction first
• ABGs orders are a must to diagnose effectively
• Fluid shifts into the alveoli which results in edema and decreases in surfactant
• Worsening V/Q mismatch, tachypnea, crackles, and increased work of breathing
• Mucosal barrier of the GI system becomes ischemic
• Ulcers and GI bleeding
• Risk of migration of bacteria which could lead to peritonitis
• Decreased ability to absorb nutrients
• Hypoperfusion of the renal system which results in damaged renal tubules
• Potentially worsened by nephrotoxic drugs (abx)
• Decreased urine output and elevated BUN and serum creatinine
• Metabolic acidosis caused because of aerobic and anaerobic changes resulting in the increased levels in lactic acid
• Renal and respiratory systems are therefore the first that show signs of failing
• Liver fails to metabolize drugs and waste, further decreasing perfusion to it
• Jaundice, elevated enzymes as cells fail to break down bacteria and waste building up in the blood stream
• Loss of immune function leads to a risk for DIC and bleeding significantly

Refractory Stage of Shock

• Anaerobic metabolism is exacerbated
• Lactic acid and waste products accumulate
• Capillary permeability increases more
• Recovery for the patient is almost impossible in this stage
• Profound hypotension and hypoxemia lead to worsening tachycardia
• Failure of one organ system starts effecting all the others, effecting and ending recovery very rapidly

Diagnostic Studies

• Thorough history and physical examination should be conducted, as there is no single study used to definitively identify shock
• Assess blood studies, specifically lactate levels and base deficit
• A 12-lead ECG should be obtained, in addition to continuous ECG monitoring
• Chest X-ray
• Hemodynamic monitoring

Interprofessional Care

• Identification of patients at risk for developing shock, is a successful management strategy
• Integrate patient history, physical examination, and clinical findings to help establish diagnosis
• Control or eliminate decreased perfusion
• Protecting vital organs from any dysfunction and to maximize oxygen delivery
• Optimize breathing with a patent airway
• High-flow oxygen with a nonrebreather
• Interventions to control or eliminate cause of decreased perfusion
• Interventions to protect target and distal organs from dysfunction
• Provisions for multisystem supportive care

General Management and Oxygenation Strategies

• Ensure patient airway is kept patent and is alert and responsive
• Maximize oxygen in the blood for delivery
• Maximize oxygen by optimizing CO with fluid and drug interventions
• If the fluid resuscitation is not helping vasopressors should be started
• Hemoglobin should be at correct levels by transfusion
• Increase the blood oxygen using supplemental oxygen or support mechanicaly

Planning and Volume Replacement

• A plan of care should avoid disrupting oxygen supply and demand with the cornerstone therapy being volume expansion for septic, hypovolemic, and anaphylactic shock
• At least 1/2 large bore IV's a intraosseous accsess device and or central venous catheter
• A starting fluids used are isotonic such as normal saline or ringers that move to colloids, like albumin, if not effective on increasing levels
• Reassess to make sure the therapy working on capillary refill temperature and urine output
• Fluid responsiveness determined by clinical examination
• Vital signs with the cerebral pressures placed within the brain parenchyma and monitoring any capillary and skin temperature variations and urine output
• Potential complications with large volumes include hypothermia and coagulopathy due to fluid and dilutions effecting the coagulation factors ability to work
• Persistent hypotension after adequate fluid may require the addition of vasopressors
• Maintaining the fluid by warming crystalloids and colloids, can also include replacement of clotting factors like platelets

Drug Therapy and Nutritional Support

• The primary goal of drugs is to correct any decreased tissue perfusion
• Vasopressor drugs and norepinephrine maintenance while monitoring end organ perfusion
• Monitor arterial pressure and implement hemodynamic perimeters
• Nutrition is one the most vital aspects to decreasing a patients morbidity from shock with intervention of enteral nutrition with in the first days
• Trophic amounts slowly drip the amount of enteral nutrition while parenteral is contraindicated
• Weigh the patient daily and monitor labs while they are in a hyper-metabolic state

Hypovolemic Shock Interprofessional Care

• Managing and stopping any loss in the patients volume by resuscitation of the fluid circulation
• Resuscitation is calculated using a 3:1 ratio or crystalloid's isotonic solution for the blood loss
• Drug vasopressors such as, Dubutamine and Nor-epinephrine are the medications that helps to increase or restore the perfusion throughout the body
• Some shock causes can effect the electrolyte/glucose or trigger the VTE and so all must be supported to a certain degrees dependent to the type

Nursing Implementation and Assessment

• A, B,C and focused assessment of the skins perfusion temperature color, skin moisture, peripheral pulses, the patients consciousness
• Note the events that leds towards shock, and health history of any allergies, medications and vaccination records
• With any impaired tissue perfusion and changes with anxiety the goals is to improve base line through constant monitoring

Body Composition & Evaluation

• Adequate assessment and management is the key for the evaluation of both physical and phycological changes dependent to the shock
• Many intubation are necessary as well for the proper saturation

SIRS and MODS

• SIRS, caused by inflammation in organs remote from the initial site of insult and requires aggressive infections strategies due to mechanical trauma, abscesses and necrotic tissues
• SIRS will lead towards the MODS with dysfunction in the cardio, resp, renal systems etc
• MODS shows several effects that can lead to a series of imbalances, DIC and metabolic dysfunction
• MODs, a failure is 2 or more of the body's organ is required for diagnosis because homeostasis can no longer be upheld through just intervention to maintain oxygen and decrease risk of infection

MODS & DIC

• Oxygen consumption and delivery becomes dependent so all should and will usually need care for multiple failing organs With a large chance that clots throughout can result in consumptions from DIC leading to bleeding, this is treated directionally in hopes will help the underlying pathological conditions