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What is shock
IT is a conditiong or a syndrome that is a widespread abnormal cellular metabolism that occurs when the human need for oxygenation and tissue perfusion is not met to the level needed to maintain cell function. Produce a whole body response. Organs either adapt or fail to function due to hypoxia. It is a syndrome becuase it happens in a predictable sequence
4 clasifications of shock and thier respective causes. (Spacific causes in the outline)
Hypovolemic shock - total bady fluid decreased ( in all compartments)
Cardiogenic shock - direct pump failure, fluid is not effected
Distributive - Fluid shifted from central vascular space. Total body fluid volume normal or increased.
Obstructive - Cardiac function decreased by noncardiac factors. Total body fluid volume not affected. Central volume decreases
Describe mechanisms involved in the regulation of normal blood pressure. CH 42 in Lehne
- Tissue and organ perfusion is related to mean arterial pressure (MAP). Because the cardiovascular system is a closed but continuous circuit, the factors that influence MAP include:
- _ Total blood volume
- _ Cardiac output
- _ Size of the vascular bed
- Total blood volume and cardiac output are directly related to MAP, so increases in either total blood volume or cardiac output raise MAP. Decreases in either total blood volume or cardiac output lower MAP.
- The size of the vascular bed is inversely (negatively) related to MAP. This means that increases in the size of the vascular bed lower MAP and decreases raise MAP.
- When blood vessels dilate and total blood volume remains the same, blood pressure decreases and blood flow is slower. When blood vessels constrict and total blood volume remains the same, blood pressure increases and blood flow is faster.
Hypovolemic shock occurs when too little circulating blood volume causes a MAP decrease(loss of blood volume through vascular space), resulting in the body's total need for oxygen not being met. Common problems leading to hypovolemic shock are hemorrhage (external or internal) and dehydration.
Decreae in MAP of 5-10 below baseline trigger baroreceptors to compansate and to provide vital organs with oxygen while limiting blod flow to others.
If MAP continue to decrase som tissues function anaerobicly releasing lactric acids and metaobolities leading to acid-bace imbalance and electrolye imbalance and if not corrected withing 1-2 hr some serioes tissue damage will be done (MODS)
- Distributive shock is the type of shock that occurs when blood volume is not lost from the body but is distributed to the interstitial tissues where it cannot circulate and deliver oxygen. It can be caused by a loss of sympathetic tone, blood vessel dilation, pooling of blood in venous and capillary beds, and increased blood vessel permeability (capillary leak). All these factors can decrease mean arterial pressure (MAP) and may be started by nerve changes (neural-induced) or the presence of chemicals (chemical-induced)
- Neural-induced distributive shock: is a loss of MAP that occurs when sympathetic nerve impulses controlling blood vessel smooth muscle are decreased and the smooth muscles of blood vessels relax, causing vasodilation. This blood vessel dilation can be a normal local response to injury, but shock results when the vasodilation is widespread or systemic.
- Chemical-induced distributive shock: has three common origins: anaphylaxis, sepsis, and capillary leak syndrome. It occurs when certain chemicals or foreign substances within the blood and blood vessels start widespread changes in blood vessel walls. The chemicals are usually exogenous (originate outside the body), but this type of shock also can be induced by substances normally found in the body (endogenous).
Sepsis is a widespread infection that triggers a whole-body inflammatory response. It leads to distributive shock when infectious microorganisms are present in the blood. This form of shock is most commonly called septic shock.
Capillary leak syndrome
Capillary leak syndrome is the response of capillaries to the presence of biologic chemicals (mediators) that change blood vessel integrity and allow fluid to shift from the blood in the vascular space into the interstitial tissues. Once in the interstitial tissue, these fluids are stagnant and cannot deliver oxygen or remove tissue waste products. These fluid shifts result from increased size of capillary pores, loss of plasma osmolarity, and increased hydrostatic pressure in the blood. Problems causing fluid shifts include severe burns, liver disorders, ascites, peritonitis, paralytic ileus, severe malnutrition, large wounds, hyperglycemia, kidney disease, hypoproteinemia, and trauma.
caused by problems that impair the ability of the normal heart muscle to pump effectively. The heart itself remains normal, but conditions outside the heart prevent either adequate filling of the heart or adequate contraction of the healthy heart muscle. The most common causes of obstructive shock are pericarditis and cardiac tamponade
Initial stage of Shock
When MAP decrease by less then 10 mm HG. Compansatory mechanisms working well in maintainig blood flow to all vital organs.
Slight increase in heart rate and resp rate, slight increase diastolic blood pressure, mild anxiety or restlessness.
- MAP decreased by 10-15 mmHg.
- Now renins system and ADH released to compansate
- kidney cause water and sodium reabsorptions and systematic vasoconstriction
- ADH - water reabsorptions and peripheral vasoconstriction.
Epinephrien and norepinephrin released
Tissue hopoxia occurs in nonvital organs but no permanent damage - can run anaerobicly
Acidosis and hyperkalemia occurs
Symptoms: anxiety, thirst sensation, increase in systolic and dicrease in diastolic blood pressure, restlesness, tachycardia, incrased respiratory rate, cool skin, slagish capilary refil, decreased urine output
- MAP decreased by more than 20mmHg
- Cells are dying
- systems are startin to fail
- pale/mottled/cyanotic skin, decreased level of consciousness, little urine output, low central venouse pressure, low pulse.
Usually a person can be saved in this stage if the conditions that casuing shock are corrected withing 1 hour of the unset of this stage.
- Organs are failing
- Cyanotic, cold skin, diminished or absent pulses, unconsciousness, no urine output, significant hypotension, shallow slow respiration
Person cannot be saved even with intervensions.
MODS: - The sequence of cell damage caused by the massive release of toxic metabolites and enzymes. Once the damage has started, the sequence becomes a vicious cycle as more dead cells break open and release harmful metabolites. The metabolites trigger small clots (microthrombi) to form. The clots block tissue oxygenation and damage more cells, thus continuing the devastating cycle. MODS occurs first in the liver, heart, brain, and kidney. The most profound change is damage to the heart muscle.
Changes in cell metabolism that occur during shock
cell damage caused by the massive release of toxic metabolites and enzymes. More dead cells break open and release harmful metabolites. The metabolites trigger small clots (microthrombi) to form. The clots block tissue oxygenation and damage more cells.
Changes in cardiovascular status during progression of shock
- It is the first clinical sign of hypovelmic shock.
- Decreased MAP leading to adaptive responses.
- Assess central and peripheral pulses for rate and quality - in the initial stage, the pulse rate increases to kep cardiac ouput and MAP at normal level, even though the actual stroke volume per beat is decreased and it is the earliest manifestation of shock.
Peripheral pulses are difficult to palpate and are easily blocked with light pressure and as shock progressess pulses can be absent
- 90/50 may indicate shock but be normal in some people
- When vasoconstriction is present, diastolic presure increae but systolic pressure remains the same leading to narrower pulse pressure.
Systolic blood pressure decreases as schock progresses and cardiac output decreases. Further narrowing pulse pressure. When shock continues and intervensiont are not adequate, then both systolic and diastolic pressure decreas.
Changes in respiratory status
- Resp reate increases
- When shock progresses to the stage at which lactic acidosis is present, the respiratory depth also increases.
A decrease in urine output is a sensitive indicator of early shock. Measure urine output at least every hour. In severe shock, urine output is decreased (compared with fluid intake) or even absent. Of the four vital organs (heart, brain, liver, and kidney), only the kidney can tolerate hypoxia and anoxia for up to 1 hour without permanent damage. When hypoxia or anoxia persists beyond this time, patients are at risk for acute tubular necrosis (ATN) and kidney failure.
With shock, it feels cool or cold to the touch and is moist. As shock progresses, color changes are first evident in the mucous membranes and in the skin around the mouth. Pallor or cyanosis is best assessed in the oral mucous membranes in dark-skinned patients. Color changes in patients with lighter skin are noted first in the extremities and then in the central trunk area. The skin feels clammy or moist to the touch, not because sweating increases but because the normal fluid lost through the skin does not evaporate quickly on cold skin. As shock progresses, skin becomes mottled. Lighter-skinned patients have an overall grayish blue color, and darker-skinned patients appear darker, without an underlying reddish glow.
Capilary refil may be absent
CHanges in neurological status
Thirst is stimulated
- assess LOC and A&O status
- The central nervous system changes of hypovolemic shock are caused by cerebral hypoxia. In the initial and nonprogressive stages, patients may be restless or agitated and may be anxious or have a feeling of impending doom that has no obvious cause. As hypoxia progresses, confusion and lethargy occur. Lethargy progresses to somnolence and loss of consciousness as cerebral hypoxia worsens.
Laboratory findings in shock
- In hemorrhage - Hemato and hemog decreased
- In dehydration - H&M elevated
Potassium - increased : dehydration, acidosis
Nursing intervensions indicated in hypovolemic shock
- _ Ensure a patent airway.
- _ Start an IV catheter, or maintain an established catheter.
- _ Administer oxygen.
- _ Elevate the patient's feet, keeping his or her head flat or elevated to a 30-degree angle.
- _ Examine the patient for overt bleeding.
- _ If overt bleeding is present, apply direct pressure to the site.
- _ Administer drugs as prescribed.
- _ Increase the rate of IV fluid delivery.
- _ Do not leave the patient
Chrystalloid fluids (nonprotein subs) - given to help maintainand adequate fluid and electrolyte balance. Normal saling increases plasma volume and can also be infused with any blood product. Ringer's lactate contains sodium, chlrodie, calcium, potassium and lactate. This isotonic solutions expands volume and the lactate buffers any acidosis - cannot be infused with blood products since calcium induces clotting of the infussin blood.
Colloid fluids (whole blood, packed red blood cells, plasma, plasma fractions, and synthetic plasma exapnders) - help restore osmotic pressure and fluid volume. Used for hemorrhage.
The actions of drugs for shock increase venous return, improve cardiac contractility, or improve cardiac perfusion by dilating the coronary vessels.
Vasoconstricting drugs stimulate venous return by constricting blood vessels and decreasing venous pooling of blood. These actions increase cardiac output and mean arterial pressure (MAP), which help improve tissue perfusion and oxygenation. Such agents include dopamine (Intropin) and norepinephrine (Levophed).
Drugs enhancing myocardial perfusion help ensure that the heart is well perfused, especially when giving drugs to improve cardiac contraction, so that aerobic metabolism is maintained in the heart cells and maximum contractility can occur. Drugs that dilate coronary blood vessels while minimally dilating systemic vessels are used for this purpose. A common drug with this action is sodium nitroprusside (Nitropress)
Sepsis and septic shock is a complex type of distributive shock that usually begins as a bacterial or fungal infection and progresses to a dangerous condition over a period of days.
Sepsis: is a widespread infection coupled with a more general inflammatory response, known as systemic inflammatory response syndrome (SIRS), that is triggered when an infection escapes local control.
At the tissue level, the WBCs are producing many pro-inflammatory cytokines as a result,there is widespread vasodilation and pooling of blood in some tissues. Pt has mild hypontension, a urine output that is lower than expceted for fluid intake, and an increased respiratory rate. These actions result in a hypodynamic state with decreased cardiac output.
Microthrombi begin to form whithin the capillaries fo some orans, causing some cell hypoxia and reducing organ function. The problem is hard to detect but if sepsis is stopped at this point, the organ damage is completely reversible.
- Cell anoxia, cell death
- Organ failure
- Release of metabolites
- Microthrombin form, consumingplatelets and clotting factors
- Trigger more pro-inflammatory cytokines which increase capillary leakness, injure cells.
- This stage last for 24 hr and can be missed due to cardiac function is hyperdynamic in this phase. The pooling of blood and the widespread capillary leak stimulate the heart, and cardiac output is increased with a more rapid heart rate and elevated systolic blood pressure. Extremities may feel warm and a little or no cyanosis.
Major manifistations: lower oxygen saturation, rapid respiratory rate, decreased to absent urine output, and a change in the patient's cognition and affect.
- is the stage of sepsis and SIRS when multiple organ failure is evident and uncontrolled bleeding occurs. Even with appropriate intervention, the death rate among patients in this stage of sepsis exceeds 60%. Severe hypovolemic shock is present with hypodynamic cardiac function. This is the result of an inability of the blood to clot because the platelets and clotting factors were consumed earlier, capillary leak continues and cardiac contractility is poor from cellular ischemia and the presence of myocardial depressant factor. The clinical manifestations resemble the late stage of hypovolemic shock (hymorrhage)
- When sepsis progresses to septic shock and circulation is severely compromised, the skin is cool and clammy and pallor, mottling, or cyanosis is present. In patients with DIC, petechiae and ecchymoses can occur anywhere. Blood may ooze from the gums, other mucous membranes, and venipuncture sites, as well as around IV catheters.
Nursing intervention in septic shock
- Oxygen therapy - mechanically ventilated
- Drug therapy to enhance cardiac output and restore vascular volume is essentially the same as that used in hypovolemic shock. In addition, drug therapy is needed to combat sepsis, adrenal insufficiency, hyperglycemia, and clotting problems.
- Blood replacement therapy is used when septic shock progresses to hemorrhage.
Nursing measures used to control hemorrhage
inhancing CO by circulatory volume replacement, cessation of bleeding, and reversing the shock syndrome.
- Administer O2 and monitor for hopoxia such as changes in LOC
- IV - crystalloid solutions such as Ringer'r and normal saline to maintaint fluid and electrolyte level and lactate is a buffer in presence of acidosis. Nurse will monitor input and output.
- Surgical repair of soucre of bleeding.
- IV - colloid solutions - blood products to restore plasma volume and osmotic pressure
- Drug - dopamine and norepinephrine can be used in patietns that don't respone to fluid and blood repalcement therapy. This will vasoconstrict and increae MAP and CO.
- -nitroprusside - inhances venous return and increase MAP, thus insurig maocardila perfusion, by systemic vasodilation
- Slowing of the heart rate
- Increased gastric secretion
- Emptying of the bladder
- Emptying of the bowel
- Focusing the eye for near vision
- Constricting the pupil
- Constracting brohcial smooth muscle
- It conserves energy by reducing cardiac work
- Help control vision
- 1. Regulating the cardiovascular system (increase CO, vasoconstriction by epi in most vascular beds and vasodilation on others)
- - Maintenance of blood flow to the brain
- - Redistribution of blood flow during exercise
- - Compensation for loss of blood, primarily by causing vasoconstriction
- 2. Regulating body temprature
- - by regulating blood flow to the skin, increase or decrease heat loss. Dilate - heat loss, constricting - conserving heat.
- - sweat glands innervated to promote secretion of sweat, helping the body to cool.
- - By inducing piloerection (erection of heir) to promote heat conservation.
- 3. Implementing the "fight-or-flight" reaction
- - Increase HR and BP
- - Shunting blood away from skin and viscera and into skeletal muscle
- -dilating brochi
- -Dilating pupils
- - Mobilized stored energy, glucose for brain and fatty acid for muscles.
In most organs, the parasympathetic NS provides the predominant tone. THe vascular system, which is regulated almost exclusively by the sympathetic NS, is the principal exception.
Drug acting sites of Parasympathetic NS
- Ganglion - the junction(synapse) where of two neurons one from brain to ganglion and the other from ganglion to effector organ.
- Two sites at which drugs can act
- 1. the synapses between preganglionic neurons and postanglionic neruons
- 2. Junctions between postanglionic neruons and theri effector organs.
Drug acting sites of Sympathetic NS
- Medula is similar to ganglion in parasympathetic NS so that the spinal cord send massages to medula via preganglionic neurons and then medula sends the responds (like epinephrine) via ponstganglionic neuron to effector organs, Even though there is no ganglion, as such, in this pathway.
- Two general drug acting sites:
- 1. thy synapses between preganglionic and postganglionic neurons (including the adrenal medulla)
- 2. junction between postganglionic neurons and their effector organs.
Transmitter of peripheral NS
- 1. All preganglionic neurons of the parasympathetic and sympathetic nervous systems release acetylcholine as their transmitter.
- 2. All postganglionic neurons of the parasympathetic nervous system release acetylcholine as their transmitter.
- 3. Most postganglionic neurons of the sympathetic nervous system release norepinephrine as their transmitter.
- 4. Postganglionic neurons of the sympathetic nervous system that innervate sweat glands release acetylcholine as their transmitter.
- 5. Epinephrine is the principal transmitter released by the adrenal medulla.
- 6. All motor neurons to skeletal muscles release acetylcholine as their transmitter.
Cholinergic and Adrenergic Receptors
- Cholinergic receptors: mediate responses to acetylcholine at the junctions where acetylcholine is trasmited.
- Adrenergic receptors: mediate responses to epinephrine and norepinephrine at all junction where norepi and epi is the trasnmiter.
Subtypes of Adrenergic receptors
5th one is dopamine receptor: responds only to dopamine, a neurotransmiter found primarily in the CNS
Location of adrenergic receptor sybtypes
Adrenergic receptors—alpha, beta, or both—are located on all organs (except sweat glands) regulated by the sympathetic nervous system (ie, organs innervated by postganglionic sympathetic nerves). Adrenergic receptors are also located on organs regulated by epinephrine released from the adrenal medulla.
Receptor specificity of adrenergic Trasmitters
- Epinephrine can activate - Alpha1, Alpha2, Beta1, Beta2, but not dopamine ( Beta 2 will only be activate in fight or flight response)
- Norepinephrine activates - Alpha 1 and 2, Beta 1
- Dopamine activates - Alpha 1, Beta 1 and dopamine