Advanced Concepts of Clinical Decision

8/8/2019 Advanced Concepts of Clinical Decision

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Advanced Concepts of Clinical Decision-Making: Unit VII: Shock

Shock can be identified as early or late, depending onthe signs and symptoms and the overall severity oforgan dysfunction: stages: compensatory (stage 1),

progressive (stage 2), and irreversible (stage 3). Thewindow of opportunity that increases the likelihood ofpatient survival occurs when aggressive therapybegins within 6 hours of identifying a shock state,especially septic shock.

acute, widespread process of impaired tissue perfusion

results in cellular, metabolic, and hemodynamicmalfunction

in other words, all body systems are affectedfrom the cellular level all the way up to organsystems.

Eventually, if shock continues without being interrupted,it causes cellular dysfunction, and multiple organdysfunction syndrome (MODS), and death.

Etiology

5 Classifications (according to most literature) based on

the underlying cause:

Hypovolemic shock: loss of circulating volume

From whatever shock including: gunshotwound, postpartum hemorrhage, knifing.

Cardiogenic shock: impaired pumping of theheart

You have enough volume but its just not

getting to where its supposed to go Septic shock: caused by infection

Massive dilation that causes a drop in bloodpressure from not having enough pressurein the system anymore


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Neurogenic shock: altered vascular tone causedby CNS injury, medications, or anesthesia.

Sympathetic vascular tone where you onlyhave unopposed parasympathetic impulses

left and the vascular bed doesnt constrict,just stays dilated of course then you losethe pressure in your vasculature.

Anaphylactic shock: hypersensitivity reaction.

Caused by a histamine release as areaction to an allergen or multiple allergens

Other Classifications seen in the literature where types ofshock are grouped according to whats going on with the

blood supply because a lot of the initial stages of shockhas to do with blood pressure:

Distributive shock: mal-distribution ofcirculating blood volume d/t massive vasodilation(loss of symathetic tone); a.k.a. circulatory orvasoactive shock

Septic, Anaphylactic, or Neurogenic (mal-distrubtion of blood volume)

Again, theres enough volume but its notgoing where its supposed to go

Obstructive shock: external forces arecompressing the heart or obstructing the outflowof blood from the heart

Can be caused by tension pneumothorax,cardiac tamponade, a massive pulmonaryembolism, severe pulmonary hypertension,severe aortic stenosis

Traumatic shock: (usually from trauma) canstart with hypovolemia; ends with massivecellular swelling causing obstruction tomicrovascular blood flow (cause there is so muchpressure from all of this fluid being sequesteredeverywhere in the tissues) even though


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macrovascular flow (large vessels) may benormal. (When it gets to the capillary levelswhere the exchange of oxygen and carbondioxide occurs) this is where the problem is andthis state of affairs causes MODS and death.

Pathophysiology

Cellular Changes

Poor perfusion and as a consequence, there ispoor oxygenation of the cells causing:

The cell to swell and cell membrane tobecome more permeable so that differentelectrolytes and fluids move in and out of the cell

much more easily than normal which causes bigfluid and electrolyte shifts and in the meantime,these cellular changes create a demand forglucose.

Cellular effects of shock. The cell swells and the cellmembrane becomes more permeable; fluids and electrolytesseep from and into the cell. Mitochondria and lysosomes are

damaged, and the cell dies.

Depletion of glycogen stores

If the patient has been in a shock state formore than 48 hours, all of their glycogen


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stores, what you store for energy in yourliver, gets all used up because the bodyneeds more and more energy to keepgoing. Mainly one of the problems is thatthere is not enough glucose so some of this

energy has to be put towards makingglucose out of other things like protein andcarbohydrates and thats calledgluconeogenesis and in order to do that,you have to expend energy and all of thiscauses a buildup of metabolic waste.

Build-up of metabolic waste in cells andinterstitial spaces

Because there is poor perfusion to be ableto exchange waste products and get themaway from the cells and because of all thecellular swelling and the fluid shifts causingimpaired cellular metabolism.

Impaired cellular metabolism and cellulardeath eventually if it keeps going on

Vascular responses

Release of biochemical mediators (cytokines)

These trigger vasodilation andvasoconstriction as part of thecompensatory mechanisms that the bodyhas to deal with shock and because thesecells keep putting out these chemicalmediators that basically say to the otherbody systems, give us oxygen, give usblood flow because we are not gettingenough so more and more cytokines get

produced and these are implicated in thedevelopment of systemic inflammatoryresponse syndrome (one of themechanisms which causes MODS) which isa massive generalized inflammation thatwont stop and one of the things that ishighly implicated are the cytokines, these


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circulating cytokines seem to take a life oftheir own and go do things that the bodydoesnt really need them to do.

Regulation of blood pressure

Catecholamine release

Because the body knows that it is notgetting enough blood perfusion and enoughoxygenation so their signal is sent to thebrain which releases adrenal corticotropicshormone (ACTH)from the pituitary whichtells the adrenal glands to release cortisol,glucagon, and catecholamines likeglucocorticoids, epinephrine, and

norepinephrine.

Activation of Renin-Angiotensin-Aldosteronesystem (sensed by the kidneys very quickly thatthe b/p is not being maintained by homeostasis.)

When Renin is released, it goes to the lungsand converted from Angiotensin I toAngiotensin II which is the most potentvasoconstrictor known so the bodyattempts to raise the blood pressure with

Angiotensin by vasoconstriction

Aldosterone is also released and thisbasically tells the kidneys to conserveSodium and Water, so that you are notlosing anymore blood volume (if thats theproblem) and this conservation also raisesthe blood pressure

Release of ADH (anti-diuretic hormone) from the

brain which also tells the kidneys to conservewater

Aerobic vs. Anaerobic metabolism

Aerobic

more efficient; produces more energy


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requires strong heart and effective circulation tokeep it going

requires ability (at the cellular level) to exchangeO2 and CO2 through the capillary membranes

meets typical body demands of typical ordinarylife

by-products are CO2 and H2O

Anaerobic (without oxygen)

body switches to this pathway when energydemands or O2 levels are low

meant to be used for short periods

when you need to run away fromsomething or exercising intensely andwhen your muscle have used up theavailable oxygen in the muscle tissue andthey switch to anaerobic metabolism. Thisis why the muscles start hurting becausethere is a build-up of lactic acid fromanaerobic metabolism.

by-product is lactic acid

requires healthy, well oxygenated muscle tissueto clear lactic acid

So if you are not healthy, and not welloxygenated, the lactic acid will build-up in yourblood


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Compensatory (initial) Stage

In the compensatory stage of shock, the BPremains within normal limits. Vasoconstriction,increased heart rate, and increased contractility ofthe heart contribute to maintaining adequate


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cardiac output. This results from stimulation of thesympathetic nervous system and subsequentrelease of catecholamines (epinephrine andnorepinephrine). Patients display the often-described fight or flight response. The body

shunts blood from organs such as the skin, kidneys,and gastrointestinal tract to the brain, heart, andlungs to ensure adequate blood supply to thesevital organs. As a result, the skin is cool andclammy, bowel sounds are hypoactive, and urineoutput decreases in response to the release ofaldosterone and ADH.

Homeostatic mechanisms attempt tissue perfusion inresponse to insult: attempts to increase tissue perfusionin response to all of this and attempt to compensate.

neural (sympathetic): increases HR andcontractility, vasoconstriction- shunts blood tovital organs. This is why peoples skin becomegetting cool and clammy because the blood hasbeen shunted away from the periphery and gointo the core where all the vital organs are.

hormonal: renin-angiotensin-aldosteronemechanism activated; ADH secreted; ACTHsecreted adrenals secrete glucocorticoids

(epinephrine, norepinephrine, cortisol, andglucagon) and aldosterone (which tells thekidneys to save Sodium and Water)

chemical: hyperventilation- body attempts toblow off CO2 to counteract the lactic acidosis(which is the metabolic acidosis) and so the bodytries to compensate with the respiratory system.

fluid shifts: are occurring in response to

intravascular volume Progressive Stage

In the second stage of shock, the mechanisms thatregulate BP can no longer compensate, and the MAP fallsbelow normal limits. Patients are clinically hypotensive;


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this is defined as a systolic BP of less than 90 mm Hg or adecrease in systolic BP of 40 mm Hg from baseline

Irreversible Stage

Clinical Findings in Stages of Shock

Finding

StageCompensatory Progressive Irreversible

Bloodpressure

Normal Systolic 100 bpm >150 bpm Erratic or asystole

Respiratory status

>20breaths/minPaCO2


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Cardiac output (CO) normal (however there may bechanges that are occurring to keep it that way)

HR > 100 and RR > 20 bpm or both INCREASED

aerobic anaerobic metabolism and lactic acidosis hasstarted to occur.

respiratory alkalosis (happens as a compensatorymechanism to the lactic acidosis: blowing off a lot ofCO2) metabolic acidosis being compensated withrespiratory alkalosis.

urine output drops (as the Renin AngiotensinAldosterone system and the ADH release from the braintells the kidneys to save H2O) so there wont be as much

urine excreted cool, clammy skin :as blood is shunted from the

periphery (which is the skin) and the extremities towardthe core where all the vital organs are.

hypoactive bowel sounds (as blood is shunted away fromthe peristalsis)

mental status: confusion (may become confused andcombative) and is usually caused by the blowing off of a

lot of CO2 and respiratory alkalosis Medical Management of the Compensatory Stage

identify cause of shock and correct it as soon as possible

support compensatory mechanisms because they will notcontinue forever

re-establish and maintain adequate tissue perfusion doneby:

medications

fluid resuscitation

Nursing Management of the Compensatory Stage

meticulous assessment for those at risk (because earlyintervention is absolutely critical: by the time the blood


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pressure begins to fall, in other words, before the ptstarts going into the progressive stage, thecompensatory mechanisms fail, and damage has alreadybeen done at the microcirculatory level so tissue damagehas already started. EARLY INTERVENTION AND

IDENTIFICATION IS CRITICAL.

recognize early signs, particularly in the elderly becausethey dont have too much reserve and theircompensatory mechanisms tend to burn out quicker.

monitor tissue perfusion:

vital signs and neuro checks

calculating pulse pressure (normal 30-40) and

narrowing pulse pressure is an early indicator ofthe onset of shock, monitoring pulse pressure isimportant.

monitoring labs in the early stages of shock. TheSodium levels will increase and the Glucose levelswill increase. The base deficit of ABGs will fall andthat is related to lactic acidosis, the body is usingup as much bicarbonate as it can to buffer thelactic acidosis.

continuous central venous oximetry

urine output

sublingual capnometry: a sublingual probe (like atemperature probe) used to measure tissuecarbon dioxide: increased levels of carbon dioxidein the tissue indicate poor tissue perfusion (doneunder the tongue)

near infra-red spectroscopy (NIRS): uses light tomeasure the oxygenation of skeletal muscle andthey use it on the palm of the hand, on themuscle that is right below the thumb. The normalis greater than 80% oxygenation and anythingless than that is an indicative of tissue hypoxia.


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reduce anxiety and promote patient safety:particularly of the patient is confused orcombative.

Progressive Stage:

Compensatory mechanisms begin to fail- affects everyorgan system

Heart is overworked and begins to malfunction

There may be arrhythmias and/or evidence ofmyocardial ischemia on the EKG (ST segmentdepression)

Microcirculation fails d/t release cytokines and chemical

mediators: which cause increased capillary permeabilitywhich leads to fluid leakage and microcirculatory failurebecause the fluid leakage creates a lot of pressure at themicrocirculatory level. Fluids are supposed to stay withinthe capillaries; they arent supposed to leak between/inthe interstitial spaces between the cells; and as this fluidleakage gets bigger and bigger, more and more pressureoccurs on the microcirculation and eventually shuts offmicrocirculatory blood flow.

Inflammatory response to whatever injury begins which

affects coagulation

Vicious cycle continues even if precipitating cause issuccessfully treated.

For example, even if hypovolemic shock iscorrected, the shock syndrome will continue andbecomes a self-perpetuating thing and theunderlying reasons for this are poorly understood.

Neuro: SNS dysfunction (we need these mechanisms to

aid in the compensatory process), coma and or lethargic,thermoregulation in the brain may fail, cardiac andrespiratory centers may become depressed in the brain

Respiratory: acute respiratory failure and ARDS: there iscapillary damage and damage to the alveolar membrane:and all this is getting traced to the inflammatory


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response, blame is on the cytokine releases and thecapillary leakage which occurs and causes an increase inpressure at the microcirculatory level which eventuallyshuts off the microcirculatory circulation.

CV: lack of adequate perfusion rapid HR whicheventually causes chest pain from myocardial ischemia,cardiac enzymes may become elevated, dysrhythmias,cardiac failure

Hematologic: DIC

GI: hepatic (liver), pancreatic and intestinal becomeischemia and stop functioning the way theyre supposedto and particularly with the intestines and the liver: theliver quits filtering bacteria out of the mesenteric

circulation and the intestinal wall, the capillaries, becomemore permeable, and eventually they become sopermeable that they become damaged and it allows failure; bacterial toxins to translocate into the systemiccirculation which can cause SEPSIS even if the initialinsult wasnt sepsis.

Renal: ARF occurs when MAP < 70 (if less than 70, thebrain starts becoming ischemic; oliguria

Capillary permeability is increased- leads to thirdspacing with massive swelling and further inintravascular volume. So you as the nurse, find yourselfgiving the pt more fluids because of this increasedcapillary permeability; the fluid eventually leaks out intothe interstitial space as the pt becomes very swollen buttheir intravascular space (inside of the pipes) is dry

Skin: mottled; petichiae may show particularly if they arehaving a problem with DIC

Mental status: very lethargic, and/or difficult to arouseleading to coma

Metabolic acidosis continues: r/t switch from aerobic tomore anaerobic metabolism; the respiratory-blowing offof CO2 to compensate-cant keep up with the massiveamounts of lactic acid


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Medical Management of the Progressive Stage

Use meds and IV fluids to:

Restore tissue perfusion

Support myocardial contractility

Improve vascular tone (to get that sympathetictone back)

Support the respiratory system (may getintubated and mechanically ventilated at thispoint)

Nutritional support: start it early! Because the pt doesntneed any negative nitrogen imbalance on top of

everything else; in fact, the pts nutritional needs getmore and more demanding up to over 3000 calories/daydepending on their condition but also because of theincreased energy demands of anaerobic metabolism andgluconeogenesis.

Aggressive glycemic control may be attemptedwith IV insulin because of the high glucose levelfrom all the stress hormones.

Prevent GI bleeding (another priority): H2blockers, PPIs, and/or antacids

Nursing Management of the Progressive Stage

Careful, frequent assessments/monitoring

Prevention of additional complications:

VAP (Ventilator Associated Pneumonia)

UTI (Urinary Tract Infection)

Decubitus Ulcers

Or any complication that the pt didnt comein the ICU with

Promote rest and comfort


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Family support: provide information!

Information is the families #1 need.

Irreversible Stage of Shock

Irreversible process: shock has gone on long enough,patient doesnt respond to treatment; severe organdamage continues; patient cannot survive

At this time, the pt has MODS: 2 or more organ systemsfail

Only 10-20% of patients survive MODS

Death

B/P: maintained by mechanical or pharmacologic means

Cardiac: Arrhythmias; terminal heart failure agonalrhythms; asystole

Respiratory: maintained on mechanical ventilation andcannot breathe on their own anymore

Skin: grey pallor; jaundice from liver damage

Renal: oliguria; anuria; requires dialysis

Neuro: pt is unconscious most of the time or may be in acoma

Profound metabolic acidosis which is refractory totreatment

Medical Management of Irreversible Shock

Same as in Progressive stage

Experimental therapies do exist

Nursing Management

Same as in Progressive stage

But the FOCUS becomes palliative; making the ptcomfortable and giving support to the family.


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Explanation of prognosis to family AFTER they have beengiven the prognosis from the physician; correct anymisconceptions including the fact that many families mayget a false hope as they see all those machines and you,the nurse, working with their loved one, and they may

interpret that as if there may still be hope for this pt., butat this stage, there really isnt any hope

Allow family to visit and participate in care wheneverthey desire

Ask about living wills, advance directives, durable powerof attorney for health care because the pt will not be inany condition to make their own choices at this point.

Encourage family to express their wishes

General Management Strategies for ALL forms ofSHOCK

Fluid Replacement

Crystalloids vs. colloids

Isotonic Crystalloid: fluid replacement forshock: includes 0.9% NS and LR

The disadvantage of Crystalloidreplacement is that they are easily third-spaced (they third-space faster thancolloids)

Hypertonic Crystalloid: 3% NS is sometimesused that pulls fluid into the vascular spacefrom the interstitial space because of thehigher amount of Sodium.

Colloids: have larger particles that are

harder to pass through the capillarymembranes so the effect of colloid fluidreplacement lasts longer; however, theyreexpensive and there is a danger of allergywith some colloids particularly albumin andplasmanate


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Other non-blood product colloids includeDextran which is heavy sugar and itscontraindicated in people with bleedingproblems because Dextran interferes withplatelet aggregation. They may also use

Heterstartch and its a carbohydratemolecule.

Complications

Cardiovascular overload

Abdominal Compartment syndrome

Vasoactive Medications (see chart)

Vasoactive Agents Used in Treating Shock


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MedicationDesired Action inShock Disadvantages

Inotropic Agents

Dobutamine(Dobutrex)Dopamine(Intropin)Epinephrine(Adrenalin)Milrinone(Primacor)

Improve contractility,increase strokevolume, increasecardiac output

Increase oxygen demand ofthe heart

Vasodilators

Nitroglycerin(Tridil)Nitroprusside(Nipride)

Reduce preload andafterload, reduceoxygen demand ofheart

Cause hypotension

Vasopressor Agents

Norepinephrine (Levophed)Dopamine(Intropin)Phenylephrine(Neo-Synephrine)Vasopressin(Pitressin)

Increase bloodpressure byvasoconstriction

Increase afterload, therebyincreasing cardiacworkload; compromiseperfusion to skin, kidneys,lungs, gastrointestinal tract

Inotropes

Vasodilators


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Vasopressors

Nutritional support: EARLY INTERVENTION

Increased energy requirements

Enteral feeding IS PREFFERED vs. parenteralnutrition: unless the pt has some difficulty withtheir GI system either from ischemia or necrosisthat precludes from giving enteral feedings.

Stress ulcers (Curlings Ulcer)

Hypovolemic Shock

Absolute: e.g. blood loss from the vascular space, non-blood fluid loss (massive diarrhea: CHOLERA: can kill in

less than 24 hrs if fluid is replenished)

Relative: e.g. third spacing : fluid that should be in thevascular space that isnt because it is third spaced, sothe intravascular space has become very dehydrated.

Pathophysiology of Hypovolemic Shock

Loss of circulating blood volume

Risk Factors of Hypovolemic Shock are listed in CH. 15

THIS IS HOW HYPOVOLEMIC SHOCK WORKS:

There is decreased blood volume from whatever reason

Which causes a decreased venous return which basicallycauses decreased preload

Decrease preload means decreased stroke volume

A decreased stroke volume means a decreased cardiac output

A decreased cardiac output causes due to not enough bloodcirculating around you get decreased tissue perfusion


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Assessment and Diagnosis of Hypovolemic Shock

Initial stage: signs may go undetected unless looked for

Especially pts that are at high risk

Later stages:

significant fall in BP, (very obvious) narrowingpulse pressure, urine flow of < 30 mL/h, and aprogressive increase in the arterial lactic acidconcentration (metabolic acidosis)

Signs related to compensatory mechanisms thatthe body uses to keep the vital organs perfusedsuch as:

Tachycardia, tachypnea, and thirst

Signs related to organ hypo-perfusion

Decreased/altered mental status, cool-clammy skin, renal failure, hepatic failure,respiratory failure.


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Hemodynamic Assessment

Normal or reduced ventricular filling pressure with a lowcardiac output in a patient with shock is diagnostic. Aright ventricular filling pressure or central venous

pressure (CVP) < 7 cm H2O (< 5 mmHg) suggestshypovolemia.


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Clotting disorders may occur becausebanked blood, particularly packed red bloodcells, dont have any clotting factors in it;those you have to get by getting freshfrozen plasma; the plasma has been taken

away.

Cellular debris is always present in bankedblood and after 4 units of blood the ptneeds to have a blood filter (an extramicrofilter) that is used to remove thisdebris because it has been postulated thatpts with hypovolemic shock who have hadmassive blood transfusions may developsuch problems as: DIC and ARDS: because

of the presence of cellular debris in theircirculation and it sets up moreinflammatory processes.

Infectious agents that can be transmittedby blood transfusions include (althoughincidences have gone down since testinghas been initiated): hepatitis, risk ofcontracting HIV (very low), CMV(cytomegalovirus), and ebola virus(hemorrhagic fever) can be passed to bloodrecipients by asymptomatic carriers(although in the US, it doesnt seem to be abig of a problem as it is in other parts of theworld.

Nursing Management of Hypovolemic Shock

Prevention of hypovolemic shock to begin with

Prompt detection and identification of at risk pts

Minimize and/or preventing further fluid losses

Enhance volume replacement by keeping the pt warm,monitoring their I&Os, monitoring their hemodynamicvalues by monitoring their vital signs, and monitoringand managing CVP lines and pulmonary artery catheters-monitor those readings, monitoring for dysrhythmias,


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and making sure that the pt has at least 2 IV large boresites at all times during the acute phase.

Above: MODIFIED TRENDELENGBURG POSITION: will help inHYPOVOLEMIC SHOCK!

This will help to shunt blood that has pooled in the lowerextremities up into the core and its a temporarymeasure so YOU the nurse, still have to replace the fluidvolume that has been lost. It is called MODIFIED

TRENDELENGBURG because the pts head and shoulderare flat on the bed. COMPLETE TRENDELENBURG- headwill be lowered and not flat.

Complications of massive blood transfusion:

Hypothermia

Hyperkalemia

Hypocalcemia

Acidosis

Alkalosis

Clotting disorders

Cellular debris

Infectious agents

CARDIOGENIC SHOCK


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Failure of the heart to pump blood around the bodyeffectively.

The cardiac output becomes inadequate for themetabolic and oxygen needs of the body and

shock ensues.

Etiology

Usually caused by Primary ventricular ischemia, e.g. MI:and it does not have to be a HUGE MI, although it seemslike pts that have a large area of heart muscle affectedare more likely to go into cardiogenic shock. Sometimespeople with a smaller MI; just because of their ownphysical makeup, their heart is unable to pumpeffectively for a period of time and they will go into

cardiogenic shock.

Structural problems: e.g. penetrating trauma, myocardialrupture, valve disorders particularly acute mitralregurgitation, which is an emergency, is usually causedby papillary muscle rupture (from a very large MI or aninfarction that involves the papillary muscles that controlthe opening and the closing of the mitral valve and whenit happens its been known to be uniformly fatal. Survivalis very low.

Dysrhythmias may cause cardiogenic shock: e.g.profound bradycardia (down to 30bpm caused by A-V-blocks: third degree heart block), VT & VF (where noblood is moving at all).

Pathophysiology

Characterized by an impaired ability of the ventricle topump blood

The shock syndrome is caused by a heart problemNOTby blood volume, not by sepsis, not by a problemwith the neurologic system, then the dominoes effecttakes place and everything else begins to fall.

Assessment and Diagnosis of Cardiogenic Shock

Low CO and low BP


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Compensatory mechanisms develop

Hemodynamic Assessment

Diagnosis usually requires demonstration of reduced

cardiac output with increased ventricular filling pressureswhere there is increased preload and increased afterloadand reduced cardiac output.

CARDIOGENIC SHOCK

First there is a decreased cardiac contractility thatstarts everything and is caused by ischemia, infarction orarrhythmia.

Then causes decreased stroke volume and cardiacoutput

Which then causes pulmonary congestion (blood/fluidgets backed up in the lungs which starts to leak out from

the higher pressures into the alveoli), decreasedsystemic tissue perfusion (because not enough bloodis being pumped out to the body), and decreasedcoronary artery perfusion (the heart has its ownneeds for blood and that alone makes the myocardialcontractility problem worse.


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Medical Management of Cardiogenic Shock

Correcting the underlying cause of pump failure if possible

By using anti-dysrythmics, inserting a pacemaker, by

doing percutanous coronary interventions like PTCA(Percutaneous Transluminal Coronary Angioplasty)and stent placement, coronary bypass surgery, anemergency replacement of a cardiac valve, andthrombolytic therapy.

Increasing myocardial oxygen supply by supportingrespiration and usually intubation and mechanicalventilation is required.

Decrease cardiac workload by promoting rest, giving

nitroglycerin (will decrease preload and afterload),morphine (will decrease preload and afterload), sometimesbeta-blockers to slow the heart but you have to be carefulwith beta-blockers because they tend to depress myocardialcontractility, and diuretics to decrease preload andafterload.


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Improve contractility with the use of inotropic agents

IABP or VAD

Intra-aortic balloon pump (IABP) is a mechanicaldevice that decreases myocardialoxygen demandwhile at the same time increasing cardiac output.Increasing cardiac output increases coronary bloodflow and therefore myocardial oxygen delivery)

Ventricular assist device, or VAD, is a mechanicalcirculatory device that is used to partially orcompletely replace the function of a failing heart.Some VADs are intended for short term use, typicallyfor patients recovering from heart attacks or heartsurgery, while others are intended for long term use

(months to years and in some cases for life), typicallyfor patients suffering from congestive heart failure).

Restore tissue perfusion by doing all of the above

Nursing Management of Cardiogenic Shock

Preventing cardiogenic shock by identifying at risk patientsearly so that appropriate interventions can be done for ptsthat need: a pacemaker, a PTCA, bypass surgery (becausethey are having so much pain), or pts that have very

hemodynamicly significant arrhythmias.

Limit myocardial oxygen consumption by decreasing the ptsactivity by making sure that they have adequate paincontrol and decreasing their anxiety.

Enhancing their oxygen supply by proper positioning and byadministering oxygen and/or maintaining them onmechanical ventilation.

Knowledge of usage and side effects of medications

because almost all of them are titratables.

Inotropes, Vasodilators, Thrombolytics (need to knowhow to give them and how to take care of the pt whilethey are on this therapy: for example: if they arehaving an MI and need to have thrombolytic therapyto restore circulation into their heart)
http://en.wikipedia.org/wiki/Myocardiumhttp://en.wikipedia.org/wiki/Oxygenhttp://en.wikipedia.org/wiki/Cardiac_outputhttp://en.wikipedia.org/wiki/Bloodhttp://en.wikipedia.org/wiki/Machinehttp://en.wikipedia.org/wiki/Machinehttp://en.wikipedia.org/wiki/Hearthttp://en.wikipedia.org/wiki/Myocardial_infarctionhttp://en.wikipedia.org/wiki/Cardiac_surgeryhttp://en.wikipedia.org/wiki/Cardiac_surgeryhttp://en.wikipedia.org/wiki/Heart_Failurehttp://en.wikipedia.org/wiki/Myocardiumhttp://en.wikipedia.org/wiki/Oxygenhttp://en.wikipedia.org/wiki/Cardiac_outputhttp://en.wikipedia.org/wiki/Bloodhttp://en.wikipedia.org/wiki/Machinehttp://en.wikipedia.org/wiki/Machinehttp://en.wikipedia.org/wiki/Hearthttp://en.wikipedia.org/wiki/Myocardial_infarctionhttp://en.wikipedia.org/wiki/Cardiac_surgeryhttp://en.wikipedia.org/wiki/Cardiac_surgeryhttp://en.wikipedia.org/wiki/Heart_Failure


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IABP, VAD (knowing how to use these)

DISTRIBUTIVE SHOCK:

Anaphylaxis Shock, Sepsis Shock, and Neurogenic Shock

All of which have the same mechanism

Massive vasodilation which then causes

Maldistribution of blood volume: a lot of plasma fluid (not thecells but the fluid) crosses into the interstitial spaces that causesswelling, edema, which then causes

Decreased venous return to the heart so preload is down andthat causes

Decreased stroke volume which causes

Decreased cardiac output a low cardiac output will give you a

Decreased tissue perfusion!

Distributive Shock: Anaphylaxis

Etiology


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Antigen-antibody reaction where the immune system isstimulated for poorly understood reasons by a release ofhistamine and bradykinin (causes a massive peripheraldilation and constriction of the airways)

Pathophysiology

Immunologic stimulation

Peripheral vasodilation

Assessment and Diagnosis

CV: tachycardic, hypotension, and may have chest pain

Respiratory: wheezing; stridor (if they have edema of thelarynx: VERY ALARMING); may have edema of the lips andtongue; bronchospasm (because of narrowing of the largerairways); and may end up with complete airway obstruction.

Cutaneous on the skin: urticaria (hives), erythema (ptturns pink or red), pruritus (very common because the hivesitch), or angioedema (edema of the eyes and face); eyeitching and conjunctival injection (where you can see all theblood vessels and the eye (conjunctiva) turns red.

Neurologic: makes them really anxious, tremors, sense of

being cold; behavior changes may occur if the pt is havingbreathing difficulties and they will become very anxious andupset, altered LOC (with worsening hypoxia or hypotension)

GI, GU: will have cramplike abdominal pain with nausea,vomiting, or diarrhea (more common w/food allergies)

Medical Management of Anaphylactic Shock

Remove antigen if you can and/or possible depending onthe antigen.

If its a bee stinger/stinger from an insect, REMOVE IT.

If its an atopical substance, REMOVE IT.

Reversing the effects of biochemical mediators likehistamine and bradykinin with antihistamine medication for


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example Benadryl IV, Hydramine, and Epinephrine forincreasing the blood pressure with vasoconstriction.

Fluid replacement is indicated particularly if the pt ishypotensive.

Oxygen may be needed for hypoxia.

Epinephrine for vascular tone by causing vasoconstrictionso you increase the sympathetic tone.

Corticosteriods may be used to decrease inflammationwhich seem to be helpful.

Nebulized bronchodilators (likeAlbuterol) may be used toreverse some of the effects of histamine and bradykinin onthe large airways.

Nursing Management

Prevention of anaphylactic shock by assessing for allergiesand teaching patients how to manage their allergies andprevent exposure to allergens.

Note all allergies whenever they are admitted to thehospital and whenever they come in contact with thehealthcare system.

Facilitate ventilation by giving oxygen, by intubation ifnecessary: but if the pts throat is completely closed, theymay not be able to be intubated if the swelling is that badand they may need a cricotomy (incision of the cricoidcartilage) and assisting them in HIGH FOWLERS to helpthem breathe better.

Enhance volume replacement by insuring IV access.

Promote comfort such as helping them to deal with itchingand usually the Benadryl will help the itching go away.

Patients might have scratches on themselves fromscratching the hives.

Assessing their Hemodynamics: Vital Signs: B/P, CVP, PA(pulmonary artery) pressures; bio-impendancecardiography; trans-thoracic or trans-esophagealultrasound; FloTrac which is CO and SVR via A-line.


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Hemodynamic monitoring will only be used if patients areREALLY REALLY shocky and doesnt respond to thetreatments.

Patient teaching

Distributive Shock:NeurogenicShock

Etiology

Disruption of SNS: spinal anesthesia, certain drugs,emotional stress, severe pain, and CNS dysfunction, e.g.spinal cord injury.

Most common of neurogenic shock IS spinal cord injuryabove the level of T-6: and you NEED to KNOW that!

Pathophysiology

Loss of sympathetic tone


Hypotension

Bradycardia: because the sympathetic nervous system isnot working; the parasympathetic is the only thing workingand it slows the heart rate.

Hypothermia

Warm dry skin: meaning that they are not going to be coldand clammy.

Hemodynamic Assessment: B/P, CVP, PA pressures; bio-impendance cardiography; trans-thoracic or trans-esophagealultrasound; FloTrac: CO and SVR via A-line: SAME AS THEANAPHYLACTIC SHOCK: used if patients are REALLY REALLYshocky and doesnt respond to the treatments.

Medical Management

Removing the cause of the neurogenic shock if possible.

Correct positioning after spinal anesthesia oreliminating/decreasing the drugs that can cause this


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such as barbiturates (can highly cause neurogenicproblems).

Restore tissue oxygenation and perfusion by intubation ormechanical ventilation, giving oxygen, vasopressor agents.

Nursing Management

Basic Life Support (ABCs)

Immobilizing spinal cord injuries

Vasoactive medications

Particularly vasopressors like: epinephrine, dopamine,neosynephrine, or norepinephrine.

Fluid resuscitation

Hemodynamic monitoring: B/P, CVP, PA pressures; bio-impendance cardiography; trans-thoracic or trans-esophageal ultrasound; FloTrac: CO and SVR via A-line.SAME AS THE OTHER FORMS OF DISTRIBUTIVE SHOCK: usedif patients are REALLY REALLY shocky and doesnt respondto the treatments.

DVT prevention

Nutritional support

Keeping the pt ALIVE to survive medical treatment.

Distributive Shock:Septic Shock

Etiology

Septic origin(caused by organisms or the bodys responsedorganisms): most common cause of circulatory shock.

Risk Factors of Septic Shock include:

Intrinsic factors: e.g. immunosuppression,malnutrition, age, & diabetes

Extrinsic factors: e.g. invasive lines, catheters, surgicalincisions, & intubation.

Pathophysiology


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Stimulation of the immune and inflammatory system ofbiochemical mediators

Causes a Systemic Response

activation of plasma enzyme cascades

activation of platelets, neutrophils, macrophages

damage to endothelial cells in the blood vessels

immune system becomes overwhelmedveither byorganisms themselves or organisms killing cellsoutright and/or toxins being produced by theorganisms killing cells outright and the immunesystem gets overwhelmed and cant keep up with it.

massive peripheral vasodilation in response to all ofthe above

causing increased capillary permeability

formation of microemboli

hyper-metabolic state

activation of sympathetic nervous system (SNS)

mal-distribution of circulating blood volume d/t all ofthe above so now this pt becomes MASSIVELY third-spaced (very swollen).


Phase 1: hyperdynamic state warm

Massive vasodilation occurs

Widening pulse pressure

HR and CO increased because of the hyperdynamicstate that doesnt last.

Febrile; warm flushed skin

Bounding pulses: label better than 4+ because thepulse is lifting your finger off the pts skin.


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Increased respiratory rate to get rid of CO2 because ofmetabolic acidosis d/t an anaerobic metabolism hasstarted because the aerobic metabolism cant keep upwith the oxygen demands of the body.

GI: n/v, diarrhea may occur

Urine output: normal or somewhat decreased

Neuro: restlessness and confused


Phase 2: hypodynamic state cold

Vasoconstriction as the SNS tries to compensating

B/P and CO falling

Temp normal or (becomes normal); cold, pale,clammy skin

weak, thready pulses as the CO and B/P continue todrop

respiratory rate, HR continue to rise and pt may needto be put on the ventilator as this phase progresses

Renal Failure will ensue as CO drops

Neuro: LOC, coma

MODS may start to develop.

Medical Management

Aimed at Controlling/Identifying (the pathogen) andeliminate infection

Reverse pathophysiologic responses to the organism(s)

Support CV system with drugs usually vasopressors to keepthe pts blood pressure up.

Fluid administration to keep the pts circulating volumeadequate

Provide oxygenation and ventilation


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Initiate nutrition (must be aggressive)

Enteral nutrition is preferred

Pharmacologic therapy

Recombinant human activated protein C- dotrecoginalfa (Xigris): has been used with some success for ptswith Septic Shock.

Nursing Management

Prevention of septic shock

Hand-washing, strict asepsis with any invasives thatwe do with pts, strict asepsis with wound care,preventing vulnerable pts from nosocomial infections

from the hospital setting, if we cant prevent sepsisthen we need to identify it early and start treatmentbefore the pt becomes so SICK that they end up in theterminally stages of shock before we get things going.

Maintain patent airway and adequate ventilation bymaintaining the patient on the ventilator, making sure thattheir airway is open, analyzing their ABGs, and making surethat the appropriate ventilator changes are made.

Promote restoration of circulating blood volume byadministering IV crystalloids and colloids as ordered andkeeping STRICT I&Os and DAILY WEIGHTS.

Administer vasoactives, antibiotics, and other drugs asordered

Maintaining continuous, careful assessment of client (thesewill be some of the physically demanding patients that youwill take care of because they are very sick and they willrequire a lot of assessment and care.

Provide psychological support: reassure client tominimize anxiety; keep family informed and supported.

Provide nutritional support

The nurse will be the one that will need to suggest anutritional consult early.


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Prevent secondary complications such as skin breakdowns,malnutrition, DVT, and the toxic effects of antibiotics, andthat everyone is kept informed of drug levels.

Obstructive Shock

pump failure caused by forces that compress heart: outflowobstruction or increased resistance to ventricular filling

Etiology

resistance to ventricular filling, e.g. tension pneumothorax,cardiac tamponade

outflow obstruction: e.g. massive pulmonary embolism,aortic stenosis

Pathophysiology

forces external to the heart prevent ventricular filling orobstruct outflow

Obstructive Shock

Medical Management

identify and correct source of obstruction/resistance

support organ function

ABCs

O2 and intubation/mechanical intubation

IV access and IV fluid replacement

Specific interventions depending on the cause forexample:

Massive pulmonary embolism: may use

trithrombolytics and/or surgery

Aortic stenois: may try surgery and valvereplacement, and/or commissurotomy (is asurgical incision of a commissure in the body, asone made in the heart at the edges of thecommissure formed by cardiac valves, or one
http://en.wikipedia.org/wiki/Surgicalhttp://en.wikipedia.org/wiki/Commissurehttp://en.wikipedia.org/wiki/Cardiac_valvehttp://en.wikipedia.org/wiki/Surgicalhttp://en.wikipedia.org/wiki/Commissurehttp://en.wikipedia.org/wiki/Cardiac_valve


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made in the brain to treat certain psychiatricdisorders.

Cardiac tamponade: relieving the fluid aroundthe heart

Tension pnuemothorax: by quickly relieving thepneumothorax

Nursing Management

same as other forms of shock

specifics depend on the cause of what caused theobstruction.

AND THIS IS THE END OF THIS PRESENTATION!! HAHA!!

STUDY!! STUDY!! STUDY!!

Advanced Concepts of Clinical Decision

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