shock - ncm 106

7/29/2019 SHOCK - NCM 106

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By: Yamon, Abigail Faye A.

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7/29/2019 SHOCK - NCM 106


Circulatory System Review

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Adequate blood flow to the tissues

and cells requires the following:

Adequate cardiac pump

Effective vasculature or circulatory system

Sufficient blood volume

If one component is impaired, perfusion to the tissues is

threatened or compromised.

Without treatment, inadequate blood flow to the tissues

results in poor delivery of oxygen and nutrients to the cells,

cellular starvation, cell death, organ dysfunction

progressing to organ failure and eventual death

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The cell swells & the cell membrane becomes more permeable; fluids & electrolytes seep from

& into the cell. Mitochondria & lysosomes are damaged & the cell dies

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Nutrients

Metabolically broken down

Stored in a form of

Adenosine Triphosphate (ATP)

Stored in Mitochondria

Transports substances

(Sodium, Potassium,Calcium) through the

cell membrane

Synthesize chemical

compounds

(cholesterol & protein)

Supplies energy for

mechanical work like

muscle contraction

Energy metabolism

within the cell

Mitochondria - cell's power producers, they convert

energy into forms that are usable by the cell.

Normal Cellular Function

Specialized cellular

function, conductionof electrical impulses

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http://slidepdf.com/reader/full/shock-ncm-106 7/99Decrease energy & performance

ATP production

slows down

Lactic acid goes through the bloodstream and the muscles

Body attempts to produce ATP to fuel the cells

Build up of lactic acid

Accumulation of the toxic end product, lactic acid

Anaerobically metabolism

(in the absence of oxygen)

Lactic acid diffuses out of the cell membrane

Cell’s response to nerve

stimulation is inhibited

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CARDIAC CYCLE

Systole100 – 120 mmHg

Diastole60 – 80 mmHg

Relaxation & filling of

the atria & ventricles

Contraction &

emptying of the atria

& ventricles

Systolic BP – Diastolic BP = Pulse Pressure

120 mmHg – 80 mmHg = 40 mmHg

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70mls X 70bpm =

4,900 mls or

approximately 5L

Approx. 5L/min.

(average)

- volume of blood

ejected from the

left ventricle intothe aorta per

minute

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StrokeVolume

Determined by 3 factors:

- the amt. of blood ejected by the

left ventricle into the aorta per

beat (60-100ml/beat)

Contractility

-refers to the force of

contraction, it is

related to the number

and status of myocardial cells.

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MAP = Systolic BP + 2 (diastolic BP)

3

Mean Arterial BP = CO X Peripheral Resistance(Peripheral Resistance is determined by the diameter of arterioles)

Normal Range: 70 – 105 mm Hg

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Definition

SHOCK

A condition in which tissue

perfusion is inadequate to deliveroxygen and nutrients to support

vital organs and cellular function

(Hameed, Aird, & Cohn, 2003).

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TYPES OF SHOCK

Hypovolemic Occurs when there is a decrease

in the intravascular volumeCardiogenic Occurs when the heart has an

impaired pumping ability

Distributive:

Anaphylactic Caused by hypersensitivity

reactionSeptic Caused by an infection

Neurogenic Caused by alterations in

vascular smooth muscle tone

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Initiating

stimulus

( BP)

Symphatetic

stimulation

RAAS

Activation

Unresolved process

Failure of

Compensatory

Mechanisms

Cellular hypoxia, anaerobic

metabolism, lactic acidosis

Myocardial

contractility &

bradycardia

SVR

Peripheral

vasodilation

Permeability

capillary bed

& pooling

CO

Irreversible tissue

& organ damage

Failure of organs &

systems of body

DeathHR, SVR

Compensated

Shock

Decompensated

Shock

Irreversible

Shock

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Decrease in cardiac output & tissue perfusion

Sympathetic nervous system activation

Renin-

angiotensin

activation

Vascular compliance, blood volume, & cardiac output

Restoration of tissue perfusion

Initial physiologic insult leading to shock state

Endocrine response

Vasoconstriction & activation of

ADH Preload

Blood pressure,

heart rate &

myocardial

contractilityRenal system conserves

Na & H2O Preload

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CO

Fluid moves from

tissues into vascular

system

Hydrostatic pressure

w/in capillaries

Compensatory Stage

Circulating volume

Sympathetic stimulation

Epinephrine &

norepinephrine released

Vasoconstriction

Systemic vascularresistance

BP maintained

Tachycardia

Capillary blood flow

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SVR

Systemic BP

Vascular tension

Reduced tension in afferent arteriole of kidneys

JG cells release renin

Stretch receptors in JG cells of kidneys respond to volume & pressure

Renin acts to split angiotensinogen (a protein release by liver)

Generation of angiotensin I

Converts to angiotensin II (vasoactive peptide)

Stimulates zona glomerulosa of adrenal

cortex to form & release aldosterone

Aldosterone causes Na+ & H20

reabsorption by the kidneys Restoration of blood volume Increased BP

Converted in

some tissues to

angiotensin III

Arteriolar diameter

(vasoconstriction)

Converting

enzyme from lung

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Clinical Manifestations

• Increased respiratory rate – in response tometabolic acidosis

• Increased pH

•

Compensatory respiratory alkalosis• Change mental status (confusion or

combativeness) – alkalotic state

• Arteriolar dilation

If treatment begins in this stage of shock, theprognosis for the patient is good.

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Medical Management

• Directed toward identifying the cause of the

shock

• Correct the underlying disorder so that shock

does not progress

• Support physiologic process

• Fluid replacement & medication therapy to

maintain adequate BP & reestablish, &

maintain adequate tissue perfusion

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Management

• Directed toward identifying the cause of the

shock, correcting the underlying disorder so

that shock does not progress, and supporting

those physiologic processes that thus far haveresponded successfully to the threat.

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Nursing Management

• Monitor tissue perfusion

- Monitor hemodynamic status & promptly

report deviations to the physician

- Report a systolic BP lower than 90mmHg

or a drop of 40mmHg

- Administer prescribed fluids &

medications and promote patient’s safety,

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Nursing Management

• Several new technologies to detect changes in

tissue perfusion before changes in classic signs

(BP, HR, UO) indicate hypoperfusion

-SUBLINGUAL CARBON DIOXIDE

-GASTRIC TONOMETRY

-CENTRAL VENOUS or MIXED VENOUS BLOOD

OXYGEN SATURATION (SvO2)

-CAPNOGRAPHY

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Nursing Management

• Reducing Anxiety

– Provide brief explanations about the diagnostic

and treatment procedures

– Support the patient during diagnostic procedures,

and provide information about the outcomes of

diagnostic procedures

–

Speak in calm manner, reassuring voice & usinggentle touch

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Nursing Management

• Promoting Safety

- Monitor potential threats to the patient’s

safety because a high anxiety level & altered

mental status typically impair judgment

- Close monitoring & frequent reorientation

because patient may disrupt IV lines &

catheters that may complicate their condition

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Recognizing early signs of shock in

older patients•

Medications such as beta-blocking agents (metoprolol[Lopressor]) may mask tachycardia a primary compensatory

mechanism to increase CO during hypovolemic states.

• Aging immune system may not mount a truly febrile response,

but an increasing trend in body temperature should beaddressed.

• The heart does not function well in hypoxemic states & the

aging heart may respond to decreased myocardial

oxygenation with dysrhthmias that may be misinterpreted as

normal part of the aging process

• Changes in mentation may be inappropriately misinterpreted

as dementia. Older people with a sudden change in mentation

should be aggressively treated for the presence of infection &

organ hypoperfusion.

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Progressive Stage

• Mechanisms that regulate BP can no longer

compensate

• MAP falls below normal limits

• Hypotensive (systolic BP <90 mm Hg)

• Prognosis worsens

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Progressive Stage

• Overworked heart dysfunctional

• Body’s inability to meet increased O2 requirements ischemia

• Biochemical mediatorsmyocardial depression failure of cardiac pump (even if the underlying cause of shock is not of cardiac origin)

• Autoregulatory function of the microcirculation fails inresponse to the numerous biochemical cytokines &mediators released by the cells increased capillarypermeability with areas of arteriolar & venousconstriction compromising cellular perfusion

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Progressive Stage

• Relaxation of precapillary sphincters causes fluidto leak from the capillaries interstitial edema& return of less fluid to the heart

•

Inflammatory response to injury is activated &proinflammatory & antiinflammatory cytokinesmediators are released activate coagulationsystem in an effort to reestablish homeostasis

• Body mobilizes energy stores & increases oxygenconsumption to meet increased metabolic needsof underperfused tissues & cells

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Progressive Stage

• Chances of survival depend on the patient’s

general health before the shock state as well

as the amount of time it takes to restore tissue

perfusion.

• Organ systems decompensates (respiratory,

cardiovascular, neurologic, renal, hepatic, GI,

hematologic)

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Medical Management

• Optimize intravascular volume

• Support the pumping action of the heart

• Improve the competence of the vascular system

•

Support the respiratory systemOther aspects:

• Early enteral nutritional support

• Aggressive hyperglycemic control with IV insulin

• Antacids, histamine – 2 (H2) blockers, orantipeptic agents reduce the risk of GIulcerations & bleeding

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Nursing Management

• Prevent complications

• Promote rest & comfort

• Support family members

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Irreversible Stage

• “refractory stage”

• Does not respond to treatment & cannot survive

• Despite treatment BP remains low

•

Renal & liver failure compounded by the release of necrotic tissue toxins overwhelming metabolicacidosis

• Anaerobic metabolism contributes to a worsening

lactic acidosis• Reserves of ATP almost totally depleted & mechanisms

for storing new supplies of energy have been destroyed

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Irreversible Stage

• Respiratory system failure prevents adequate

oxygenation & ventilation despite mechanical

ventilatory support

• Cardiovascular system is ineffective in

maintaining MAP for tissue perfusion

• MODS complete organ failure death

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Medical Management

• Same as for the progressive stage

• Antibiotic agents & immunomodulation

therapy may be tried to reduce or reverse the

severity of shock

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Medical Management

• Depends on the type of shock & its underlying cause• Medications that are common to all types of shock:

- optimize intravascular volume

-support the pumping action of the heart

-improve the competence of the vascular system

-support the respiratory system

Other aspects of management:

-early enteral nutritional support

-aggressive hyperglycemic control with IV insulin

-antacids, histamine – 2 (H2) blockers, antipeptic agentsto reduce the risk of GI ulcerations & bleeding

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Nursing Management

• Preventing complications

• Promoting rest & comfort

• Supporting family members

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Finding COMPENSATORY PROGRESSIVE IRREVERSIBLE

BP Normal Systolic <80-90mmHG

Requires mechanical orpharmacologic support

HR >100bpm >150bpm Erratic or asystole

Respiratory

Status

>20 breaths/min Rapid, shallow

respirations;

crackles

Requires intubation

Skin Cold, clammy Mottled, petechiae Jaundice

Urinary output Decreased 0.5mL/kg/hr Anuric, requires

dialysis

Mentation Confusion Lethargy Unconscious

Acid-base

balance

Respiratory

alkalosis

Metabolic acidosis Profound acidosis

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SIGNS AND SYMPTOMS

Early Stage

(SNS

activation)

Restlessness , confusion

Tachycardia

TacypneaDiaphoresis; cold clammy skin

Decrease body temperature

Decrease urine output

Thirst, dry mucous membraneHypokalemia

Respiratory alkalosis (due to tachypnea, there is loss of

carbon dioxide)

Late Stage Hypotension, oliguria anuriaShallow respiration

Hypothermia

Decreased bowel sounds

Hyperkalemia, respiratory & metabollic acidosis

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Diagnostic Assessment

• Spirometry, pulse oximeter – respiratory status• ABG analysis – to determine whether the metabolic

acidosis that occurs with shock is being effectivelycombated by hyperventilation

• CVP - to estimate fluid loss• Pulmonary artery or Swan-Ganz catheter – to assist

with assessments of fluid status, cardiac function, &tissue oxygen consumption

•

Monitoring tools: cardiac monitor & the 12-lead ECG• Laboratory studies: CBC, blood chemistry, blood and

body fluid cultures

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• CVP- Pressure within the superior vena cava, or a

balloon flotation catheter in the PA

- Normal CVP Pressure: 2 – 12 mm Hg

- Decreased CVP decrease circulating volume

- Client should be relaxed (straining, coughing orany other activity that increases intrathoracic

pressure can cause falsely high measurements)- If with ventilator – readings at the point of endexpiration for greatest accuracy

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Assessing CVP Readings

ToAssess

Increased CVP(>11cm H2O)

Decreased CVP(<3cm H2O )

Blood

Volume

Increased

circulatingvolume

Decreased

circulatingvolume

Vascular

Tone

Vasoconstriction

HPN

Vasodilation,

peripheral

pooling

Septic Shock

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• Pulmonary Artery or Swan-Ganz catheter

- Via percutaneous puncture of the brachial,

subclavian, jugular, or femoral vein using

sterile technique

- Catheter is connected to a transducer & a

fluid-filled pressure monitoring system

- Potential complications: PA infarction, PE,

injury to the heart valves and myocardium

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Potential

complications:

PA infarction, PE,injury to the

heart valves &

myocardium

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Nursing Diagnosis

• Ineffective Tissue Perfusion

Other potential nursing diagnosis:

• Decreased Cardiac Output

• Risk for Impaired Gas Exchange

• Deficient Fluid Volume

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TYPES OF SHOCK

• Hypovolemic Shock

a. Hemorrhagicb. Dehydration

c. Burn

• Cardiogenic Shock

a. Excessive preload

b. Reduced preload

c. Excessive afterload

• Distributive Shock

a. Neurogenic (Vasogenic)

b. Septic Shock

c. Anaphylactic/Anaphylactoid

HYPOVOLEMIC SHOCK

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HYPOVOLEMIC SHOCK

Due to inadequate circulating blood volume resulting from:

*Hemorrhagic Results from a significant loss of whole bloodfrom trauma, GI bleeding, coagulation defects

*Dehydration Results from an extensive loss of body fluid

that depletes tissue fluid

*Burn Results from loss of plasma proteins, which

alters colloid osmotic pressure & leads to

edema. Chemical mediators in tissues enhance

fluid exudation to tissues. Central blood

volume is markedly depleted

The most common type of shock and develops when the intravascular

volume decreases to the point where compensatory mechanisms are

unable to maintain organ & tissue perfusion

CAUSES/Ri k F t

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CAUSES/Risk Factors:

EXTERNAL FLUID

LOSSES

INTERNAL FLUID

SHIFTS

Trauma

SurgeryVomiting

DiarrheaDiuresis

Diabetes Insipidus

Hemorrhage

BurnsAscites

PeritonitisDehydration

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Pathophysiology of HypovolemiaDecreased intravascular volume

Decreased CO

SNS stimulationInterstitial fluid

shiftsintravascularly vasoconstriction Increased HR

Increased renin,

aldosterone, ADH

Volume retention

Increased BP, blood volume

Continued loss of volume

Failure of compensatory mechanisms

Cellular hypoxia

Anaerobic metabolismImpaired cellular metabolism Irreversible changes

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Management of HYPOVOLEMIC SHOCK

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Management of HYPOVOLEMIC SHOCKEtiology Clinical Situation Intervention

Blood loss Massive trauma

GI bleeding

Ruptured aortic

aneurysm

Surgery

Erosion of vesselfrom lesion, tubes,

or other devices

Stop external bleeding with direct

pressure, pressure dressing,

tourniquet (as last resort)

Reduce intra-abdominal or

retroperitoneal bleeding by applying

MAST garment or prepare foremergency surgery

Administer Lactated Ringer’s or NS

(isotonic)

Transfuse with fresh whole blood,

packed cells, fresh frozen plasma, or

other clotting factors (if significant

improvement does not occur with

crystalloid administration)


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Blood loss Massive trauma

GI bleedingRuptured aortic

aneurysm

Surgery

Erosion of vessel fromlesion, tubes, or other

devices

Use non-blood plasma expanders

(albumin, hetastarch, dextran) untilblood is available

Conduct autotransfusion if

appropriate

Plasma

loss

Burns

Accumulation of intra-abdominal fluid

Malnutrition

Severe dermatitis

DIC

Administer low-dose cardiotonics

(dopamine: dose range 5-20mcg/kg/min; begin infusion at

5mcg/kg/min; increase infusion

rate according to BP & other

clinical responses; dobutamine:

usual dose is 2-20mcg/kg/min IV)


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Crystalloid

loss

Dehydration (ex. DKA,

heat exhaustion,protracted vomiting,

diarrhea, nasogastric

suction)

Administer isotonic or hypotonic

saline with electrolytes as neededto maintain normal circulating

volume & electrolyte balance

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• Trendelenburg position

Etymology: Friedrich Trendelenburg

• a position in which the head is low and the

body and legs are on an inclined plane. It issometimes used in pelvic surgery to displacethe abdominal organs upward, out of thepelvis, or to increase the blood flow to thebrain in hypotension and shock.

Mosby's Medical Dictionary, 8th edition. © 2009, Elsevier.

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Modified Trendelenburg - the lower extremities are elevated to

an angle of about 20 degrees; the knees are straight, the trunk is

horizontal & the head is slightly elevated.

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- Modified trendelenburg is the desired

position of the client during shock. The patient

is placed in supine position with the legs

elevated at 20-30 degree angle, the hipsslightly higher than the torso. To increase

venous return to the heart & to strengthen

contractility of the heart. Provide head pillowsupport to prevent cerebral venous

congestion & an increase ICP

CARDIOGENIC SHOCK

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CARDIOGENIC SHOCKDue to inadequate pumping action of the heart because of

primary cardiac muscle dysfunction or mechanical

obstruction of blood flow caused by:

*Excessive preload

-Acute MI,

Myocarditirs,mitral/aortic valvular

insufficiency,

ventricular septal

defects, congenital

conditions causingright heart failure, COPD

Poor cardiac contractility leads to increased

end-diastolic pressure and decreased BP. SNS is

activated to increase afterload; renin-angiotensin increases preload (aldosterone) and

after load (angiotensin II). Heart unable to

pump under increased stress. CO decreases, BP

decreases, tissue perfusion declines & acidosis

impairs cardiac functioning further.

Occurs in 10 % - 15% of all clients after MI & carries associated

mortality rate of up to 80%. Cardiogenic shock after MI usually occurs

when 40% or more of the myocardium has been damaged.

CARDIOGENIC SHOCK

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CARDIOGENIC SHOCK*Reduced

Preload-Pericardial

tamponade, RVI,

tension

pneumothorax

Restriction of input to the heart occurs

with tamponade and tensionpneumothorax. RVI causes decreased

blood flow to left ventricle due to poor

contractility. Standard SNS responses occur,

but increased HR does not compensate forfilling defect.

*Excessive

afterload

- Massivepulmonary

embolism, systemic

hypertension,

aortic stenosis

Gradual onset of heart failure and shock occurs

when heart cannot maintain the pressures

required from hypertension & aortic stenosis, thehypertrophied left ventricle decompensates, heart

failure ensues, BP declines. In massive PE, sudden

right heart failure develops from obstruction to

flow

Causes/Risk Factors:

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Causes/Risk Factors:

Excessive preload

-Acute MI,Myocarditirs,

mitral/aortic

valvular

insufficiency,

ventricular septal

defects, congenital

conditions causingright heart failure,

COPD

Reduced

Preload-Pericardial

tamponade,

RVI, tension

pneumothorax

Excessive

afterload- Massive

pulmonary

embolism,

systemic

hypertension,

aortic stenosis

Pathophysiology of Cardiogenic Shock

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Pathophysiology of Cardiogenic Shock

Renin, aldosterone, ADH,

catecholamine release

Pulmonary

or systemiccongestion

Decrease CO

Decreased coronary

artery perfusion

Decreased O2 &

nutrients available

to tissues & organs

Compensatory response

Increased blood

volume, SVR

Increased HR, stroke volume, & preload

Inability toovercome

increase

afterload

Increasedmyocardial

oxygen

demands

Decrease BP

Decreased

further

contractility

Impaired cellular

metabolism

Anaerobic

metabolism

Lactic acidosis&

depressed organ

function

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Management of CARDIOGENIC SHOCK

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Management of CARDIOGENIC SHOCKEtiology Clinical Situation Intervention

Myocardial

disease orinjury

Acute MI,

Myocardialcontusion

Cardiomyopathies

Fluid-challenge with up to 300ml of

NSS or Ringer’s lactate to rule outhypovolemia, unless HF or PE is present

Monitor CO, pulmonary artery

pressure & PCWP; administer IVF to

maintain left ventricular filling pressureof 15-20mmHg

Administer inotropics (dopamine or

dobutamine)

Vasodilators , diuretics, cardiotonics,

betablockers, glucocorticosteroids

Intra-aortic balloon pump or external

counterpulsation device if

unresponsive to other therapies


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Valvular

disease orinjury

Ruptured aortic

cusp (sudden heart

failure)

Ruptured capillary

muscle

Thrombus

Fluid-challenge with up to 300ml of NSS or

Ringer’s lactate to rule out hypovolemia, unlessHF or PE is present

Monitor CO, pulmonary artery pressure &

PCWP; administer IVF to maintain left

ventricular filling pressure of 15-20mmHg

Administer inotropics (dopamine ordobutamine)

Vasodilators , diuretics, cardiotonics,

betablockers, glucocorticosteroids

Intra-aortic balloon pump or external

counterpulsation device if unresponsive to

other therapies

If rapid response does not occur, prepare for

prompt cardiac surgery


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External

pressure onthe heart

interferes

with heart

filling oremptying

Pericardial

tamponade due totrauma, aneurysm,

cardiac surgery,

pericarditis

Massive pulmonaryembolus

Tension

pneumothorax

Ascites

Relieve tamponade with ECG-assisted

pericardiocentesis; repair surgically if itrecurs

Thrombolytic (streptokinase) or

anticoagulant (heparin) therapy; surgery

for removal of clot (embolectomy)

Relieve air accumulation with needlethoracostomy or chest tube insertion

Relieve fluid accumulation with

paracentesis

Cardiac

dysrhythmias

Tachydysrhythmias

Bradydysrhythmias

Pulseless electrical

activity

Treat dysrhthmias; be prepared

to initiate CPR, cardiac pacing

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Needle Thoracostomy

DISTRIBUTIVE SHOCK

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DISTRIBUTIVE SHOCKAlso called “VASOGENIC SHOCK”

Due to changes in blood vessel tone that increase inthe circulating blood volume.

*Neurogenic Shock

(Vasogenic)

- CNS damage tovasomotor center,

cerebral edema,

general anesthetic

medullary

depression,

cervical, spinal cord

injury

Interference with nervous system

control of the blood vessels, such as

with spinal cord injury (esp. cervicalspine injury), spinal anesthesia or severe

vasovagal reactions caused by pain or

psychic trauma

DISTRIBUTIVE SHOCK

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DISTRIBUTIVE SHOCK*Septic Shock

- endotoxinmediated,

exotoxin

mediated

Widespread sepsis from gram-

negative or gram-positiveorganisms. Toxins produce

vasodilation & peripheral pooling.

Mediators of inflammationpotentiate the vasodilation. SNS

response cannot overcome

vasodilation. Capillary endothelial

damage, microemboli, myocardial

depression & organ failure are

common effects.

DISTRIBUTIVE SHOCK

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DISTRIBUTIVE SHOCK*Anaphylactic Shock

- IgE mediated:certain drugs, foods,

insect venoms,

pollens

-Non-IgE mediated:iodinated contrast

material, dextran,

opiates, mannitol,

NSAIDs, polymixin B,BT to IgA-deficient

patients, & local

anesthetic

Drastic, acutely developing &

progressing type of shock.Occurs with IgE mediated reactions.

Molecules of IgE bind with allergen &

tissue mast cells, releasing histamine ,

which causes vascular permeability &smooth muscle constriction . Occurs

on re-exposure to an antigen. Non-IgE

mediated reactions can be induced on

first contact. Physiologic response isvasodilatation, & peripheral edema &

bronchoconstriction, SNS cannot

overcome vasodilating stimulus.

Neurogenic Shock(Vasogenic)

Septic Shock-immuno

Anaphylactic Shock-Penicillin sensitivity

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Precipitating event

VasodilationActivation of

inflammatory

response

Decreased venous

return

Maldistribution of blood volume

(Vasogenic)

-Spinal cord injury

-spinal anesthesia

-depressant action of medications

-glucose deficiiency

immuno

suppression

-extremes of age (<1

yr. & >65 yr.)-malnourishment

-chronic illness

-invasive procedures

Penicillin sensitivity

-Transfusion reaction

-Bee sting allergy

-Latex sensitivity-Severe allergy to some

foods or medications

Decreased cardiac

output

Decreased tissue

perfusion

Management of DISTRIBUTIVE SHOCK

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gEtiology Clinical Situation Intervention

Anaphylactic

shock

Allergy to food,

medicines, dyes,insect bites, stings,

or latex

Prepare for surgical management

of the airwayDecrease further absorption of

antigen (stop IV fluid, place

tourniquet between injection or

sting site)Epinephrine (1:100) 2 inhalations

q3O or

Epinephrine (1:1000) 0.2-0.5ml q

5mins. Given at a rate of 1mg/min

IV fluid resuscitation with

isotonic solution

Diphenhydramine HCL or H1 –

receptor antagonist IV


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Anaphylactic

shock

Allergy to food,

medicines, dyes,insect bites, stings,

or latex

Theophylline IV drip for

bronchospasmSteroids IV

Vasopressors (norepinephrine,

metaraminol bitartrate, high

dosage dopamine)Gastric lavage for ingested

antigen

Ice pack to injection or sting site

Meat tenderizer paste to sting

site


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Septic shock Often gram-

negative septicemiabut also caused by

other organisms in

debilitated,

immunodeficient orchronically ill

patients

Identify origin of sepsis; culture

all suspected sourcesVigorous IV fluid resuscitation

with normal saline

Empirical antibiotic therapy until

sensitives are reportedIf suspected organism is gram-

positive, vancomycin is used; if

gram-negative, give expanded

spectrum penicillin or a

cephalosporin & aminoglycoside

Administer cardiotonic agents

(dopamine or dobutamine,

norepinephrine, isoproterenol,

digitalic, calcium)


7/29/2019 SHOCK - NCM 106



Septic

shock

Often gram-

negativesepticemia but

also caused by

other organisms

in debilitated,immunodeficient

or chronically ill

patients

Naloxone (narcotic antagonist) --

capillary bed vasodilationProstaglandins

Monoclonal antibodies

Temperature control (both

hypothermia & hyperthermia arenoted)

Heparin, clotting factors, blood

products if DIC develop

Neurogenic

shock

Spinal anesthesia

Spinal cord injury

Normal saline to restore volume

Treat bradycardia with atropine

Vasopressors (norepinephrine,

metaraminol bitartrate, high dosage

dopamine, phenylephrine

Place in modified trendelenburg position

7/29/2019 SHOCK - NCM 106


SHOCK

Inadequate

tissue/organ

perfusion

affecting all

organs of body

Failure of compensatory mechanisms

Damage to

the capillaryendothelial

lining

Activation of

clotting factors

Lead to complications

7/29/2019 SHOCK - NCM 106


Drug Therapy in Shock

7/29/2019 SHOCK - NCM 106


Vasoconstrictors Vasodilators

To maintain normal BP:

NorepinephrineEpinephrine

Dopamine

Dobutamine

To improve circulation:

NitroglycerineHydralazine

Na bicarbonateTo reverse acidosis:

Antibiotics – sepsis

Heparin – DIC

Steroids – to reduceantiinflammatory effect

Glucagon – to increase

blood sugar

Cimetidine – to prevent stress ulcer

Naloxene (Narcan) – to block endorphin –

mediated hypotension

Diphenhydramine (Benadryl) – foranaphylaxis

Narcotics – to relieve pain (used with

great care because these may cause

respiratory depression)

Drug Therapy in Shock

7/29/2019 SHOCK - NCM 106


g pyCardiotonic Medications

To improve myocardial contraction:Digitalis – evidence of cardiac failure

Amiodarone, lidocaine, bretylium, quinidine, &

procainamide – to treat dysrhythmias that tend toreduce cardiac efficiency

Atropine – may treat bradycardia

7/29/2019 SHOCK - NCM 106


QUESTIONS

1. Which of the following best describes

neurogenic shock?

a. Results from circulating volume

b. Results from compromised cardiac output

c. Results from loss of vasomotor tone that

includes arteriolar & venous dilatation

d. Results from severe allergic reaction

7/29/2019 SHOCK - NCM 106


• Answer: letter c

- neurogenic shock results from loss of

vasomotor tone that includes arteriolar &

venous dilation

7/29/2019 SHOCK - NCM 106


2. During the initial stage of shock, the

following manifestations are expected

EXCEPT:

a. Elevated BP, elevated temperature

b. Tachycardia, restlessness

c. Tachypnea, respiratory alkalosis

d. Diaphoresis, pallor

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• Answer: Letter a

- Elevated BP, elevated temperature are not

expected manifestations during initial stage of

shock. There is hypotension & decreased bodytemperature

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3. During the decompensated stage of shock,the following signs and symptoms occur

EXCEPT:

a. oliguria

b. elevated BUN

c. hyperkalemia

d. metabolic alkalosis

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• Answer: letter d

- metabolic alkalosis is not expected during

decompensated stage of shock. Instead

metabolic acidosis occurs. This is due to bloodstasis that enhances lactic acid production

7/29/2019 SHOCK - NCM 106


4. The following are causes of altered LOC inshock EXCEPT:

a. cerebral hypoxia

b. acidosis

c. accumulation of waste products

d. release of blood from the liver

7/29/2019 SHOCK - NCM 106



- release of blood from the liver is not a cause

of altered LOC in shock. Cerebral hypoxia,

acidosis, accumulation of waste products arecauses of altered LOC in shock

7/29/2019 SHOCK - NCM 106


5. The desired position during shock is:

a. Modified trendelenburg

b. Flat position

c. Semi – Fowlers’s position

d. Lateral position

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• Answer : letter a

- Modified trendelenburg is the desired position

of the client during shock. The patient is placed in

supine position with the legs elevated at 20-30degree angle, the hips slightly higher than the

torso. To increase venous return to the heart & to

strengthen contractility of the heart. Provide

head pillow support to prevent cerebral venous

congestion & an increase ICP

7/29/2019 SHOCK - NCM 106


6. The most commonly used plasma expander is:

a. 0.9% NaCl

b. Dextran

c. Lactated Ringer’s

d. Whole blood

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• Answer: letter b

- Dextran is most commonly used plasma

expander

7/29/2019 SHOCK - NCM 106


7. Which of the following is administered toreverse acidosis?

a. Na bicarbonate

b. Heparin

c. Steroids

d. Cimetidine

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• Answer: Letter a

- Sodium bicarbonate is administered to

reverse acidosis

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8. Hypovolemic shock occurs when blood loss is:

a. 5% - 10%

b. 15% - 25%

c. 10% - 15%

d. 1% - 5%

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• Answer: letter b

- hypovolemic shock occurs when blood loss is

15% - 25%

7/29/2019 SHOCK - NCM 106


9. The client has intra-aortic ballooncounterpulsation device. This is primarily

meant to:

a. decrease cardiac workload

b. decrease stroke volume

c. increase preload

d. maintain current coronary circulation

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• Answer: letter a- intra-aortic balloon counterpulsation deviceincreases coronary artery and myocardial

tissue perfusion & reduces left ventricularworkload. During diastole, the balloon isinflated to allow more blood from the aorta tofill the coronary artery. During systole, the

balloon is deflated to allow free flow of bloodvia the aorta

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10. The following are assessment parametersthat indicate adequate fluid replacement in

shock EXCEPT:

a. urine output is 50 ml/hr

b. CVP = 10cm water

c. Hct = 48 vol. %

d. Serum potassium = 6 mEq/L

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- serum potassium of 6mEq/L is elevated.

This may indicate dehydration, causing

retention of electrolytes. Therefore, fluidreplacement is not adequate.

shock - ncm 106

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