Shock

NEUROGENIC SHOCK is a result of...

DECREASED VASOMOTOR TONE with generalized VASODILATION

STAGES of SHOCK

Initial Compensatory Progressive Refectory

INTRINSIC CARDIOGENIC SHOCK results from?

LV FAILURE: heart CANNOT PUMP (Sys) or CANNOT FILL properly (Dias)

What happens to CELLS?

METABOLIC WASTE accumultion

*Clinical manifestations* of shock

NOT LINKED to the CAUSE of shock *Result of COMPENSATION by the body*

EXTRINSIC CARDIOGENIC SHOCK results from?

PHYSICAL OBSTRUCTION that reduces cardiac output (despite normal contractility and intravascular volume)

Pathophysiology of DISRUPTVE SHOCK

POOR DISTRIBUTION of BLOOD d/t ACUTE VASODILATION. Simultaneously NO EXPANSION of INTRAVASCULAR VOLUME or LEAKAGE from Intravascular space to interstitial space.

SEPSIS

Presence of both INFECTIONS and a SYSTEMIC INFLAMMATORY RESPONSE

BACTEREMIA

Presence of viable bacteria in the blood; demonstrated by positive blood cultures

SEPTIC SHOCK

State of ACUTE CIRCULATORY FAILURE.

STAGES of SHOCK

hypotension and shock are caused by a problem with HR, STROKE VOLUME or PERIPHERAL RESISTANCE *progresses in a predictable sequence*

Characteristics of SEPTIC SHOCK

persistent ARTERIAL HYPOTENSION despite fluid resuscitation unexplained by other causes

Stages HYPERVOLEMIC SHOCK

results in DEATH

Stages of CARDIOGENIC SHOCK

results in DEATH

manifestations of SEPSIS

temp: >38 or <36; HR: >90 RR: >20 increased WBC + documented infection

Ongoing monitoring

vital signs level of consciousness cardiac rhythm oxygen saturation urine output respiratory effort quality of peripheral pulses skin colour and temperature effects of medications administered

*Stimulation of alpha1‐adrenergic fibres* (compensatory)

*SELECTIVE VASOCONSTRICTION* 1) lungs= *hypoxemia & increased RR* 2) kidneys= *RAAS* 3)skin= *pale, cool, clammy (warm, flushed in sepsis)* 4) GI organs= decreased bowel sounds 5)Muscles= increased lactic acid *shunting of blood to heart & brain

*Drug Therapy-Vasodilators* (cardiogenic)

*i.e. nitroglycerin or nitroprusside* Usually in *cardiogenic shock* excessive vasoconstriction & poor tissue perfusion in spite of adequate BP

What is SHOCK?

*inadequate perfusion* relative to tissue demands

*O2 Therapy*

*supplement* inspired oxygen concentration to *prevent tissue hypoxia* (and resultant cellular dysfunction) Titrated to achieve targeted oxygen saturation levels (i.e. *94-98%* in most patients) *decrease oxygen demand*

*Drug therapy-Other drugs*

*treat symptomatically* - i.e. antibiotics in septic shock -drugs to help cardiac & CV function in cardiogenic & neurogenic shock (diuretics)

CLASS III Hypervolemic shock

-30 - 40 % LOSS OF BV -Marked TACHYPNEA & TACHYCARDIA -↓ systolic BP -OLIGURIA -significant changes in MENTAL STATUS -Most patients require BLOOD TRANFUSIONS. Decision to administer blood is based on the initial response to fluids

CLASS IV Hypervolemic shock

-> 40% LOSS OF BV - Marked TACHYCARDIA -↓ systolic BP -narrowed PULSE PRESSURE (or immeasurable diastolic pressure) -↓ (or no) URINARY OUTPUT -↓ LOC -COLD & PALE SKIN -immediately LIFE THREATENING

ANAPHYLACTIC SHOCK is a result of...

-Acute widespread (massive) DILATION of ARTERIOLES and CAPILLARY BEDS -Release of VASOACTIVE MEDIATORS -Increase in CAPILLARY PERMEABILITY

Causes of ANAPHYLACTIC SHOCK

-acute HYPERSENSITIVITY REACTION -RELEASE of HISTAMINE into bloodstream

*Drug Therapy-Vasopressors* (norepinephrine alone)

-only *after fluid resuscitation* -goal is to achieve & *maintain a MAP *> 65 mmHg* for *end organ perfusion* -*Epinephrine* added to supplement -*Vasopressin* added if above does not Increase MAP

*Fluid resuscitation*

1) *CRYSALLOIDS* -Usually *isotonic* -*Normal saline* 2) *COLLOIDS* -*Volume expanders* -large molecules that stay in the intravascular space & exert oncotic force to maintain plasma volume (e.g.. *albumin*)

factors that *disrupt tissue perfusion*

1) *HEART function* 2) *BLOOD VOLUME* 3) *BP*

*HYPOPERFUSION* of cells

1) *HYPOVOLAEMIC* shock 2) *CARDIOGENIC* shock

*Nursing Actions compensatory stage*

1) *Report changes* to RN/Physician 2) continuous *VS monitoring* 3) identify *probable cause* (i.e. resolve hemorrhage) 4) measures to *reduce anxiety* 5) *symptomatic Tx* - provide oxygen, positioning to improve RR or perfusion 6) Anticipate *collaborative care* - fluids, blood work, medications, transfer to another unit

*Stimulation of beta‐adrenergic fibres* (compensatory)

1) *increased HR* 2) *increased force of myocardial contraction* 3) *increased cardiac output* 4) *increased O2 demand by myocardium* *vasodilation of coronary and cerebral arteries*

*Manifestation* of *Compensatory stage*

1) *restlessness* 2) *normal/decreasing BP* 3) *tachycardia* 4) *bounding/thready pulse* 5) *tachypnea* 6) *normal/hypoactive bowel sounds* 7) *slightly ↓ urine output* 8) *pale, cool skin (flushed, warm skin with sepsis and neurogenic)*

*Manifestations* of *refractory stage*

1) *tachypnea, crackles and increased WOB*->slow, shallow, irregular respirations 2) *tachycardia*-> slow irregular HR; absent pulses 3) *respiratory & cardiac arrest*

*Manifestations* of *progressive stage*

1) *↓ body temperature* (increased with sepsis) 2) *tachycardia/arrhythmias* 3) *weak thready/absent pulses* 4) *↓ BP w/ narrowed pulse pressure* 5) *Rapid, shallow resps* 6) *absent bowel sounds* 7) *anuria* 8) *cold, clammy skin*

Types of DISRUPTIVE SHOCK

1) ANAPHYLACTIC shock 2) SEPTIC shock 3) NEUROGENIC shock

Causes of ABSOLUTE HYPOVOLEMIC SHOCK

1) BLOOD LOSS (external bleeding) 2) LOSS OF PLASMA (burns) 3) LOSS OF WATER from the body (severe diarrhea or vomiting, excessive sweating or urination) hemorrhage 4) GI lOSSES 5) DIABETES MELLITUS 6) DIABETES INSIPIDUS 7) DIURETIC THERAPY

*Clinical markers* of shock

1) Brachial systolic blood pressure: *<110mmHg* 2) Sinus tachycardia: *>90 beats/min* 3) Respiratory rate: *<7 or >29 breaths/min* 4) Urine Output: *<0.5mL/kg/hr* 5) Metabolic acidemia: *[HCO3]<31mEq/L or base deficit >3mEq/L; serum lactate >4mmol/L* 6) Hypoxemia: *0-50yr: <90mmHg; 51-70yr: <80mmHg; >71yo: <70mmHg* 7) *Cutaneous vasoconstriction vs. vasodilation* 8) Mental status changes: *anxiousness, agitation, indifference, lethargy, obtundation*

S&S of SHOCK

1) Change in mental status (restless, decreased LOC; "don't feel right") 2) Pallor 3) Sudden and ongoing rapid heartbeat 4) Decreased BP 5) Weak or thready pulse 6) Rapid breathing 7) Clammy or moist skin 8) Cool hands and feet 9) Decreased or no urine output

CATAGORIES of SHOCK

1) LOW blood flow (*HYPOPERFUSION* of cells) 2) MALDISTRIBUTION of blood flow (*DISRUPTIVE SHOCK*)

Causes of EXTRINSIC CARDIOGENIC SHOCK

1) PULMONARY EMBOLISM (acute/severe) 2)DISSECTING AORTIC ANEURYSM 3)CARDIAC TEMPONADE 4)TENSION PNEUMOTHORAX 5)PERICARDITIS (severe/restrictive) 6) SUPPRESION OF MYOCARDIAL CONTRACTILITY by drugs (eg betablockers, or due to metabolic disturbance, eg acidosis, hypokalaemia or hyperkalaemia, hypocalcaemia. Thyrotoxic crisis)

Nursing management summary

1) Recognize who is at risk for shock 2) Learn how to recognize early indicators of shock 3) Prevent or treat the underlying cause 4) Provide immediate support 5) ABCs 6) Adequate oxygenation 7) Maintain hemodynamic stability 8) Anticipate assessment & treatment of complications

some causes of SPETIC SHOCK

1) Urinary tract infection (UTI) 2) Catheter Associated (CAUTI) 3) Immunosuppression 4) Catheter‐related bloodstream infection (CLBSI)

*Compensatory Stage* of shock

1) body's attempt to *regain homeostasis* & *improve tissue perfusion* 2) *Decreased cardiac output* ->*decreased mean arterial pressure (MAP)* 3) SNS stimulated *(stress response)* -stimulation of alpha1‐adrenergic fibres -stimulation of beta‐adrenergic fibres

INITIAL stage of SHOCK

1) metabolic changes at *cellular level* 2) *not clinically apparent* *Followed by three clinically apparent stages (continuum)*

Some cause of NEUROGENIC SHOCK

1) spinal anaesthesia 2) epidural block 3) spinal cord injury 4) vasovagal syncope

*HYPOVOLEMIC SHOCK*

1)*ABSOLUTE*: *fluid leaves* the body 2)*RELATIVE*: *Capacity of circulatory system increases*, and *BV becomes insufficient*. OR *fluid leaves* the circulatory system, but *not the body*

Causes of INTRINSIC CARDIOGENIC SHOCK

1)Acute MYOCARDIAL INFARCTION (MI). 2) MYOCARDIAL CONTUSION (often d/t steering wheel impact) 3) acute ARRHYTHMIAS (compromising cardiac output) 4)STRUTURAL FACTORS (i.e. cardiac or septal rupture, sever mitral regurgitation) 5)MYOCARDITIS. 6)POST-CARDIAC SURGERY requiring prolonged cardioplegia and cardiopulmonary bypass. 7) MEDICATIONS (rare)

CARDIOGENIC SHOCK

1)INTRINSIC: d/t intrinsic heart problem 3)EXTRINSIC: d/t anything external to the heart that disrupts hearts functioning

INITIAL NURSING PRIORITIES

1)Major focus is on maintaining or restoring tissue perfusion 2)ASSESSMENT is ALWAYS an initial nursing action (vital signs & initial physical assessment) 3) Establish and maintain a patent airway 4) Initiate oxygen administration 5) Obtain an IV access 6) Additional interventions will be specific to the type of shock

COMPLICATIONS of SHOCK

1)Neurological damage 2)Arrhythmias, MI, cardiac failure 3)ARDS d/t decreased perfusion to pulmonary capillaries 4)GI ulceration d/t increased acid production from reduced blood flow 5)Hepatic insufficiency from poor perfusion (leads to recirculation of bacteria and cellular debris) 6)Renal failure d/t prolonged hypoperfusion causes acute tubular necrosis (ATN) 7)DIC from excessive consumption of clotting factors

Causes of RELATIVE HYPOVOLEMIC SHOCK

1)VASODILATION (increases volume in intravascular space) 2)INTERNAL BLEEDING 3)VENOUS OR ARTERIAL POOLING 4)DECREASED BLOOD VOLUME in the arteries-arterial hypovolemia-in heart failure 5)DECREASED ONCOTIC PRESSURE of the blood plasma due to low blood protein levels and hypoalbuminemia 6)PERITONITIS with a loss of fluid into the abdominal cavity 7)FLUID SHITD (burns acites) 8)CAPILLARY LEAKAGE into extravascular space (i.e. sepsis)

CLASS II Hypervolemic shock

15 - 30 % LOSS OF BV -TACHYCARDIA & TACHYPNEA -↓ PULSE PRESSURE -COOL CLAMMY SKIN -DELAYED CAP REFILL -ANXIETY -(↓ pulse pressure d/t increased catecholamine levels) ->increase in PERIPHERAL VASCULAR RESISTANCE & increase in DIASTOLIC BP

CLASS I Hypervolemic shock

<15% LOSS OF BV (~750 mL) -ABSENCE OF COMPLICATIONS -MINIMAL TACHYCARDIA -little /no changes in BP, pulse pressure, or RR -Cap refill >3 sec=volume loss of approximately 10%

General Management of Shock

*ABC's* *Airway* establish & maintain patent airway *Breathing* Admin high flow O2 & ventilate PRN *Circulation* control bleeding, positioning & IV access

*Refractory stage* of shock Irresversible

*Compensatory mechanisms fail* 1) *Continued ↓ cellular perfusion & altered capillary permeability* 2) *↓ circulating volume* as fluids shift into interstitial spaces 3) *leakage of fluids and proteins into interstitial space*-> diffuse, profound edema 4) *Decreased perfusion to end organs* ->end organ failure

*Progressive stage* of shock

*Compensatory mechanisms ineffective* (possibly counterproductive) example: 1) Renal ischemia->RAAS->further vasoconstriction 2)↓ CO-> vasoconstriction 3) increased lactic acid->m. acidosis->fluid shifts -> ↓ circulating volume

What happens to TISSUES?

*Deprived of O2*

*Nursing actions progressive stage*

*Resuscitation measures* (fluids, vasopressors, O2) *family support*