Upload
jocelyn-chapman
View
218
Download
2
Tags:
Embed Size (px)
Citation preview
2
Definition of shock
A disorder characterized by hypoperfusion coupled with hypo-oxygenation
Leads to anaerobic metabolism, ischemia and cell death if uninterrupted also called multiple organ dysfunction syndrome
Can be classified according to site of origin or functional impairment
6
Pathophysiology of shock overview
Decreased vasculartone
Capillary leaking Volume depletion
Pump failure
Renin AngiotensinAldosterone released
oliguria
Anaerobic metabolism
AcidosisHyperkalemia
Toxic metabolitesCausing endothelial damage
& tissue death
MODS
7
Complications of shock MODS (multiple organ dysfunction syndrome) Anoxic encephalopathy ARDS Myocardial pump failure
myocardial depressants known as MDF which are released from the pancreas
Acute tubular necrosis result of decreased renal perfusion
DIC platelet consumption
Rhabdomyolysis skeletal muscle breakdown
Profound sepsis from decreased macrophage effectiveness
Paralytic ileus from decreased peristalsis
Liver failure
8
Clinical manifestations of shock
Cardiovascular Manifestations ▪ Decreased cardiac output ▪ Increased pulse rate ▪ Thready pulse ▪ Decreased blood pressure ▪ Narrowed pulse pressure ▪ Postural hypotension ▪ Low central venous pressure ▪ Flat neck and hand veins in dependent positions ▪ Slow capillary refill in nail beds ▪ Diminished peripheral pulses
Respiratory Manifestations ▪ Increased respiratory rate ▪ Shallow depth of respirations ▪ Decreased Paco2 ▪ Decreased arterial Pao2 ▪ Cyanosis, especially around lips and nail beds
9
Clinical manifestations of shock
Neuromuscular Manifestations ▪ Early Anxiety Restlessness Increased thirst ▪ Late Decreased central nervous system activity (lethargy to
coma) Generalized muscle weakness Diminished or absent deep tendon reflexes Sluggish pupillary response to light
Renal Manifestations ▪ Decreased urine output ▪ Increased specific gravity ▪ Sugar and acetone present in urine
10
Clinical manifestations of shock
Integumentary Manifestations ▪ Cool to cold ▪ Pale to mottled to cyanotic ▪ Moist, clammy ▪ Mouth dry; paste like coating present
Gastrointestinal Manifestations ▪ Decreased motility ▪ Diminished or absent bowel sounds ▪ Nausea and vomiting ▪ Constipation
14
BEST PRACTICE for The Client in Hypovolemic Shock
Ensure a patent airway. Start an IV catheter or maintain an established
catheter. Administer oxygen. Elevate the client's feet, keeping his or her head
flat or elevated to a 30-degree angle. Examine the client for overt bleeding. If overt bleeding is present, apply direct pressure
to the site. Administer medications as prescribed. Increase the rate of IV fluid delivery. Do not leave the client.
15
INTERVENTION ACTIVITIES for The Client with Hypovolemic Shock
Shock Management: Volume: Promotion of adequate tissue perfusion for a client with severely compromised intravascular volume
Monitor for signs and symptoms of persistent bleeding (e.g., check all secretions for frank or occult blood).
Monitor the client closely for hemorrhage. Prevent blood volume loss (e.g., apply pressure to site of
bleeding). Administer IV fluids, as appropriate. Note hemoglobin/hematocrit level before and after blood loss, as
indicated. Administer blood products (e.g., platelets or fresh frozen plasma),
as appropriate. Monitor coagulation studies, including prothrombin time (PT),
partial thromboplastin time (PTT), fibrinogen, fibrin degradation/split products, and platelet counts, as appropriate.
16
Drug therapy in Hypovolemic shock
IV agents to do replace appropriate volume and blood product replacement. They are used as a supportive intervention until volume depletion is corrected
18
Cardiogenic
Pump failure results in inadequate tissue perfusion
DECREASE IN CARDIAC OUTPUT CAUSES A DECREASE IN MEAN ARTERIAL PRESSURE
Seen in: MI Exacerbation of CHF restrictive pericarditis tamponade dysrhythmia Valvular disease
19
Management of cardiogenic shock
Reversal of underlying cause Arrhythmia, structural anomaly, acute
coronary syndrome Supportive care
Airway management Hemodynamic monitoring Vasoactive agents
22
Management of septic shock
Surviving sepsis campaign guidelines for management of severe sepsis and septic shock.
25
BEST PRACTICE for The Client in Sepsis-Induced Distributive Shock
Ensure a patent airway.▪ Start or maintain an established IV catheter.▪ Administer oxygen.▪ Administer antibiotics.▪ Obtain specimens of blood, urine, wound drainage, and sputum for
culture.▪ Increase the rate of IV fluid delivery.▪ Use aseptic technique for any invasive procedure.▪ Handle the client gently.▪ Examine the client for overt bleeding, especially of gums, injection
sites, and IV sites.▪ Elevate the client's feet, keeping his or her head flat or elevated to
a 30-degree angle.▪ Take the client's vital signs every 5 minutes until they are stable.▪ Administer medications as prescribed: Heparin during phase 1 Clotting factors, platelets, and plasma during phase 2
27
NEUROGENIC SHOCK
PARASYMPATHETIC NS OVERSTIMULATION
SYMPATHETIC NS UNDERSTIMULATION SUSTAINED VASODILATION RESULTS IN
DECREASED SYSTEMIC VASCULAR RESISTANCE
HYPOTENSION BRADYCARDIA MENTAL STATUS CHANGES
Associated with Spinal cord injury
28
Management of Neurogenic shock
Follow shock management protocols Maintain spinal immobilization Administer vasopressors
30
Anaphylaxis care
Ensure airway Administer epinephrine Establish IV access Provide supportive care as required
Intubation Vasopressors Corticosteroids H2 antagonists
32
Can you name which shock is most likely responsible?
Diffuse edema to extremities, skin reddened with wheals noted, just started on new antibiotic
Acute mental status change, decreased heart rate, skin cool and dry
s/p radiation and chemotherapy with neutropenia refractory to Neupogen. rectal temp 96.5 BP 100/60 HR 133
PMH of MI X 4, IDDM, CHF with Harsh systolic murmur at 2nd intercostal space at the right sternal border
S/P exploratory laparotomy POD#1 with a history of COPD on PO steroids X 10 years whose skin is pale and cool. Client c/o fatigue and unable to participate in ADLs
33
ADDITIONAL DIAGNOSES/COLLABORATIVE PROBLEMS PC:MODS PC: ARDS PC:DIC PC;PARALTYIC ILEUS PC: HEPATIC FAILURE PC:SEPSIS PC:RHABDOMYOLYSIS RISK FOR INJURY PAIN ANXIETY VS FEAR PC: NEGATIVE NITROGEN BALANCE INTERRUPTED FAMILY PROCESSES RISK FOR IMPAIRED VERBAL COMMUNICATION ACTIVITY INTOLERANCE VS FATIGUE INADEQUATE TISSUE PERFUSION:PERIPHERAL RISK FOR IMPAIRED SKIN INTEGRITY
34
Monitor/Prevent potential complications of shock
Remember risk for MODS, ARDS, DIC, Rhabdomyolysis, ATN, anoxia, sepsis, ileus, liver failure, ulcers identified as potential complications
Develop assessment/monitoring strategies that are broad-sweeping and repeated frequently until stable Mon vital signs (VS), cardiac monitoring (CM) pulse
oximetry, I/O, peripheral pulses, neurochecks Mon CMP, CK, CBC,PT/PTT and bleeding times, type and
cross, total protein, albumin, LFTs Insert NG tube to prevent ileus Administer anti-ulcer therapy and antibiotic
prophylaxis
35
Shock Summary
Disorder of impaired tissue perfusion secondary to decreased circulating volumes caused by cardiac, neurogenic, inflammatory, obstructive and infectious etiologies
Manifests with AMS, agitation, thirst, Increased HR (except neurogenic shock) and normal to slightly lower BP in initial phase
Can progress to irreversible refractory phase Treatment focuses on ABC’s, reversal of underlying cause,
and prevention of complications Evaluation of outcomes focus on tissue perfusion and
oxygenation, cardiac pump effectiveness, fluid/electrolyte balance and avoidance of systemic complications such as MODS, ARDS, DIC, ATN, Rhabdomyolysis, sepsis, ileus, liver failure and ulcers