Pharmacology Lecture Slides on Therapy of Shock by Sanjaya Mani Dixit Assistant Professor of Pharmacology at Kathmandu Medical College

1. Therapy of Shock
Sanjaya Mani Dixit
Assistant Prof of Pharmacology

2. Learning Objectives
• Define shock
• Stages of shock
• Classifications of shock
• Approach to the Patient in Shock
• ABCDEs

3. What is shock?
• Inadequate perfusion to meet tissue demands.
A progressive process.
– Occurs in 2% of hospitalized patients.
– Mortality 10% in children, vs. 30-40% in adults.
• In other words, a systemic reduction in tissue
perfusion  decreased tissue O2 delivery.
– A shift to less-efficient anaerobic metabolism, leading to lactic acidosis.
• Initially, effects are reversible. Eventually:
– Cell membrane ion pump dysfunction
– Cellular edema, leakage of cells’ contents
– Inadequate regulation of intracellular pH
–  Cell death, organ failure, cardiac arrest, and death.

4. Stages of Shock
A progressive process: Intervene early
• Compensated Shock: Cardiac output
(HR x SV) and systemic vascular resistance (peripheral
vasoconstriction) work to keep BP within normal.
– On exam: Tachycardia; decreased pulses & cool extremities in cold shock;
flushing and bounding pulses in warm shock; oliguria; labs may show mild
lactic acidosis
• Hypotensive (Uncompensated) Shock: Compensatory
mechanisms are overwhelmed.
– On exam: As above, plus hypotension, altered mental status; labs may show
increased lactic acidosis
– Generally quick progression to cardiac arrest.
• Irreversible Shock: Irreversible organ damage, cardiac arrest,
death occur.

5. Multiorgan Dysfunction Syndrome (MODS)
• Progression of physiologic effects as shock
ensues
• Cardiac depression
• Respiratory distress
• Renal failure
• DIC
• Result is end organ failure

6. Classifications of Shock
• Hypovolemic Shock
– Decreased preload due to
internal or external losses.
• Distributive Shock
– Decrease in SVR, with
abnormal distribution
of blood flow 
functional
hypovolemia,
decreased preload.
– Typically, NL or  CO.
 Cardiogenic Shock
 “Pump failure.”  CO,
systolic function.
 Obstructive Shock
 Outflow from left or right
side of heart physically
obstructed.
 Anaphylactic shock
Anaphylaxis is a severe, life-
threatening, generalised or
systemic
hypersensitivity reaction.

7. Physiologic profiles of shock states
Type of Shock Preload
(PCWP)
Cardiac
Output
Afterload
(SVR)
Tissue
Perfusion
(Mixed venous sat)
Hypovolemic     
Distributive  Or
=
 Or
=
  
Cardiogenic   *   
Obstructive     

8. Approach to the Patient in Shock
• ABCs
• Cardiorespiratory monitor
• Pulse oximetry
• Supplemental oxygen
• IV access
• ABG, labs
• Foley catheter
• Vital signs including rectal temperature

9. Approach to the Patient in Shock
• History
• Recent illness
• Fever
• Chest pain, SOB
• Abdominal pain
• Comorbidities
• Medications
• Toxins/Ingestions
• Recent hospitalization or
surgery
• Baseline mental status
• Physical examination
• Vital Signs
• CNS – mental status
• Skin – color, temp, rashes,
sores
• CV – JVD, heart sounds
• Resp – lung sounds, RR,
oxygen sat, ABG
• GI – abd pain, rigidity,
guarding, rebound
• Renal – urine output

10. Is This Patient in Shock?
• Patient looks ill
• Altered mental status
• Skin cool and mottled or
hot and flushed
• Weak or absent
peripheral pulses
• SBP <110
• Tachycardia
Yes!
These are all signs and
symptoms of shock

11. Goals of Treatment
• ABCDE-- Airway, Breathing, Circulation, Disability, Exposure
• Airway
• control work of Breathing
• optimize Circulation
• assure adequate oxygen Delivery
• achieve End points of resuscitation

12. Airway
• Determine need for intubation but remember:
intubation can worsen hypotension
• Sedatives can lower blood pressure
• Positive pressure ventilation decreases preload
• May need volume resuscitation prior to
intubation to avoid hemodynamic collapse

13. Control Work of Breathing
• Respiratory muscles consume a significant
amount of oxygen
• Tachypnea can contribute to lactic acidosis
• Mechanical ventilation and sedation decrease
WOB and improves survival

14. Optimizing Circulation
• Isotonic crystalloids
• Titrated to:
• CVP 8-12 mm Hg
• Urine output 0.5 ml/kg/hr (30 ml/hr)
• Improving heart rate
• May require 4-6 L of fluids
• No outcome benefit from colloids
• Elevating lower limbs helps increase venous return with
vasodilatation.

15. Maintaining Oxygen Delivery
• Decrease oxygen demands
• Provide analgesia and anxiolytics to relax muscles
and avoid shivering
• Maintain arterial oxygen saturation/content
• Give supplemental oxygen
• Maintain Hemoglobin > 10 g/dL
• Serial lactate levels or central venous oxygen
saturations to assess tissue oxygen extraction

16. End Points of Resuscitation
• Goal of resuscitation is to maximize survival
and minimize morbidity
• Use objective hemodynamic and
physiologic values to guide therapy
• Goal directed approach
• Urine output > 0.5 mL/kg/hr
• CVP 8-12 mmHg
• MAP 65 to 90 mmHg
• Central venous oxygen concentration > 70%

17. Anaphylactic shock
• Anaphylaxis is a severe, systemic allergic
reaction
• multisystem involvement, including the skin,
airway, vascular system, and GI
• Severe cases may result in complete
obstruction of the airway, cardiovascular
collapse, and death

19. Drugs Inducing Anaphylaxis
– Antibiotics (especially parenteral penicillins and
other ß-lactams),
(Because they are obtained from microbes)
Aspirin and NSAIDs
 intravenous (IV) contrast agents are the most
frequent medications associated with life-
threatening anaphylaxis.

20. Epinephrine
• Administer epinephrine by IM injection early
to all patients with signs of a systemic
reaction, especially hypotension, airway
swelling, or definite difficulty breathing.
• Use a rapid progression to high dose without
hesitation in patients in full cardiac arrest.
• A commonly used sequence is 1 to 3 mg IV (3
minutes), 3 to 5 mg IV (3 minutes), then 4 to
10 µg/min infusion

21. • Administer IV epinephrine if anaphylaxis
appears to be severe with immediate life-
threatening manifestations
• Use epinephrine (1:10 000) 0.1 mg IV slowly
over 5 minutes. Epinephrine may be diluted to
a 1:10 000 solution before infusion.
• An IV infusion at rates of 1 to 4 µg/min may
prevent the need to repeat epinephrine
injections frequently

22. The Use of Adrenaline in Anaphylaxis
The problems with its use:
•Variable Absorption - give I.m. AVOID s.c.
•Arrhythmogenic in high dose - NEVER give 1:1000 ADRENALINE I.v.
If using ADRENALINE as an IVI, it must be diluted and do not delay
administration of ADRENALINE to set up IVI and gain IV access.
Therefore:
1. Give ADRENALINE I.m promptly (can repeat at 5-10 min intervals)
2. Gain IV access
3. If patient remains in shock resort to IV Iine thus ….
Dilute 0.5ml of 1:1000 ADRENALINE in 50ml of N/saline
(1:100,000)
4. Infuse at 0.1-2ml/min (1-20ug/min) until haemodynamically
stable
5. If using prolonged IVI, add renal-dose of DOPAMINE IVI.

23. Other Drugs
• Antihistamine IV. There is little data about the value of
antihistamines in anaphylactic cardiac arrest, but it is
reasonable to assume that little additional harm could result
• Administer antihistamines slowly IV or IM (eg, 25 to 50 mg of
diphenhydramine)
• Corticosteroids Infuse high-dose IV
corticosteroids early in the course of therapy.
Beneficial effects are delayed at least 4 to 6
hours.

24. Aggressive volume expansion
 profound vasodilation
 Increases intravascular capacity
 Massive volume replacement is needed.
At least 2 large-bore IVs with pressure bags to
administer large volume (typically between 4
and 8 L) of isotonic crystalloid (infusions of
NS, DNS, )as quickly as possible

25. Potential Therapies
• Vasopressin. There are case reports that vasopressin may
benefit severely hypotensive patients.
• Atropine. Case reports suggest that when relative or severe
bradycardia is present, there may be a role for administration
of atropine.
• Glucagon. For patients who are unresponsive to epinephrine,
especially those receiving ß-blockers, glucagon may be
effective. This agent is short-acting; give 1 to 2 mg every 5
minutes IM or IV. Nausea, vomiting, and hyperglycemia are
common side effects

29. Triggers of fatal Anaphylactic reactions in UK

30. Thank you for your Attention

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32. That’s All
ENJOY
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