1. SHOCK Complications & Approach to Patient
Dr.Mohammed Sharique Ahmed Quadri
Assistant Prof.Physiology
Almaarefa College

2. Complications of Shock
Acute respiratory distress syndrome
Acute renal failure
Gastrointestinal complications
Disseminated intravascular coagulation
Multiple organ dysfunction syndrome

3. Acute Respiratory Distress Syndrome (ARDS)
Potentially life threatening form of lung injury
Characterized by
Severe dyspnea of rapid onset
Respiratory rate increases
Profound hypoxemia (cyanosis) refractory to supplemental oxygen
Results from greatly reduced diffusion of gases across the thickened alveolar membranes.
Pulmonary infiltration ( x-ray chest)
Exact cause is unknown

4. Pathophysiology of (ARDS)
cytokines
Accumulates in pulmonary vasculature
Activation of
neutrophils
Injury to endothelial cells
Leakage of fluid and plasma proteins in alveolar spaces
Atelectasis
Impaired gas exchange
Decrease compliance (stiffness)
Decrease surfactant

5. X-ray chest (ARDS)- GROUND GLASS APPEARANCE

6. Clinical features OF ARDS
Tachypnea, tachycardia, hypoxia, and respiratory alkalosis are typical early clinical manifestations
Usually followed by the appearance of diffuse pulmonary infiltrates and respiratory failure within 48 hours.

7. Acute Renal Failure (ARF)
Renal vasoconstriction cuts off urine production
Results in Acute renal failure
Continued vasoconstriction cuts off renal oxygen supply
Renal tubular cells die leading to
Acute tubular necrosis

8. Acute Renal Failure (ARF)
Frequent monitoring of urine out put provided a means of assesing renal blood flow.(urine out put of 20 ml/hr or less indicate impaired renal perfusion)
Serum creatinine and blood urea nitrogen levels provided valuable information regarding renal status

9. G.I Complication
Constriction of vessels supplying GIT for redistribution of blood flow
Severe Decrease mucosal perfusion
GIT ulceration
Bleeding

10. Disseminated Intravascular Coagulation (DIC)
pathways
activated
clots in
platelets
many
and
small
clotting
blood
proteins
vessels
used up
ORAGAN FAILURE
microinfarcts,
bleeding
ischemia
problems

11. Multiple Organ Dysfunction Syndrome (MODS)
The most frequent cause of death in the noncoronary intensive care unit
Affects multiple organ system (kidney, heart lungs, liver & brain.
Mortality rates vary from 30% to 100%
Pathogenesis not clearly understood

12. Major risk factor for development of MODS are
Severe trauma
Sepsis
Prolonged periods of hypotension
Hepatic dysfunction
Infarcted bowel
Advanced age
Alcohol abuse

13. Approach to the Patient in Shock

14. Avoid over reliance on invasive haemodynamic monitoring
Pulse rate
Capillary fill time
temperature
Blood pressure
Level of consciousness
Blood-gas estimation
Assess
Intervene
RE-assess
Seek help

15. Practically Speaking….
Keep eye on these patients
Frequent vitals signs:
Monitor success of therapies
Watch for decompensated shock
Let your nurses know that these patients are sick!

16. Is this the appropriate environment?

17. Approach to the Patient in Shock
ABCs
Cardiorespiratory monitor
Pulse oximetry
Supplemental oxygen
IV access
ABG, labs
Foley catheter
Vital signs

18. Diagnosis
Physical exam (Vital Signs, mental status, skin color, temperature, pulses, etc.)
Surveillance for Infectious source
Labs:
CBC
Chemistries ( urea, creatinin ,etc)
Lactate
Coagulation studies
Cultures
ABG ( arterial blood gas analysis)

19. Further Evaluation
CVP( central venous pressure)and PCWP(pulmonary capillary wedge pressure)
CT of head/sinuses
Lumbar puncture
Wound cultures
Abdominal/pelvic CT or USG
Cortisol level
Fibrinogen, FDPs(fibrin degradation product), D-dimer
D-dimer is a fibrin degradation product (or FDP), a small protein fragment present in the blood after a blood clot is degraded by fibrinolysis. It is so named because it contains two crosslinked D fragments of the fibrin protein.
D-dimer concentration may be determined to help diagnose thrombosis
Its main use, therefore, is to exclude thromboembolic disease where the probability is low. In addition, it is used in the diagnosis of the blood disorder disseminated intravascular coagulation, Deep vein thrombosis (DVT) ,Pulmonary embolism (PE) ,Strokes
CVP = 0-6 mmHg
Pulmonary capillary wedge pressure (PCWP) provides an indirect estimate of left ... value that is very similar to left atrial pressure (normally about 8-10 mmHg).
The jugular venous pressure is usually assessed by observing the right side of the patient's neck. The normal mean jugular venous pressure, determined as the vertical distance above the midpoint of the right atrium, is 6 to 8 cm H2O .

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

21. 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

22. Shock Do you remember how to quickly estimate blood pressure by pulse?60
by palpating a pulse,
you know SBP is at
least this number 70 80 90

23. Goals of Treatment ABCDE Airway control work of Breathing
optimize Circulation
assure adequate oxygen Delivery
achieve End points of resuscitation

24. 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

25. Control Work of Breathing
Respiratory muscles consume a significant amount of oxygen
Mechanical ventilation and sedation decrease WOB and improves survival

26. Optimizing Circulation
Isotonic crystalloids
Titrated to:(aims to achieve)
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
Crystalloids passed readily through the membrane, whereas colloids (from the Greek word for glue) did not. Intravenous fluids are similarly classified based on their ability to pass through barriers separating body fluid compartments, particularly the one between intravascular and extravascular (interstitial) fluid compartments
The principal component of crystalloid fluids is the inorganic salt sodium chloride (NaCl).
The prototype crystalloid fluid is 0.9% sodium chloride (NaCl), also called isotonic saline or normal saline. The latter term is inappropriate because a one normal (1 N) NaCl solution contains 58 g NaCl per liter
Other crystalloids are , R.L and dextrose solutions
As mentioned earlier, colloids are large molecules that do not pass across diffusional barriers as readily as crystalloids. Colloid fluids infused into the vascular space therefore have a greater tendency to stay put and enhance the plasma volume than do crystalloid fluids( albumin, dextrans etc )

27. 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
SmvO

28. 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%

29. Treatment objectives
Specific treatment will depend on the underlying cause
ABC approach
Volume replacement: Hypovolemic or septic
Inotropes: Cardiogenic
Vasopressors: Septic
Adrenaline: Anaphylactic

30. Break !!

31. What Type of Shock is This?
68 yo M with hx of HTN and DM presents to the ER with abrupt onset of diffuse abdominal pain with radiation to his low back. The pt is hypotensive, tachycardic, afebrile, with cool but dry skin
Types of Shock
Hypovolemic
Septic
Cardiogenic
Anaphylactic
Neurogenic
Obstructive
Hypovolemic Shock

32. Hypovolemic Shock ABCs Establish 2 large bore IVs or a central line
Crystalloids
Normal Saline or Lactate Ringers
Up to 3 liters
PRBCs
O negative or cross matched
Control, if any bleeding
Arrange definitive treatment

33. What Type of Shock is This?
An 81 yo F resident of a nursing home presents to the ED with altered mental status. She is febrile to 39.40C, hypotensive with a widened pulse pressure, tachycardia, with warm extremities
Types of Shock
Hypovolemic
Septic
Cardiogenic
Anaphylactic
Neurogenic
Obstructive
Septic

34. Sepsis Two or more of SIRS criteria
Temp > 380C or < 360C
HR > 90 beats /min
RR > 20 /min
WBC > 12,000 or < 4,000 / mm3
Plus the presumed existence of infection
Blood pressure can be normal!

35. Treatment of Septic Shock
2 large bore IVs
NS IVF bolus- 1-2 L wide open (if no contraindications)
Supplemental oxygen
Empiric antibiotics, based on suspected source, as soon as possible

36. Persistent Hypotension
If no response after 2-3 L IVF, start a vasopressor (norepinephrine, dopamine, etc) and titrate to effect
Goal: MAP > 60
Consider adrenal insufficiency: hydrocortisone 100 mg IV

37. What Type of Shock is This?
A 55 yo M with hx of HTN, DM presents with “crushing” sub sternal Chest Pain, diaphoresis, hypotension, tachycardia and cool, clammy extremities
Types of Shock
Hypovolemic
Septic
Cardiogenic
Anaphylactic
Neurogenic
Obstructive
Cardiogenic

38. Cardiogenic Shock Signs: Defined as: Cool, mottled skin
Tachypnea
Hypotension
Altered mental status
Narrowed pulse pressure
Rales, murmur
Defined as:
SBP < 90 mmHg
CI < 2.2 L/m/m2
PCWP > 18 mmHg
Normal value for PCWP mmHg
CI = 3.2 L/m/m2

39. Ancillary Tests ECG Chest X-Ray
CBC, Chemistry , cardiac enzymes, coagulation studies
Echocardiogram

40. Treatment of Cardiogenic Shock
Goals- Airway stability and improving myocardial pump function
Cardiac monitor, pulse oximetry
Supplemental oxygen, IV access
Intubation may decrease preload and result in hypotension
Be prepared to give fluid bolus

41. What Type of Shock is This?
A 34 yo F presents to the ER after dining at a restaurant where shortly after eating the first few bites of her meal, became anxious, diaphoretic, began wheezing, noted diffuse pruritic rash, nausea, and a sensation of her “throat closing off”. She is currently hypotensive, tachycardic and ill appearing.
Types of Shock
Hypovolemic
Septic
Cardiogenic
Anaphylactic
Neurogenic
Obstructive
Anaphylactic

42. Anaphylactic Shock- Diagnosis
Clinical diagnosis
Defined by airway compromise, hypotension, or involvement of cutaneous, respiratory, or GI systems
Look for exposure to drug, food, or insect
Labs have no role

43. Anaphylactic Shock- Treatment
ABC’s
Angioedema and respiratory compromise require immediate intubation
IV line , cardiac monitor, pulse oximetry
IVFs, oxygen
Epinephrine
Second line
Corticosteriods
H1 and H2 blockers
Epi – the single most important step in treatment

44. What Type of Shock is This?
Types of Shock
Hypovolemic
Septic
Cardiogenic
Anaphylactic
Neurogenic
Obstructive
A 41 yo M presents to the ER after an RTA complaining of decreased sensation below his waist and is now hypotensive, bradycardic, with warm extremities
Neurogenic

45. Neurogenic Shock- Treatment
A,B,Cs
Remember c-spine precautions
Fluid resuscitation
Keep MAP at mm Hg
If crystalloid is insufficient use vasopressors
Search for other causes of hypotension
For bradycardia
Atropine
Pacemaker

46. What Type of Shock is This?
A 24 yo M presents to the ED after an RTA c/o chest pain and difficulty breathing. On Physical examination, you note the patient to be tachycardic, hypotensive, hypoxic, and with decreased breath sounds on left
Types of Shock
Hypovolemic
Septic
Cardiogenic
Anaphylactic
Neurogenic
Obstructive
Obstructive

47. Any Questions?