MBBS 3: Internal Medicine > Shock > Flashcards

Shock Flashcards

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1
Q

What is shock?

A

circulatory failure leading to decreased perfusion and thus tissue dysfunction due to decreased O2
- an impaired cardiac pump, circulatory system, and/or volume can lead to compromised blood flow to tissues

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2
Q

Consequences of inadequate tissue perfusion?

A
  1. generalized cellular hypoxia (starvation)
  2. widespread impairment of cellular metabolism
  3. tissue damage
  4. organ failure
  5. death
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3
Q

What are the stages of schock?

A
  1. initial stage
  2. compensatory stage
  3. progressive stage
  4. irreversible or refractory stage
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4
Q

Initial stage of shock?

A
  1. tissues are under perfused, decreased CO
  2. increased anaerobic metabolism, lactic acid is building
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5
Q

Compensatory stage of shock?

A

SNS activated by low CO, attempting to compensate for the decrease tissue perfusion
Note: this stage is reversible

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6
Q

Progressive stage of shock?

A

Failing compensatory mechanisms:
1. profound vasoconstriction from the SNS
2. ISCHEMIA - Lactic acid production is high > metabolic acidosis

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7
Q

Irreversible/refractory stage?

A

Cellular necrosis and Multiple Organ Dysfunction Syndrome may occur

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8
Q

Net results of cellular shock?

A
  1. systemic lactic acidosis
  2. decreased myocardial contractility
  3. decreased vascular tone
  4. decrease blood pressure, preload, and cardiac output
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9
Q

What are the shock syndromes?

A
  1. hypovolemic
    - blood volume problem
  2. cardiogenic
    - blood pump problem
  3. distributive
    - blood vessel problem
    e.g. septic; anaphylactic; neurogenic
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10
Q

What is hypovolemic shock?

A

Loss of circulating volume
- “Empty tank ” decrease tissue perfusion leading to general shock response

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11
Q

Causes of hypovolemic shock?

A

Internal or External fluid loss
- Intracellular and extracellular compartments
1. Hemorrhage
2. Dehydration from excessive diarrhea or vomiting

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12
Q

Causes of external loss of fluid causing hypovolemic shock?

A
  1. Fluid loss
    - Dehydration
    e.g. Nausea & vomiting, diarrhea, massive diuresis, or extensive burns
  2. Blood loss
    - Trauma: blunt and penetrating
    - BLOOD YOU SEE
    - BLOOD YOU DON’T SEE
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13
Q

How internal fluid loss leads to hypovolemic shock?

A
  1. Loss of Intravascular integrity
  2. Increased capillary membrane permeability
  3. Decreased Colloidal Osmotic Pressure (third spacing)
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14
Q

Pathophysiology of hypovolemic shock?

A

Decreased intravascular volume leads to:
1. Decreased venous return (Preload, RAP) leads to
2. Decreased ventricular filling (Preload, PAWP) leads to
3. Decreased stroke volume (HR, Preload, & Afterload) leads to
4. Decreased CO leads to (Compensatory mechanisms)
5. Inadequate tissue perfusion

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15
Q

Clinical presentation of hypovolemic shock?

A
  1. Tachycardia and tachypnea
  2. Weak, thready pulses
  3. Hypotension
  4. Skin cool & clammy
  5. Mental status changes
  6. Decreased urine output: dark & concentrated
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16
Q

Signs and symptoms related to the severity of fluid loss?

A
  1. Less than 15% [750ml]
    - compensatory mechanism maintains cardiac output
  2. 15-30% [750-1500ml]
    - Hypoxemia, decreased BP & UOP
  3. 30-40% [1500-2000ml]
    - Impaired compensation
    - profound shock along with severe acidosis
  4. 40-50%- refractory stage
    - loss of volume = death
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17
Q

What is cardiogenic shock?

A

Syndrome of inadequate tissue perfusion associated with normal circulating blood volume but a low cardiac output

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18
Q

Symptoms of cardiogenic shock?

A
  1. dyspnea
  2. poor exercise tolerance
  3. confusion
  4. sweating
  5. PND
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19
Q

Signs of cardiogenic shock?

A
  1. tachycardia
  2. cold skin
  3. raised JVP
  4. Added heart sounds
  5. engorged liver
  6. peripheral oedema
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20
Q

Causes of cardiogenic shock?

A
  1. complications of myocardial infarction
    - Papillary Muscle Rupture!!!!
    - Ventricular aneurysm
    - Ventricular septal rupture
  2. Cardiomyopathies
  3. Tamponade
  4. Tension pneumothorax
  5. Severe arrhythmias
  6. Severe valve disease
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21
Q

Pathophysiology of cardiogenic shock that leads to decreased tissue perfusion?

A
  1. Impaired pumping ability of LV
  2. Decreased stroke volume
  3. Decreased CO
  4. Decreased BP
  5. Compensatory mechanism which may lead to Decreased tissue perfusion
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22
Q

Pathophysiology of cardiogenic shock that leads to pulmonary interstitial and intra-alveolar edema?

A
  1. Impaired pumping ability of LV
  2. Inadequate systolic emptying
  3. Increased Left ventricular filling pressures (preload)
  4. Increased Left atrial pressures
  5. Increased Pulmonary capillary pressure
  6. Pulmonary interstitial & intra-alveolar edema
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23
Q

Clinical presentation of cardiogenic shock?

A
  1. Tachycardia and tachypnea
  2. Weak, thready pulses
  3. Hypotension
  4. Skin cool & clammy
  5. Mental status changes
  6. Decreased urine output: dark & concentrated
    Note: May not show typical tachycardic response if on Beta blockers, in heart block, or if bradycardic in response to nodal tissue ischemia
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24
Q

What is mean arterial pressure?

A

(MAP = SBP + (2) DBP/3)

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25
Mean arterial pressure that compromises coronary and renal perfusion?
1. below 70 mmHg compromises coronary perfusion 2. Below 65mmHg compromises renal perfusion
26
Clinical features of cardiogenic shock in regards to abnormal heart sounds?
1. murmurs 2. pericardial tamponade 3. tension penumothorax
27
Murmurs heard in cardiogenic shock?
1. Pathologic S3 (ventricular gallop) 2. Pathologic S4 (atrial gallop)
28
Features of pericardial tamponade?
1. muffled heart tones 2. elevated neck veins 3. low blood pressure
29
Features of tension pneumothorax?
1. Raised JVP 2. tracheal deviation 3. decreased or absent unilateral breath sounds 4. chest hyperresonance on affected side
30
How do you optimize the pump in cardiogenic shock in terms of management?
1. Increasing myocardial O2 delivery 2. Maximizing CO 3. Decreasing LV workload (Afterload)
31
How can you limit/reduce myocardial damage during myocardial infarction?
Increased pumping action & decrease workload of the heart 1. Inotropic agents 2. Vasoactive drugs 3. Intra-aortic balloon pump 4. Cautious administration of fluids 5. Transplantation - Consider thrombolytics, angioplasty in specific cases
32
How do you optimize pump function in cardiogenic shock?
1. Aggressive airway management - Mechanical ventilation if needed 2. Judicious fluid management 3. Morphine as needed - Decreases preload, anxiety 4. Cautious use of diuretics in CHF - Unless they are on continuous inotropic infusion 5. Short acting beta blocker, esmolol, - for refractory tachycardia 6. Vasoactive agents - Dobutamine - Dopamine
33
Describe the mode of action of dobutamine?
> primarily a β1-receptor agonist (cardiac stimulation), but it also has mild β-2 effects (vasodilation) 1. causes a dose-dependent increase in stroke volume 2. decrease in cardiac filling pressures > An alkaline pH inactivates catecholamines such as dobutamine - Dose 2-20 mcg/kg/min
34
What is distributive shock?
- Inadequate perfusion of tissues through maldistribution of blood flow - Intravascular volume is maldistributed because of alterations in blood vessels - Cardiac pump & blood volume are normal but blood is not reaching the tissues
35
Causes of distributive shock?
1. Septic Shock (Most Common) 2. Anaphylactic Shock 3. Neurogenic Shock
36
What is anaphylactic shock?
A type of distributive shock that results from widespread systemic allergic reaction to an antigen NB: This hypersensitive reaction is LIFE THREATENING
37
Pathophysiology of anaphylaxis?
1. Antigen exposure - body stimulated to produce IgE antibodies specific to antigen e.g. drugs, bites, contrast, blood, foods, vaccines 2. Re-exposure to antigen - IgE binds to mast cells and basophils e.g. Anaphylactic response
38
Describe the anaphylactic response?
1. Vasodilatation 2. Increased vascular permeability 3. Bronchoconstriction 4. Increased mucus production 5. Increased inflammatory mediators 6. recruitment to sites of antigen interaction
39
Clinical presentation of anaphylactic shock?
1. Almost immediate response to inciting antigen 2. Cutaneous manifestations e.g. urticaria, erythema, pruritis, angioedema 3. Respiratory compromise e.g. stridor, wheezing, bronchorrhea, resp. distress 4. Circulatory collapse e.g. tachycardia, vasodilation, hypotension
40
Management of anaphylactic shock?
Early Recognition, treat aggressively 1. airway support 2. IV epinephrine (open airways) 3. antihistamines - diphenhydramine 50 mg IV 4. Corticosteroids - Hydrocortisone 100-200mg iv stat 5. immediate withdrawal of antigen if possible 6. prevention 7. judious crystalloid administration 8. Vasopressors to maintain organ perfusion 9. Positive inotropes 10. Patient education
41
What is neurogenic shock?
- A type of distributive shock that results from the loss or suppression of sympathetic tone - Causes massive vasodilatation in the venous vasculature, ↓ venous return to heart, ↓ cardiac output Note: rarest form of shock
42
Most common etiology of neurogenic shock?
spinal cord injury above T6
43
Pathophysiology of neurogenic shock?
1. Disruption of sympathetic nervous system 2. Loss of sympathetic tone 3. Venous and arterial vasodilation 4. Decreased venous return 5. Decreased stroke volume 6. Decreased cardiac output 7. Decreased cellular oxygen supply 8. Impaired tissue perfusion 9. Impaired cellular metabolism
44
Features of neurogenic shock?
1. Hypotension 2. Bradycardia 3. Hypothermia 4. Warm, dry skin 5. CO ↓ 6. Flaccid paralysis below level of the spinal lesion
45
Mnagement of neurogenic shock?
1. Hypovolemia - tx with careful fluid replacement for BP<90mmHg, UO<30cc/hr 2. Changes in LOC 3. Observe closely for fluid overload 4. Vasopressors may be needed 5. Hypothermia - warming txs - avoid large swings in pts body temperature 6. Treat Hypoxia - Maintain ventilatory support 7. Observe for Bradycardia - major dysrhythmia 8. Observe for DVT - venous pooling in extremities make patients high-risk>>P.E. - Use prevention modalities [Sequential stockings, anticoagulation 9. may need transcutaneous or transvenous pacing temporarily
46
How to diagnose neurogenic shock?
1. Fluid Volume Deficit r/t relative loss 2. Decreased CO r/t sympathetic blockade 3. Anxiety r/t biologic, psychologic or social integrity
47
Treatment for tissue perfusion and bradycardia in neurogenic shock?
perfusion - Alpha agonist to augment tone if perfusion still inadequate - dopamine at alpha doses (> 10 mcg/kg per min) - ephedrine (12.5-25 mg IV every 3-4 hour) bradycardia - Treat bradycardia with atropine 0.5-1 mg - doses to maximum 3 mg
48
What is sepsis?
life threatening organ dysfunction  caused by a dysregulated host response to infection
49
What is septic shock?
subset of sepsis in which particularly profound circulatory, cellular and metabolic abnormalities are associated with a greater risk of mortality than with sepsis alone
50
Features of septic shock?
1. Syndrome of profound hypotension due to release of endotoxins / TNF / vasoactive peptides following bacterial destruction 2. Usually associated with normal blood volume, high / low CO, and low SVR 3. Re-distribution of blood to splanchnic vessels, with resultant poor skin perfusion
51
What is SIRS?
A clinical response arising from a nonspecific insult, including > 2 of the following: Temperature >38oC or <36oC HR >90 beats/min Respirations >20/min WBC count >12,000/mm3 or <4,000/mm3 or >10% immature neutrophils
52
Sepsis and SIRS?
SIRS with a presumed or confirmed infcerious process
53
What is severe sepsis?
Sepsis with >1 sign of organ failure 1. Cardiovascular (refractory hypotension) 2. Renal 3. Respiratory 4. Hepatic 5. Hematologic 6. CNS 7. Metabolic acidosis
54
Risk factors for sepsis?
1. Extremes of age (old and young) - Can’t communicate, need careful assessment - Patients with developmental delay - Cerebral Palsy 2. Recent surgery, invasive procedure, illness, childbirth/pregnancy termination/miscarriage 3. Reduced immunity
55
Diseases that increase the risk for sepsis?
1. DIABETES, DIABETES, DIABETES 2. Liver cirrhosis 3. Autoimmune diseases (lupus, rheumatoid arthritis) 4. HIV/AIDS 5. Sickle cell disease 6. Splenectomy patients
56
Pathophysiology of septic shock?
1. Initiated by gram-negative (most common) or gram positive bacteria, fungi, or viruses 2. Cell walls of organisms contain Endotoxins 3. Endotoxins release inflammatory mediators (systemic inflammatory response) causes…... 4. Vasodilation & increase capillary permeability leads to - Shock due to alteration in peripheral circulation & massive dilation
57
Clinical presentation of septic shock?
2 phases 1. warm shock 2. cold shock
58
Warm septic shock?
1. early phase 2. hyperdynamic response, 3. VASODILATION
59
Cold septic shock?
1. late phase 2. hypodynamic response 3. DECOMPENSATED STATE
60
Clinical manifestations of the early compensated stage of septic shock?
Massive vasodilation Pink, warm, flushed skin Increased Heart Rate Full bounding pulse Tachypnea Decreased SVR Increased CO & CI SVO2 will be abnormally high Crackles on lung auscultation
61
Clinical manifestations of late/decompensated stage of septic shock?
Vasoconstriction Skin is pale & cool Significant tachycardia Decreased BP Increase SVR Decreased CO Decreased urine output Metabolic & respiratory acidosis hypoxemia
62
qSOFA?
1. RR > 22BPM 2. SBP < 100mmHg 3. altered GCS < 13
63
qSOFA scoring?
0 = mortality < 1% 1 = mortality 2-3% >2 = mortality >10%
64
Initial management of septic shock?
Administer oxygen Aim SpO2 >94% Start I.v. line, and take bloods for culture Give 20ml/kg boluses of colloid Aim MAP of 65mmHg Observe rise in BP, CVP line if possible Aim CVP 8-12 cm If > 60ml/kg (4200mL) consider ICU referral For initiation of inotropes Broad spectrum antibiotics urgently while awaiting blood culture results
65
ICU care of septic shock?
Adequate oxygenation and ventilation CVP and PA line Broad spectrum antibiotics Drive oxygen delivery towards 600ml/min/m2 Attempt to identify source of sepsis Septic screen
MBBS 3: Internal Medicine
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