Download Shock principle

Shock
“A rude unhinging of the machinery of life”
“A brief pause in the act of
dying”
Shock
Profound and widespread
reduction of effective tissue
perfusion leading to cellular and
circulatory dysfunction
Shock
Determinants OF Effective Tissue Perfusion
Cardiovascular performance
Preload
Afterload
Contractility
Heart rate
Distribution of cardiac output
Microvascular function
Local oxygen unloading &diffusion
Shock
Adequate Cellular Oxygenation
Red Cell Oxygenation
Red Cell Delivery To Tissues
Fick Principle
Fick Principle
Air’s gotta go in and out.
Blood’s gotta go round and round.
Any variation of the above is not a good
thing!
Shock
Red Cell Oxygenation
Oxygen delivery to alveoli
Adequate FiO2
Patent airways
Adequate ventilation
Shock
Red Cell Oxygenation
Oxygen exchange with blood
Adequate oxygen diffusion into blood
Adequate RBC flow past alveoli
Adequate RBC mass/Hgb levels
Adequate RBC capacity to bind O2
– pH
– Temperature
Shock
Red Cell Delivery To Tissues
Adequate perfusion
Blood volume
Cardiac output
– Heart rate
– Stroke volume (pre-load, contractility, after-load)
Conductance
– Arterial resistance
– Venous capacitance
Shock
Red Cell Delivery To Tissues
Adequate RBC mass
Adequate Hgb levels
Adequate RBC capacity to unbind O2
pH
Temperature
Distance between capillaries and cells
Shock
VO2<DO2
VO2=QTX13.4XHgbX(SaO2-SvO2)
DO2=CIXCaO2
=CIX1.34(Hgb)SaO2+PaO2X0.003
Shock
Inadequate oxygenation or
perfusion causes:
Inadequate
cellular oxygenation
Shift from aerobic to anaerobic
metabolism
AEROBIC METABOLISM
6 CO2
6 O2
METABOLISM
GLUCOSE
6 H2O
36 ATP
HEAT (417 kcal)
Glycolysis: Inefficient source of energy production; 2
ATP for every glucose; produces pyruvic acid
Oxidative phosphorylation: Each pyruvic acid is
converted into 34 ATP
ANAEROBIC METABOLISM
2 LACTIC ACID
GLUCOSE
METABOLISM
2 ATP
HEAT (32 kcal)
Glycolysis: Inefficient source of energy production; 2
ATP for every glucose; produces pyruvic acid
Ultimate
Effects of
Anaerobic
Metabolism
Inadequate
Energy
Production
Metabolic
Failure
Inadequate
Cellular
Oxygen
Delivery
Anaerobic
Metabolism
CELL
DEATH
Lactic
Acid
Production
Metabolic
Acidosis
Shock
Markers Of Hypoperfusion
S.Lactate
Base deficit
Perfusion related acidemia
↓ScVO2
Gastric pH
Hypotension
Maintaining perfusion requires:
Volume
Pump
Vessels
Failure of one or more of these
causes shock
Classification of Shock:
Hypovolemic Shock = Low Volume
–Trauma
–Non-traumatic
blood loss
Vaginal
GI
GU
–Burns
–Diarrhea
–Vomiting
–Diuresis
–Sweating
–Third space losses
Pancreatitis
Peritonitis
Bowel obstruction
Shock
Cardiogenic Shock = Pump Failure
Myopathic
MI
CHF
Cardiomyopathy
Arrhythmic
Tachy or
bradyarrhythmias
–Mechanical
Valvular Failure
HOCM
Shock
Distributive Shock ( Low Peripheral Resistance)
Septic Shock
– Toxic Shock Syndrome
Anaphylactic
Histamine is released
– Blood vessels
» Dilate (loss of resistance)
» Leak (loss of volume)
– Extravascular smooth muscle spasm
» Laryngospasm
» Bronchospasm

Neurogenic/Vasogenic(spinal cord)
Endocrinologic
Shock
Obstructive shock

Impaired diastolic filling
Cardiac tamponade
Constrictive pericarditis
Tension pneumothorax
 Increased
ventricular afterload
Pulmonary embolism
Hemodynamics in Shock
Type
Preload
CO
SVR
Hypovolemic
↓
↓
↑
Anaphylactic
↓or nl
Cardiogenic
↑↑
↑↑or ↓ ↓
nl
↓↓ ↑
Septic (Hyperdynamic)
↓or nl
↑↑
↓↓
Septic (Hypodynamic)
↓
↓
↑
Shock
Progressive syndrome
Three phases
Compensated
Decompensated
Irreversible
Shock
Signs and symptoms due to:
Hypoperfusion
–
–
–
–
–
–
Altered mental state
Impaired capillary filling
Urine output
Skin temperature
BP(narrow pulse pressure)
Skin colour
Compensatory responses
Decompensated Shock
Presentation
Listlessness, confusion, apathy, slow speech
Tachycardia; weak, thready pulse
Decreased blood pressure
Moderate to severe orthostatic hypotension
Decreased body temperature
Tachypnea
Key Issues In Shock
Tissue ischemic sensitivity
Heart, brain, lung: 4 to 6 minutes
GI tract, liver, kidney: 45 to 60 minutes
Muscle, skin: 2 to 3 hours
Resuscitate Critical
Tissues First!
Key Issues In Shock
Recognize & Treat during
compensatory phase
Restlessness, anxiety, combativeness =
Earliest signs of shock
Best indicator of
resuscitation effectiveness =
Level of Consciousness
Key Issues In Shock
Falling BP = LATE sign of shock
BP is NOT same thing as perfusion
Pallor, tachycardia, slow capillary
refill = hypoperfusion, until proven
otherwise
General Shock Management
Goals and Monitoring
MAP
CVP
PCWP
CI
sCVO2
Hypovolemic Shock
Control severe external bleeding
Elevate lower extremities
Avoid Trendelenburg
Two large bore IV lines/central line
Cardiogenic Shock
Supine, or head and shoulders slightly
elevated
Do NOT elevate lower extremities
Keep open line, micro-drip set
Fluid challenge based on
cardiovascular mechanism and history
Titrate to BP ~ 90 mm Hg
Cardiogenic Shock
Treat the underlying cause if possible
Treat rate, then rhythm, then BP
 Correct bradycardia or tachycardia
 Correct irregular rhythms
 Treat BP
Cardiac contractility(inotropes)
– Dobutamine, Dopamine
Cardiogenic Shock
Obstructive Shock
Treat the underlying cause
Tension Pneumothorax
Pericardial Tamponade
Isotonic fluids titrated to BP w/o pulmonary
edema
Control airway
Intubation
Neurogenic Shock
Patient supine; lower extremities
elevated
Avoid Trendelenburg
Infuse isotonic crystalloid
Maintain body temperature
Distributive Shock
Anaphylaxis
Suppress inflammatory response
Antihistamines
Corticosteroids
Oppose histamine response
Epinephrine
– bronchospasm & vasodilation
Replace intravascular fluid
Isotonic fluid titrated to BP ~ 90 mm
Shock Management
Avoid vasopressors until
hypovolemia ruled out, or
corrected
Squeezing partially empty
tank can cause ischemia,
necrosis of kidney and bowel
ADRENERGIC RECEPTORS
 Alpha receptors:
 vascular walls
 heart
contraction
vasoconstriction
increase the duration of
ADRENERGIC RECEPTORS
 Dopamine receptors:
renal, splanchnic (Mesentric)
coronary, cerebral vascular beds
vasodilation
Second subtype induces norepinephrines
release
vasoconstriction
VASOACTIVE MEDICTION RECEPTOR ACTIVITY
AND CLINICAL EFFECTS
Receptor activity
Predominant clinical
effects
Alpha 1
Beta 1
Beta 2
Dopaminergic
Phenylephrine
+++
0
0
0
SVR
, CO
/
Norepinephrine
+++
++
0
0
SVR
, CO
/
Epinephrine
+++
+++
++
0
Drug
Dopamine
CO
SVR
, SVR (low dose)
/ (higher dose)
(mcg/kg/min)*
0.5 to 2.0
0
+
0
++
CO, SVR
5.0 to 10.0
+
++
0
++
CO
10.0 to 20.0
++
++
0
++
SVR
Dobutamine
0/+
+++
++
0
CO
Isoproterenol
0
+++
+++
0
CO , SVR
, SVR
VASOACTIVE AGENTS IN SEPTIC SHOCK
Effect on
Effect on
Arterial constriction
heart rate
contractility
effects
Dobutamine
+
+++
-(dilates)
Dopamine
++
++
++
Epinephrine
+++
+++
++
Norepinephrine
++
++
+++
Phenylephrine
0
0
+++
Amrinone
+
+++
-- (dilates)
Drug
I. Non-Adrenergic Agents
a. Vasopressin:
 (ADH) hormone analogue
 refractory septic shock as second agent
b.
Terlipressin:
Side effects: coronary, mesentric ischemia, hyponatremia,
pulm. Vaso constriction
c.
Phosphodiestrase inhibitors
Amrinone and milrinone are inotropic and vasodilator
agents (similar to dobutamine but with less dysrhythmias
used for refractory heart failure but not in hypotension
d.
Nitric oxide synthase inhibitors
CN – monomethyl – L – Arginine)
SVR but
CI and
HR
C O M PLI CATI O N S
 hypoperfusiosn
 dysrhythmias
Myocardial ischemia
Local effects
hyperglycemia
CONTRAINDICATIONS
 Dobutamine in hypertrophic subaortic stenosis
 Pheochromacytoma & monoamine oxidase
inhibitor
e.
Levosimendan
 Mode of action
 Dual:
 calcium sensitization for positive inotrope effect
 activation of ATP-dependent potassium channels
for vasodilation and cardioprotective effect
 Clinical effects
i. Increase in cardiac index
ii. Decrease in pulmonary capillary wedge pressure
i. Others: reduce preload and afterload, improve coronary
blood flow, no adverse effect on diastolic function,
decreased potential for arrhythmia, improved cardiac
function in stunned myocardium
Clinical uses
Treatment of decompensated cardiac
failure (level of evidence: B)
Treatment of ischaemic heart failure
(level of evidence: B)
Short term treatment appears to be safer
than dobutamine for acute worsening of
chronic heart failure (level of evidence: B
Adverse effects
 Most common adverse reaction is headache and
hypotension (both 5%)
 No increase risk of hypotension and ischaemia in
patients with heart failure due to acute myocardial
infarction
 No increase risk for arrhythmias
 No attenuated effects with beta-blockers
 Caution in renal, hepatic or torsades de pointes.
Controversies
 Renal dose dopamine
 Optimal selection and dosage
 Supranormal cardiac index
 Vasopressors in septic shock
PRACTICAL CONSIDERATIONS
 Volume resuscitation
 Selection and titration
 Cardiogenic
 Septic
 Tachyphylaxis
 Hemodynamic interaction
 MAP in relation to (SVR) and (CO)
 Frequent re-evaluation