Download - Acute medicine Lecture Series 2010
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ACUTE MEDICINE LECTURE SERIES 2010
Ahmad F. Mady MD
SHOCKHOW TO WATER A GARDEN?
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Before we go anywhere, let’s start at the beginning
What do you need to maintain a nice garden?
WATER
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What do you need to get the water to the garden ?
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4 things
Water pump Release valve Hose Water amount
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What is Shock?
Theoretical:Inability to meet cellular requirements for
oxygen Practical:When the nurse calls you for a low blood
pressure
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what are the types of shock?Think about the garden:The garden will die without enough water Pump failure Release valve failure Hose failure Water failure
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What the hell are you talking about?
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Aetiological Shock Categories Pump failure = Cardiogenic shock Release valve failure = Obstructive
shock Hose failure = Distributive shock Water failure = Hypovolemic shock
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Hypovolemic Shock
Not enough stuff Blood plasma
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Hemorrhagic Shock
Parameter I II III IV
Blood loss (ml) <750 750–1500 1500–2000 >2000
Blood loss (%) <15% 15–30% 30–40% >40%
Pulse rate (beats/min) <100 >100 >120 >140
Blood pressure Normal Decreased Decreased Decreased
Respiratory rate (bpm) 14–20 20–30 30–40 >35
Urine output (ml/hour) >30 20–30 5–15 Negligible
CNS symptoms Normal Anxious Confused Lethargic
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Cardiogenic Shock
The heart cannot pump enough blood to meet the metabolic demands of the body
CausesMuscleValveHeart rate
Too fastToo slowPoor coordination
Mortality ( 60-90%)
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Obstructive Shock
• Tension pneumothorax• Cardiac tamponade• Pulmonary embolism• Aortic stenosis
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Distirutive shock
Caused by systemic vasodilatation from Infection -Septic shock (35-40% ,1 month
mortality) Spinal / Neurogenic Shock Anaphylaxis
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Septic shock
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Pathophysiology
DO2 = Q X CaO2
DO2 = Q X (1.34 X Hb X SpO2)
Normal DO2 is 520 to 570 mL/min/m2
VO2 = Q X (CaO2 - CvO2)
VO2 = Q X 13.4 X Hb X (SpO2-SvO2)
Normal VO2 is 110-160 ml/min/ m2
O2ER = VO2 / DO2 X 100
Normal O2ER = 0.2-0.3 (20 to 30%)
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Pathophysiology
MRO2 : The metabolic demand for oxygen at the tissue
level. The rate at which oxygen is utilized in the
conversion of glucose to energy and water through glycolysis and Kreb’s cycle.
VO2 ≥ MRO2 = Normal Metabolism
VO2 < MRO2 =
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Pathophysiology
When demand is insufficient the first compensatory mechanism is increase in CO.
autonomic responses.1. Arteriolar vasoconstriction.2. Increase in HR and contractility .3. Constriction of venous capacitance, which
augments VR.4. Release of vasoactive hormones epi, norepi,
dopamine, and cortisol to increase arteriolar and venous tone.
5. Release of ADH and activation of the renin-angiotensin axis
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Pathophysiology
The cellular response to a decrease in systemic O2 delivery is ATP depletion leading to ion-pump dysfunction (influx Na+ and efflux K+) leading to membrane instability and cellular dysfunction.
When compensatory mechanisms failure the body starts anaerobic metabolism forming lactic acid.
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Clinical manifestation
Characterized by three stages Preshock (warm shock, compensated
shock) Shock End organ dysfunction
Compensated shock Low preload shock – tachycardia,
vasoconstriction, mildly decreased BP Low afterload (distributive) shock –
peripheral vasodilation, hyperdynamic state
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ShockInitial signs of end organ dysfunction Tachycardia Tachypnea Metabolic acidosis Oliguria Cool and clammy skin
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End Organ DysfunctionProgressive irreversible dysfunction Oliguria or anuria Progressive acidosis and decreased CO Agitation, obtundation, and coma Patient death
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Invasive hemodynamic monitoring
Etiology of shock
Example Filling p. CO SVR VO2 sat
Preload Hypovolemic Low Low High Low
Contr, Cardiogenic High Low High Low
Afterload Distributive
Hyperdynamic Septic
Low/High High Low High
Hypodynamic Septic
Low/High Low High Low/High
Neurogenic Low Low Low Low
Anaphylactic Low Low Low Low
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Also diagnosis of hyperdynamic septic shock optimizing fluids/intorops/vasopressors
Arterial line CVP Is CVP or PAOP reliable in shock ??? Is there a role for Swan-Ganz in shock ?!
PAOP PAP
Cardiogenic Increased Decreased
Obst PE Normal Increased
Obst C. Tamponad
Increased Increased
Invasive hemodynamic monitoring
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Treatment
General objectiveRapid recognition and restoration of perfusion
Hypovolemic
Volume resuscitation by crystaloids and blood
obstructive Maxmize preload +relife of obstruction
cardiogenic Maximize preload and cardiac performance + reducing afterload
distributive Supplement preload+augment BP+TTT cause
Fluids vasopressors inotrops
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Fluids
Two broad categories related to a shock discussion Crystalloids Colloids
Crystalloids Hypoosmolar D5, 1/4, ½ NS
not helpful for our patient in shock Iso-osmolar NS, RL
RL has lower chloride concentration vs. NS so tendency
of non-AG metabolic acidosis Hyper: mannitol, 3%NS no great advantage..cell
dehydration
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Fluids
Colloids Natural vs Synthetic Natural
Blood FFP Platelets Human albumin
Drawbacks: Limited supply High cost Possible allergic reactions Risk of infection
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Fluids
Synthetic Dextran HES high MW , medium MW , low MW
Drawbacks: Alterd hemostasis if large dose relative High cost Hyperamylesmia....? misinterpretation Dextrane (bleeding,x-matched
RBCs,anaphylaix,renal)
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Which is best ?
Crystalloid vs Colloid
Evidence has been conflicting
Tailoring the type of resuscitation fluid to the specific clinical condition seems a more logical approach than using the
same type of fluid without exception for all ICU patients
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Vasopressors / Inotropes
Essential few principles to remember Alpha Peripheral squeeze on vessels Beta Inotropic and/or chronotropic effect . with most beta effect, comes a
degree of vasodilation >decreased afterload Other pathways exist c AMP Phosphodiesterase inhibitors
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Vasopressors / Inotropes
epinepherin Alpha and beta effect Great increase on cardiac O2 demand Splanchnic vasoconstriction Should be 2nd or 3rd line trope
Dopamine Alpha and beta depending on dose BUT Overall
alpha effect is weaker than levo Beta effect increases cardiac O2 requirements Beta also increases amount of dysrhythmias works indirectly at nerve endings to release
norepi and epi.
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Vasopressors / Inotropes
Norepinepherine (levophed) Mostly alpha, some beta Potent vasoconstrictor, less effect on increase in HR Reflex bradycardia in response to increase in MAP,
HR remains unchanged or even slight decreaseVasopressin Vasoconstriction of peripheral blood vessels via V1
receptor Weak pressor in normal patients Patel 1999, Sharshar 2003- 1/3 of septic patients
have relative vasopressin deficiency Although used commonly, needs future studies.
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Vasopressors / Inotropes
Dobutamine Mostly beta effect Increase in inotropy Increase in chronotropy Peripheral vasodilation Overall will increase cardiac output and
decrease afterload
Others
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So…
Now we discuss shock types We discuss fluid principles We discuss pressors/tropes
Let’s put it all together to treat “shock”
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Case 1
52 yr old male with crushing retrosternal chest pain, diaphoresis.
ECG: depression in V56, II, III, aVF BP 110/70, HR 110, in CCU BP drops to
80/60
Cardiogenic shock Treatment
Judicious fluidInotropesLittle need for pressors
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Case 2
60 yr female with chest pain and shortness of breath Sa02 82% BP 75/50 Elevated JVP, S1Q3T3 CT chest: massive saddle pulmonary embolism
Obstructive ShockTreatment: Fluids + pressors or tropes ? RELIEVE THE OBSTRUCTION
Pulmonary embolism ThrombolysisTension pneumo Needle
decompression and ICTTamponade Pericardiocentesis
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Case 3
78 yr female with productive cough, fever, confusion
BP 85/35, HR 125 CXR: RLL infiltrate, 25% bands, urea 19
Distributive Shock
Treatment: fluids, pressors, inotropes? ANTIBIOTICS (in under one hour)
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Septic Shock
Rivers et al. Early Goal Directed Therapy in the Treatment of Severe Sepsis and Septic Shock.
NEJM 2001; 345:1368-77 randomized partially blinded 263 patients; 130 Tx, 133 control Standard therapy vs. six hours of EGDT
CVP 8-12 MAP >65
SvO2 >70 UOP >0.5cc/kg/hr
Total fluids(L)
0-6hr 7-72hr 0-72hr
Standard 3.5L 10.6L 13.3L
EGDT 5.0L 8.6L 13.4L
Inhospital mortality
46.5%
30.5%
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So...
You have to Fill the tank...earlyA dry patient not in heart failure will die much sooner than a resuscitated patient in heart failure
What about pressors/inotropes ?
If your MAP <65, likely will need vasopressor If your MAP>65, and Scv02<70, may benefit
from inotrope
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Treatment Algorithm
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Case 4
53 yr old male on GI ward, Hx of Portal HTN, esophagealvarices, recent sever hematemesis HR 135, BP 80/60, 8L 02. Anxious, confused, diaphoretic
Hypovolemic shockTreatment
Your staff will bring the scope in about 30 minutesThe MET team will respond in 15 minutesYour patient will be dead in 10 minutes
Stop the bleeding fluids, pressors, inotropes?
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Resuscitation endpoints....?? Blood pressure Heamatocrite/Hb Filling pressures All of the above Non of the above
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Resuscitation endpoints
Lactic acid production Elevated serum lactate is an indirect measure of the oxygen debt, and an approximation of the magnitude and duration of the severity of shock. The rate of clearance of lactate is a better marker of adequate resuscitation rather than absolute value. Base deficit
BD is the amount of base in millimoles that is required to
titrate 1 L of whole blood to a pH of 7.40 with the sample fully saturated with O2 at 37°C and a PaCO2 of
40. Elevated BD correlate with the severity of shock. Correction of BD is a guide for resuscitation.
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Resuscitation endpoints
Intramucosal pH monitoringMesenteric organs have earlier and greater
hypoperfusion than other organs.
Gastric tonometry measure intragastric intramucosal pH and is an early indicator of hypoperfusion in shock and correlate with the mortality.(technically difficult to use)
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So…what was our objective ?
Have a nice garden
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So…our objectives were
Definition of shock Pathophysiology Shock Categories Management of shock Case scenarios
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?
any question..
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Thank you
A H M
A D F. M A
D y