ACUTE MEDICINE LECTURE SERIES 2010

Ahmad F. Mady MD

SHOCKHOW TO WATER A GARDEN?

Before we go anywhere, let’s start at the beginning

What do you need to maintain a nice garden?

WATER

What do you need to get the water to the garden ?

4 things

Water pump Release valve Hose Water amount

What is Shock?

Theoretical:Inability to meet cellular requirements for

oxygen Practical:When the nurse calls you for a low blood

pressure

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

What the hell are you talking about?

Aetiological Shock Categories Pump failure = Cardiogenic shock Release valve failure = Obstructive

shock Hose failure = Distributive shock Water failure = Hypovolemic shock

Hypovolemic Shock

Not enough stuff Blood plasma

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

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%)

Obstructive Shock

• Tension pneumothorax• Cardiac tamponade• Pulmonary embolism• Aortic stenosis

Distirutive shock

Caused by systemic vasodilatation from Infection -Septic shock (35-40% ,1 month

mortality) Spinal / Neurogenic Shock Anaphylaxis

Septic shock

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%)

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 =

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

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.

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

ShockInitial signs of end organ dysfunction Tachycardia Tachypnea Metabolic acidosis Oliguria Cool and clammy skin

End Organ DysfunctionProgressive irreversible dysfunction Oliguria or anuria Progressive acidosis and decreased CO Agitation, obtundation, and coma Patient death

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

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

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

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

Fluids

Colloids Natural vs Synthetic Natural

Blood FFP Platelets Human albumin

Drawbacks: Limited supply High cost Possible allergic reactions Risk of infection

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)

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

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

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.

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.

Vasopressors / Inotropes

Dobutamine Mostly beta effect Increase in inotropy Increase in chronotropy Peripheral vasodilation Overall will increase cardiac output and

decrease afterload

Others

So…

Now we discuss shock types We discuss fluid principles We discuss pressors/tropes

Let’s put it all together to treat “shock”

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

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

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)

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%

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

Treatment Algorithm

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?

Resuscitation endpoints....?? Blood pressure Heamatocrite/Hb Filling pressures All of the above Non of the above

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.

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)

So…what was our objective ?

Have a nice garden

So…our objectives were

Definition of shock Pathophysiology Shock Categories Management of shock Case scenarios

?

any question..

Thank you

A H M

A D F. M A

D y