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Presentor : Dr.

Kumar
Moderator: Dr.Vamsidhar
History
term shock (Fr, choke) was first used by French
physician Le Pran in 1773 todescribe the clinical
characteristics of patients after severe gunshot
trauma.
Definitions:
Shock is a state in which failure of the circulatory
system to maintain adequate cellular perfusion
results in wide spread reduction in delivery of
oxygen and other nutrients to tissues.
( OR )
Shock is a syndrome of failure of heart to pump
blood in sufficient quantity or under sufficient
pressure to maintain pressure flow relationship
necessary for adequate tissue perfusion
( OR )
Shock denotes circulatory failure leading to
inadequate vital organ perfusion ,oxygen delivery
and other tissues
Stages of Shock
Compensated
15-25% of fluid loss from the vessels
Signs are subtle
Patient may show signs of an adrenaline rush
Decompensated
25-35% of fluid loss from the vessels
The body cells are profoundly hypoxic
Classic signs of shock
Irreversible
> 35% fluid loss from the vessels
Body cells die
All vital signs bottom out
Compensatory ( Reversible )
SYMPATHOADRENAL STIMULATION

PRE CAPILLARY SPINCTER CONSTRUCTION

CAPPILARY HYDROSTATIC
PRESSURE.(Increase )

FLUID MOVES INTO INTRAVASCULAR SPACE


IRREVERSIBLE
IF HYPOPERFUSION CONTINUES

HYPOXIA – ANAEROBIC METABOLISM

INCREASE IN LACTIC ACID + INCREASE [H+]

DECREASE IN CAP. HYDR. PRES

INCREASE IN POST CAP. SPHINCTER TONE

WEAKENING OF PRE CAP SPHINCTER TONE

FLUID MOVES INTO EXTRA VASCULAR SPACE


Fluid loss into extra vascular space.
Adhesion of activated leukocytes to endothelial
cells – increase in cap. Permeability
obstruction to micro vessels
Accumulation of micro thrombi because of
activation of coagulation system with fibrin
deposition.
Types of Shock
Cardiogenic (intracardiac vs extracardiac)
Hypovolemic
Distributive
sepsis****
neurogenic (spinal shock)
adrenal insufficiency
anaphylaxis
Pathophysiology: Overview
Tissue perfusion is determined by Mean Arterial
Pressure (MAP)

MAP = CO x SVR

Heart rate Stroke Volume


Cardiogenic Shock:
Pathophysiology
Heart fails to pump blood out

MAP = CO x SVR

HR Stroke Volume
as a consequence of cardiac pump failure, resulting in decreased
cardiac output (CO).
Pump failure can occur both as a result of an abnormality of the
Heart rate or the Stroke volume
Cardiogenic Shock: Causes
↓MAP = ↓ CO (HR x Stroke Volume) x ↑SVR
Decreased Contractility (Myocardial Infarction,
myocarditis, cardiomyopathy, Post resuscitation
syndrome following cardiac arrest)

Mechanical Dysfunction – (Papillary muscle rupture


post-MI, Severe Aortic Stenosis, rupture of ventricular
aneurysms etc)

Arrhythmia – (Heart block, ventricular tachycardia,


SVT, atrial fibrillation etc.)

Cardiotoxicity (B blocker and Calcium Channel


Obstructive Shock:
Pathophysiology
Heart pumps well, but the output is decreased
due to an obstruction (in or out of the heart)

MAP = CO x SVR

HR x Stroke volume
If the blood outflow from the heart is decreased
because there is decreased return to the heart (due
to an obstruction) or “obstructed” as the blood leaves
the heart the stroke volume diminishes, with the
overall effect of decreasing the cardiac output
Obstructive Shock: Causes
↓MAP = ↓ CO (HR x Stroke Volume) x ↑SVR
Heart is working but there is a block to the
outflow
Massive pulmonary embolism
Aortic dissection
Cardiac tamponade
Tension pneumothorax

Obstruction of venous return to heart


Vena cava syndrome - eg. neoplasms, granulomatous
disease
Sickle cell splenic sequestration
Hypovolemic Shock:
Pathophysiology
Heart pumps well, but not enough blood volume
to pump

MAP = CO x SVR

HR x Stroke volume
Hypovolemic shock is a consequence of
decreased preload due to intravascular volume
loss.
-The decreased preload diminishes stroke
volume, resulting in decreased cardiac output
(CO).
Hypovolemic Shock: Causes
↓MAP = ↓ CO (HR x Stroke Volume) x ↑SVR

Decreased Intravascular volume (Preload)


leads to Decreased Stroke Volume
Hemorrhagic - trauma, GI bleed, AAA rupture,
ectopic pregnancy
Hypovolemic - burns, GI losses, dehydration,
third spacing (e.g. pancreatitis, bowel
obstruction), Adesonian crisis, Diabetic
Ketoacidosis
Distributive Shock:
Pathophysiology
Heart pumps well, but there is peripheral
vasodilation due to loss of vessel tone

MAP = CO x SVR

HR x Stroke volume
Distributive (vasodilatory) shock is a consequence of
severely decreased SVR.
Distributive Shock: Causes
↓MAP = ↑CO (HR x SV) x ↓ SVR

Loss of Vessel tone


Inflammatory cascade
Sepsis and Toxic Shock Syndrome
Anaphylaxis
Post resuscitation syndrome following cardiac arrest
Decreased sympathetic nervous system function
Neurogenic - C spine or upper thoracic cord injuries
Toxins
Due to cellular poisons -Carbon monoxide,
methemoglobinemia, cyanide
Drug overdose (a1 antagonists)
To Summarize

Type of Insult Physiologic Compensation


Shock Effect
Cardiogenic Heart fails to pump ↓CO BaroRc
blood out ↑SVR

Obstructive Heart pumps well, but ↓CO BaroRc


the outflow is obstructed ↑SVR

Hemorrhagic Heart pumps well, but ↓CO BaroRc


not enough blood ↑SVR
volume to pump

Distributive Heart pumps well, but ↓SVR ↑CO


there is peripheral
vasodilation
Type of Insult Physio Compen Compensation Compensation
Shock logic sation Heart Rate Contractility
Effect
Cardiogenic Heart fails to ↓CO BaroRc ↑ ↑
pump blood ↑SVR
out
Obstructive Heart pumps ↓CO BaroRc ↑ ↑
well, but the ↑SVR
outflow is
obstructed
Hemorrhagic Heart pumps ↓CO BaroRc ↑ ↑
well, but not ↑SVR
enough blood
volume to
pump
Distributive Heart pumps ↓SVR ↑CO ↑ ↑
well, but
there is No Change - No Change -
peripheral in neurogenic in neurogenic
vasodilation shock shock
Additional Compensatory
Mechanisms
Renin-Angiotensin-Aldosterone Mechanism
AII components lead to vasoconstriction
Aldosterone leads to water conservation

ADH leads to water retention and thirst

Inflammatory cascade
Hypovolemic Distributive Cardiogenic Obstructive
Shock Shock Shock Shock

HR Increased Increased May be Increased


(Normal in increased or
Neurogenic decreased
shock)
JVP Low Low High High

BP Low Low Low Low

SKIN Cold Warm (Cold Cold Cold


in severe
shock)
CAP Slow Slow Slow Slow
REFILL
Symptoms and Signs of Shock
Level of consciousness

Initially may show few symptoms


Continuum starts with
Anxiety
Agitation
Confusion and Delirium
Obtundation and Coma

In infants
Poor tone
Unfocused gaze
Weak cry
Lethargy/Coma
(Sunken or bulging fontanelle)
Symptoms and Signs of Shock
Pulse
Tachycardia HR > 100
Rapid, weak, thready distal pulses

Respirations
Tachypnea
Shallow, irregular, labored
Symptoms and Signs of Shock
Blood Pressure
May be normal!
Definition of hypotension
Systolic < 90 mmHg
MAP < 65 mmHg
40 mmHg drop systolic BP from from baseline

Children
Systolic BP < 1 month = < 60 mmHg
Systolic BP 1 month - 10 years = < 70 mmHg + (2 x age in years)

In children hypotension develops late, late, late


A pre-terminal event
Symptoms and Signs of Shock
Skin
Cold, clammy (Cardiogenic, Obstructive,
Hemorrhagic)
Warm (Distributive shock)
Mottled appearance in children
Look for petechia
Dry Mucous membranes
Low urine output <0.5 ml/kg/hr
Empiric Criteria for Shock
4 out of 6 criteria have to be met

Ill appearance or altered mental status


Heart rate >100
Respiratory rate > 22 (or PaCO2 < 32 mmHg)
Urine output < 0.5 ml/kg/hr
Arterial hypotension > 20 minutes duration
Lactate > 4
Management of Shock
History
Physical exam
Labs
Other investigations
Treat the Shock - Start treatment as soon as you
suspect Pre-shock or Shock
Monitor
Historical Features
Trauma?
Pregnant?
Acute abdominal pain?
Vomiting or Diarrhea?
Hematochezia or hematemesis?
Fever? Focus of infection?
Chest pain?
Physical Exam
Vitals - HR, BP, Temperature, Respiratory rate,
Oxygen Saturation
Capillary blood sugar
Weight in children
Physical Exam
In a patient with normal level of
consciousness - Physical exam can be
directed to the history
Physical Exam
In a patient with abnormal level of
consciousness
Primary survey
 Cardiovascular (murmers, JVP, muffled
heart sounds)
 Respiratory exam (crackles, wheezes),
 Abdominal exam
 Rectal and vaginal exam
 Skin and mucous membranes
 Neurologic examination
Laboratory Tests
CBC, Electrolytes, Creatinine/BUN, glucose
+/- Lactate
+/- Capillary blood sugar
+/- Cardiac Enzymes
Blood Cultures - from two different sites
Beta HCG
+/- Cross Match
Other investigations
ECG
Urinalysis
CXR
+/- Echo
+/- FAST(focused abdominal sonography for
trauma)
• Do you remember how to
60
quickly estimate blood
pressure by pulse?
• If you palpate a pulse, 70
you know SBP is at 80
least this number

90
Goals of Treatment
• ABCDE
• Airway
• control work of Breathing
• optimize Circulation
• assure adequate oxygen Delivery
• achieve End points of resuscitation
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
Control Work of Breathing

• Respiratory muscles consume a significant


amount of oxygen
• Tachypnea can contribute to lactic acidosis
• Mechanical ventilation and sedation
decrease WOB and improves survival
Optimizing Circulation

• Isotonic crystalloids
• Titrated to:
• 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
• No outcome benefit from colloids
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
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%
Persistent Hypotension

• Inadequate volume resuscitation


• Pneumothorax
• Cardiac tamponade
• Hidden bleeding
• Adrenal insufficiency
• Medication allergy
Management of hypovolemic
shock:
AIM: To restore cardiac filling pressure promptly and
adequately without inducing pulmonary edema.
Measures:
1. Arresting ongoing blood loss.
2. Restoration of blood volume.
3. Correction of metabolic acidosis
Arresting ongoing blood loss:
External haemorrage by pressure elevation and tourniquet.
Internal haemorrhage by immediate surgical exploration.

Restoration of circulating blood volume:


Start two large bore I.V. cannula,
Debate still exists over the type, amount and rate of infusion
of fluids.
Fluid challenge test is the guideline for rate of infusion.
End point of resuscitation should be based on factors
reflecting adequacy of perfusion
1. Establishing urine output > 0.5 ml/kg/Hr.
2. Reappearance of peripheral pulses.
3. Correction of hypothermia, with reduction of core to
peripheral temp gradient to< 10C.
4. Improvement of mental status.
5. Return of B.P. to normal
6. Capillary refill < 3 sec
7. Correction of metabolic acidosis (blood lactate
level <1.5 mmol/l) with normalization of pH.
Management of cardiogenic
shock:
Three steps:
1. Initial stabilization
2. Evaluation of the patient
3. Definitive therapy
Initial stabilization:
1. Establishment of ventilation and oxygenation to
maintain PaO2> 70 mm Hg.
2. Restore MAP > 70 mm Hg with volume
correction and vasopressors.
3. Treatment of pain, arrhythmias and acid base
abnormality.
Evaluation of the patient:
Brief history, physical examination and
investigations.
ECG-look for ischemic changes, cardiac enzymes
Cardiac filling pressure – CVP, PCWP, LVEDP
Chest x-ray, ABG
2D echo for ventricular function
Arterial O2 saturation
Starling function curve.
Definitive therapy
Goals of treatment
1. CI -4.5 l/min/ m2 (N – 3.0 – 3.4 l/min /m2).
2. DO2- 600 ml/min/ m2 (N – 480 – 600 ml/min
/m2)
3. VO2 – 140 – 180 ml/min /m2 (N – 130 – 160
ml/min/ m2)
Achieved by,
1. Pharmacological support and / or
2. Surgical intervention
1) Pharmacological support:
Aimed at – increase C.O., improving coronary blood flow and
decrease transudation of fluid into the lung.
Done by – modifying preload, after load and by increase inotropic
function of the myocardium.

Reduction in preload (diuretics):


Decrease volume where excusive preload exists.
Over use may result in organ hypoperfusion and renal failure.
Loop diuretics

Improving myocardial contractility (inotropes):


Inotropes are indicated where preload is optimal but low cardiac
output and
hypotension exists.
Sympathomimetic amines are potent inotropes which act via a and b
adrenergic
Epinephrine:
Powerful cardiac stimulant
Increase HR, shortens systole.
Increase cardiac work and O2 consumption.
1-2 mcg / min - b stimulation
2-10 mcg/min – mixed a and b stimulation
10 mcg / min - a stimulation.
Dopamine: (3-4 di-hydroxy phenyl ethylamine)
1-5 mg/kg/min – dopaminergic receptors – renal and
mesenteric vasodilation.
5-10 mg/kg/min - b action, receptor positive inotropic and
positive chronotropic effects on heart.
10 mg/kg/min - a receptor– vasoconstriction.
Dobutamine: synthetic sympathomimetic
amine
Acts mainly on b1 receptor with little effects on b2
/a
Useful in cardiogenic shock due to MI with
tachycardia.
Increase CO without increasing infarct size or
causing malignant arrhythmias.
Dose – 5-20 mg/kg/min.
Reduction in after load (vasodilators):
Vasodilators decrease after load by decrease
SVR and decrease PVR which improves cardiac
output.
Useful in patient with
Normal / increase preload-PCWP > 15 mm Hg.
Adequate perfusion pressure SBP > 110 mm Hg.
High vascular resistance
Low cardiac output
SNP:
Both arteriolar and Venodilators
Onset of action within 2 mins
Rapidly metabolized to Thiocyanate and cyanide
Dose 1-10 mg/kg/min (20-500 mg/min)
NTG:
·Venodilators, + coronary vasodilator treatment
myocardial ischemia
Onset within sec
½ life – 4 mins
Dose 1-10 mg/kg/min (10-400 mg/min)
II. Surgical intervention:
IABP
Angioplasty
CABG
Cardiac transplant.
The Sepsis Continuum
Severe Septic
SIRS Sepsis Sepsis Shock

 A clinical response
arising from a SIRS with a Sepsis with Refractory
nonspecific insult, with presumed organ failure hypotension
2 of the following: or confirmed
 T >38oC or <36oC infectious
 HR >90 beats/min process
 RR >20/min
 WBC >12,000/mm3 or
SIRS = systemic inflammatory
<4,000/mm3 or >10%
response syndrome
bands
Severe Sepsis Screening Tool

Are any 2 of the following SIRS criteria present and new to


your patient?

Obs: Temperature >38.3 or <36 0C Respiratory rate >20 min-1

Heart rate >90 bpm Acutely altered mental


state

Bloods: White cells <4x109/l or >12x109/l Glucose>7.7mmol/l


If yes, (if patient is not
diabetic)
patient has SIRS
Is this likely to be due to an infection?
For example

Cough/ sputum/ chestpain Dysuria

Abdo pain/ diarrhoea/distension Headache with neckstiffness

Line infection Cellulitis/wound infection/septic arthritis

Endocarditis

If yes,
patient has SEPSIS
Start SEPSIS BUNDLE
Check for SEVERESEPSIS

BP SBP< 90 / Mean < 65 mmHg


(after initial fluid challenge)
Lactate > 4 mmol/l

Urine output < 0.5 ml/kg/hr for 2 hrs

INR > 1.5

aPTT > 60 s

Bilirubin > 34 μmol/l

O2 Needed to keep SpO2 > 90%

Platelets < 100 x 109/l

Creatinine > 177 μmol/l or UO < 0.5 ml/kg/hr

Severe Sepsis
What is a Bundle?

 Specifically selected care elements


 From evidence based guidelines
 Implemented together provide improved
outcomes compared to individual elements
alone
6 Hour Resuscitation
Bundle

 Early Identification
 Early Antibiotics and
Cultures
 Early Goal Directed
Therapy
6 - hour Severe Sepsis/
Septic Shock Bundle

 Early Detection: • Vasopressors:


 Obtain serum lactate level. – Hypotension not responding to
fluid
– Titrate to MAP > 65 mmHg.
 Early Blood Cx/Antibiotics:
 within 3 hours of • Septic shock or lactate > 4
mmol/L:
presentation. – CVP and ScvO2 measured.
– CVP maintained >8 mmHg.
 Early EGDT: – MAP maintain > 65 mmHg.
 Hypotension (SBP < 90, MAP
• ScvO2<70%with CVP > 8 mmHg,
< 65) or lactate > 4 mmol/L: MAP > 65 mmHg:
 initial fluid bolus 20-40 ml of – PRBCs if hematocrit < 30%.
crystalloid (or colloid equivalent) – Inotropes.
per kg of body weight.
EGDT
Call for specialist support

<8mmHg Crystalloid
CVPline
Colloid

>8
mmHg

< 65 or <90 mmHg


MAP VasoactiveDrugs

>65 &
>90mmHg

<70% Transfuse red cells


ScvO2
until Hb > 10 g/dl

YES ScvO2
>70% >70%

NO
Goals
Inotropic agents
Achieved

Rivers et al 2001, NEJM; 345, 1368-1377


Activated protein C
Known inflammatory and procoagulant host
responses to infection.
TNF-alpha, IL-1, IL-6, thrombin
Diffuse endovascular injury, multiorgan dysfunction
and death.
Activated Protein C
anticoagulant, modulates the inflammatory response
reduced levels of protein C found in majority of patients with
sepsis and are associated with increased risk of death.
STEROIDS

IVcorticosteroids (hydrocortisone
200-300 mg/day,
for 7 days in three or four divided
doses or by continuous infusion)
who, despite adequate fluid
replacement, require vasopressor
therapy to maintain adequate blood
pressure.
Blood Product Administration
PRBC transfusion if Hb <7.0 g/dL ; target 7.0-
9.0 g/dL.
Erythropoietin only accepted reasons for
administration of erythropoietin such as renal
failure induced anemia.

No Routine use of fresh frozen plasma to


correct laboratory clotting abnormal

Platelets administered <5,000/mm3 (5 x


109/L) regardless of apparent bleeding.

Higher platelet counts (>50,000/mm3 [50 x


109/L])for surgery or invasive procedures
Management of anaphylactic
shock
Generally a clinical diagnosis
a.The offending agent can often be difficult to
identify (eg. Latex, metabisulfites, food
allergy, etc) and sometimes drugs

b.Seurmtryptase may be useful in difficult


diagnostic cases.
Initial Therapy
1. Maintain Adequate Ventilation
a) Oxygen
b) Establish an airway if needed
2. Stop absorption
3. Epinephrine
a) This remains the most important pharmacological
management of anaphylaxis (J All Clin Innunol, 1994;
94:666-8)
b) 0.3 – 0.5 mg IV or SQ
a) Use 0.3 – 0.5 ml of 1:1,000 dilution SQ
b) Use 3 – 5 ml of 1:10,000 dilution IV
4. Inhaled beta-agonists
5. Establish Adequate Venous Access
Secondary Therapy
1. Antihistamines (H1 & H2 blockers)
a) 25-50mg hydroxyzine or diphenhydramine Q6 hours
b) Cimetidine 300mg every 8-12 hours
2. Corticosteroids (may shorten protracted
reactions but do not provide immediate benefit)
a) 250 mg hydrocortisone Q6 hours IV
3. Aminophylline (probably not as useful as
inhaled b-agonists)
a) Load with 6 mg/kg/hr IV
b) Maintain with 0.3 – 0.6 mg/kg/hr IV
4. Observation in the hospital for at least 24 hours
(for relapse)
5. Glucagon (1 mg IV) can be useful in patients
which anaphylactic shock on beta-blockers as
these patients may be resistent to epinephrine