Etiology, signs and symptoms and management of hypovolemic and cardiogenic shock

1. HYPOVOLEMIC AND
CARDIOGENIC Shock
PRESENTER: DR.ANNAMALAI
MODERATOT: DR.M.V.SRINIVAS

2. HYPOVOLEMIC SHOCK
 Hypovolemic shock encompasses
disease process that reduces CO and
oxygen delivery via reduction in preload.

3. DETERMINANTS OF OXYGEN DELIVERY (DO2)
 The two major components of DO2 are cardiac output(CO) and arterial oxygen
content(cao2):
DO2=CO X Cao2
 The two major components of CO are heart rate (HR) and stroke volume (sv)
DO2 = (HR X SV) x Cao2
 The major determinants of SV are preload, afterload(SVR) and cardiac contractility
SV = (preload x contractility)xSVR
 The Cao2 is composed of oxygen carried by convection with hemoglobin and
oxygen dissolved in blood
Ca02 = (Hb x 1.39 x Sa02) + (pao2 x 0.03)

4.  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).

5. etiology
Haemorrhagic causes:
1. internal
 Hematoma
 Hemothorax
 Hemoperitoneum
2.external
 Trauma
 bleeding

6. Non haemorrhagic causes
1.internal
 Third space loss
 Pancreatitis
 Ascitis
2.external
 Vomitting
 Diarhea
 burns

7. Clinical features
 Cold clammy pale skin
 Thready pulse
 Tacchycardia & tacchypnea
 Hypotension
 Oliguria
 Confusion
 Decreased CVP
 Decreased CO
 Decreased PCWP
 Elevated SVR
 Decreased CVP

8. AMERICAN COLLEGE OF SURGEON CLASSIFICATION OF ACUTE
HAEMORRHAGE
PARAMETERS GRADE I GRADE II GRADE III GRADE IV
%Blood loss <15% 15-30% 30-40% >40%
ml blood loss <750 750-1500 1500-2000 >2000
PR/min <100 >100 >120 >140
SBP N N 90-70 <60
Pulse pressure 36 30 20-3. 10-20
RR 14-20 20-30 30-40 >40
Urine output ml/hr 30-35 25-30 5-15 <5
Mental status oriented anxious confusion lethargic

10. management
 Resuscitation of these patients should be considered in two phases:
 Early, while active bleeding is still ongoing
 Late, once all hemorrhage has been controlled

11. GOALS OF THE TREATMENT
• ABCDE
• Airway
• control work of Breathing
• optimize Circulation
• assure adequate oxygen Delivery
• achieve End points of resuscitation

13.  Fluid administration is the cornerstone of resuscitation
 rapid infusion of up to 2 L of warmed isotonic crystalloid
solution in any hypotensive patient with the goal of restoring
normal blood pressure

14. Goals of early resuscitation
 Maintain systolic blood pressure at 80 to 100 mm Hg
 Maintain hematocrit at 25% to 30%
 Maintain the prothrombin time and partial thromboplastin time in normal ranges
 Maintain the platelet count at greater than 50,000 per high-power field
 Maintain normal serum ionized calcium

15. crystalloids
 Isotonic crystalloids (normal saline, lactated Ringer's solution [LR], Plasma-Lyte A)
are the initial resuscitative fluids administered to any trauma patient .
 advantage of being inexpensive, readily available, nonallergenic, noninfectious,
and efficacious in restoring total-body fluid.
 easy to store and administer, mix well with infused medications, and can be
rapidly warmed to body temperature.
 Disadvantages of crystalloids include lack of oxygen-carrying capacity, lack of
coagulation capability, and limited intravascular half-life.

16.  Hypertonic saline solution will draw fluid into the vascular space from the
interstitium and thereby reverse some of the non hemorrhagic fluid loss caused by
shock and ischemia.

17. colloids
 Colloids, including starch solutions and albumin, have been advocated for rapid
plasma volume expansion.
 Like crystalloids, colloids are readily available, easily stored and administered
 colloids will increase intravascular volume by drawing free water back into the
vascular space.

18.  colloid resuscitation will restore intravascular volume more rapidly than crystalloid
infusion will and at a lower volume of administered fluid.
Disadvantage:
 expensive, allergic reaction
 If there is any endothelial injury colloids leaks out . It will increase the oncotic
pressure in extravascular space which worsen the condition.
 It takes 12-24hrs for endothelial cells to repair

19.  Red blood cells are the mainstay of treatment of hemorrhagic shock.
 With an average hematocrit of 50% to 60%, a unit of RBCs will predictably restore
oxygen-carrying capacity and expand intravascular volume as well as any colloid
solution.

20.  When the patient is in shock,and blood loss is likely to be substantial, platelets
should be empirically administered in proportion to RBCs and plasma (1 : 1 : 1)

21. ASSESMENT OF INTRAVASCULAR VOLUME STATUS
PASSIVE LEG RAISE TEST:
 Predict the responsiveness to additional intravenous fluid by providing the patient
with endogenous volume bolus
 While the patient is resting in a semirecumbent position at 45 degree angle, the
bed is placed in Trendelenburg such that the patients head becomes horizontal
and the legs are extended at 45 degree angle
 There is an immediate assesement of changes in CO or pulse pressure variation
occur.

22.  The most commonly used parameters to assess the adequacy of volume
resuscitation are IVC diameter and IVC collapse using echocardiography.

23. OXYGENATION AND VENTILATION
 In addition to cellular hypoxia caused by circulatory failure patient with shock may
present with hypoxemia
 In shock there can be development of ARDS and subsequent V/Q mismatch and
shunt.
 Supplement oxygen should be initiated and titrated to maintain spo2 of 92-95%
 If patient requires intubation this should be provided promptly so as to minimize
the duration of tissue hypoxia
 Patient with shock may have need high minute ventilatory needs to compensate
for metabolic acidosis.

24.  It is important to provide ventilation with lung protective stratergies focussed on
low tidal volume ventilation and optimization of positive end expiratory pressure
to minimize ventilator induced lung injury.

25. Cardiogenic shock
 Cardiogenic shock results from cardiac failure with the inability of the heart to maintain
adequate tissue perfusion.
 The clinical definition of cardiogenic shock is evidence of tissue hypoxia due to
decreased cardiac output (cardiac index < 2.2 L/min/m2)and sustained systolic arterial
hypotension (<90 mmHg) in the presence of adequate intravascular volume.
 This is most often caused by cardiac dysfunction due to myocardial infarction ..
 The initiating event in cardiogenic shock is a primary pump failure.

26. etiology
1.compressive type
Associated with external compression to the heart
 Cardiac tamponade
 Tension pneumothorax
 Positive pressure ventilation
2.obstructive type:
Associated with obstruction to outflow or inflow to the heart
 AS
 MS
 TS
 PS

27. 3.Functional type
Overall most common type
 IHD
 arryhthmias

28. Hemodynamics
 The pulse is typically weak and rapid,
 Often in the range of 90–110 beats/min,
 elevated PCWP
 Elevated CVP
 Decreased CO

29. MANAGEMENT
 Correction of hypovolemia
The first priority in treating cardiogenic shock is
to expand the circulating blood volume with IV fluids ,
 Treatment of arrhythmias
 Treatment of hypotension
 Treatment of metabolic acidosis
 Treatment of electrolyte disturbances

30.  Therapy should minimize myocardial oxygen demand and raise oxygen delivery to
the ischemic area;
 This goal is complicated by the fact that many resuscitative approaches to correct
hypotension (preload augmentation, inotropes, and vasopressors; increase
myocardial oxygen consumption.
 In patients without hypotension, pharmacologic vasodilatation using nitrates or
sodium nitroprusside may reduce myocardial oxygen consumption and improve
ventricular ejection by reducing left ventricular afterload and possibly produce a
shift of blood from the lungs to the periphery by reducing venous tone.

31. Medications:-
1. Vasoactive therapy—
Vasopressors and inotropic agents are administered only after adequate fluid
resuscitation.
 Choice of vasoactive therapy depends on the presumed etiology of shock as well as
cardiac output.
 If there is evidence of low cardiac output with high filling pressures, inotropic support
is needed to improve contractility.
 If there is continued hypotension with evidence of high cardiac output after adequate
volume resuscitation, then vasopressor support is needed to improve vasomotor tone.

32. Dobutamine,
 predominantly ß-adrenergic agonist,
 1st line of drug for cardiogenic shock,
 Increasing contractility and decreasing afterload.
 Initial dose is 0.5–1 mcg/kg/min as a continuous iv infusion,
 Which can be titrated every few minutes as needed to hemodynamic effect;
 The usual dosage range is 2–8 mcg/ kg/min intravenously.

33.  Epinephrine:
 Increases the myocardial contractility
 Powerful cardiac stimulant
 Increases the heart rate

34. End points of resucitation
1.clinical:
most important: urine output
 Adults:>0.5ml/kg/hr
 Children:1-1.5ml/kg/hr
 Infants:>2ml/kg/hr

35.  2.check for arterial blood lactate level
 3.mixed venous oxygen saturation:
 It is a measure of oxygen saturation at right atrium
 It indicates the utilisation of oxygen by the organs
 Normal value is 70%
 In hypovolemic shock: blood volume is l,ow, so the oxygen is overutilized by the
organs so M.V.O.S - < 50%
 In cardiogenic shock: blood volume is normal but heart cannot pump enough
blood so oxygen is over utilized so M.V.O.S <50%

36.  Refference: MILLERS ANAESTHESIA
HARRISON