shock
DESCRIPTION
A Detail explanation regarding pathophysiology and treatment modalities of different types of shock.TRANSCRIPT
1GOOD MORNING
2
SHOCK
Dr.Mehul JaniMAXILLOFACIAL SURGEON
3
4
ShockShock
DIFINITION
Shock is a physiologic state characterized by systemic reduction in tissue perfusion, resulting in decreased
tissue oxygen delivery.
It is a condition in which circulation fails to meet the nutritional needs of the cells &
at the same time fails to remove the metabolic waste products.
5
ETIOLOGIES
6
7
Basic Physiology• Unit of life = cell
• Cells get energy (ATP) from cellular respiration:
O2 + Glucose ATP + water + CO2
No O2 = no energy
No energy = no lifeRemember:
Cell Tissues Organ
Body Organ System
Damage to Damage to Damage to
Damage to Damage to
8
Review of the Cardiovascular System
9
Cardiovascular System
• Transports oxygen (fuel) to cells
• Removes carbon dioxide and other waste products
• Cardiovascular system must be able to maintain sufficient flow through capillary beds to meet cell’s oxygen and fuel needs
Flow = Perfusion
Inadequate Flow = Inadequate Perfusion = Hypoperfusion
Adequate flow = Adequate Perfusion
SHOCK
Types of shock
10
11
12
Shock
CardiogenicHypovolaemic
Anaphylactic Septic
Distributive
Neurogenic
Classification of Shock
Hypovolaemic shock
13
Clinical featuresClinical features
14
Mild shock
15
Clinical features are due to adrenergic constriction of blood vessels.•Pale and cool extremities because of collapse of s.c veins.•May be sweat in forehead,hand and feet.•U.O, B.P, pulse may remain normal at this stage.
Moderate shock
16
oliguriaMild shock features +
In the initial stage B.P remains normal and falls in later stage.SO PULSE AND B.P ARE NEVER THE MAIN SIGNS OF SHOCK.
SHOCK MAY BE PRESENT EVEN WITH NORMAL PULSE AND B.P
Sever shock
17
•Rapid pulse•Low urinary output•Pallor of extremities•Low B.P
Clinical monitoring
• Blood pressure::
It is essential to monitor B.P though it is normal in mild shock.
• Respiration::
Increase in rate & depth of respiration is an important indicator of shock.
• Urine output::
It is a good indication of severity of shock and good index of adequacy of replacement therapy. 18
• Central venous pressure (CVP)::
It is important in assessing shock.
CVP decreases in hypovoleamic shock
Where remain constant in cardiogenic shock.*
19
SWAN-GANZ CATHETER
• It is used to get valuable information about the precise diagnosis and circulatory derangement of shock.
• It provides 3 types of information:
1:flow in CVS
2:sampling of blood from pumonary artery to measure the accurate amount of blood gases in venous bllod.
3:filling pressure of rt.<. Side of heart 20
Management Management ofof
hypovolaemic shock hypovolaemic shock
21
General Treatment of Shock– Remember your ABC’s– Administer airway– 100% O2– Assist ventilations if necessary– Position patient to assist perfusion(in tredelenburg position )– Keep patient warm– Perform focused assessment – Monitor and adjust O2,– gain IV access, cardiac monitor, pulse oximetry– Fluid replacement of LR or NS– Need 3 liter of fluid to replace 1 liter of blood loss– Apply pressure to IV or blood to facilitate faster infusion
22
MX
• Resuscitation.
• Control of bleeding
• Extracellular fluid replacement
• Drugs.
23
Resuscitation
24
Goal of treatment
So,
• Maintain airway
• If require intubate the patient
• Maintain adequate ventilation and oxygenation.
25
Bleeding control
• Find out the cause of bleeding and control the bleeding either by raising the foot end of the bed or compression bandage or by surgical intervention if require.
26
ECF replacement
• Most important point in Mx ..
• Non sugar,non protein,crystalloid solution with Na concentration that of plasma is best fluid for replacement.
• Normal saline
• Ringer’s lactate* NaHCo3 **
• Ringer’s acetate*
27
• 3 litres of fluid given over 45 minutes should resuscitate any pt.with arrested haemrrhage.
• Resuscitation should always start with crystalloid solution even if blood is available.*
28
Drugs • Sedatives:Morphine:use to alleviate pain.
:should adminnistrate I.V
should not be use in children,in head injury pt.,pt.with acute abdomen
Berbiturate are preferred in children.
• Vasoconstrictors:help full in hypovolaemic shock.
29
Drug Indication Dose MOA Principal actionsDopamine Renal perfusion 2-5 mcg/kg/min Dopaminergic Renal a. dilation
hypotension 5-10 mcg/kg/min 1 &dopaminergic
+ inotrope
Hypotension >10 mcg/kg/min 1 vasoconstrictionDobutamine Cardiogenic shock 2.5-25 mcg/kg/min Selective 1 + inotropeNorepinephrine Hypotension 2-4 mcg/min 1 & 1 VasoconstrictionPhenylephrine Hypotension 40-180 mcg/min Selective 1 Vasoconstriction
• Cardiogenic shock
30
31
32
Etiology
33
,Chronic congestive heart failure
34
Clinical features:• In beginning : skin is pale,cool & U.O is
low.
• Gradually pulse become rapid & B.P becomes low.
• In the case of rt.ventricular dysfunction the neck veins become distended & liver may also be enlarged.
• In case of lt.ventricular dysfunction third heart sound is heard.
35
Mx
• Airway must be clear with adequate oxygenation.
• In a case of rt.sided failure caused by pulmonary embolism should be treated by large dose of heparine I.V.
• Diuretics can be help full in cardiogenic shock by reducing volume and decrease filling pressure.
36
• Neurogenic shock
37
Spinal cord trauma causes a loss of blood
vessel tone and results in widespread vasodilation.
38
•is one type of distributive shock.•injury may damage the sympathetic nerve fibers that control vessel tone.*
Clinical features:
• Skin remains WARM, PINK, WELL PERFUSED.*
• U.O normal.
• Heart rate is rapid
• B.P is LOW.
39
Mx• Protect and stabilize c-spine.*
• Maintain airway.
• Keep pt.in trendelenburg position.
• Administrate fluid but it is not much important as in hypovolaemic shock.
• Vasoconstrictor drugs by which this shock can be treated safely.
40
•Septic shock
41
42
Most frquent organisms are,Gm +ve ,Gm-ve bacteria,And any agent capable of producing infection like viruses,parasites,fungi
Clinical features:• Recognized Initially by chills and temp.>1000F.*• 2 types: early warm shock & late cold shock.
• Early warm shock:Toxins from infected tissue increase body temperature.to bring this down vasodilatation occurs which decrease systemic vascular resistance.
• LV has minimal resistance + adrenergic discharge again increase CO.
• So skin will become WARM-PINK-WELL PERFUSED.
43
• LATE COLD SHOCK: due to vasodilatation hypovolaemia takes place which reduces cardiac output .
Clinically it is difficult to differentiate it from hypovolaemic or traumatic shock.
Only guide remains is the knowledge of existence of a septic focus.
44
Mx
45
• Use of steroids is questionable because it impaires the immunity responce of body. It also improves the cardiac,pumonary,renal functions which is life saving.
• If steroids given SHORT TERM –HIGH DOSE is recommended.
• 15-30 mg /kg- methyl prednisolone or equivalent dexamethasone.(I.V in 5-10 min)
• Same dose repeat at 4 hours if benificial effect have been not achieved.
46
Systemic Inflammatory Response Syndrome (SIRS)
• Defined as when generalized inflammation occurs and threatens vital organs
• Causes: multiply transfusions, massive tissue injury, burns, and pancreatitis, severe infections or sepsis
• Effects: endothelium is damaged and allows fluid to leak into the body tissues, results in poor perfusion of blood to organs
• Body is in a hypermetabolic state
• Diagnosis made when 2 or more of the following are seen:– Temperature less than 97 or greater than 100.4– Heart rate more than 90– Respiratory rate more than 20 or PaCO2 less
than 32mm Hg– WBC count less than 4000 cells or more than
12,000– Sepsis is used if patient has SIRS with and
infection
Treatment for SIRS/MODS
• Critical care nursing
• Goals– Prevent and treat infections– Maintain tissue oxygenation– Provide nutritional and metabolic response– Support failing organs
• Anaphylactic shock
50
Vasodilation moves blood from the central core to the periphery, causing distributive
shock.
51
• Mass release of histamine and slow release substance of anaphylaxis due to allergic hypersensitivity reaction (foods, insect bites, blood transfusion, drugs).
• Causes bronchospasm,laryngeal edema,and respiratory distress which leads to hypoxia.
• Increased capillary permeability with vasodilation reduces venous return and BP.
•HypoAdrenal shock
52
53
54
55
• Now that we have an understanding of what shock is and the different types, lets look at the physiology behind shock.
• To understand the physiology of shock we need to understand the following formula:
Blood Cardiac Systemic
Pressure = Output x Vascular Resistance
56
• By applying a mathematical aspect to the formula we can start to identify how blood pressure can be maintained.
BP = CO x SVR
• We need to keep both sides balanced.
• If one side of the formula changes, the other side needs to change in the opposite direction to balance this out.
• i.e. If BP increases, we need to decrease CO, SVR or both to bring it back down again
If BP decreases, we need to increase CO, SVR or both to bring it back up again
57
What happens if you get a drop in BP?
BP = CO x SVR
• We need to maintain homeostasis so need to increase BP.
• We can increase BP by increasing:
- CO
- SVR
- CO & SVR
to increase BP back up again.
58
What happens if you get a rise in BP?
BP = CO x SVR
• We need to maintain homeostasis so need to decrease BP.
• We can decrease BP by decreasing:
- CO
- SVR
- CO & SVR
to bring BP back down again.
59
Key Issues In Shock
• Recognise and treat early (during compensatory phase)
Increased resp. rate,Restlessness, EarlyAnxiety, signs of
Argumentative shock
• Falling BP = Late sign of shock
• Pallor, tachycardia and slow capillary refill = Shock until proven otherwise
Hallmark symptoms are:Decreased BPIncreased HR
60
61
Inadequate cellular Oxygen Delivery
Inadequate Energy Production
Anaerobic Metabolism Lactic Acid
Production
Metabolic Failure
CELL DEATH
Metabolic Acidosis
• What happens in compensated shock???
62
63
Compensated shock
• Baroreceptors detect fall in BP• Sympathetic nervous system activated
(see diagram 1)
1. Cardiac Effects
- increased force of contractions
- increased rate (tachycardia)
- increased cardiac output
2. Peripheral Effects
- arteriolar constriction
- increased peripheral resistance
- shunting of blood to main core organs (causing cold clammy skin)
64
sympathetic innervation of myocardium
sympathetic innervation of arterioles
Baroreceptors on aorta and carotid sinus send information about
changes in BP to cardiovascular centre
cardiovascular centre
sympathetic and parasympathetic innervation
of Sino-atrial node
Control of Blood Pressure via the Baroreceptor Reflex
brain
key parasympathetic nerves sympathetic nerves afferent sensory nerves
arterioles
heart
© Roger McFadden – University of Central England 2003
65
3. Respiratory Effects
Tachypnoea is one of the first signs that reflects reduced blood flow and oxygen transport.
the cardiovascular and respiratory systems work together-
If blood flow around the body is compromised in any way, oxygen delivery to tissues is reduced.
To compensate for this, ventilation will increase to attempt to increase oxygen uptake in the lungs.
66
So how does this happen ??
respiratorycentres in medulla
chemoreceptorson aorta and carotid
artery
heart
brain
intercostal nerve to externalintercostal muscles
phrenic nerve to diaphragm
ribs
The Baroreceptors not only stimulate the cardiovascular control centre but also the respiratory centre in the medulla, increasing the respiratory rate.
67
4.Renal Effects
68
Renin – Angiotensin – Aldosterone Pathway
THIRST
ANGIOTENSIN II
ADRENAL CORTEX
KIDNEYS increase Na+ reabsorption from filtrate
BP
VASOCONSTRICTION
BLOOD PRESSURE
ALDOSTERONE
BLOOD VOLUME
ANGIOTENSIN CONVERTING ENZYME
JUXTAGLOMERULAR cells in the kidney respond to a REDUCTION
IN BLOOD VOLUME from EXCESS VOMITING,
SWEATING, & HAEMORRHAGE etc.
RENIN released into blood
ANGIOTENSINOGEN ANGIOTENSIN I
. 5.Hypothalamus Effects
- decreased blood flow to hypothalamus- release of ADH from post pituitary (see diag 3)results in retention of salt, waterand peripheral vasoconstriction
69
70
osmoreceptors in hypothalamus detect increase in osmolarity of
bloodand release ADHinto blood stream
ADHFILTRATE
ADH
water
urine blood
nephron capillary
ADH increases the amount of water
reabsorbed from the filtrate to the blood
urine output is reduced as more water is returned to the blood
Role of ADH in dehydrationRole of ADH in dehydration
71
6. Hormonal Effects
- Glucagon (contributes to hyperglycaemia)
- ACTH (stimulates cortisol release and glucose production)
72
Progressive Shock
1. Cardiac Effects- decreased RBC oxygenation- decreased coronary blood flow- myocardial ischaemia-decreased ventricular filling- decreased force of contraction
2. Peripheral Effects- peripheral pooling of blood- plasma leakage into interstitial
spaces- cold, grey waxy skin- confusion, slow speech- tachycardia, weak thready pulse- decreased BP- decreased body temperature
73
3. Respiratory effects
If oxygen delivery to tissues continues to be inadequate, cells must do anaerobic respiration to continue ATP production.
Anaerobic respiration produces lactic acid as a waste product – this must be removed.
Central chemoreceptors will detect a fall in pH and stimulate the respiratory centre to increase ventilation.
This allows the excess acid to be ‘blown off’ in the form of CO2
.
74
Anaerobic respiration
Lactic acid
PCO2 and
H+ in blood
expiration of PCO2
H+ in CSF
stimulation ofcentral
chemoreceptors
frequency of impulses to medullary rhythm generator
rate and depth of ventilation
Response to acidosis
75
Irreversible Shock• Loss of peripheral vascular resistance
• Confusion, slurred speech, unconscious
• Slow, irregular, thready pulse
• Falling BP (diastolic is zero)
• Cold, clammy cyanotic skin
• Slow, shallow, irregular respirations
• Dilated, sluggish pupils
• Severely decreased body temperature
76
Irreversible Shock leads to:
• Renal failure
• Hepatic failure
• Multiple organ systems failure
• Adult respiratory distress syndrome
• Death
77
THANK YOU