Transcript Vaginitis: Diagnosis approach and Treatment

SHOCK
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Life is provided through a variety of mechanisms, however all of them
depend on proper circulation. Circulation itself consists of 2 parts: work of
heart (pump of the body) and vessels, through which blood is pumped to the
most remote organs and tissues. During every systolic contraction heart
pump 70-80 ml of blood 9so called stroke volume). Thus in case of heart
rate 70 beats per minute heart pumps nearly 5 liters of blood, what makes
more than 7 tones per day.
From the left ventricle blood gets to the arterial system of the systemic
circuit. Arteries contain 15% of the whole circulating blood volume; they
carry blood from the heart to their distal departments – arterioles (vessels of
resistance). Arterioles themselves are defining blood distribution: in
condition of constriction (spasm) they make blood supply of the capillaries
impossible (ischemia appears). On the contrary, in condition of dilatation
they provide maximal oxygenation. When arterioles are blocked due to the
spasm blood is flowing through the arterio-venous anastomosis directly to
the venous system.
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Distribution of blood in the vascular bed (% of CBV).
heart cavity 3%
arteries 15%
capillaries 12%
venous system 70%
Among the natural vasoconstrictors (agents, which cause
constriction of the blood vessel) are epinephrine, norepinephrine,
serotonin, angiotensin II. Stress enhances the secretion of
cathecholamines, their blood concentration increases and arterioles
constrict. Spasm of the arterioles is the basis of blood flow
centralization: peripheral flow is disregarded in order to provide
brain with the oxygenated blood as long as possible.
• To the group of vasodilatators (agents, which provide dilatation of
the vessels) belong “acid” metabolites (lactate, pyruvate, adenylic
acid, inosinic acid), bradykinin, acetylcholine, different medicines
(neuroleptics, α-adrenergic antagonists, peripheral vasodilatators,
ganglionic blocking agents, etc.), some exogenous poisons. All of
them cause blood flow decentralization: opening of arterioles and
distribution of the blood from central vessels to the capillary bed.
• Capillaries are the interweaving network of the smallest body
vessels with the general length of 90-100 thousands of kilometers.
However simultaneously work only 20-25% of them. They provide
metabolic exchange bringing oxygen and nutrients to the tissues
and take back wastes of metabolism.
• Periodically, every 30-40 seconds one of them get closed and others
open (vasomotion effect). Capillaries contain 12% of the whole
circulating blood volume, but different pathological conditions can
increase this amount even 3 and more times.
• “Used” blood from the capillaries flows to the venous system. Veins
are the blood reservoir, which contains 70% of the total circulating
blood volume. Unlike arteries they are capable of volume control
and thus they influence the amount of blood, which returns to the
heart.
• The most important haemodynamic index of venous system is
central venous pressure. CVP represents the pressure which blood
causes to the walls of cava veins and right atrium. This parameter is
an integral index of circulating blood volume, systemic vascular
resistance and pump function of the heart. It can be measure with a
special device called “phlebotonometer” (pic. 4.9) or with a usual
infusion set and a ruler. Normally CVP measured from the sternum
point is 0-14 cm H2O and from midaxillary line is 8-15 cm H2O.
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Central venous pressure decreases (sometimes even to negative) in case
of:
- blood loss
- excessive water loss (dehydration)
- distributive shock (decrease of peripheral resistance due to venous and
arterial dilatation)
In those conditions decreases volume of blood returning to the heart and
thus suffers cardiac output. In case of negative CVP cardiac arrest is highly
probable.
Central venous pressure increases in case of:
- heart failure (insufficiency of left or right ventricle)
- hypervolemia (excessive blood infusion, improper infusion therapy)
- obstructions to blood flow (pulmonary embolism, cardiac tamponade, etc.)
When CVP over 15-16 cm H2O is combined with left ventricle insufficiency
the risk of pulmonary edema is very high.
• Blood pressure is an integral index of arterial part of
systemic haemodynamics. Talking about blood pressure
we may refer to systolic, diastolic, pulse and mean
arterial pressure. Systolic (Psyst) and diastolic (P diast)
pressures are measured with the manometer (method
with the usage of phonendoscope was invented by M.
Korotkoff). Pulse pressure (PP) is a difference between
systolic and diastolic blood pressure.
• Mean arterial pressure (MAP) is calculated according to
the formula:
• MAP= P dias + 1/3 PP
mm Hg
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• MAP defines the level of pressure necessary for the
metabolic exchange in the tissues. Its measurement
allows the evaluation of tissue perfusion level.
• Blood pressure depends on different factors, but the
most important are cardiac output and vascular
resistance (mostly arterioles). This dependence is direct,
thus you can increase blood pressure using:
• infusion of vasoconstrictors - solutions of
epinephrine, phenylephrine (mesaton), etc. (they will
increase the vascular resistance);
• infusion of hydroxyethyl starch solutions or saline
(they will increase circulating blood volume)
• infusion of cardiac glycosides or other medicine
which stimulate myocardium
• General volume of blood in the body of a healthy adult is
nearly 7% from the body weight: 70 ml per kilogram for
male and 65 mil per kilogram of body weight for female.
Of course circulating blood volume is lower, because
part of blood is out of metabolic processes as a reserve.
CBV can be measured with the infusion of coloring
substance to the blood flow (Evans blue, polyglucin) and
later evaluation of its dissolution degree.
• Therefore measurement of CVP, BP, cardiac output and
circulating blood volume allow to evaluate condition of
circulation system of the patients and to provide
adequate correction.
• Shock is a pathological state which can be
described as a tissue hypoxia caused by
hypoperfusion. Pathogenetic basis of
shock depends on its reason (trauma,
toxins, thermal injury) and at the same
time on reactivity of the organism (level of
defense mechanisms mobilization).
• Stimulation of sympathetic nervous system - production
of catecholamines and other vasoactive substances by
hypothalamus and adrenal glands are the universal
response of the body to the stress. Those mediators
interact with the receptors of peripheral vessels causing
their constriction and at the same time they dilatate the
vascular bed of life-important organs. This is so called
“centralization of the flow”: rational decrease of blood
flow in less important tissues (skin, organs of abdominal
cavity, kidneys) in case of aggressive external influence
for protecting life itself (brain, heart, lungs).
• However influence of shock agents (pain,
hypovolemia, destroyed cells, toxic metabolites),
extended microcirculation violations (vascular
spasm, microthrombosis and sludge) and
caused by them tissue ischemia lead to hypoxic
affection and cellular death of the internal
organs. Further it can bring multiple organ
dysfunction syndrome.
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• Collapse is a vascular failure. It occurs when body is not
able to provide blood flow according to the new level of
its needs (either because reaction is not fast enough or
because sympathetic activation fails).Vascular bed
volume and circulating blood volume are disproportional:
too much blood gets to the microcirculation vascular
reserve and the amount, which returns to the heart is not
enough for the systemic needs (so called
“decentralization” of the blood flow). Cardiac output and
blood pressure decrease, that causes hypoperfusion of
the central nervous system and thus unconsciousness
and life-threatening complications.
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Pathogenetic classification of shock (according to P. Marino, 1998):
hypovolemic
cardiogenic
distributive
mixed (two and more factors).
Clinical classification of shock:
traumatic shock;
haemorrhagic shock;
dehydration shock;
burn shock;
septic shock;
anaphylactic shock;
cardiogenic shock;
exotoxic shock.
Outline
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Definition
Epidemiology
Physiology
Classes of Shock
Clinical Presentation
Management
Controversies
Definition
• A physiologic state characterized by
– Inadequate tissue perfusion
• Clinically manifested by
– Hemodynamic disturbances
– Organ dysfunction
Epidemiology
• Mortality
– Septic shock – 35-40% (1 month mortality)
– Cardiogenic shock – 60-90%
– Hypovolemic shock – variable/mechanism
Pathophysiology
• Imbalance in oxygen supply and demand
• Conversion from aerobic to anaerobic
metabolism
• Appropriate and inappropriate metabolic
and physiologic responses
Pathophysiology
• Cellular physiology
– Cell membrane ion pump dysfunction
– Leakage of intracellular contents into the
extracellular space
– Intracellular pH dysregulation
• Resultant systemic physiology
– Cell death and end organ dysfunction
– MSOF and death
Physiology
• Characterized by three stages
– Preshock (warm shock, compensated
shock)
– Shock
– End organ dysfunction
Physiology
• Compensated shock
– Low preload shock – tachycardia,
vasoconstriction, mildly decreased BP
– Low afterload (distributive) shock –
peripheral vasodilation, hyperdynamic state
Pathophysiology
• Shock
– Initial signs of end organ dysfunction
– Tachycardia
– Tachypnea
– Metabolic acidosis
– Oliguria
– Cool and clammy skin
Physiology
• End Organ Dysfunction
– Progressive irreversible dysfunction
– Oliguria or anuria
– Progressive acidosis and decreased CO
– Agitation, obtundation, and coma
– Patient death
Classification
• Schemes are designed to simplify
complex physiology
• Major classes of shock
– Hypovolemic
– Cardiogenic
– Distributive
Hypovolemic Shock
• Results from decreased preload
• Etiologic classes
– Hemorrhage - e.g. trauma, GI bleed,
ruptured aneurysm
– Fluid loss - e.g. diarrhea, vomiting, burns,
third spacing, iatrogenic
Hypovolemic Shock
• Hemorrhagic Shock
Parameter
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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
Normal
Anxious
Confused
Lethargic
CNS symptoms
Crit Care. 2004; 8(5): 373–381.
Cardiogenic Shock
• Results from pump failure
– Decreased systolic function
– Resultant decreased cardiac output
• Etiologic categories
– Myopathic
– Arrhythmic
– Mechanical
– Extracardiac (obstructive)
Distributive Shock
• Results from a severe decrease in SVR
– Vasodilation reduces afterload
– May be associated with increased CO
• Etiologic categories
– Sepsis
– Neurogenic / spinal
– Other (next page)
Distributive Shock
• Other causes
– Systemic inflammation – pancreatitis, burns
– Toxic shock syndrome
– Anaphylaxis and anaphylactoid reactions
– Toxin reactions – drugs, transfusions
– Addisonian crisis
– Myxedema coma
Distributive Shock
• Septic Shock
SIRS
2 or more of the following:
Temp >38 or <36
HR > 90
RR > 20
WBC > 20K
>10% bands
Sepsis
SIRS in the presence of suspected or documented infection
Severe Sepsis
Sepsis with hypotension, hypoperfusion, or organ dysfunction
Septic Shock
Sepsis with hyotension unresponsive to volume resuscitation,
and evidence of hypoperfusion or organ dysfunction
MODS
Dysfunction of more than one organ
Clinical Presentation
• Clinical presentation varies with type and
cause, but there are features in common
• Hypotension (SBP<90 or Delta>40)
• Cool, clammy skin (exceptions – early
distributive, terminal shock)
• Oliguria
• Change in mental status
• Metabolic acidosis
Evaluation
• Done in parallel with treatment!
• H&P – helpful to distinguish type of
shock
• Full laboratory evaluation (including
H&H, cardiac enzymes, ABG)
• Basic studies – CxR, EKG, UA
• Basic monitoring – VS, UOP, CVP, A-line
• Imaging if appropriate – FAST, CT
Treatment
• Manage the emergency
• Determine the underlying cause
• Definitive management or support
Manage the Emergency
• Your patient is in extremis – tachycardic,
hypotensive, obtunded
• How long do you have to manage this?
• Suggests that many things must be done
at once
• Draw in ancillary staff for support!
• What must be done?
Manage the Emergency
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One person runs the code!
Control airway and breathing
Maximize oxygen delivery
Place lines, tubes, and monitors
Get and run IVF on a pressure bag
Get and run blood (if appropriate)
Get and hang pressors
Call your senior/fellow/attending
Determine the Cause
• Often obvious based on history
• Trauma most often hypovolemic
(hemorrhagic)
• Postoperative most often hypovolemic
(hemorrhagic or third spacing)
• Debilitated hospitalized pts most often
septic
• Must evaluate all pts for risk factors for
Determine the Cause
• What if you’re wrong?
• 85 y/o M 4 hours postop S/P sigmoid
resection for perforated diverticulitis is
hypotensive on a monitored bed at 70/40
• Likely causes
• Best actions for the first 5 minutes?
Definitive Management
• Hypovolemic – Fluid resuscitate (blood
or crystalloid) and control ongoing loss
• Cardiogenic - Restore blood pressure
(chemical and mechanical) and prevent
ongoing cardiac death
• Distributive – Fluid resuscitate, pressors
for maintenance, immediate abx/surgical
control for infection, steroids for
adrenocortical insufficiency
Controversies
• IVF Resuscitation
– Limited resuscitation in penetrating trauma
– Use of hypertonic saline resuscitation in
trauma
– Endpoints for prolonged resuscitation
• Pressors
– Best pressors for distributive shock
• Monitoring
– Most appropriate timing and use for PA