NCM 118 LECTURE NOTES FOR STUDENTS

Week 8
October 4 - 8, 2021

Shock, Systemic Inflammatory Response Syndrome (SIRS), Multi Organ Dysfunction

Syndrome ( MODS )
TERMS:
DaO2 = oxygen delivery
VO2 = oxygen consumption
RAAS = renin-angiotensin-aldosterone system
ScvO2 = central mixed venous oxygen saturation
SIRS = systemic inflammatory response syndrome
PaO2 = partial pressure of oxygen
TNFα = tumor necrosis factor alpha
MODS = multiple organ dysfunction syndrome
MvO2 = myocardial oxygen consumption
CVP = central venous pressure
NO = nitric oxide
ARDS = acute respiratory distress syndrome
PEEP = positive end expiratory pressure
SaO2 = arterial oxygen saturation
CO = cardiac output
ATP = adenosine triphosphate
ADH = antidiuretic hormone
SVR = systemic vascular resistance dioxide
PaCO2 = partial pressure of carbon
IL-1 = interleukin-1
DIC = disseminated intravascular coagulation
LVEDP = left ventricular end-diastolic pressure
SBP = systolic blood pressure
SvO2 = mixed venous oxygen saturation
MAP = mean arterial pressure
EtCO2 = end-tidal CO2

I. PATHOPHYSIOLOGY OF SHOCK
SLIDE 2
Shock is the result of a decrease in BP. If BP goes down, there is less blood going to your tissues and
therefore there is less O2 and nutrients. This is called decreased perfusion. Meaning oxygen delivery
(DO2) is less than oxygen consumption (VO2). This decreased tissue perfusion causes an imbalance
between oxygen supply and demand, anaerobic metabolism, lactic acidosis, cellular and organ
dysfunction, and metabolic acidosis. If this situation is not immediately alleviated, this can cause cell
death, irreversible organ damage, and eventually death.

SLIDE 3
SHOCK IS A LIFE THREATENING SITUATION.

Primary goal in shock: maximize DaO2 to meet cellular oxygen requirements to prevent tissue and cell
death and maintain end-organ perfusion.
How: by maintaining BP.

SLIDE 4
Important concept to remember throughout this discussion:
BP = CO x SVR, where CO is further computed as HR x SV.

Although MAP is actually a better indicator of perfusion to vital organs than SBP, let’s keep it simple
and remember this equation. If BP goes down, this means either CO or SVR has decreased. And to
compensate, we need to raise the other factors in the equation.
SLIDE 5
The major organs: the heart (SA & AV nodes, aorta), the brain (medulla oblongata, posterior
pituitary), and the kidneys (adrenal glands).

SLIDE 6
SA and AV nodes are part of the electro conduction system. The electrical signals travel down to the
bundle of His, then on to the left and right bundle branches, then of course, to the Purkinje fibers.

The aortic arch branches off into 3 vessels. The first being the brachiocephalic which then branches
off into the right subclavian artery and the right common carotid artery. The right common carotid
artery further branches off into the internal and external carotid arteries.

The middle main branch coming off the aorta is the left common carotid artery, which further
branches into the internal and external carotid arteries on the left. The third and last branch is the left
subclavian artery.

There are two important primary receptor sites that play major roles in blood pressure. These are
called baroreceptor and chemoreceptor sites. One of these primary receptor cites is located at the
aortic arch, and the other located on the carotid sinus of both sides.

Baroreceptors pick up on arterial stretch or to arterial pressure, to regulate BP.

Chemoreceptors respond to arterial levels of O2, CO2, and pH to regulate and maintain normal ABG.

SLIDE 7
Under normal conditions, the cells go through aerobic metabolism, when they receive enough oxygen
to produce ATP. In a state of lowered perfusion, with less O2, cells switch to anaerobic metabolism,
resulting in less ATP and this ultimately leads to cell death. Also, anaerobic metabolism results in a
build-up of lactic acid and other waste products including CO2, which leads to a state of metabolic
acidosis. If the condition remains uncorrected, cell death also ensues.

SLIDE 8
MAP = [SBP + (2 x DBP)] / 3

Mean arterial pressure is the average blood pressure in an individual during a single cardiac cycle.

* The cardiac cycle comprises all of the physiological events associated with a single heartbeat,
including electrical events, mechanical events (pressures and volumes), and heart sounds. The atria
and ventricles alternately contract in each cardiac cycle.

SLIDE 9
This decreased MAP leads to a decrease in baroreceptor firing. Normally, our baroreceptors, which
are also called stretch receptors, stay stretched because of the pressure exerted by the blood against
the aorta. When these baroreceptors are stretched out, they end up firing. The vagus nerve (CN 10)
picks up the firing from the baroreceptor and chemoreceptor sites in the aortic arch. The
glossopharyngeal nerve or (CN 9) picks up the signals from the carotid sinuses. Both nerves lead to
the medulla oblongata.

Within the medulla, we have the cardio-regulatory center (which regulates the heart) and the
vasomotor center (which regulates the blood vessels).

The cardio-regulatory center has two parts: the cardio-inhibitory (which inhibits cardiac activity,
thereby lowering our HR) and the cardio-acceleratory (which increases cardiac activity, resulting in an
increased HR and an increased SV). So when both HR and SV are increased, cardiac output also
increases. In terms of sympathetic and parasympathetic nervous systems, cardio-inhibitory falls under
parasympathetic while the cardio-acceleratory goes under sympathetic nervous system.

These sympathetic and parasympathetic nerve fibers from both cardio-regulatory centers in the
medulla travel back down to the heart along different pathways. The sympathetic nerve fibers arise
from the cervical ganglia then enter the heart and act on the sinoatrial node, speeding up the
depolarisation rate, and therefore increasing the heart rate. The parasympathetic system works in
reverse in order to slow the heart rate down. The parasympathetic nerve fibers travel from the
medulla to the heart by way of the efferent vagus nerve.

* Trivia: The sinoatrial node, which is the heart’s natural pacemaker, does not need a nervous supply
to function. If you sever all the nerves to the heart, it will continue to beat. In fact, it will beat faster
than normal, since there is normally a parasympathetic supply slowing the heart down.

When there is a decrease in BP, as seen in shock, there is less stretch which leads to less baroreceptor
firing. These get transmitted to the medulla’s cardio-regulatory center and the inhibitory center gets
inhibited, thereby inhibiting the decreasing heart rate. Simultaneously, the acceleratory center is
activated so that there is an increase in the sympathetic response, thereby increasing HR and SV, in an
effort to increase cardiac output, therefore increasing MAP.

Aside from activating the cardio-regulatory center in the medulla, the vasomotor center also gets
activated. Activation of this vasomotor center is another sympathetic response. So the impulse here
travels down another sympathetic nerve along the spinal column and eventually reaches the adrenal
glands. Here the nerve synapses with the adrenal medulla, releasing catecholamines, adrenaline and
noradrenaline, which play vital roles in vasoconstriction of arteries and veins.

These catecholamines enter the blood vessels and there, bind to alpha receptors. This results in
vasoconstriction which eventually leads to an increase in systemic vascular resistance and ultimately
increasing MAP. These events involving the catecholamines happen only in the blood vessels and not
in the heart nor the brain, since the body wants more blood feeding these vital organs and
vasoconstriction is not going to make that happen.

The aforementioned events occur in the early phase of shock.

SLIDE 10
If shock persists, the RAAS System is activated. There is an increase in renin production from the
adrenal gland. Renin enters the blood stream, makes its way to the liver where it interacts with the
precursor angiotensinogen. When renin and angiotensinogen combine, angiotensin I is produced.
This angiotensin I eventually makes its way to the lungs where there are high concentrations of
angiotensin converting enzymes (ACE). So these two combine and are converted to angiotensin II.

Angiotensin II increases thirst , thereby increasing fluid volume to increase BP or MAP. Angiotensin II
also increases vasoconstriction, which again increases MAP. Aside from these, angiotensin II triggers
the release of aldosterone from the adrenal cortex.

Aldosterone also increases Na reabsorption in the kidneys, which leads to water reabsorption. This
then increases the circulating plasma volume to ultimately increase MAP. This increased intravascular
volume also leads to an increase in venous return to the heart. If preload increases, cardiac output
also increases and this ultimately increases MAP.

In response to the increased osmolality due to the increase in Na, the posterior pituitary in the brain
releases ADH to increase reabsorption of Na, thereby increasing fluid retention, eventually increasing
MAP.

SLIDE 11
II. SYSTEMIC INFLAMMATORY RESPONSE SYNDROME
As shock states progress, there is a systemic activation of the inflammatory response. Although the
inflammatory response is meant to be protective, it has the potential to produce detrimental effects
that lead to damage to tissues and organs. The term systemic inflammatory response syndrome (SIRS)
describes patients in whom the inflammatory response is fully and systemically activated. (not
SYSTEMATICALLY!)

SLIDE 12
SIRS may be caused by any type of shock. It can also be caused by other conditions such as massive
blood transfusion, traumatic injury, brain injury, surgery, burns, and pancreatitis and infection.

SLIDE 13
Normally, endothelial cells that line blood vessels provide an anticoagulant surface, are tightly
wedged, and control permeability of vessels.

During proinfalmmatory conditions, activated endothelial cells express proteins on their surface that
attract platelets and neutrophils, forming a procoagulant endothelial surface. Cytokines cause these
tight spaces to widen and this increases capillary permeability, which allows plasma to leak out from
inside the blood vessel and into the interstitial space.

SLIDE 14
Systemic inflammation results in the activation of endothelial cells, an immune response, and the
coagulation cascade.

Aside from this happening, these activated endothelial cells express proteins on their surface that
attract platelets and neutrophils, forming a procoagulant endothelial surface, resulting in the
formation of platelet plugs in this area. Also, the coagulation cascade is activated, where fibrin forms
strands around these clots, giving them stability and strength.
Microthrombi form in the capillaries to obstruct blood flow to repair injury. Proinflammatory
cytokines also attract phagocytic white blood cells (WBCs) to the area and activate the complement
cascade. The goal of the combined activity of WBCs and complement proteins is the elimination of the
invading microorganism.

WBCs, platelets, and activated endothelial cells release vasodilating substances such as nitric oxide
(NO), histamine, and bradykinin to enhance blood flow to the site of injury to promote healing. What
these substances do is that they also allow capillary leak from blood vessels, resulting in additional
extravasation of plasma and coagulation factors.

SLIDE 15
This inflammatory response is helpful, if isolated. However, in SIRS, the inflammatory response is
systemic. It is seen all over the body. Endothelial cells are activated in many vessels throughout the
body, causing widespread extravasation of fluid into the interstitial compartment and systemic
activation of the immune system and coagulation cascade. This means that there is a considerable
amount of fluid accumulating in the extravascular space, with a lot of microthrombi forming in
capillaries and the interstitium.

SLIDE 16
The combination of this intravascular coagulation and decreased circulating blood volume results in
reduced perfusion of vital organs, which can progress to multiple organ dysfunction (MODS) and
death.

SLIDE 17
III. STAGES OF SHOCK

The progression of shock is thought to have three overlapping and increasingly severe phases. The
last, unfortunately, cannot be reversed. The difficulty in determining which phase of shock a
particular person is in, at a particular time, lies in three reasons:
1. Shock has varied causes
2. The exact time of onset is unknown in many cases
3. There is a lack of diagnostic tests that provide a clear measure of the extent of shock at a given
time.

To prevent the development of shock to progress into multiple organ failure and death, early
identification and timely reversal of the shock state is essential. So, here are the stages of shock:

SLIDE 18
Stage 1: Initial, Non-Progressive Stage
 Compensatory mechanisms are still effective in maintaining relatively normal vital signs and
tissue perfusion.
 At this stage, shock is poorly diagnosed and often goes unrecognized.
SLIDE 19
Stage 2: Intermediate, Progressive Phase
 Compensatory mechanisms that maintain normal perfusion begin to fail
 Metabolic and circulatory derangements become more pronounced
 Activation of the inflammatory and immune responses may develop
 Signs of failure in one or more organs become apparent
 To save the patient, interventions that target both the cause of the shock and the resultant
metabolic, circulatory, and inflammatory responses, must be instituted

SLIDE 20
Stage 3: Final, Irreversible Stage
 Severe cellular and tissue injury
 Correction of metabolic, circulatory, and inflammatory derangements is difficult or impossible
 Cellular hypoxia and death may follow
 Development of Multiple Organ Dysfunction Syndrome (MODS), resulting in demise of the
patient. We will discuss MODS later.

SLIDE 21
IV. CLASSIFICATION OF SHOCK

The classification of shock includes hypovolemic, cardiogenic, or distributive. Hypovolemic and

distributive occur due to inadequate venous return to the heart. This results from hypovolemia as
seen in dehydration and hemorrhage, or widespread vasodilation which cause a relative hypovolemia
as seen in sepsis, anaphylaxis, or loss of sympathetic tone with spinal cord injury (neurogenic shock).

Cardiogenic shock is caused by the heart’s failure to effectively pump blood. Pump failure may result
from myocardial infarction, abnormal heart rate or rhythm, or impaired diastolic filling. (Diastolic
filling is the period in which the ventricle fills with blood from the left atrium -- from the onset of mitral
valve opening to mitral valve closure.)

SLIDE 22
V. HYPOVOLEMIC SHOCK

In hypovolemic shock – hypo means “below” and volemic refers to volume, the circulating fluid
volume of the body is reduced. This fluid can be blood or non-blood.

For blood loss, this may come about from hemorrhage like from a GI bleed, post-partum hemorrhage,
trauma, or an abdominal aortic aneurysm for example. Non-blood fluid can be lost through vomiting,
diarrhea, polyuria (like in diabetes where there is too much glucose, which pulls more water into the
urinary tract and which is eventually excreted as urine). Another way to lose non-blood fluid is
through burns.

SLIDE 23
With this drop in volume, the amount of blood ejected in every contraction also drops. In
hypovolemic shock, the problem is the decrease in SV. Remember, BP = CO x SVR. In an effort to
maintain blood pressure, the body needs to compensate. So, looking at the equation, if stroke volume
is down, the body will have to increase any or all the other factors in the equation.

In hypovolemia, the body increases HR to compensate for the decrease in SV. So the patient here
presents with tachycardia. But even as the heart tries to work faster to try and maintain CO, CO will
still be low because the stroke volume is less.

Another way the body will try to compensate for this decrease in fluid volume is to increase the SVR
by constricting blood vessels. And if you remember, if blood vessels are constricted, the space for
blood to move is narrowed, thereby increasing blood pressure. However, if SVR stays up for a longer
period, the cells in the tissues and organs will get less blood resulting in hypoperfusion, meaning less
oxygen for the cells, which will eventually lead to cell death.

SLIDE 24
Signs and symptoms:
 Altered mentation, ranging from lethargy to unresponsiveness
 Rapid and deep respirations, which gradually become labored and more shallow as the
condition of the patient deteriorates
 Cool and clammy skin, with weak and thready pulses
 Tachycardia from activation of the sympathetic nervous system
 Hypotension
 Decreased urine output; urine is darker and more concentrated because the kidneys are
conserving fluid

SLIDE 25
Laboratory studies:
 Serum lactate. A serum lactate level that remains elevated after initial resuscitation is a poor
prognostic indicator.
 Arterial pH and base deficit to assess the presence of anaerobic metabolism as a marker of
inadequate DaO2.
 Metabolic laboratory studies and serum electrolyte measures assist with adjustment of fluid
and electrolytes.
 Serial hemoglobin and hematocrit and coagulation panels to assess need for blood or blood
product replacement.

SLIDE 26
Medical Management:
 Focus would be on restoring circulating volume and resolving the cause of volume loss.
 Composition of volume replacement therapy is determined by what was lost.
o Crystalloid solutions are used as first-line therapy for volume resuscitation. Isotonic
solutions, like lactated Ringer’s solution or 0.9% NSS, are preferred over hypotonic
solutions (like 5% dextrose solution).
o To replace RBCs, platelets, and clotting factors lost in severe bleeding, blood and blood
products are also administered.
 o Colloid solutions, such as albumin and synthetic volume expanders, may also be
administered, particularly if the primary cause hypovolemia is blood loss.
o Note: Colloid solutions, administered in the early phase of fluid resuscitation, is
controversial. Normally colloids are supposed to remain within the intravascular space
compared to crystalloids. So, patients generally need smaller amounts of colloids for
resuscitation. But remember, capillary permeability is increased in shock. This leads to
the large colloid molecules leaking out from the vascular vessels and into the
intravascular space. This results in more fluid volume being shifted out of the
intravascular space and into tissues.

So the result is a worsening of the hypovolemia we wanted to fix in the first place. This
suggests that colloids, although they provide swifter volume expansion in the
intravascular space over crystalloids, are not superior to crystalloids in treating critically
ill patients with hypovolemia.

SLIDE 27
Nursing Management:
 Focuses on the restoration of circulating volume through volume administration.
 Obtaining and maintaining adequate IV access is imperative. Large-bore (16-gauge or larger) IV
catheters are inserted into large veins or central veins to make rapid infusion of fluids more
efficient.
 When administering fluids rapidly, precautions must be taken to prevent compromising the
pulmonary system. When large volumes of fluid are given too quickly, this may cause
pulmonary congestion which in turn inhibits adequate ventilation. This situation only adds
insult to injury to the already problematic delivery of oxygen (DaO2) to the tissues.
 Another thing is to be sure fluids are warmed during infusion to limit the negative effects of
hypothermia.
 Patients may be placed in modified trendelenburg position as well to improve return of
venous circulation.
 Monitoring and documentation of vital signs must be done frequently. These include BP, HR,
RR and depth, O2 saturation, urine output, and mentation.
 Lab results and interventions must also be monitored and properly documented.

SLIDE 28
Hypovolemic Shock Summary

SLIDE 29
VI. CARDIOGENIC SHOCK

In cardiogenic shock, the problem lies within the heart itself. The heart is a muscular pump that
pushes blood around the body. If something is wrong with the pump, what happens is a decrease in
heart rate or in stroke volume or both, resulting in a decrease in cardiac output.
SLIDE 30
The causes of cardiogenic shock fall intrinsically in any abnormality that affects the pumping action of
the heart. In other words, there is a loss of the contractile function of the heart. So these causes
include:
 myocardial infarctions (especially extensive left ventricular myocardial infarction
 cardiomyopathy (conditions that affect the heart muscle)
 acute myocarditis (inflammation of heart muscle which affects the heart’s electrical conduction
system)
 cardiac valve disease
 papillary muscle rupture (located at the ventricles, attached to cusps of AV valves via chordae
tendinae and contract to prevent inversion or prolapse of valves on systole or ventricular
contraction)
 ventricular septal rupture
 dysrhythmias (which can be caused by so many conditions such as hypertension, coronary
artery disease, MIs, electrolyte imbalances—Na and K, valve disorders, and so on)

SLIDE 31
How does the body compensate? Looking back at the equation, (BP = CO X SVR) since cardiac output
has dropped, what needs to be adjusted would be the systemic vascular resistance. So the body
increases SVR.

SLIDE 32
The same as in hypovolemic shock, neuroendocrine compensatory mechanisms are activated to
improve perfusion. So stimulation of RAAS and sympathetic nervous system causes that
vasoconstriction and increases afterload.

Preload is the intitial stretching of the cardiac myocytes just before contraction and is associated with
ventricular filling. Afterload on the other hand is the force or load against which the heart has to
contract to eject the blood.

The increase in afterload presents other problems. Although the vasoconstriction increases BP to
push that blood forward, this increase in afterload causes an increase in myocardial workload,
intraventricular filling pressures, and myocardial oxygen requirements.

Elevated afterload ends up reducing effective contraction and inhibits ejection. The increased preload
causes an increase in ventricular filling pressures, but because there is something wrong with the
heart’s ability to pump, we don’t see successful or efficient ejection of that blood out of the ventricle.

The ventricle then becomes distended, because of all that blood accumulating in it, and this further
impairs effective contraction, which inadvertently results in a continued decrease in CO.

In addition, pulmonary vascular pressures increase as left ventricular function declines, resulting in
pulmonary congestion. Fluid leaks into the interstitium and alveoli, impairing the diffusion of O2 from
the alveoli into the pulmonary capillaries.
This vicious cycle, related to decompensation further impairs myocardial contraction, worsens
pulmonary congestion, and results in a more inadequate DaO2 to the heart and other organs. These
compensatory mechanisms were supposed to support aerobic metabolism.

If the cells cannot make ATP from aerobic metabolism, the body is forced to switch to the inefficient
and worrisome anaerobic metabolism.

All these stressors imposed on an already failing heart will eventually lead to cardiac arrest.

SLIDE 33
Signs and Symptoms:
 We will observe that the patient will exhibit dyspnea, increased RR, thready and rapid pulse,
distended neck veins, dysrhythmias, chest pain, pale and cool skin, low urinary output, mental
changes.
 Recurrent chest pain, which may be indicative of the spreading of infarcted tissue.

SLIDE 34
Laboratory Studies:
 Elevated myocardial tissue markers : creatine phosphokinase (CPK) and cardiac troponin I are
released into the blood by dying cardiac cells)
(Creatine phosphokinase = released when there has been injury or stress to
muscle tissue
Cardiac troponin I = a protein released in blood that indicates damage to heart
muscles if seen in detectable amounts)
 Progressive hemodynamic compromise and clinical deterioration (SBP less than 90 mmHg;
MAP less than 70 mmHG; cardiac index less than 2.2 L/min/m2 (cardiac index reflects the
amount of blood the left ventricle ejects into the systemic circulation in one minute, measured
in liters per minute; pulmonary artery wedge pressure greater than 18 mmHg (provides an
indirect measure of the left arterial pressure))
 The above are hallmarks for acute MI and extensive myocardial necrosis, which may progress
on to cardiogenic shock

SLIDE 35
Medical Management:
 Aimed at increasing myocardial DaO2, maximizing CO, and decreasing left ventricular
workload.
 The goals are to protect and preserve myocardium and improve tissue perfusion by reversing
hypoxemia due to pulmonary congestion and metabolic acidosis.
 Reducing preload with diuretics or nitrate infusion since left ventricular filling pressures are
often elevated.
 Vasodilators and intra-aortic balloon pumps are directed at reducing afterload, thus improving
left ventricular emptying and reducing myocardial workload.

(Intra-aortic balloon pump or IABP: a catheter is inserted via the left or right femoral artery into the
upper aorta. Tip of balloon stops a couple of centimeters from the origin of the left subclavian
artery in the aortic arch. The balloon can deflate during systole. This deflation creates suction,
which pulls blood from the ventricle into the aorta, which reduces the workload of the left ventric le
since it does not have to use so much force to contract. This way, coronary arteries also get
oxygenated blood.

During diastole, the balloon is inflated. This creates positive pressure within the aorta, pushing
blood back towards the ventricle. Since aortic valve is closed during diastole, oxygen-rich blood is
pushed into the coronary arteries, further improving flow into the myocardium. The inflation and
deflation of the balloon is synchronized with the patient’s heartbeat by an external control unit.
The gas used in inflating the balloon is helium gas because of its low viscosity and is less likely to
embolize if the balloon ruptures. The IABP is only a temporary measure and stays in the patient for
only a few days.)

SLIDE 36
VIDEO: Dr. Cal Shipley, M.D. (May 31, 2016). Cardiogenic Shock and Intra-aortic Balloon Pump by
Dr. Cal Shipley, M.D. Retrieved from https://www.youtube.com/watch?v=mADxD7C8jBw

SLIDE 37
Nursing Management:
 Goal is to conserve myocardial energy and decrease the workload of the heart
 Provide periods of rest and help with ADLs to minimize myocardial energy expenditure
 Use opioid analgesics and sedatives to minimize sympathetic nervous system response so that
venous capacitance is increased and resistance to ejection is decreased. Also use opioids to relieve
ischemic pain.
 Administer supplemental O2 to optimize arterial oxygen content and diffusion. Might have to start
mechanical ventilation.
 Use of antiarrhytmic agents, cardioversion to help restore stable cardiac rhythm and enhance
cardiac output.
 Give sympathomimetic drugs adrenalin and noradrenaline to try to enhance CO by increasing
contractility, HR, or SVR, but this may at the same time increase cardiac work.
 Administer agents with positive inotropic effects that may have less activity on vascular tone
include low-dose dopamine, dobutamine, amrinone, and milrinone.
 Give vasodilators such as sodium nitroprusside, nitroglycerin, or angiotensin-converting enzyme
(ACE) inhibitors to reduce SVR and LVEDP in an effort to increase CO and improve left ventricular
function.
 Assist and support use of intra-aortic balloon pump and left ventricular assist device. These two
devices help reduce workload of the left ventricle by supplementing pumping ability.

(left ventricular assist device or LVAD is implanted in the client’s chest to help pump blood
from the left ventricle of the heart on to the rest of the body. It is connected to a control unit
and battery pack worn outside the body.)

SLIDE 38
Cardiogenic shock summary
SLIDE 39
VII. OBSTRUCTIVE SHOCK

Obstructive shock may be due to either an internal or external obstruction that impedes or blocks
blood flow out of the heart or into the great vessels, thus decreasing CO.

Common conditions that result in obstructive shock include: tension pneumothorax (PTX), cardiac
tamponade, massive pulmonary embolism (PE).

SLIDE 40
Tension PTX
 Increased intrapleural pressure due to atmospheric air entering the interpleural space from an
injury
 Intrapleural pressure exceeds pressure within the lungs and pushes the lungs toward the
mediastinum
 Mediastinal shift can displace the trachea and heart
 Compression of heart and major blood vessels (SVA, IVA)
 Decreased CO due to less blood entering the heart and the heart’s inability to push blood out
due to the compression of these structures brought about by mediastinal shift
 S/S: hypotension; tympanic sound upon percussion during PE of lungs; decreased breath
sounds due to lung collapse; distended neck veins due to high jugular venous pressure caused
by compression of SVA
 Management: needle decompression (insertion of needle into interpleural space to equalize
the pressure by withdrawing air out of the pleural cavity

SLIDE 41
Cardiac Tamponade
 Increased amount of fluid developing within the pericardial cavity (for whatever reason)
compresses or strangulates the heart
 Heart is unable to expand and fill with blood because of the decrease in volume capacity
within the chambers
 S/S: Beck’s Triad (high jugular venous pressure distended jugular veins; low BP due to
decreased CO; muffled or distant heart sounds due to accumulation of fluid around the heart)
 Management: pericardiocentesis (use of a needle and catheter to remove excess fluid in
pericardium)

SLIDE 42
Massive PE
 Presence of massive PE, especially along the pulmonary trunk, blocking blood flow from the
heart to the lungs
 Less blood flow into the lungs less blood flow into the left atria and left ventricle 
decreased end diastolic volume (EDV)  decreased SV  decreased CO  decreased BP
 S/S: difficulty breathing; hypoxia; ABG (PaO2 less than 80mm Hg): elevated lactic acid (as body
shifts from aerobic to anaerobic metabolism)
  Management: thrombolytics (“clot busters”; emergency ttt for strokes and heart attacks to
dissolve blood clots to clear blood flow); heparin (anticoagulant); embolectomy (surgical
removal of an embolus from an artery or vein)

Because of decreased in BP, there is less O2 to the cells, leading to ischemia, necrosis, and eventually
organ failure.

SLIDE 43
Management:
 Treat underlying condition
 Administer oxygen
 Give isotonic fluids
 Give vasopressors (to increase vasoconstriction of blood vessels to increase BP)

SLIDE 44
Nursing Management:
 Provide adequate oxygenation
 Institute and support fluid and/or drug therapy
 Monitor vital signs and labs
 Provide a safe environment (patient may be at risk for altered LOC and deteriorating vital
signs)

SLIDE 45
VIII. DISTRIBUTIVE SHOCK STATES

SLIDE 46
Distributive shock states are due to a decreased venous return from the displacement of blood
volume away from the heart because the vascular compartment enlarges and there is loss of blood
vessel tone. This loss of blood vessel tone is caused by a loss of sympathetic innervation of blood
vessels, as in neurogenic shock, or because of vasodilating substances in the blood, as seen in
anaphylactic and septic shock.

Looking at the equation BP = CO X SVR, these distributive shock states fall under the last part of the
equation, the SVR.

SLIDE 47
A. NEUROGENIC SHOCK

In neurogenic shock, the problem lies in an injury to the spinal cord sustained by the patient. The site
of spinal cord injury is at the cervical or upper thoracic regions (above T6). This injury affects the
autonomic nervous system, specifically the sympathetic nervous system, which is supposed to help
constrict the blood vessels to increase BP. So when BP drops, the sympathetic nervous system needs
to be activated in order to increase that BP. However, due to the spinal cord injury, nerve fibers that
innervate the blood vessels don’t work. So we end up with blood vessels dilating because they cannot
constrict, leading to a drop in SVR.
Neurogenic shock can also happen in patients who received spinal anesthesia, or have taken drugs
that affect the autonomic or sympathetic nervous system.

Characteristics of neurogenic shock include hypotension, bradycardia, and hypothermia.

Because of the loss of sympathetic tone, there is nothing to oppose parasympathetic response; the
result is uncontrolled arterial vasodilation and a decrease in SVR. At the same time, vasodilation in
the veins result in blood pooling and therefore decreases preload because the blood cannot
efficiently enter the heart.

Unopposed parasympathetic stimulation leads to bradycardia, even in the presence of falling blood
pressure. When BP drops, as in other forms of shock, HR increases to compensate. But because of
the disruption of the sympathetic nervous, in neurogenic shock, there is an inhibition of the
stimulation of baroreceptors in the aortic arch and carotid sinus. Vasodilation causes decreased
preload and thus stroke volume. We end up with a decreased CO, resulting in inadequate tissue
perfusion.

SLIDE 48
Signs and Symptoms:
 Decreased central venous pressure (CVP), CO, and SVR combined with bradycardia
 Hypothermia as a result of uncontrolled heat loss from excessive vasodilation. Skin is warm, unlike
other shock states where the patient may feel cold and clammy.

SLIDE 49
Management:
 Careful fluid resuscitation to prevent and treat hypotension
 Administer α-adrenergic agents such as norepinephrine to promote vasoconstriction
 Administer β-adrenergic agonists such as dopamine to increase heart rate and contractility

SLIDE 50
Nursing Management:
 Immobilizing the spine
 Managing airways and circulation
 Administering IV fluids or vasopressors
 Prevent DVTs (deep vein thrombosis)
 Foley catheter placement
 Rewarming devices for hypothermia
 Administrating atropine for bradycardia

SLIDE 51
B. ANAPHYLACTIC SHOCK
Moving on, there is anaphylactic shock. This is a life threatening allergic response that can be caused
by an allergen. Allergens may come in the form of foods, insect stings, blood products and
medications. Anaphylaxis is an emergency situation.

Antigens are substances that can be introduced through injection, ingestion, inhalation or through
skin absorption. These antigens are proteins that are recognized by the immune system and elicit the
allergic response.

Anaphylaxis may be either immunoglobulin E (IgE) mediated or non-IgE mediated.

SLIDE 52
When there is an immune response to a specific antigen, what happens is IgE-mediated anaphylaxis.
The first time the immune system is exposed to the antigen, a very specific IgE antibody is formed and
this IgE antibody circulates in the blood.

When a second exposure to this same antigen occurs, the antigen in this second exposure binds to
the circulating IgE formed from that first exposure. What happens then is that mast cells and
basophils are activated. These mast cells then release biochemical mediators such as histamine,
prostaglandins and leukotrienes that initiate anaphylaxis.

On the other hand, anaphylactoid or non-IgE-mediated reactions occur without the presence of IgE
antibodies. So there is a direct activation of mediators that cause this response. An example of a
common anaphylactoid reaction is associated with your nonsteroidal anti-inflammatory drugs
(NSAIDs), including aspirin. When this happens, staying away from all other NSAIDs would be wise
since any of them could elicit a second reaction.

SLIDE 53
Going back to the antigen-antibody reaction causing mast cells and basophils to secrete histamines,
prostaglandins and leukotrienes, also secreted are eosinophil chemotactic substance, platelet-
activating factor 2, and others.

Histamine, prostaglandins, and leukotrienes are particularly problematic since they cause systemic
vasodilation, increased capillary permeability, bronchoconstriction, coronary vasoconstriction, and
urticaria (hives). A continued downward progression of myocardial depression, inflammation,
excessive secretion of mucus , and peripheral vasodilation are precipitated by some of the other
substances.

Diffuse arterial vasodilation creates a maldistribution of blood volume to tissues, and venous dilation
decreases preload, thereby decreasing CO. Then there is the increased capillary permeability that
leads to the loss of vascular volume, which further decreases CO and of course, impairs tissue
perfusion.

SLIDE 54
Signs and Symptoms:
 Initially there is generalized erythema, urticaria, and pruritus (itchiness)
  Anxiety, restlessness, dyspnea, wheezing, chest tightness, a warm feeling, nausea and
vomiting, angioedema (swelling underneath the skin), and abdominal pain
 Severe respiratory manifestations, such as laryngeal edema or severe bronchoconstriction
with stridor, as allergic reaction progresses
 Hypotension from vasodilation which progresses to circulatory collapse or hypoxemia, leading
to a deteriorating LOC that worsens into unresponsiveness

SLIDE 55
Management:
 Early recognition and treatment of anaphylaxis is vital.
 Therapeutic goals: removal of offending antigen, reversal of effects of the biochemical
mediators, restoration of adequate tissue perfusion
 For mild symptoms: administer oxygen and subcutaneous or IV antihistamine, such as
diphenhydramine, to block the effects of histamine.
 For life-threatening changes in airway, breathing, or circulation: immediate administration of
epinephrine to reverse vasodilation and bronchoconstriction caused by anaphylactic shock
 If patient is severely hypotensive or does not immediately respond to epinephrine: rapid
infusion of crytalloid fluids
 Corticosteroids, bronchodilators, vasoconstrictors and positive inotropic agents to combat
circulatory collapse
 NOTE: Epinephrine Dosage in Anaphylaxis in Adults
Epinephrine 1:1,000 dilution (1mg/ml), 0.2 to 0.5 ml intramuscularly or
subcutaneously every 5 minutes, as necessary, should be used to control symptoms and
increase BP in patients experiencing anaphylaxis.

SLIDE 56
Nursing Management:
 Maintain adequate airway
 Monitor patient response to antigen
 Monitor vital signs and level of anxiety
 Comfort measures related to dermatologic manifestations
 Evaluate for allergies and future risk for anaphylaxis
 Educate patient regarding prevention and treatment

SLIDE 57
C. SEPTIC SHOCK

Septic shock falls under problems related to SVR as expressed in the equation BP = CO x SVR. So, we
need to look at what is happening in the blood vessels.

Sepsis starts off from an infection, which may be caused by a variety of microorganisms such as gram-
negative or gram-positive bacteria, fungi and viruses.
In some patients, sepsis may be caused by several organisms; some of which may never be identified.
Portals of entry include the pulmonary system, the urinary tract, the gastrointestinal system, wounds,
or through invasive devices.

In septic shock, complex interactions among invading microorgansims and immune, inflammatory,
and coagulation systems, result in a pro-infalmmatory and hypercoagulable state.

SLIDE 58
Gram-positive bacteria release exotoxins, sometimes called enterotoxins, while gram-negative
bacteria release endotoxins called lipopolysaccharides. Fungi also release several kinds of toxins. Both
gram-negative and gram-positive organisms may directly stimulate the inflammatory response and
other aspects of the immune system that activate cytokines, complement, and coagulation systems.

The presence of these microorganisms cause macrophages and helper T cells to secrete
proinfalmmatory cytokines, such as TNFα and IL-1β. As discussed in SIRS, these cytokines induce
endothelial dysfunction that result in increased capillary permeability.

Normally, anti-inflammatory cytokines are also released to balance the proinfalmmatory response.
Type 2 helper T cells secrete the anti-inflammatory cytokines IL-4 and IL-10. However, in some
patients, anti-inflammatory cytokines fail to balance the proinfalmmatory cytokines, and excessive
proinfalmmatory response activates the coagulation cascade.

In sepsis, there is an imbalance between procoagulant and anticoagulant factors.

Endotoxins embedded in the cell walls of the invading microorganisms, stimulate endothelial cells to
release tissue factor, which activate the coagulation cascade, converting fibrinogen to fibrin. As
previously discussed, we end up with these fibrin clots also known as microthrombi.

These microthrombi form throughout the microvasculature and cause obstruction of vessels, which
leads to more injury and ischemia to distal tissues. Under normal conditions, anticoagulant factors
modulate coagulation, preventing microthrombi formation from spreading all over.

In sepsis, however, the levels of these anticoagulant factors are decreased, resulting in a procoagulant
state that increases microthrombi formation and contributes to futher inflammation. Recognizing that
proinfalmmatory and procoagulant responses result in a loss of homeostasis of almost every organ is
key to understanding what happens in the body during sepsis.

Long story short, because there is less blood within the vessel walls, vascular resistance cannot be
maintained. With more space in the blood vessels because of the dilation of the blood vessels and
that leakage of blood, SVR in septic shock drops. To compensate, the body then tries to increase the
HR and tries to increase the SV.

SLIDE 59
Signs and Symptoms:
 Early signs: warm flushed skin, increased HR and RR, restlessness, fever, decreased SVR,
decreased BP
  Late: cold/clammy skin, severe hypotension, respiratory failure, oliguria (renal failure), low
cardiac output and increase systemic vascular resistance, coma

SLIDE 60
Laboratory Studies:
 Cultures: blood, sputum, urine, surgical or nonsurgical wounds, sinuses, and invasive catheters;
positive results are not necessary for diagnosis.
 CBC: WBCs usually will be elevated and may decrease with progression of shock.
 Chemistry panel: hyperglycemia may be evident, followed by hypoglycemia in later stages.
 Arterial blood gases: metabolic acidosis with mild hypoxemia (PaO2 less than 80 mm Hg) and possibly
compensatory respiratory alkalosis (PaCO2 less than 35 mm Hg).
 CT scan: may be needed to identify sites of potential abscesses.
 Chest and abdominal radiographs: may reveal infectious processes. (SvO2 or ScvO2: can assist in the
assessment of adequacy of oxygen delivery and consumption. (Central venous oxygen saturation
(ScvO2) is a useful surrogate for SvO2 and is measured in the superior vena cava through an ordinary
central venous catheter. ScvO2 only measures venous blood returning from the upper half of the body,
while SvO2 samples the true mixed venous blood leaving the right heart)
 Lactate level: decreasing levels of serum lactate indicate aerobic metabolism is able to meet cellular
energy requirements. Elevated levels indicate inadequate perfusion and utilization of anaerobic
metabolism to meet cellular energy requirements.
 Base deficit: elevated levels indicate inadequate perfusion and anaerobic metabolism.
 EtCO2: decreasing EtCO2 is an early indicator of inadequate regional and global tissue perfusion.
(EtCO2: end-tidal CO2 monitoring is a noninvasive technique which measures the partial pressure or
maximal concentration of CO2 at the end of an exhaled breath, which is expressed as a percentage of
CO2 or mmHg. Normal values are 5% to 6%, which is equivalent to 35-45 mmHg.)

SLIDE 61
Management:
The Surviving Sepsis Campaign, established by the Society of Critical Care Medicine and the American
College of Chest Physicians, aims to disseminate clinical guidelines to standardize the care of patients with
sepsis and align practice with the most current evidence. The campaign regularly updates their
recommendations based on the latest research.
 Initial interventions: Large-volume fluid resuscitation, obtaining serum lactate level and blood
cultures, and antibiotic administration
 Subsequent interventions: continuing resuscitation and assuring adequate perfusion (e.g., invasive
hemodynamic monitoring, blood administration, and use of vasoactive medications), nutritional
supplementation

At the end of this lecture, are attached infographics on The Surviving Sepsis Campaign.

SLIDE 62
Nursing Management:
 Infection control. All invasive procedures must be carried out with aseptic technique after
careful hand hygiene.
  Collaboration. The nurse must collaborate with the other members of the healthcare team to identify
the site and source of sepsis and specific organisms involved.
 Management of fever. The nurse must monitor the patient closely for shivering.
 Pharmacologic therapy. The nurse should administer prescribed IV fluids and medications including
antibiotic agents and vasoactive medications.
 Monitor blood levels. The nurse must monitor antibiotic toxicity, BUN, creatinine, WBC, hemoglobin,
hematocrit, platelet levels, and coagulation studies.
 Assess physiologic status. The nurse should assess the patient’s hemodynamic status, fluid intake and
output, and nutritional status.

SLIDE 63
IX. MULTIPLE ORGAN DYSFUNCTION SYNDROME

MODS is defined as a progressive physiologic failure of several organ systems in acutely ill patients.
Exact etiology of MODS is unknown, however it is suspected that the release of systemic
inflammatory mediators found in SIRS contribute to the etiology of MODS.

This condition results from the body’s inability to maintain end-organ perfusion and oxygenation
because of SIRS or any type of shock. The inflammatory and procoagulant effects on systemic
vasculature cause tissue hypoxia and necrosis at end organs. Also, inflammatory mediators disrupt
cell junctions, not only in the endothelium as was explained earlier, but also in the gut mucosa. What
happens is, this loss of integrity of gut mucosal barrier liberates bacterial toxins from the gut by a
process called translocation. Gastrointestinal toxins circulate systemically, causing further damage to
multiple organs.

SLIDE 64
Pathophysiology of MODS is a combination of the following mechanisms:
 Bacterial factors
 Endothelial injury
 Inflammatory mediator release
 Disturbed hemostasis
 Microcirculatory failure

Organ failure is closely associated with mitochondrial dysfunction and reduced ATP production. In
MODS, dysfunction and the inflammatory response in one organ may cause a snowball effect in other
organs. Usually the first organs to manifest signs of dysfunction are the lungs, heart, and kidneys.
Because the liver has better compensatory mechanisms, liver failure tends to occur later.

Interventions should be directed toward increasing end-organ perfusion and oxygenation and to
lessen the inflammatory response to prevent or limit MODS.

SLIDE 65
Signs and Symptoms: (some)
 Hypotension, tachycardia, tachypnea, hypothermia
 Increased WBC
 Altered mental state
  Decreased renal perfusion

SLIDE 66
Management:
 Early identification of at-risk patients and early normalization of ScvO2, arterial lactate
concentration, base deficit and pH help shorten hospital stay and decrease inpatient mortality
 Enforcement of measures to prevent nosocomial infections: HOB elevated during mechanical
ventilation, oral care, turning and skin care, invasive catheter care, and wound care.

SLIDE 67
CONSIDERATIONS FOR THE OLDER PATIENT: RESPONSE TO SHOCK STATES
 Nurse should be aware of physiologic changes of aging and monitor closely for changes in the
older patient’s baseline assessments.
 Patient’s medical history may reveal other chronic diseases or conditions that further
compromise normal physiologic changes seen with aging
Cardiovascular system: Increased dysrhythmias, increased atrial size and irritability, left ventricular
myocardial thickening leading to decreased compliance and lower ejection fraction; thickened heart
valves that interfere with forward flow; decreased response to sympathetic nervous system;
decreased sensitivity of baroreceptors; generalized stiffening of arterial vessels, including aorta

Pulmonary system: Decreased tidal volume and respiratory muscle strength, decreased alveolar
surface area, increased dead space at end expiration, decreased elastic recoil of lungs, increased
resting respiratory rate, increased risk for infection as a result of decreased number of cilia, blunted
response to hypoxemia, decreased gag and cough reflex leading to increased risk for infection,
aspiration
Hematologic system: Decreased ability of bone marrow to produce cells (red blood cells, WBCs,
platelets), increased anemia, decreased immune function (decreased production of T and B
lymphocytes) leading to increased infections, lower baseline temperature, blunted temperature
response, and increased risk for adverse drug reactions

SLIDE 68
SUMMARY

To summarize, there are different types of shock. And these can be explained in the equation: BP =
CO X SVR
Some of these fall under CO, others under SVR. Ultimately what happens in shock is BP goes down
because either of the factors in the equation decreases.

The equation of CO x SVR determines the blood pressure which we want to keep at normal levels.
Cardiac output is the amount of blood the heart ejects every minute. CO is the heart rate (HR)
multiplied by the stroke volume (SV). Again, heart rate refers to the number of heartbeats in one
minute, while stroke volume refers to the amount of blood ejected by the heart in every beat.

SVR refers to how much resistance the blood is experiencing as it courses through the blood vessels. If
a blood vessel constricts, the blood then has a harder time going through and this increases the
systemic vascular resistance (SVR). While if the blood vessel dilates, there is more space for the blood
to move, which makes it easier for the blood, therefore SVR is decreased. This means that the
diameter of the blood vessel plays a role in determining SVR.

If BP drops, then this means that there was a drop in either the CO or the SVR, or a drop in both of
these factors.

SLIDE 69
4 WAYS OF NOT GETTING GAS (FUEL)

SLIDE 70 – 71
SURVIVING SEPSIS CAMPAIGN

SLIDE 72
THANK YOU

SLIDES 73 - 74
REFERENCES:

Dr Matt & Dr Mike. (Mar 6, 2020). Types of Shock. Retrieved from

https://www.youtube.com/watch?v=3wa8jGDyhS8

ICU Advantage. (May 22, 2019). What is Shock? I Shock Pathophysiology I Shock (Part 1). Retrieved
from https://www.youtube.com/watch?v=n77OH16wztk
Marianne Belleza, RN. Nurselabs. (April 22, 2021). Sepsis and Septic Shock. Retrieved from
https://nurseslabs.com/sepsis-and-septic-shock/

Morton, P. G., & Fontaine, D. K. (2018). Critical Care Nursing: A Holistic Approach. Wolters Kluwer.

Ninja Nerd. (Aug 5, 2017). Types of Shock I Hypovolemic, Cardiogenic, & Obstructive Shock. Retrieved
from https://www.youtube.com/watch?v=t_RLS6sSFrE

Ninja Nerd. (Aug 5, 2017). Types of Shock I Septic, Anaphylactic, & Neurogenic Shock. Retrieved from
https://www.youtube.com/watch?v=UbJRZTFLKdw&t=1165s

RegisteredNurseRN. (Dec 9, 2018). Shock Stages Nursing NCLEX: Initial, Compensatory, Progressive,
Refractory. Retrieved from https://www.youtube.com/watch?v=cybqmtsqvGs&t=29s

RegisteredNurseRN. (Dec 9, 2018). Shock Stages Nursing NCLEX: Initial, Compensatory, Progressive,
Refractory. Retrieved from https://www.youtube.com/watch?v=cybqmtsqvGs&t=29s

RegisteredNurseRN. (Jan 8, 2019). Hypovolemic Shock Nursing, Treatment, Management,

Intervention NCLEX. Retrieved from https://www.youtube.com/watch?v=yZ7AXi_pkOg&t=6s

RegisteredNurseRN. (Dec 23, 2018). Cardiogenic Shock Nursing Management, Pathophysiology,

Interventions NCLEX Review. Retrieved from https://www.youtube.com/watch?v=VJdygiX_pyY&t=2s
RegisteredNurseRN. (Feb, 2019). Septic Shock Nursing (Sepsis) Treatment, Pathopysiology, Symptoms
Distributive. Retrieved from https://www.youtube.com/watch?v=XuGPoQWzIco

RegisteredNurseRN. (Mar 1, 2019). Neurogenic Shock Nursing NCLEX (Distributive) Treatment,

Interventions, Signs and Symptoms. Retrieved from
https://www.youtube.com/watch?v=TNSvqLoN_3U&t=4s

RegisteredNurseRN. (Feb 19, 2019). Anaphylactic Shock (Anaphylaxis) Treatment, Nursing

Interventions, Symptoms NCLEX. Retrieved from
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