Ana de Luca
Shock The stroke volume is found by taking the total volume of blood
left over after contraction, which is called the end-systolic
volume, and subtracting it from the total volume in the heart
Whole body circulatory failure → blood ow to the tissues is low after lling, or the end-diastolic volume.
→ celular injury → damage to multiple organs → can lead to
multiple organ failure if not treated immediately. Classification
Decline in cardiac output or systemic vascular resistance. 3 three main categories with some subcategories.
- Decline in output can be due to low preload, low contractility
or HR too fast or too slow. I. Hypovolemic shock
- Decrease in preload can be due to 1. extracellular uid
volume depletion → like diarrhea, excessive diuresis, Hypo means “low,” vol refers to “volume,” and emia refers to the
dehydration or hemorrhage → hypovolemic shock or 2. blood; thus, hypovolemic shock is shock induced by a low uid
obstructing entry of blood → obstructive shock (like in volume of blood.
tension pneumothorax, pericardial tamponade, This could be either non-hemorrhagic or haemorrhagic.
pulmonary embolism. NON-HEMORRHAGIC means that the loss of uid volume isn’t
- Cardiogenic shock is when decrease in cardiac output is from bleeding → ex: dehydration → loss of uid from sweating
due to a decrease in contractility! Like in ICC, MI, reduces blood volume to the point that it isn’t enough to supply
contusion. the body’s organs → hypovolemic shock.
- Decline in SVR causes peripheral vasodilation → anaphylactic,
septic or neurogenic shock. HEOMMORRHAGIC hypovolemic shock → loss of blood volume
through ruptured blood vessels. A loss of about 20% of total
Normally, blood perfuses through tissue and delivers oxygen blood volume (1L) → can be enough to induce hypovolemic
because there’s enough pressure in the circulatory system to shock.
push it through; so, blood pressure majorly a ects the amount of
blood perfusing through tissues. When that liter of blood leaves circulation, the total volume lling
into the heart goes down → the end-diastolic volume goes
Now, blood pressure is determined by two components: down → stroke volume goes down as well → low cardiac output
the resistance to blood ow in the blood vessels, which is → low blood pressure.
a ected by things like vessel length, blood viscosity, and vessel
diameter; and the cardiac output, which is the volume of blood When cardiac output goes down, catecholamines such
pumped by the heart through the body per minute. as epinephrine and norepinephrine, ADH, and angiotensin II
are released. These all cause vasoconstriction of blood vessels,
Cardiac output is determined by heart rate, or the number of which increases vascular resistance and heart rate, and in
beats per minute, multiplied by stroke volume, or the amount turn, this increases cardiac output. These combined e ects
pumped out each beat. increase blood pressure.
A super important indicator that tissues are not getting enough
oxygen due to hypovolemia is a decreased mixed venous
oxygen saturation, or MVO2.
- MVO2 is the amount of oxygen bound to hemoglobin in the
blood coming to the right side of the heart from the tissues.
- It’s like the amount of oxygen left over, or not extracted and
used by the tissues. So, if blood volume is down, it means
that oxygen is down, and there’s going to be less left over,
right? So MVO2 will be down with hypovolemic shock.
Considered a cold shock → skin is cool and clammy.
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, Ana de Luca
II. Cardiogenic shcok - Endotoxins (LPS) found in the outer membrane of gram-
negative bacteria cause a cascade of events that lead to
The most common cause is acute myocardial infarction, or heart lowered perfusion.
attack.
- First, it directly damages endothelial cells and cause
them to release vasodilators, such as nitric oxide.
Or congestive heart failure, myocardial contusion and
- They also activate the complement pathway in the blood,
dysrhythmias. which stimulates mass cell release of histamine, another
vasodilator.
When the heart’s muscle cells die, it can’t contract as hard, which
- The LPS molecules also activate immune cells,
means the amount of blood pumped out, or stroke volume, goes like macrophages and neutrophils, which help create a
down; therefore, cardiac output goes down as well. In the same bunch of pro-in ammatory cytokines, such as tumor
way as with hypovolemic shock, the body releases necrosis factor and interleukin 1. These help the immune
vasoconstrictors to increase vascular resistance and help system destroy the invaders, but they also stimulate the
maintain blood pressure. endothelial cells to release more in ammatory
molecules, like platelet activating factor and reactive
Also, similar to hypovolemic shock, in cardiogenic shock MVO2 oxygen species.
will be down because since there’s less oxygen being pumped
- All of these in ammatory chemicals damage the
out, less will be left over. endothelial cells and increases their vascular
Sometimes, there might be an obstruction that doesn’t allow the permeability, making the blood vessels “leaky.”
heart to ll properly with blood. For example, we might have
the pericardial sac ll up with uid from an infection or with Endothelial cells also express a procoagulant called tissue
blood from trauma, like getting stabbed in the chest → can be factor. Procoagulants are molecules that increase blood
subclassi ed as OBSTRUCTIVE shock. coagulation, or blood clotting. These procoagulants combine with
an overall decrease in anti-coagulants, which decrease clotting
Preload decreases if there is something obstructing the entry of and seem to be often depleted or used up during sepsis, to
blood into or out of a cardiac chamber, and this is create a net increase in coagulation and clotting in the
called obstructive shock. microvasculature → decreases perfusion.
- Tension pneumothorax and pericardial tamponade can
compress the vena cana → obstructs blood ow to the right This widespread vasodilation means very little vascular
ventricle and decreases cardiac output. resistance. Blood can’t get the chance to unload as much oxygen
- A massive pulmonary embolism can obstruct blood from as it cruises through the vasculature, and it gets back to the right
circulating through the pulmonary vessels and getting to the left side of the heart with leftover oxygen. Thus, in this case, in
ventricle. contrast to cardiogenic and hypovolemic shock, MVO2 can be
normal or even increased
III. Distributive shock
Also contrary to hypovolemic and cardiogenic shock, there’s an
increase in ow in the peripheral blood vessels, so the skin
Leakiness of blood vessels and excessive amount of arteriole
becomes warm and ushed; therefore, distributive shock is a
vasodilation, or widening of the peripheral blood vessels.
kind of warm shock.
Decreases systemic vascular resistance → result in peripheral
vasodilation!
The combined e ects of widespread vasodilation, increased
vascular permeability, and microvascular blood
If he arterioles dilate, vascular resistance to blood ow goes down
clotting contribute to decreased perfusion of blood to vital
→ blood pressure goes down → less perfusion and distribution of
organs.
blood to organs and tissues.
Distributive shock has two subcategories → ANAPHYLACTIC
The most common type of distributive shock is SEPTIC shock,
shock (alergic reaction that causes dangerously low blood
which is from pathogens in the blood, and most commonly, gram-
pressure) and NEUROGENIC shock (nervous system is damaged
negative pathogens.
and can’t control the body’s blood pressure).
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Shock The stroke volume is found by taking the total volume of blood
left over after contraction, which is called the end-systolic
volume, and subtracting it from the total volume in the heart
Whole body circulatory failure → blood ow to the tissues is low after lling, or the end-diastolic volume.
→ celular injury → damage to multiple organs → can lead to
multiple organ failure if not treated immediately. Classification
Decline in cardiac output or systemic vascular resistance. 3 three main categories with some subcategories.
- Decline in output can be due to low preload, low contractility
or HR too fast or too slow. I. Hypovolemic shock
- Decrease in preload can be due to 1. extracellular uid
volume depletion → like diarrhea, excessive diuresis, Hypo means “low,” vol refers to “volume,” and emia refers to the
dehydration or hemorrhage → hypovolemic shock or 2. blood; thus, hypovolemic shock is shock induced by a low uid
obstructing entry of blood → obstructive shock (like in volume of blood.
tension pneumothorax, pericardial tamponade, This could be either non-hemorrhagic or haemorrhagic.
pulmonary embolism. NON-HEMORRHAGIC means that the loss of uid volume isn’t
- Cardiogenic shock is when decrease in cardiac output is from bleeding → ex: dehydration → loss of uid from sweating
due to a decrease in contractility! Like in ICC, MI, reduces blood volume to the point that it isn’t enough to supply
contusion. the body’s organs → hypovolemic shock.
- Decline in SVR causes peripheral vasodilation → anaphylactic,
septic or neurogenic shock. HEOMMORRHAGIC hypovolemic shock → loss of blood volume
through ruptured blood vessels. A loss of about 20% of total
Normally, blood perfuses through tissue and delivers oxygen blood volume (1L) → can be enough to induce hypovolemic
because there’s enough pressure in the circulatory system to shock.
push it through; so, blood pressure majorly a ects the amount of
blood perfusing through tissues. When that liter of blood leaves circulation, the total volume lling
into the heart goes down → the end-diastolic volume goes
Now, blood pressure is determined by two components: down → stroke volume goes down as well → low cardiac output
the resistance to blood ow in the blood vessels, which is → low blood pressure.
a ected by things like vessel length, blood viscosity, and vessel
diameter; and the cardiac output, which is the volume of blood When cardiac output goes down, catecholamines such
pumped by the heart through the body per minute. as epinephrine and norepinephrine, ADH, and angiotensin II
are released. These all cause vasoconstriction of blood vessels,
Cardiac output is determined by heart rate, or the number of which increases vascular resistance and heart rate, and in
beats per minute, multiplied by stroke volume, or the amount turn, this increases cardiac output. These combined e ects
pumped out each beat. increase blood pressure.
A super important indicator that tissues are not getting enough
oxygen due to hypovolemia is a decreased mixed venous
oxygen saturation, or MVO2.
- MVO2 is the amount of oxygen bound to hemoglobin in the
blood coming to the right side of the heart from the tissues.
- It’s like the amount of oxygen left over, or not extracted and
used by the tissues. So, if blood volume is down, it means
that oxygen is down, and there’s going to be less left over,
right? So MVO2 will be down with hypovolemic shock.
Considered a cold shock → skin is cool and clammy.
ff fi fl fl flff fl fl ff flfi
, Ana de Luca
II. Cardiogenic shcok - Endotoxins (LPS) found in the outer membrane of gram-
negative bacteria cause a cascade of events that lead to
The most common cause is acute myocardial infarction, or heart lowered perfusion.
attack.
- First, it directly damages endothelial cells and cause
them to release vasodilators, such as nitric oxide.
Or congestive heart failure, myocardial contusion and
- They also activate the complement pathway in the blood,
dysrhythmias. which stimulates mass cell release of histamine, another
vasodilator.
When the heart’s muscle cells die, it can’t contract as hard, which
- The LPS molecules also activate immune cells,
means the amount of blood pumped out, or stroke volume, goes like macrophages and neutrophils, which help create a
down; therefore, cardiac output goes down as well. In the same bunch of pro-in ammatory cytokines, such as tumor
way as with hypovolemic shock, the body releases necrosis factor and interleukin 1. These help the immune
vasoconstrictors to increase vascular resistance and help system destroy the invaders, but they also stimulate the
maintain blood pressure. endothelial cells to release more in ammatory
molecules, like platelet activating factor and reactive
Also, similar to hypovolemic shock, in cardiogenic shock MVO2 oxygen species.
will be down because since there’s less oxygen being pumped
- All of these in ammatory chemicals damage the
out, less will be left over. endothelial cells and increases their vascular
Sometimes, there might be an obstruction that doesn’t allow the permeability, making the blood vessels “leaky.”
heart to ll properly with blood. For example, we might have
the pericardial sac ll up with uid from an infection or with Endothelial cells also express a procoagulant called tissue
blood from trauma, like getting stabbed in the chest → can be factor. Procoagulants are molecules that increase blood
subclassi ed as OBSTRUCTIVE shock. coagulation, or blood clotting. These procoagulants combine with
an overall decrease in anti-coagulants, which decrease clotting
Preload decreases if there is something obstructing the entry of and seem to be often depleted or used up during sepsis, to
blood into or out of a cardiac chamber, and this is create a net increase in coagulation and clotting in the
called obstructive shock. microvasculature → decreases perfusion.
- Tension pneumothorax and pericardial tamponade can
compress the vena cana → obstructs blood ow to the right This widespread vasodilation means very little vascular
ventricle and decreases cardiac output. resistance. Blood can’t get the chance to unload as much oxygen
- A massive pulmonary embolism can obstruct blood from as it cruises through the vasculature, and it gets back to the right
circulating through the pulmonary vessels and getting to the left side of the heart with leftover oxygen. Thus, in this case, in
ventricle. contrast to cardiogenic and hypovolemic shock, MVO2 can be
normal or even increased
III. Distributive shock
Also contrary to hypovolemic and cardiogenic shock, there’s an
increase in ow in the peripheral blood vessels, so the skin
Leakiness of blood vessels and excessive amount of arteriole
becomes warm and ushed; therefore, distributive shock is a
vasodilation, or widening of the peripheral blood vessels.
kind of warm shock.
Decreases systemic vascular resistance → result in peripheral
vasodilation!
The combined e ects of widespread vasodilation, increased
vascular permeability, and microvascular blood
If he arterioles dilate, vascular resistance to blood ow goes down
clotting contribute to decreased perfusion of blood to vital
→ blood pressure goes down → less perfusion and distribution of
organs.
blood to organs and tissues.
Distributive shock has two subcategories → ANAPHYLACTIC
The most common type of distributive shock is SEPTIC shock,
shock (alergic reaction that causes dangerously low blood
which is from pathogens in the blood, and most commonly, gram-
pressure) and NEUROGENIC shock (nervous system is damaged
negative pathogens.
and can’t control the body’s blood pressure).
fi fi flfl flff fi fl fl fl fl fl
