Shock Flashcards
(33 cards)
What is Hypovolemic shock?
- due to excessive blood/fluid loss
- loss of >20% of the blood volume (1000mL) results in shock
- excessive fluid loss can be due to sweating, diarrhea, severe burns, vomiting
What happens due to Hypovolemic Shock?
- decreased cardiac output (due to decreased volume of the blood)
- increased peripheral vascular resistance (PVR)
- due to vasoconstriction of arterioles from catecholamines and angiotensin II which are released in response to decreased Cardiac output - Decreased left ventricular end diastolic volume (LVEDV)
- due to decreased volume of blood
(angiotensin II causes vasoconstriction and increased release of aldosterone from adrenal glands cortex)
- decreased intravascular volume leads to decreased venous return and decreased cardiac output – this stimulates RAAS and causes shock
What Clinical Symptoms do we see in Hypovolemic Shock?
- cold and clammy skin due to vasoconstriction of blood vessels, altered mental state, elevated blood lactate
- hypotension due to decreased cardiac output
- rapid and weak pulse (tachycardia) which is a response due to decreased cardiac output
What is Cardiogenic Shock?
- due to myocardial pump failure, which is a result of damage to cardiac muscle and left heart dysfunction (contractility problem NOT volume problem)
- examples of cardiac problems can arise due to myocardial infarction (MI) and arrhythmias
- there is acute hypoperfusion and hypoxia of the tissues and organs
Why does Cardiogenic Shock happen?
- decreased cardiac output due to decreased force of contraction from the left ventricle (can be due to MI), this causes an increased LVEDV because blood has accumulated in the left ventricle, and increased pulmonary vascular resistance (PVR) because its leading to left sided HF that leads to right sided HF
- So in both, the body tries to keep blood pressure up by vasoconstricting, but the causes are different:
- Cardiogenic = bad pump
- Hypovolemic = not enough fluid
What is similar between Hypovolemic and Cardiogenic Shock?
Both have one key mechanism in common:
They both cause decreased perfusion (less blood getting to tissues), which leads to compensatory vasoconstriction to maintain blood pressure.
What is Obstructive Shock?
- physical and mechanical obstruction to the flow of blood through the central circulation which impedes cardiopulmonary blood flow (less oxygenated blood reaches tissues and can lead to acute hypoperfusion and tissue hypoxia). We might see small ventricles.
Extrinsic compression (outside of the heart problem): cardiac tamponade, tension pneumothorax
Outflow Obstruction: Pulmonary embolism
🧠 Obstructive Shock (overall)
This is a type of shock where something physically blocks blood flow, preventing the heart from pumping effectively — even though the heart itself may be okay.
- Extrinsic Compression
- The heart is squeezed from the outside, so it can’t fill properly.
- Examples:
- Cardiac tamponade (fluid in the pericardium compresses the heart)
- Tension pneumothorax (air in chest compresses heart & vessels)
- Massive pulmonary embolism (blocks return to left heart and adds back pressure)
⏺️ Problem: The heart can’t fill = less output = shock.
- Outflow Obstruction
- Blood can fill the heart, but it can’t leave the heart properly due to a block in the exit path.
- Examples:
- Massive pulmonary embolism (also fits here — blocks flow from right ventricle to lungs)
- Aortic stenosis (narrow valve prevents blood from exiting left ventricle)
- Hypertrophic cardiomyopathy (thickened wall blocks outflow tract)
⏺️ Problem: The heart fills, but blood can’t get out = less output = shock.
Why can Electrocardiogram show smaller ventricles in Obstructive shock? (wouldn’t we suspect larger ventricle due to greater afterload?)
It depends on the type of obstruction. But in some forms of obstructive shock, you might see small ventricles — especially in extrinsic compression cases like:
Example: Cardiac Tamponade or Tension Pneumothorax
- These cause external pressure on the heart.
- That pressure prevents the ventricles from filling properly.
- So on echo, the chambers look small — not because the muscle is weak, but because they’re being squeezed and can’t expand.
- Less filling = lower stroke volume = shock.
Example: Massive Pulmonary Embolism
- The right ventricle (RV) might actually be dilated due to increased afterload from the clot in the lungs.
- The left ventricle (LV) might be small because it’s not getting much blood from the lungs — so low preload.
On echocardiogram:
- RV: Dilated and struggling.
- LV: Small and underfilled (because not enough blood is returning from the lungs).
What is Distributive Shock?
- characterized by Hypovolemia and Hypotension because there is vasodilation that releases inflammatory mediators
- systemic vasodilation and decrease in blood flow to vital organs
- loss of blood volume through capillary leakage
What are the Subcategories of Distributive Shock?
- Septic shock
- Anaphylactic shock
- Neurogenic Shock
Septic Shock
Cause: A severe infection (usually bacterial) that triggers an overwhelming inflammatory response.
Mechanism:
- Bacteria (GRAM NEGATIVE most common) → immune system releases cytokines (like TNF, IL-1)
- These cause massive vasodilation
- Also increases capillary leak, leading to fluid loss into tissues
Signs:
- Fever, warm skin (early)
- Later: cold skin, low BP, organ failure
Labs: High lactate, possible positive blood cultures
What is the most common type of shock? What is it caused by?
Septic Shock (microbial infection overwhelmingly high)
- due to microbial infection most cases are by endotoxin producing Gram Negative bacteria (E.COLI most likely) and is therefor known as ENDOTOXIC SHOCK
What are the common causes of septic shock?
- E.Coli Sepsis can be from urinary catheter which is the MAIN cause of septic shock (MCC)
- Urinary retention secondary to prostate hyperplasia is also a common cause (Urinary retention from prostate hyperplasia (also called benign prostatic hyperplasia, or BPH) happens because:
👉 The prostate surrounds the urethra, which is the tube that carries urine from the bladder out of the body.
👉 When the prostate enlarges, it squeezes or narrows the urethra.
👉 This makes it harder for urine to pass, so the bladder can’t fully empty.
Over time, the bladder muscle gets weaker from working harder, which worsens the problem and can lead to urinary retention—meaning urine gets trapped in the bladder).
- Spread of a localized infection into the blood stream. This can be from an abscess or pneumonia
What is released from Gram-Negative bacteria (such as E.Coli) during Septic Shock? What does it cause?
- Endotoxins (LPS- Lipopolysaccharides) are a component of the cell wall of Gram (-) bacteria. They are released when bacterial cell wall is degraded.
- Endotoxins bind to CD14 receptor on WBC and endothelial cells which causes
1. activation of the alternative complement pathway which results in the release of C3a and C5a (leading to vasodilation and chemotaxis)
- Macrophages to release IL-1/TNF, this results in increased neutrophil adhesion to endothelial cells (eg. increased neutrophils in pulmonary capillaries)
- Direct injury to endothelial cells results in the release of chemical mediators Nitric Oxide (NO) and prostoglandin-12 (vasodilator)
What does Nitric Oxide do?
causes vasodilation of peripheral resistance arterioles
What does C5a and C3a do?
- causes release of histamine from mast cells which leads to vasodilation
What are the most important cytokines? What is SIRS?
SIRS stands for Systemic Inflammatory Response Syndrome.
SIRS = Body is in “full-body inflammation mode”
It’s not always bad, it’s the body trying to respond to danger. But if uncontrolled, it can damage tissues and lead to sepsis, shock, or organ failure.
- TNF-alpha
- IL-1
- IL-6
- Platelet activating factor
What is the pathogenesis of endotoxic shock?
- explanation of the pathogenesis of endotoxic shock (which is a form of septic shock, usually caused by Gram-negative bacteria)
1.Bacteria release endotoxin (LPS)
- LPS = lipopolysaccharide, found in the outer membrane of Gram-negative bacteria
- When bacteria die or multiply, LPS is released into the blood
- LPS activates immune cells
- It binds to receptors on immune cells like monocytes/macrophages - Big immune response: TNF-α is released
- This is a powerful inflammatory signal that kicks everything off
What does vasodilation due to septic shock result in?
- initial increase in cardiac output due to rapid flow through dilated arterioles causing increased return to the heart
- increased blood flow through microcirculation and the tissue is unable to remove O2 because of increased blood flow can lead to tissue hypoxia
- reduced peripheral vascular resistance (PVR)
Why does high-output cardiac failure happen due to vasodilation and septic shock?
💔 What is High-Output Cardiac Failure?
- It’s when the heart pumps more than normal, but still can’t meet the body’s needs.
- So even though cardiac output is high, tissues are still not getting enough oxygen.
Why does this happen in septic shock (due to vasodilation)?
1.Sepsis causes massive vasodilation
→ Blood vessels get very wide (due to inflammatory mediators like nitric oxide)
2.Vasodilation drops blood pressure
→ Even though there’s enough blood, it spreads out too much = not enough pressure to perfuse organs
3.Heart tries to compensate
→ Pumps harder and faster to keep up = increased cardiac output
4.Still not enough perfusion
→ Because blood keeps pooling in dilated vessels and leaking into tissues (due to leaky capillaries)
5.Leads to high-output failure
→ Heart can’t keep up with the excessive demand, even though it’s working hard
🧠 Bottom Line:
Septic shock = low resistance + leaky vessels → heart overworks → high-output failure
→ Tissues still suffer from low oxygen delivery, despite strong heart effort.
Why is Nitric Oxide released during sepsis?
- What is Nitric Oxide (NO)?
- It’s a gas made by the body.
- It causes vasodilation = makes blood vessels wider.
Why is NO released during sepsis?
During infections like sepsis (especially from bacteria), the body senses danger and tries to:
- Increase blood flow to fight infection.
- Dilate vessels to send more immune cells to the area.
How is NO made?
1. Immune cells detect bacteria or toxins
→ Especially lipopolysaccharide (LPS) from gram-negative bacteria.
2. This activates pattern recognition receptors (like TLR4) on immune cells.
3. These immune cells (like macrophages) then:
→ Release cytokines like TNF-α and IL-1.
4. These cytokines activate an enzyme called:
Inducible Nitric Oxide Synthase (iNOS)
5. iNOS makes nitric oxide (NO) from the amino acid arginine.
6. NO is released into the blood vessels → causes vasodilation.
In sepsis → immune system detects bacteria → cytokines trigger iNOS → nitric oxide is released → blood vessels dilate.
What are the Clinical features of Septic Shock?
- warm skin (due to vasodilation)
- Bounding Pulse: Why does it happen in high cardiac output (like in septic shock)?
- In septic shock, there’s vasodilation (widened vessels).
- The heart compensates by pumping faster and harder → ↑ cardiac output (CO).
- The increased stroke volume and rapid ejection of blood into these dilated vessels creates a forceful, bounding pulse. - Acute Respiratory Distress Syndrome (ARDS)
- What it is: A life-threatening condition where the lungs fill with fluid.
- Why it happens:
- In sepsis, the capillaries in the lungs leak fluid due to inflammation.
- This fluid fills the alveoli (air sacs), blocking gas exchange.
- Symptoms: Shortness of breath, hypoxia (low oxygen), rapid breathing. - Disseminated Intravascular Coagulation (DIC): What it is: A serious condition where the body forms tiny clots everywhere and uses up clotting factors, which paradoxically leads to bleeding.
- Why it happens in septic shock:
- Inflammation triggers tissue factor, activating clotting throughout the body.
- This causes microthrombi, ischemia, and eventual bleeding when platelets and clotting factors are depleted.
- Symptoms: Bleeding from IV lines, petechiae, bruising, organ failure. - Increased Mixed Venous Oxygen Content (MVOC)
- What it is: The amount of oxygen remaining in blood after it has passed through the body (measured in the pulmonary artery).
- Normal situation: Tissues use oxygen → venous blood has less oxygen.
- In septic shock:
- Blood moves too quickly through capillaries.
- Tissues can’t extract enough oxygen due to dysfunction or high flow.
- So, more oxygen is left in the venous blood.
- Result: SvO₂ is high, even though tissues are starved of oxygen.
What is the best predictor for tissue hypoxia?
- Swan-Ganz Catheter
- A thin tube inserted into a central vein (like the jugular) and threaded into the pulmonary artery.
It measures:
- Pulmonary capillary wedge pressure
- Cardiac output
- Mixed venous oxygen saturation (SvO₂)
- Used in septic shock to monitor how well the heart is pumping and how much oxygen is being used.
Why is MVOC decreased in Hypovolemic shock and Cardiogenic shock?
In Hypovolemic/Cardiogenic Shock:
* Cardiac output (CO) is low → not much blood gets to tissues.
* Tissues get less oxygen overall, so they extract as much as they can.
* ➜ Mixed venous O₂ (MvO₂) is LOW.
Why?
Because the tissues are hungry for oxygen and have time to grab more since the blood is flowing slowly.
In hypovolemic and cardiogenic shock, MvO₂ is low because:
1. ↓ Cardiac Output (CO):
* In hypovolemic shock, there’s not enough blood.
* In cardiogenic shock, the heart isn’t pumping effectively.
* Both → less oxygenated blood reaches tissues.
2. ↑ Oxygen extraction by tissues:
* Because tissues aren’t getting enough oxygenated blood, they try to take more oxygen from the little blood they do get.
* So by the time the blood returns to the veins, it has much less oxygen → low MvO₂.
