Shock

Question 1

What is pulsus paradoxus and its mechanism?

Answer 1

More than normal drop in BP during inspiration. This occurs during pericardial tamponade. Increased fluid around the heart (within the pericardium) decreases compliance of the walls of the heart. During inspiration, there is increased volume in the right side of the herat (due to increased venous return); however, because the walls aren’t compliant, the increase in volume makes the interventricular septum move toward the LV, which makes the LV volume smaller and decreases blood coming back to left side of the heart from the lungs. This impedes filling of the LV and subsequently low CO ⇒ lower BP than usual.

Question 2

What type of low CO shock leads to a “fall off”/ downward displacement of Frank-starling curve and why?

Answer 2

Cardiogenic shock. This is because in this type of shock, the primary issue is decrease in myocardial contractility. As a result, for a given EDV, it cannot pump out all the blood, decreasing cardiac output.

Question 3

What is the most sensitive finding in pericardial tamponade?

Answer 3

Pulsus paradoxus

Question 4

What is Beck’s triad and what is it a sign of?

Answer 4

Sign of pericardial tamponade

1) Hypotension
2) Muffled Heart sounds: sound of heart cannot be transmitted through fluid barrier
3) JVD: Pressure around heart caused by fluid impedes venous return.

Question 5

What is central venous pressure and what does this value indicate?

Answer 5

Central venous pressure (CVP) is the blood pressure in the venae cavae, near the right atrium of the heart. CVP reflects the amount of blood returning to the heart and the ability of the heart to pump the blood back into the arterial system. If CVP is high, this means that the heart cannot pump blood adequately and is not getting pushed into the venous system from the arterial system.

Question 6

What are the two factors related to cardiac output?

Answer 6

Stroke volume and HR.

Question 7

What is the compensatory response distributive shock and why?

Answer 7

Increase in CO. Distributive shock is very low BP due to low systemic vascular resistance. As a result, the heart will compensate by increasing CO.

Question 8

Common causes of loss of blood cell mass

Answer 8

Trauma, GI bleed, Post-op

Question 9

How does sepsis affect cardiac contractility over time?

Answer 9

Decreases contractility because over time, inflammatory mediators and products interfere with herat’s ability to do work

Question 10

Determinants of blood pressure

Answer 10

CO, SVR

Question 11

What is neurogenic shock?

Answer 11

Type of distributive shock (low BP); due to loss of SNS tone secondary to spinal cord injury. Loss of SNS tone → no peripheral vasoconstriction → vasodilation.

Question 12

What is anaphylactic shock?

Answer 12

Type of distributive shock (Low BP); due to Histamine release causing profound vasodilation.

Question 13

Mechanism of RAAS

Answer 13

1) Decreased blood flow to the glomerulus is sensed by JGA cells, which responds by secreting renin
2) Renin converts angiotensinogen ⇒ AT1
3) AT1 ⇒ AT2 via ACE
4) AT2 raises BP by contraction of arteriolar smooth muscle and promoting adrenal release of aldosterone, which increases resorption of Na+ in DCT ⇒ expand plasma volume

Question 14

What is tachypnea a sign of?

Answer 14

Metabolic acidosis during shock. Person breathes faster for compensatory respiratory alkalosis

Question 15

What is the main factor that can cause obstructive shock, and what conditions can cause this?

Answer 15

Decreased preload– Volume within circulatory system is fine; however, not getting to the heart properly (impaired venous return) so heart doesn’t fill.

Causes: Pericardial tamponade, tension pneumothorax

Question 16

Shock definition

Answer 16

Physiological state characterized by insufficient oxygen delivery to the tissues, resulting in accumulation of cellular energy deficit

Question 17

What are 3 physical exam findings that has a vert strong predictive value that patient has low CO? What are some other abnormal findings in physical exam that indicate this?

Answer 17

Cool skin temperature + >2 seconds capillary refill + Livedo reticularis

Other findings: Clubbing nail beds, splinter hemorrhage, peripheral cyanosis.

Question 18

What is the general problem in cardiogenic shock and what conditions can cause this??

Answer 18

Cardiogenic shock occurs due to primary pump failure (reduced contractility), which can occur due to:

1) MI
2) Cardiomyopathy (Fulminant myocarditis, dilated cardiomyopathy)
3) Rhythm disturbance
4) Valvular heart disease

Question 19

MAP formula

Answer 19

[(2 x diastolic) + systolic] / 3

Question 20

What is a common response related to all types of low cardiac output shocks (Cardiogenic shock, hypovolemic shock, obstructive shock)

Answer 20

increased HR (via baroreceptor response)

Question 21

Mechanism of barorecetor respnose

Answer 21

1) Decrease in arterial pressure ⇒ decreased baroreceptor firing in carotid sinus and aortic arch to CNS
2) Decreased firing of inhibitory neurons that suppress SNS output from CNS
3) Increased SNS tone
4) Increased vasoconstriction in peripheray + increased HR and contractiltiy

Question 22

How is CO affected in sepsis and why?

Answer 22

Increase in CO due to marked decreased in peripheral vascular resistance

Question 23

Cold clammy skin, gray pale or mottled skin, weak, thready pulse, tachycardia, altered mental status, oliguria are sx of what??

Answer 23

Hypovolemic shock

Question 24

When is capillary refill > 2 seconds seen on physical exam?

Answer 24

When there is low blood flow to the extremities. Occurs during low CO shock when blood is diverted away from hands.

Question 25

What is the problem in pericardial tamponade?

Answer 25

Fluid accumulates in potential space between wall of heart and pericardium, compressing the heart.

Question 26

What is the primary difference in physical findings between hypovolemic shock and cardiogenic shock?

Answer 26

In cardiogenic shock, there an coronary occlusion/myocardial ischemia that leads to stiffening of ventricles (due to low ATP) and impaired LV pump that can’t accommodate the volume. As a result, filling pressures will be high. Moreover, physical exam will show heart failure sx such as JVD, pulmonary edema (rales, wheezes), S4, murmurs, etc.

In hypovolemic shock, problem is not the heart itself but the volume of blood. As a result, filling pressures are low and it is not associated with physical exam findings of herat failure. Instead, there are flat neck veins with clear lungs and normal heart sounds (except tachycardia).

Question 27

Are there symptoms of pulmonary edema/congestion in pericardial tamponade?

Answer 27

No

Question 28

Pathophysiology of tension pneumothorax

Answer 28

1) Injury to lung causes dysruption of parenchyma
2) Everytime breath is taken in, air goes through airway → lungs → out of lungs → into chest (between visceral pleura and parietal pleura).
3) Lung begins to separate from chest wall and gets pushed away, progerssively getting smaller as air keeps filling that space.
4) Lung completely collapses and as pressure builds up, only flexible area is the mediastinum, which shifts away from the pressure.
5) Most susceptible structures to increased pressures in the mediastinum are the venous structures that fill the heart, which are susceptible to collapse.

Question 29

Physical exam findings of pulmonary congestion in cardiogenic shock

Answer 29

1) Elevation of JVP (JVD)
2) Pulmonary rales/ wheezes
3) Tachycardia, Third heart sounds (e.g. S4) + possible new murmur (mitral regurgitation)

Question 30

Fever, tachypnea, GI dysfunction (N/V), disorientation and confusion, and elevated blood lactate/glucose are all clinical features of what condition?

Answer 30

Sepsis

Question 31

How is peripheral oxygen utilization affected in sepsis?

Answer 31

Although there is increased peripheral blood flow due to decreased PVR (due to increased NO release), oxygen utilization is decreased because mediators of inflammation prevent the tissues from appropriately using oxygen.

Question 32

What type of shock is most common 5-7 hours most MI?

Answer 32

Cardiogenic shock. This is the leading cause of deaht for pts with acute myocardial infarction.

Question 33

How can mitral regurgitation occur in setting of cardiogenic shock?

Answer 33

As pressure/ volume of left ventricle fills, it will dilate ⇒ pulls apart leaflets of mitral valve ⇒ mitral regurgitation.

Question 34

Pathophysiology of septic shock

Answer 34

1) Components of bacterial cell wall (e.g. LPS, flagellin, fimbria, DNA, etc.) recognized by pattern recognition receptors (e.g. Toll receptor family; Nod family) that initiate inflammatory response
2) Infalmmatory response causes endothelail cell injury → vasodilation and increased permeability (fluid leaks from vasculature)
3) Leakage of fluid results in decreased perfusion or organs → multiorgan failure

Question 35

Clinical findings of cardiogenic shock (3)

Answer 35

1) Hypotention
2) Hypoperfusion
3) Congestion

Question 36

When do the first physical signs of blood loss/ hypovolemic shock (how much blood) and how do they manifest?

Answer 36

Not until Class 3, in which 1500-2000 mL of blood lost can physical sx be seen such as cold, clammy skin, reduced systolic BP, and elevated HR. However, the first real sign of blood loss/ hypovolemic shock is when 750mL-1500 mL of blood is lost.

Question 37

What occurs in bp during normal respiration and why? (Explain what happens in both RV and LV)

Answer 37

During inspiration, blood pressure drops a bit.

RV: During inspiration, there is negative intrathroacic pressure, which increases venous return to the heart. This increases RV volume and therefore takes longer to empty, closing the pulmonic valve later.

LV: As lungs inflate during inspiration, pulmonary veins stretch, increasing their volume and decreasing their capacitance. This decreases venous return to the LV. As a result, the LV can get rid fo the blood faster during systole and aortic valve closes earlier. However, there is also a decrease in CO so blood pressure also drops a little bit.

Question 38

What are the physical exam findings of hypotension in cardiogenic shock?

Answer 38

Tachycardia, faint pulses, distant herat sounds, lateral displacement of PMI (since heart is dilating due to increased volume), apical impulse

Question 39

What are the 3 factors that affect stroke volume?

Answer 39

Myocardial contractility, preload, afterload

Question 40

In what instances can patients maintain their BP despite tissue hypoperfusion?

Answer 40

Children adn young adults; they have compensatory mechanisms via high HR and BP will stay in a normal range and then suddenly have cardiac arrest.

Question 41

Physical exam findings of hypoperfusion in cardiogenic shock

Answer 41

1) Agitation, disorientation, lethargy
2) Cool, clammy, cyanotic extremities
3) Oliguria: Low urine output

Question 42

Pathophysiology of cardiogenic shock effects on the heart

Answer 42

1) Coronary occlusion/ myocardial ischemia ⇒Loss of ATP
2) Profound depression of myocardial contractility due to stiffness (both systolic and diastolic function lost due to loss of ATP)
3) Reduced CO and low BP
4) Reduced CO ⇒ reduced blood in aorta during diastole ⇒ reduced coronary blood flow from aorta to coronary arteries ⇒ poor coronary perfusion.
5) Poor coronary perfusion leads to more depression of myocardial contractility ⇒ cycle keeps going.

Question 43

What is electrical alternans?

Answer 43

Occurs when there is large amount of fluid in pericardium in pericardial tamponade. Morphology of QRS complex should be teh same in every lead because it’s a vector; however, in electrical alternans, morphology of QRS complex changes beat to beat for the same lead. This means that heart is moving around in the chest, indicating that the heart is essentially floating. Usually, the pericardium is there to keep it in position.

Question 44

What metabolic condition occurs with shock and why? What is the body’s response to this condition?

Answer 44

Metabolic acidosis- occurs bc low oxygen state causes failure of membrane pumps, which increases H+. Moreover, anaerobic metabolism wrosens the acidemia. As a response, the person will be tachypneic, a compensatory respiratory alkalosis.

Question 45

Clinical features of tension pneumothorax

Answer 45

1) Absent breath sounds: on side of pneumothorax
2) JVD: obstruction of veins in mediastinum prevents filling of heard → pressure backs up to jugular veins
3) Tracheal deviation: away from side of pneumothorax

Question 46

How is shock usually identified/ accompanied with?

Answer 46

Hypotension: MAP < 60 mm Hg (normal 70-110)

Question 47

What is the sign of blood loss/ hypovolemic shock and why?

Answer 47

At 750-1500 mL of blood loss. Once there is more than 750 mL of blood loss, peripheral vasoconstriction occurs via increased SNS tone, which is enough to raise diastolic blood pressure. Systolic pressure at this time is normal; however, diastolic pressure drops- as a result, there is a narrow pulse pressure.

Question 48

3 types of low cardiac output shocks

Answer 48

1) Cardiogenic
2) Hypovolemic
3) Obstructive

Question 49

What is the main factor that is wrong in hypovolemic shock and what can cause this?

Answer 49

Decreased preload (e.g. intravascular volume depletions)

Causes:

1) Loss of blood cell mass
2) Loss of plasma volume

Question 50

Common causes of loss of plasma volume

Answer 50

Extravascular volume fluid sequestration

GI, GU, or insensible loss (e.g. cholera)

Burn injury (Significant loss of skin integrity ⇒ loss of fluid)

Question 51

What type of low CO shock does failure of each component of SV lead to?

Answer 51

1) Decreased myocardial contractility: leads to cardiogenic shock
2) Decreased Preload (volume): leads to hypovolemic shock or obstructive shock
* 3) Increased afterload*

Question 52

How does sepsis affect peripheral vascular resistance and why?

Answer 52

Marked decrease in PVR due to increased NO production by endothelium, leading to increase in peripheral blood flow. Moreover, there is diminished vasoconstrictor response to catecholamines

Question 53

What is the compensatory response to low bp due to low CO shock? What is the function of this compensatory mechanism?

Answer 53

Increase systemic vascular resistance (to periphery). This serves to divert blood from nonessential vascular beds (e.g. skin, muscle, GI tract) to vital organs (e.g. heart and brain)

Question 54

What is distributive shock and what are the three subtypes?

Answer 54

Low bp due to low systemic vascular resistance.

Types:

1) Septic
2) Anaphylactic
3) Neurogenic

Question 55

What are EKG findings associated with pericardial tamponade? (2)

Answer 55

1) Electrical alternans
2) Tachycardia

Question 56

Pathophysiology of cardiogenic shock leading to pulmonary edema

Answer 56

1) Decreased contractility from occlusion/ischemia leads to impaired LV pump
2) Impaired pump leads to inadequate emptying of LV ⇒ increased LV EDV
3) Blood bakcs up into LA ⇒ LAV + LAP
4) Blood backs up to lungs ⇒ increased pulmonary capillary pressure
5) Pulmonary edema

Question 57

What are the 2 compensatory mechanisms to hypotension, and what happens when these mechanisms fail?

Answer 57

1) Baroreceptor response
2) RAAS

Failure of mechanisms results in irreversible shock

Question 58

What are the physical sx of low CO shock and why?

Answer 58

1) Cool, clammy skin with pale or gray color. This is because in response to low CO (low BP), the body vasoconstricts its vessels from the periphery to vital organs. Since blood supply is diverted from skin, skin temp will be cool and will appear pale/gray since the pink tone is due to capillary perfusion.
2) Mental status changes: Agitation/anxiety; sense of impending doom, confusion, obtundation

Question 59

Pathophysiologic changes in sepsis

Answer 59

1) Distributive shock: failure of VSM constriction
2) Diffuse endothelial injury resulting in microvascular leak → hypovolemia and tissue/organ edema