Exam I - Lecture VII (Fick Equation, MI compensation, Shock recap)

Question 1

In an avg healthy adult, what is their cardiac reserve?
(Liters/min and % from our baseline)

🚴🏼‍♂️ In an elite athlete, what is the maximum cardiac reserve?

❤️‍🩹 In severe cardiac disease, what’s the cardiac reserve?

Answer 1

~23-25 L/min (~400%)

~35-40 L/min, up to 600%

< 0%

08:00

Question 2

What does the redline represent?

Answer 2

A heart post MI ❤️‍🩹 (most likely L heart)
*notice the ⬆️ RAP overtime…not good.

12:00

Question 3

What does point A represent?

Answer 3

Immediate compensation post MI via SNS.
*CO: ⬇️ 2.5 L/min
*RAP: ⬆️ +2

13:30

Question 4

Immediate compensation post MI involved the SNS.

How does the body compensate overtime (days) and what effects will we see?

Answer 4

Retains fluid & lytes (B,C) > expands fluid volume (C,D) > steadily ⬆️ RAP (C,D) > stretches heart out (E) > worsens heart (if not enough healing has occurred) (F) > HF/shock, possibly death

17:00

Question 5

How much CO does the healthy, 30yr old male need to perfuse his organs?

Answer 5

5L/min

18:00

Question 6

Which type of edema is more dangerous and harder to treat?

Answer 6

Pulmonary edema 🫁

23:00

Question 7

If a patient never returns to 5L/min CO post MI, what continues to occur?

Answer 7

⬆️ fluid retention > ⬆️ RAP > ⬆️ workload on heart

24:00

Question 8

What do you think occurred from B to C?

From C to D?

Answer 8

B to C = SNS compensation (notice higher RAP)

C to D = some recovery of tissue or treatment with drug to get to normal CO.

25:00

Question 9

Days after an MI, would you use Epi or NE to aid the failing heart?
Explain your answer.

Answer 9

No. SNS endogenous compensation (NE, Epi) is exhausted. You would want to use something like Digoxin.

27:00

Question 10

Is it okay to have the RAP at point H for an extended period of time?

Answer 10

~4-5mmHg - this is okay! 👌🏼
Won’t stretch the heart too much (Thanks, Dig!)

29:00

Question 11

What is a great drug for HF to improve CO?

Answer 11

Digoxin!

29:00

Question 12

Is arterial pressure (MAP) a reliable VS during shock?

Answer 12

Not really.
*notice you can be at a 15-20% blood loss and still have a MAP of 100…(thanks to SNS and vasoconstriction)

30:00

Question 13

Swan-Ganz catheters are the GOLD STANDARD for measuring what?

What is a risk of using one?

Answer 13

CO

Risk for puncture

34:00

Question 14

What are other ways to measure CO besides the Swan-Ganz?

Answer 14

1) Flotrack
2) Dilution test (Cold saline injection & measuring temp; ⬆️ dilution = ⬆️ CO)
3) Fick Equation from arterial and venous blood gases
4) Bloodwork (lactate, pH, coag’s - clot formation)

37:00 & 42:00

Question 15

In irreversible shock, we are prone to what? (other than demise ☠️)

Answer 15

Sludgy blood flow = clots.
*think microcirculation and O2 delivery 😟

40:00

Question 16

State the Fick Equation.

Answer 16

*Schmidt may ask us this in dL, Beware!

43:00

Question 17

How many ml’s are in 1 deciliter?

Answer 17

100ml = 1dL

*5000ml = 50 dL

56:00

Question 18

How can we double our oxygen delivery to tissues without expanding blood volume?

Answer 18

Double our CO.

59:00

Question 19

In most tissues, the O2 extraction has a ΔP ~5 (or about 1/4 of arterial O2) except where?

Answer 19

The coronary circulation.
- the coronaries have the capability to extract ~3/4 of the arterial O2.
- ΔP = 15ml

73:00

Question 20

Why is it more catastrophic to ⬇ coronary oxygen delivery as opposed to anywhere else in the body?

Answer 20

The coronaries are already taking a lot of O2 (~3/4) from the arterial blood flow as opposed to the rest of the body (~1/4 = has more ‘wiggle room’ to pull from).

73:30

Question 21

Methods for measuring CO:
What does the dip after the large increase in flow represent?

Answer 21

Retrograde blood flow in the aorta (this happens as the aortic valve closes)
-this is when the coronaries get perfused 😃

78:00

Question 22

Other ways to estimate CO:
Impedance Changes can be traced as blood flows through the thorax by leads placed on the chest. This uses electromagnetic technology but is not used often bc it can be super accurate d/t interference.

How do you think the leads pick up the electromagnetic changes?

Answer 22

By the iron in the blood.

80:00

Question 23

What are all the ways to measure CO discussed in lecture?

Answer 23

1) Fick equation
2) Dilution method
3) Electromagnetic or Ultrasonic Flowmeter
4) Thoracic Impedance Changes
5) Echocardiogram

80:00

Question 24

You give a bolus of fluid to your patient.

Would you expect their pulse pressure to have more variability or less?

Answer 24

Less variation (and vice versa)

84:40

Question 25

What is the term for a >10mmHg ⬇ sBP during inspiration? What could this indicate?

Answer 25

Pulses Paradoxus That your patient is dry/hypovolemic. 88:00

Question 26

You see variable pulse pressures throughout your case. How can you easily check if your patient needs more volume?

Answer 26

Give them a lil' leg raise to see if the sBP ⬆ and PP variation ⬇ 😂 (We would push on the patients liver to see if they were dry...) 86:30

Question 26

What happens at the cellular level with the capillaries during shock and Why?

Answer 26

They get leaky. They get angry w/ the ⬇ blood flow and get ischemic > Lysosomes will start to dissolve the dead cells > ⬆ permeability > Peace out✌️colloids & fluid. 92:00

Question 26

What medications are given in shock to prevent apoptosis and capillary leaking?

Answer 26

Steroids! -stabilize cell walls 96:00

Question 27

Okay, so you gave steroids to your shock patient and they are kinda stable now. List a reason their edema can take forever to resolve.

Answer 27

Colloids that leaked out during shock are now on the wrong side of the membrane & the lymphatic system is slow AF -especially if they are laying in an ICU bed. 🛌 97:00

Question 28

Please, for the love of God, remember these pressures.

Answer 28

98:00

Question 29

Unlike you, the heart hates toxins. In shock, what will release of toxins do to your vasculature, venous return and cardiac function?

Answer 29

venodilate > ⬇ venous return > ⬇ cardiac function/CO 102:00

Question 30

What does the heart release to signal the kidneys to ⬆ salt & water excretion in response of ⬆ venous volumes & overstretching?

Answer 30

ANP (aka ANF - atrial natriuretic factor) *BNP, honorable mention by the book *prevents clotting from stagnant blood 103:00, Guyton pg. 277

Question 31

What are some options to treat shock?

Answer 31

1) maybe try to prevent it 🙃 2) pressers (NE 1st line in Septic shock) 3) steroids 4) volume - -- probably use colloids or whole blood -- colloids can cause ⬆ kidney dmg 5) positioning or you could just cut off all your patients limbs 😅 (this would actually ⬇ CO bc you are taking the venous reservoirs away) 6) probably slap on some O2 -- do they have enough hgb tho?? 105:00

Question 32

How long does the body take to activate the SNS reflexes? Where are your sensors to do this?

Answer 32

ms to < 30sec (happens when you stand up from your desk) Carotid baroreceptors & Aortic baroreceptors 110:00

Question 33

Where is the major controller of our cardiovascular system?

Answer 33

Lower brainstem - medulla 🧠 111:00

Question 34

In immediate shock states, determine if these would be ⬆ or ⬇? HR SVR Contractility NE/Epi ANP/ANF Vasopressin Thirst Blood shifting

Answer 34

HR ⬆ SVR ⬆ Contractility ⬆ NE/Epi ⬆ ANP/ANF ⬇ (we wanna keep the fluid) Vasopressin ⬆ (from posterior pit gland) Thirst ⬆ (glycerine swabs only, sir) Blood shifting ⬆ (reservoirs) 112:00

Question 35

What are the blood reservoirs called upon during shock states?

Answer 35

Spleen - RBC, hgb rich Circulatory systems - GI tract, Lungs 115:00, Guyton pg. 191

Question 36

What is the reflex that tells ALL blood vessels to constrict to ⬆ blood flow to the brain and SC?

Answer 36

CNS Ischemic Response 116:00

Question 37

Is the CNS Ischemic Response a stable response?

Answer 37

No, it oscillates unless the initial problem is fixed. **(B)** Baroreceptor: pressures ⬇ > ✅ baroreceptor reflex > pressures ⬆ > 🚫 SNS > fall in pressure > = oscillations. **(A)** CNS-IR: ⬆ ICP > compresses cerebral vessels > ⬆ 🧠 ischemia > ✅ CNS-IR > ⬆ arterial pressures > ischemia relieved > 🚫 SNS > arterial pressure falls > ⬆ 🧠 ischemia > ✅ CNS-IR... This will continue, hence oscillations, until the initial problem is fixed. 117:00