Exam I - Lecture VII (Fick Equation, MI compensation, Shock recap) Flashcards
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?
~23-25 L/min (~400%)
~35-40 L/min, up to 600%
< 0%
08:00
What does the redline represent?
A heart post MI ❤️🩹 (most likely L heart)
*notice the ⬆️ RAP overtime…not good.
12:00
What does point A represent?
Immediate compensation post MI via SNS.
*CO: ⬇️ 2.5 L/min
*RAP: ⬆️ +2
13:30
Immediate compensation post MI involved the SNS.
How does the body compensate overtime (days) and what effects will we see?
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
How much CO does the healthy, 30yr old male need to perfuse his organs?
5L/min
18:00
Which type of edema is more dangerous and harder to treat?
Pulmonary edema 🫁
23:00
If a patient never returns to 5L/min CO post MI, what continues to occur?
⬆️ fluid retention > ⬆️ RAP > ⬆️ workload on heart
24:00
What do you think occurred from B to C?
From C to D?
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
Days after an MI, would you use Epi or NE to aid the failing heart?
Explain your answer.
No. SNS endogenous compensation (NE, Epi) is exhausted. You would want to use something like Digoxin.
27:00
Is it okay to have the RAP at point H for an extended period of time?
~4-5mmHg - this is okay! 👌🏼
Won’t stretch the heart too much (Thanks, Dig!)
29:00
What is a great drug for HF to improve CO?
Digoxin!
29:00
Is arterial pressure (MAP) a reliable VS during shock?
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
Swan-Ganz catheters are the GOLD STANDARD for measuring what?
What is a risk of using one?
CO
Risk for puncture
34:00
What are other ways to measure CO besides the Swan-Ganz?
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
In irreversible shock, we are prone to what? (other than demise ☠️)
Sludgy blood flow = clots.
*think microcirculation and O2 delivery 😟
40:00
State the Fick Equation.
*Schmidt may ask us this in dL, Beware!
43:00
How many ml’s are in 1 deciliter?
100ml = 1dL
*5000ml = 50 dL
56:00
How can we double our oxygen delivery to tissues without expanding blood volume?
Double our CO.
59:00
In most tissues, the O2 extraction has a ΔP ~5 (or about 1/4 of arterial O2) except where?
The coronary circulation.
- the coronaries have the capability to extract ~3/4 of the arterial O2.
- ΔP = 15ml
73:00
Why is it more catastrophic to ⬇ coronary oxygen delivery as opposed to anywhere else in the body?
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
Methods for measuring CO:
What does the dip after the large increase in flow represent?
Retrograde blood flow in the aorta (this happens as the aortic valve closes)
-this is when the coronaries get perfused 😃
78:00
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?
By the iron in the blood.
80:00
What are all the ways to measure CO discussed in lecture?
1) Fick equation
2) Dilution method
3) Electromagnetic or Ultrasonic Flowmeter
4) Thoracic Impedance Changes
5) Echocardiogram
80:00
You give a bolus of fluid to your patient.
Would you expect their pulse pressure to have more variability or less?
Less variation (and vice versa)
84:40
What is the term for a >10mmHg ⬇ sBP during inspiration?
What could this indicate?
Pulses Paradoxus
That your patient is dry/hypovolemic.
88:00
You see variable pulse pressures throughout your case.
How can you easily check if your patient needs more volume?
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
What happens at the cellular level with the capillaries during shock and Why?
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
What medications are given in shock to prevent apoptosis and capillary leaking?
Steroids!
-stabilize cell walls
96:00
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.
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
Please, for the love of God, remember these pressures.
98:00
Unlike you, the heart hates toxins.
In shock, what will release of toxins do to your vasculature, venous return and cardiac function?
venodilate > ⬇ venous return > ⬇ cardiac function/CO
102:00
What does the heart release to signal the kidneys to ⬆ salt & water excretion in response of ⬆ venous volumes & overstretching?
ANP (aka ANF - atrial natriuretic factor)
*BNP, honorable mention by the book
*prevents clotting from stagnant blood
103:00, Guyton pg. 277
What are some options to treat shock?
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
How long does the body take to activate the SNS reflexes?
Where are your sensors to do this?
ms to < 30sec (happens when you stand up from your desk)
Carotid baroreceptors & Aortic baroreceptors
110:00
Where is the major controller of our cardiovascular system?
Lower brainstem - medulla 🧠
111:00
In immediate shock states, determine if these would be ⬆ or ⬇?
HR
SVR
Contractility
NE/Epi
ANP/ANF
Vasopressin
Thirst
Blood shifting
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
What are the blood reservoirs called upon during shock states?
Spleen - RBC, hgb rich
Circulatory systems - GI tract, Lungs
115:00, Guyton pg. 191
What is the reflex that tells ALL blood vessels to constrict to ⬆ blood flow to the brain and SC?
CNS Ischemic Response
116:00
Is the CNS Ischemic Response a stable response?
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
