Cardiac A&P

Question 1

What is the primary Calcium ion reservoir in the body?

Answer 1

The Sarcoplasmic Reticulum

Question 2

How does the SA Node stimulate an action potential?

Answer 2

-Changes in automaticity of SA node are due to ANS stimulation
-Spontaneously produces its own action potential
-Depolarizes at 90 bpm
-“Pacemaker” of the heart.

Question 3

What is Phase 0 of the SA Node Action Potential (Pacemaker Action Potential)?

Answer 3

Rapid depolarization due to Ca and Na influx.

Question 4

What is Phase 3 of the SA Node Action Potential (Pacemaker Action Potential)?

Answer 4

Repolarization due to K+ efflux

Question 5

What is Phase 4 of the SA Node Action Potential (Pacemaker Action Potential)?

Answer 5

Spontaneous depolarization from resting membrane potential (-60 mV) to threshold (-30 mV) due to Na influx (slow depolarization)

Question 6

Why is there a pause at the AV Node?

Answer 6

-To allow for coordinated contraction between Atria and ventricles.
-Allows atria to completely empty (and ventricles to fill) before ventricles contract.
-Atrial conduction is slowed by 0.1-0.13 seconds

Question 7

Which fibers have the fastest conduction velocity in the heart?

Answer 7

-His-Purkinje fibers depolarize at 20-40 BPM
-Have to create a coordinated ventricular contraction very quickly. So fast that it looks like it’s in unison.
-Lots of branches beneath the endocardium that allow ventricular ctx to happen.

Question 8

What do anesthetic gasses do to SA node activity & contractility?

Answer 8

-Anesthetic gasses depress SA nodal activity and contractility
-Depress SA nodal automaticity
-Volatiles depress contractility by decreasing entry of Ca+ into cells during depolarization

Question 9

What is Phase 0 of the Ventricular Action Potential?

Answer 9

Rapid depolarization (Na influx)

Question 10

What is Phase 1 of the Ventricular Action Potential?

Answer 10

Initial repolarization (Na channels close)

Question 11

What is Phase 2 of the Ventricular Action Potential?

Answer 11

-Plateau (Ca influx).
-Allows ventricle time to contract, push blood out, and then relax.
-Prevents tetany in ventricular cells.
-Occurs due to increased Ca influx and decreased permeability of K+
-Absolute refractory period.

Question 12

What is Phase 3 of the Ventricular Action Potential?

Answer 12

Repolarization (K efflux)

Question 13

What is Phase 4 of the Ventricular Action Potential?

Answer 13

Na-K pump restores resting membrane potential (-90mV) = diastole

Question 14

What time is sacrificed at high heart rates?

Answer 14

-Systole is relatively fixed in duration
-diastolic time is sacrificed at high heart rates
-Tachycardia not only decreases ventricular filling but also coronary filling (bad for cardiac patients)

Question 15

What is Excitation-Contraction Coupling?

Answer 15

The conversion of an action potential into a muscle contraction.
-The result of actin and myosin overlapping one another, causing shortening of the myocyte.

Question 16

What is Calcium-Induced Calcium Release?

Answer 16

-T-Tubules bring extracellular Ca in via voltage-gated receptors (DHP receptor)
-Once in the cell, Ca binds to Ryanodine receptor, causing SR to release more calcium
-As long as Ca is present, actin-myosin will stay crossed.
-When you want to relax, Calcium is pumped via Sarco/endoplasmic reticulum Ca pump (SERCA) back into the SR (uses ATP)
-Also, the Na/Ca pump puts Ca back into the ECF
-Ca release from myosin cross bridges causes heart muscle to relax

Relaxation is ATP and O2 dependent (just like contraction is).

Question 17

What does End diastolic pressure volume relationship (EDPVR) indicate?

Answer 17

Compliance (Stiffness)

Question 18

What does End systolic pressure volume relationship (ESPVR) indicate?

Answer 18

Contractility (slope)

Question 19

How do you calculate Stroke Volume?

Answer 19

SV = EDV-ESV

Question 20

How do you calculate EF?

Answer 20

EF = SV / EDV

Question 21

Review PV Loop pictures

Answer 21

Yes

Question 22

How do you calculate CO?

Answer 22

CO = HR x SV (4-6 L/min)

Question 23

How do you calculate CI?

Answer 23

CI = CO / BSA (2.5-4.2 .2 L/min/m2)

Question 24

What is Preload?

Answer 24

-EDV
-Dependent on ventricular filling.
-Venous return is the primary determinant of PL
-75% of blood volume resides in the veins
-When HR is constant, CO is directly proportional to PL to both the R & L heart.
-Inc HR = dec diastole = impaired filling

Question 25

What is the Bainbridge Reflex?

Answer 25

Increased volume in R atrium cause HR to increase by 10-20%

Question 26

Why do you want to avoid overfilling?

Answer 26

The point at which further increases in SV are not possible. -SV diminishes because actin-myosin filaments are pulled so far apart that contraction strength is reduced (sarcomere is overly stretched) -Will see pressure increase along EDPVR line

Question 27

What are the components of Afterload?

Answer 27

-Ventricular Wall Tension -Arterial Impedance to Ejection -Physical Properties of blood vessels and/or blood (viscosity) CO and SV are inversely r/t AL

Question 28

How does Ventricular Wall Tension affect AL?

Answer 28

-Law of LaPlace: T (wall tension) = P (pressure) x R (radius) -Small radius (vasoconstriction) = increased pressure. RV > LV in terms of sensitivity to AL changes (LV has larger muscle mass)

Question 29

How does Arterial Impedance to Ejection affect AL?

Answer 29

-HTN, atherosclerosis. Higher resistance to ejection. -SVR = 80 x (MAP-CVP/CO). Normal is 900-1500 dynes/cm -PVR = 80x(pap-lap/co). Normal PVR- 50-150

Question 30

How do the physical properties of blood vessels/blood affect AL?

Answer 30

Can do autologous blood transfusions and replace with crystalloid to make blood less viscous.

Question 31

What is the compliance equation?

Answer 31

Compliance = Volume / Pressure

Question 32

What factors effect Contractility?

Answer 32

-Independent of PL and AL -Calcium concentration is the most important factor (More Ca = more myosin binding sites = stronger contraction) -Also affected by Mg, O2, and acidosis -Slope of the ESPVR line corresponds with contractility -Dec slope = dec contractility (systolic failure)

Question 33

Why is the endocardium more vulnerable to ischemia?

Answer 33

Blood flows to endocardium during mainly diastole, making it the most vulnerable to ischemia. -Blood flows to epicardium during entire cardiac cycle

Question 34

What is the Coronary Sinus SvO2?

Answer 34

Coronary sinus SVO2 = 35% (i.e. large O2 extraction with little reserve in times of ischemia)