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Principles 2 > Cardiac A&P > Flashcards

Cardiac A&P Flashcards

1
Q

What is the primary Calcium ion reservoir in the body?

A

The Sarcoplasmic Reticulum

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2
Q

How does the SA Node stimulate an action potential?

A

-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.

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3
Q

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

A

Rapid depolarization due to Ca and Na influx.

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4
Q

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

A

Repolarization due to K+ efflux

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5
Q

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

A

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

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6
Q

Why is there a pause at the AV Node?

A

-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

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7
Q

Which fibers have the fastest conduction velocity in the heart?

A

-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.

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8
Q

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

A

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

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9
Q

What is Phase 0 of the Ventricular Action Potential?

A

Rapid depolarization (Na influx)

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10
Q

What is Phase 1 of the Ventricular Action Potential?

A

Initial repolarization (Na channels close)

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11
Q

What is Phase 2 of the Ventricular Action Potential?

A

-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.

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12
Q

What is Phase 3 of the Ventricular Action Potential?

A

Repolarization (K efflux)

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13
Q

What is Phase 4 of the Ventricular Action Potential?

A

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

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14
Q

What time is sacrificed at high heart rates?

A

-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)

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15
Q

What is Excitation-Contraction Coupling?

A

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

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16
Q

What is Calcium-Induced Calcium Release?

A

-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).

17
Q

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

A

Compliance (Stiffness)

18
Q

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

A

Contractility (slope)

19
Q

How do you calculate Stroke Volume?

A

SV = EDV-ESV

20
Q

How do you calculate EF?

A

EF = SV / EDV

21
Q

Review PV Loop pictures

A

Yes

22
Q

How do you calculate CO?

A

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

23
Q

How do you calculate CI?

A

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

24
Q

What is Preload?

A

-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

25
Q

What is the Bainbridge Reflex?

A

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

26
Q

Why do you want to avoid overfilling?

A

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

27
Q

What are the components of Afterload?

A

-Ventricular Wall Tension
-Arterial Impedance to Ejection
-Physical Properties of blood vessels and/or blood (viscosity)

CO and SV are inversely r/t AL

28
Q

How does Ventricular Wall Tension affect AL?

A

-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)

29
Q

How does Arterial Impedance to Ejection affect AL?

A

-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

30
Q

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

A

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

31
Q

What is the compliance equation?

A

Compliance = Volume / Pressure

32
Q

What factors effect Contractility?

A

-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)

33
Q

Why is the endocardium more vulnerable to ischemia?

A

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

34
Q

What is the Coronary Sinus SvO2?

A

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

Principles 2 (45 decks)

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