Quiz #3 (1/20-1/25)

Question 1

Cardiac Cycle

Answer 1

Diastole:75% of blood flows directly into atrial due to pressure from filling. Atrial priming is the other 25% of blood that is pushed into the ventricles after electrical current

Systole: Isometric contraction is at the beginning when pressure is increasing but blood is still in ventricle (valves closed).

Question 2

Cardiac Output (mL/min)

Answer 2

= Stroke Volume (mL/beat) * HR (bpm)
Stroke volume: blood volume ejected by ventricles/beat
Average resting cardiac output is 5 L/min. Average SV is 70 mL/beat and average resting HR is 70 bpm

Question 3

Preload and Afterload

Answer 3

Both are determinants of SV

Preload: tension of ventricular muscle before contraction. Determined by left ventricular end diastolic volume/pressure (LVEDP). Essentially is the amount of blood returned to heart from venous system.

Afterload: pressure against which ventricles pump blood. Determined by total peripheral resistance (TPR)

Question 4

SA node

Answer 4

“pacemaker”, located in right atrium, controls HR, origin of spontaneous (no external stimuli) action potential through HCN (hyperpolarization cyclic nucleotide gated channels):
Phase 0: Ca2+ enters
Phase 3: K+ leaves cell
Phase 4: Na+ and Ca2+ slowly enter through leaky ion channels

Question 5

Propagation of impulses

Answer 5

internodal pathways, Bachmann’s bundle (atria): spreads current through atria

AV node/Bundle of His: converged pathways that electrically separates atria and ventricles. Functions to delay signal long enough to fill ventricles with blood.

Also has spontaneous activity but is slower than SA node, is called an ectopic pacemaker.

Purkinje fibers (ventricle): spread currents through ventricles

Question 6

Non-spontaneous action potential

Answer 6

atrial and ventricular myocytes and requires stimulus (which is normally from the SA node)

Phase 0: Na+ enters
Phase 1: K+ and Cl- exits (little effect)
Phase 2: K+ exits and Ca2+ enters causing contraction of myocytes:
Voltage gated Ca2+ channels open, Ca2+ spreads across myocytes by transverse T-tubules
opens ryanodine receptors on SR which stimulates release of IC pools of Ca2+, “Ca induced Ca release”.
Ca2+ then binds troponin-C to release troponin from tropomyosin and increases actin-myosin cross-bridging which is contraction.

Phase 3: K+ exits
Phase 4: Resting membrane potential

Question 7

Frank-Starling Mechanism

Answer 7

Increasing LVEDP corresponds to increasing SV. Increase blood coming back to heart each heart beat will increase the SV to push it out of the heart. In HF this curve isn’t linear.

Question 8

ANS impact on cardiac output

Answer 8

Sympathetic system: Increases HR and SV. Innervation of cardiomyocytes. NE at beta-1 receptors. Increases Ca2+/Na+ channel opening increasing SA node rhythm and AV node transmission to increase force of atrial/ventricular contraction. Decreases phase 4 duration.

Parasympathetic system: Decreases HR and SV. Innervation of SA and AV nodes. ACh at M2 receptors (Gi coupled). Increases K+ channel opening to decrease SA node rhythm and AV node transmission. Increases phase 4 duration

Question 9

Baroreceptor Reflex on Cardiac output

Answer 9

Rapid, fine control of CVS to detect changes in BP. Short-term control
High BP increases parasympathetic activity to lower cardiac output
Low BP increases sympathetic activity to increase cardiac output

Question 10

RAAS on cardiac output

Answer 10

Long-term control of CVS
Decreased BP in kidney causes excretion of renin to the circulation
Renin converts angiotensin to angiotensin I
In lungs, ACE converts angiotensin I to angiotensin II
angiotensin II effects: increases aldosterone, plasma volume, BP, and cardiac output

Question 11

Angina types

Answer 11

Stable: common, follows predictable pattern, exasperated with exercise and relieved with rest

Unstable: no pattern, not relieved by rest, and is a precursor to heart attacks and acute coronary syndrome

Variant (Prinzmetal’s): rare and occurs at rest between midnight and early morning

Question 12

Coronary arteries Adventitial

Answer 12

supporting layer that contains macrophages, monocytes and fibroblasts

Question 13

CA Medial

Answer 13

contractile layer with vascular smooth muscle cells
Contraction of vascular smooth muscle: contractile G-alpha-q coupled GPCRs activate MLCK which phosphorylates myosin. Myosin binds actin to cause vessel contraction
G-alpha-q receptors: binding activates PLC which cleaves PIP2 into IP3 and DAG. IP3 increases calcium release from the SR which binds to calmodulin and activates MLCK.
Receptors: alpha-1 adrenergic, angiotensin II type 1, endothelin A, 5-HT2 serotonin and Kisspeptin 1R

Question 14

CA Intima

Answer 14

inner layer adjacent to lumen with endothelium and elastic lamina

NO production: vasodilatory GPCRs on endothelium converts eNOS and L-arginine with NADPH and O2 into L-citrulline and NO. NO diffuses into adjacent smooth muscle cells

Receptors: bradykinin, angiotensin II type 2, endothelin B, muscarinic 1/3

NO activates GC to increase cGMP levels, which activates protein kinase G (PKG). PKG activates MLCP (phosphatase) which dephosphorylates myosin light chains and PKG also phosphorylates K+ channels to cause an influx and hyperpolarization. All of this causes vasodilation.

Question 15

MLCP vs MLCK

Answer 15

MLCP: removes phosphate from myosin light chain to cause relaxation
MLCK: adds phosphate to myosin light chain to cause contraction