Glossary of Cardiology part II

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APs are longer in cardiac or skeletal muscle?
SAN conduction velocity
1 m/sec
AV node conduction velocity
0.01-0.05 m/sec
His-Purjinke conduction velocity
2-4 m/sec
- what causes depolarization of phase 0?
why is there a plateau in heart but not nerve?
(1) I-Ca absent or insignificant in nerve

(2) decrease in gK1 on depolarization limits outward current and makes it easier to maintain a plateau (does not occur in nerve)
rate of firing of pacemakers is dependent on which three factors?
(1) maximum diastolic potential

(2) threshold potential

(3) rate of diastolic depolarization
effective refractory period
ERP -- longer than ARP, a conducted action potential cannot be eilicited
supranormal period
SNP -- current required for excitation is less than required at rest, most prominent in Purkinje fibers
Is conduction velocity related to APD?
what are the three determinants of conduction velocity?
(1) amplitude of inward current

(2) passive properties -- resistive and capacitive properties of the membrane and cell-to-cell jxns

(3) excitability
Fick's 1st Law
dN/dt = DA (dc/dx) = PA x dc
why doesn't all the water leak out of capillaries?
- proteins in plasma can't fit through capillary wall, osmotic pressure (oncotic or colloid osmotic pressure) develops
lymph flow is determined by which two factors?
interstitial fluid pressure, the lymphatic "pump"
volume of interstitial fluid increases if more fluid is filtered than can be handled by the lymphatics
flow in an organ Q eqn
Q = (TPR/R) x CO
list some oxygen-linked metabolites
adenosine, H+ and lactate, CO2, K+
metabolite washout
once the metabolite enters the capillary, it is "washed away" by the blood flowing through the capillary
maintenance of a constant blood flow to an organ in the face of changing arterial P
autoregulation e.g.
kidneys, brain, heart, and skeletal muscle
active hyperemia
blood flow to an organ is proportional to its metabolic activity
reactive hyperemia
an increase in blood flow in response to a prior decreased blood flow
myogenic hypothesis
- which of the three blood flow categories can it explain?
only autoregulation
myogenic hypothesis
when vascular smooth muscle is stretched, it contracts; also the opposite is true
metabolic hypothesis
- which of the three blood flow categories can it explain?
all three: autoregulation, active hyperemia, reactive hyperemia
metabolic hypothesis
metabolic activity produces vasodilator metabolites, which help tissues meet need for O2
Normal Sinus Rhythm

for normal sinus rhythm:

(1) impulse arises in SAN

(2) 60-100 b/min and regular

(3) excitation must occur in a normal sequence with appropriate timing of excitation of various portions of the heart
via which nerve does parasympathetic innervation travel to the heart?
what neurotransmitter is released from postganglionic parasympathetic nerve terminals to the heart --> and which receptor does it interact with?
acetylcholine --> muscarinic (M2) receptors
Via what does the sympathetic innervation supply the heart?
superior cervical ganglion
what neurotransmitter is released by sympathetic post-ganglionic nerve terminals to the heart and what receptor does it interact with?
NE --> Beta-1 receptors
non-selective Beta-blocker
cardioselective beta-blockers
metoprolol and practolol
what does parasympathetic withdrawal do to HR?
strongly increases HR
What is the most important site of control of conduction velocity by the ANS?
the AV node
ventricular escape
heart beats arising from the Purjinke fibers due to their automaticity
what is the basis for faster relaxation during a symp stimulation of the heart (positive inotropic effect)
(1) increased rate of Ca2+ accumulation by SR due to NE-induced phosphorylation of phospholamban

(2) Decreased affinity of TnC for Ca2+
does cerebral blood flow increase during exercise?
NOT really, it stays pretty constant.

But coronary, skeletal and skin circulation increases
what is the dominant factor controlling coronary blood flow?
metabolic rate of myocardium
tissue hypoxia
oxygen delivery by the blood is insufficient to meet the oxygen demand of the tissue
why is/are the sympathetic receptor type(s) for skeletal smooth muscle.
alpha (constrictor) and beta-2 (vasodilator)
T/F Hypoxia plays an integral role in the autoregulatory response
subcutaneous venous plexus
holds large quantities of blood that can heat the skin
arteriovenous anastomoses
serve the useful purpose of heat removal
is the dominant factor in regulation of skin circulation local metabolites?
NO! Skin is actually the exception, since there is not much metabolism in the skin; rather, it's controlled by neural control
triple response
- skin stroked firmly with a pointed object

red line - local damage to tissues, release of histamine (vasodilator)

red flare - 20-40 s it appears, pain fiber axon reflex, vasodilation 2-3 cm from stroke line

raised wheal - inc capillary hydrostatic P and Q, 1 cm sensitivity to histamine
what are the three levels of regulation of arterial BP?
neural, humoral, intrinsic
what are the three independent variables regulating arterial blood pressure?
(1) contractility of the vascular smooth muscle

(2) contractility of the heart

(3) Renal Fxn
The Body Fluid System
heart, vascular system, and kidneys
when does the renal body-fluid system come to a steady state?
when dEo/dt = dEi/dt
of the extrinsic mechanisms, which is thought to be the most important to the minute by minute stabilization of arterial BP?
describe how pressure is transduced by baroreceptors
Baroreceptors detect pressure indirectly through stretch. Increases in pressure increase stretch and the increase in stretch produces APs carried by the afferent nerve fibers to the CNS.
how do neural impulses from the solitary tract affect the neural activity of the vasomotor center and the vagal nucleus?
inhibit the activity of the vasomotor center

stimulate the activity of the vagal nucleus
Cardiopulmonary Receptors:
A receptors
veno-atrial stretch receptors activated during tension during systole
Cardiopulmonary Receptors:
B receptors
activated by stretch either of great veins or atrial chamber during filling, are volume receptors
Bainbridge Reflex
bolus of fluid delivered rapidly to the great veins produces marked tachycardia
role of currents in action potential:
- I(Na)
responsible for upstroke (not in SAN/AVN)
role of currents in action potential:
- I(Ca)
- responsible for inward current during plateau (mostly L-type channels)

- responsible for upstroke in SAN/AVN (mostly T-type channels)
role of currents in action potential:
- I(K1)
- responsible for resting potential in ventricle, atrium
role of currents in action potential:
- I(K)
- slowly turns on during phase 2 (helps set APD)
role of currents in action potential:
- I(to)
- contributes to phase 1 repolarization
what phase primarly sets the APD, and how is this phase set?
phase 2

- set by the slow turn on of I(K) and the slow turn off of I(Ca)
myogenic hypothesis of autoregulation
in pressure --> inc blood flow --> inc radius --> inc wall tension --> stretch --> when smooth muscle is stretched it contracts --> dec radius --> dec wall tension
metabolic hypothesis of autoregulation
inc pressure --> inc blood flow --> inc O2 and inc washout of metabolites --> dec vasodilation = vasoconstriction --> inc resistance --> dec blood flow to normal
metabolic hypothesis of active hyperemia
inc tissue activity --> inc production of vasodilators --> vasodilation --> dec resistance --> inc blood flow
metabolic hypothesis of reactive hyperemiai
occlude blood vessel --> dec pressure --> dec blood flow --> dec washout --> accumulation of vasodilator metabolites --> release occlusion --> accumulated metabolites vasodilate --> dec resistance --> inc flow above normal until excess vasodilators are washed away
what does NE do to the rate of phase 4 depolarization?
increases rate
the pacemaker current


increasing inward current carried primarily by Na+
- inc If
causes inc rate of phase 4 depolarization
- inc ICa
makes TP more negative
- inc IK-ACh
causes hyperpolarization of MDP

IK-ACh behaves like IK1 but can be turned on by ACh or adenosine
describe the three main + inotropic effects NE has on contractility, specifically the tension
- inc peak tension

- inc dT/dt

- inc rate of relaxation
- an SR protein that regulates the SR Ca2+ pump

- NE-induced phosphorylation of phospholamban increases the rate of Ca2+ accumulation
NE effects on contractility:
- name 2 reasons for the basis for faster relaxation
(1) increased rate of Ca2+ accumulation by SR due to NE-induced phosphorylation of phospholamban

(2) decreased affinity of TnC for Ca2+ (makes Ca2+ more available by SR)
what does ACh do to contractility of the atrium in low and high doses?
low doses: inc IK-Ach causes hyperpolarization and decreased APD (indirectly decreases Ca2+ entry and contractility)

high doses: ACh inc IK-ACh and directly decreases ICa -- profound negative inotropic effect!
- functions
(1) inhibits adenylate cyclase

(2) directly activates K+ channels
the rate of CBF is regulated primarily by the concentration of what?
CO2 --> leads to changes in pH in the fluid that bathes the vessels and it is this change in pH that elicits alterations in vascular caliber
afferent fibers of the baroreceptor reflex:
large myelinated A fibers
lower threshold, greater sensitivity, and narrower response range
afferent fibers of the baroreceptor reflex:
small, unmyelinated C fibers
higher thersholds, lower sensitivity, and a wider range
sensory information generated by the carotid baroreceptors is transmitted from the carotid sinus --> ?

aortic baroreceptors?
over the fine carotid sinus nerve which joins the glossopharyngeal nerve (IX)

Info from the aortic baroreceptors is carried over the depressor nerve and ascends via the vagus nerve
neural impulses from the solitary tract do what to the activity of the vasomotor center? the vagal nucleus?
inhibit the activity of the vasomotor center

stimulate the neural activity of the vagal nucleus

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