Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Board Review: Physiology > Chapter 3: Cardio (not everything, mainly equations) > Flashcards

Chapter 3: Cardio (not everything, mainly equations) Flashcards

1
Q

Velocity of blood flow can be expressed as

A

V= Q/A

Q= Flow ( mL/Min)
A= Area (cm^2)

As blood flow goes up so does velocity.
As cross sectional area goes up, velocity decreases. (Low in capillaries since they have the largest cross sectional area)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Q = dP/R

A

Flow = Change in Pressure / Resistance (TPR)

dP= MAP -Right Atrial Pressure

Analogous to ohms law: I (flow) = V(voltage or Pressure) / R (resistance)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Poiseulles law

A

To determine Resistance

R = (8 x Viscosity x Length) / pi x r^4

In this, changes in radius have the larges effect on resistance.

The larger the radius the less resistance (by exponent 4)

Really just remember R= Viscosity x L / R^4 (the other crap won’t change but these will)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Is resistance in the vascular system in series or in parallel ?

A

Parallel (like the capillary bed)

With excetption of going from one organ to the next (series), blood flow is set up in parallel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Blood flow where there is no leading edge, fluid moves in a solid wall

A

Laminar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

When Reynolds Number is increased, is there an increased or decreased chance of turbulence ?

A

Increased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

As blood viscosity decreases, is there an increase or decreased chance of turbulence ?

A

Increased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

As velocity of blood flow decreases is there an increased or decreased chance of turbulence ?

A

Decreased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Capacitance

A

The distensibility of a vessel (ability of a vessel to accommodate increased volume with minimal increases in pressure)

C= V/P

Capacitance = Volume/ Pressure

decreases with age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Is capacitance higher in veins or arteries ?

A

VEINS (of course, did i really need to ask ?)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Where in the vascular system is the decreases in blood pressure most pronounced ?

A

Across the ARTERIOLES !

Aorta: 100 mmHg
Arterioles: 50 mmHg
Capillaries: 20 mmHg
Vena Cava: 4 mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Pulse Pressure

A

Systolic - Diastolic

Mainly determined by STROKE VOLUME

Decreases in capacitance leads to pulse pressure increases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

MAP

A

Diastolic + 1/3(Pulse Pressure)

Pulse pressure = Systolic - Diastolic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

P Wave

A

Atrial Depolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Atrial Repolarization

A

Burried in the QRS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

PR interval

A

Beginning of P-wave to beginning of Q

R = QRS complex, they just don’t want to say it.

PR interval varies with conduction velocity through the AV Node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

QRS Complex

A

Depolarization of the Ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

QT Interval

A

Beginning of the Q wave to the End of T-wave.

Represent Ventricular Depolarization and Repolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

ST Segments

A

End of the S-wave to the beginning of the T-wave

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

T-wave

A

Ventricular Repolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What ion determines the resting membrane potential ?

A

K+ (the equilibrium potential of -94 is close to resting membrane potential)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

In general, inward current of ions should _______ the cell

A

depolarize ( I, know this isn’t necessarily true, only with Cations)

Outward flow generally hyperpolarizes the cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Phase 0 is mediated by opening of which Voltage Gated channel ?

A

Na+ ( leads to an inward current) and depolarization of cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Phase I is mediated by

A

Brief depolarization when Na+ gates close and K+outflow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Phase II

A

Plateaus mediated by outflow of K+ and inflow of Ca++

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Phase III

A

Reolarization

K+ outflow and Ca++ channel closing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Phase IV

A

Resting membrane potential

Where inward an outward K+ channels equal each other

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

The Atria, Ventricles and Purkinje system have the same resting membrane potential , what is it ?

A

-90

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the pacemaker of the heart

A

SA node (membrane potential at around -65 mV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Along with the SA node, what other portions of the heart can be considered pace makers ?

A

AV node, His-Purkinje system (When the normal pacemakers are insufficient or absent)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Phase O of SA Node

A

Fast upstroke mediated by Ca++ influx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Phase 3 of SA node(yes, there are no phases 1 and 2)

A

Repolarization

Outward K+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Phase 4 of SA Node

A

Slow depolarization
Reason for autonomous pacemaker ability of SA node
I-f (

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What causes an upstroke in the action potential for the AV node ?

A

Ca++ (Just like the SA node, unlike the other portions of the heart in which phase O is Na+ mediated)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

An increase in the inward current will lead to an __________ in the conduction velocity of excitation in the hard.

A

Increase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Where is the conduction velocity the greatest in the heart ?

A

Purkinje System

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Where is the conduction velocity the slowest in the heart ?

A

AV node.

This is the P-R interval (beginning of P to beginning the QRS complex).. Slowing in the AV allows for ventricular filling before contraction and ejection.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Excitability

A

The ability of cardiac cells to initiate AP’s in response to inward currents.

Depends on the ability of the cells to recover from previous depolarization.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Absolute Refractory Period

A

Period in which another AP cannot be generated , even with increasing stimuli

Begins with the upstroke (0) of the AP and ends at the end of the plateau phase (2)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Effective Refractory Period

A

Slightly longer than ARP (conducted action potential cannot be elicited)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Relative Refractory Period

A

Just after the ARP , point at which a higher than normal stimulus can elicit an action potential.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Chronotropic Effects

A

Effects on heart rate (usually by modulating phase 4 of the SA node)

Increase or decrease the Ca++ influx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Dromotropic Effects

A

Cause changes in conduction velocity through the AV node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What phase do negative chronotropic effects work in ?

A 
Phase 4 (of SA node). 
Inhibits spontaneous depolarization
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

An negative dromotropic effect will ______ the PR interval

A

Elongate.

Remember, domotropic events modulate conduction velocity (through the AV normally)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

How is the cardiac Sarcomere similar to SkMu ?

A

Between Z-lines

Has Actin and Myosin filaments (also troponin and tropomyosin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What special cell communication structures are seen in the intercalated disks of cardiac myocytes ?

A

Gap Junctions (allows for portions of the heart to act as syncytium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

are mitochondria more or less frequent in cardiac muscle as compared to SkMu ?

A

Cardiac

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is the function of T-tubules ?

A

To carry the Action potential to the cell interior (more prevalent in ventricles)

50
Q

During the plateau phase Ca++ enters the cell, what kind of Channels mediate this ?

A

L-Type Ryanodine Receptors

51
Q

Like in SkMu what does Ca++ bind to to initiate excitation contraction coupling ?

A

Troponin C which pulls tropomyosin out of the binding spot allowing for myosin to bind .

52
Q

Contractility

A

Intrinsic Ability of cardiac muscle to develop force at a given muscle length.

53
Q

How is contractility often assessed ?

A

Via the ejection fraction.

54
Q

Inotropic effects

A

Those which modulate contractility

55
Q

How do sympathetic agents increase contractility ?

A
  1. Increase the amount of Ca++ that comes in during phase II of the AP
  2. Increases the activity of phospholamban which accumulates Ca++ in the SR for subsequent contractions

Ca++ modulates force of contraction

Parasympathetics do the opposite (decrease Ca++ concentrations)

56
Q

How do cardiac glycoside increase force of contraction ?

A

Inhibit the Na/K+ pump on myocytes.
This causes a disruption in the Na/Ca++ anti port (Na+ in and Ca+ out) leading to increased Na and Ca++ in the myocyte –> increased contraction

57
Q

Pre-load

A

End DIASTOLIC volume (Related to Right Atrial Pressure)

58
Q

After Load

A

For the Left Ventricle: Aortic Valve

For the Right Ventricl: Pulmonary Artery Pressure

59
Q

Frank Starling

A

increases in stroke volume and cardiac output occur in response to increased venous return and end-diastolic volume

60
Q

Ventricular Pressure Volume Loop: 1-2

A

Isovolumetric Contraction

Point 1: Diastole (140 mL) , Mitral vavle is closed when Left Vent P is greater than Right Vent P.

61
Q

Ventricular Pressure Volume Loop: 2-3

A

Ejection of ventricle

Volume ejected at this point is the Stroke Volume

62
Q

Ventricular Pressure Volume Loop: 3-4

A

Isovolumetric Relaxation

63
Q

Ventricular Pressure Volume Loop: 4-1

A

Ventricular Filling

64
Q

Increased pre-load will lead to an increased ….

A

Stroke volume

65
Q

Increased after load will lead to

A

Decreased stroke volum and an elevated Left Ventricular pressure to overcome increased load

66
Q

What are two ways in which Mean Systemic Pressure are increasesed

A

Increases in volume or decreases in compliance.

Shifts the Curve to the right

( Decreased MSP are due to low blood volume or an increase in compliance .. shifts curve to the left)

67
Q

Equillibrium

A

Cardiac Output = Venous Return

68
Q

Venous return can be altered by changing which two variables

A

Blood volume
Compliance

Increased blood volume or decreased compliance leads to increased veinous return

Decreased blood volume or increased Compliance lead to decreased Venous return

69
Q

What can you do to alter Cardiac output ?

A

Give inotropic drugs

70
Q

Stroke Volume

A

End diastole - End Systolic

71
Q

Cardiac Outpute

A

SV x HR

72
Q

Ejection Fraction

A

SV/End Diastolic Volume

Related to Contractility (increased contractility = increased SV and thus larger ejection fraction)

55% is normal Ejection Fraction

73
Q

Stroke Work

A

Aortic Pressure x Stoke volume

W = P x V

Primarily run by FATTY ACIDS !

74
Q

What 4 factors when increased, increase Cardiac Oxygen demand ?

A

Afterload
Size of the Heart
Contractility
HR

75
Q

Cardiac Output (FIck Principle)

A

O2 Consumption /([02 in pulm vein) - [O2 in pulm Artery])

76
Q

Atrial Systole

A

Preceded by P Wave (contributes but is not essential for arterial filling)

A-wave on Venous pulse curve

Leads to 4th heart sound

77
Q

Isovolumetric contraction

A

Occurs after closure of the AV valves (First Heart Sound)

Pressure in the ventricles force the AV valves shut and when the pressure reaches a point the Semilunar valves are forced open and blood is ejected into the Pulmonary Artery (right vent.) and Aorta (left ventricle)

78
Q

First Heart Sound

A

Closure of the AV valves (Lub)

79
Q

Isovolumetric Relaxation

A

Repolarization of the ventricles (T-Wave) occurs during this time

Aortic (Pulmonic) Valves close. (2nd heart sound)

80
Q

What is the event that causes the second heart sound ?

A

Closing of the Aortic (and pulmonic) Valves

81
Q

What causes the third heart sound ?

A

Rapid filling of the ventricle with atrial blood

Normal in kids, not so much in adults.

82
Q

What is the longest part of the cardiac cycle ?

A

Reduced Ventricular FIlling (diastasis)

83
Q

What are the two main ways that the Arterial Pressure is Regulated

A

Fast Barroreceptor

Slow Renin Angiotensin system

84
Q

What do barrorecptor respond to ?

A

Stretch within the walls of the Carotid Sinus near the bifurcation of the common carotid arteries.

MOST RESPONSIVE TO RAPID DECREASES IN STRETCH. (rapidly decreasing arterial)

(there are also barroreceptors in the Aortic Arch which respond to increased Stretch but not to decreased stretch)…

85
Q

When there is less stretch in the carotid barroreceptors, there will be _________ firing of the carotid sinus barroreceptor nerves.

A

DECREASED ( increased stretch leads to more firing which inhibits parasympathetic outflow to the heart)

Note: Firing of the Carotid barrorecetors –> increased parasympathetic tone. In by IX out by X with decreased Sympathetic outflow

The opposite is true for increased stretch.

86
Q

What is the sent point for the vasomotor center in the brain stem in terms of MAP ?

A

100 mmHg

Purpose of the Vasomotor center is to decrease MAP back to 100 (increase Parasympathetic outflow if above and decrease PS if below)

87
Q

What four processes are modulated to increase arterial pressure when Barroreceptors sense low BP ?

A

Bascially you increase the Sympathetic outflow while decreasing Parasympathetic

INcrease : HR, Contractility (and SV consequently), Vasoconstriction of Arterioles (Alpha 1 receptor activation by NE) , Venoconstriction.

88
Q

Valsalva Manuever

A

Increases intrathoracic pressure, thus decreasing Venous Return

89
Q

What causes a release of Renin ?

A

Decreased perfusion pressure in the kidney (really its decreased Na+ in the blood outflow)

90
Q

What rxn does Renin catalyze ?

A

Angiotensinogen –> AT1 (In plasma)

91
Q

What catalyzes AT1 –> AT II

A

ACE (in the lungs)

92
Q

ARBs block …

A

Angiotiensin Receptors (Bind Angiotensin II)

93
Q

What hormone is released in response to Angiotensin II action ?

A

Aldosterone –> Na+ Reabsorption and K+ excretion

94
Q

4 Effects of Angiotensin II binding with AT1 Receptor

A

Releases Aldosterone (Na+ reabsorption in the Distal Tubule)

Increase Na+/H+ exchange (Sodium into blood, H+ into filtrate)

Increased Thirst

Vasoconstriction –> TPR

95
Q

What is actually sensed in Cerebral Ischemia that leads to increased sympathetic outflow from the Vasomotor ?

A

Partial Pressure of CO2 (Central Chemoreceptors)

Leads to Vasoconstriction that may be dangerous !

96
Q

Where are peripheral chemoreceptors located in the body ?

A

Carotid Body

Aortic Bodies

97
Q

What are the peripheral chemoreceptors sensitive to ?

A

Decreases in Partial Pressure of O2

Low P- 02 leads to increased firing o the Chemorecptors, this will lead to vasoconstriction –> increased Arterial pressures ( increases Venous Return ?)

98
Q

Vassopressin (ADH) is released when BP is decreased due to ..

A

Hemorrhage or dehydration (DECREASED BLOOD VOLUME)

99
Q

Which Vassporessin receptors are activated and lead to vasoconstriction ?

A

V1

100
Q

Which vassopressin receptors are activated and lead to the implantation of Aquaporins into the distal tubule and collecting ducts ?

A

V2

101
Q

ANP is released from ?

A

Atria (in response to increased blood volume !!)

102
Q

What is the overall effect of ANP ?

A

Relaxation of vascular smooth muscle (decreased TPR)

Leads to excretion Na+ and H20

Inhibits Renin Secretion !

103
Q

Starling Equation

A

(Pc + Oi) - (Pi + Oc) x Kf

\+= fluid out of the capillary
- = fluid into the capillary
104
Q

What is responsible for the unidirectional flow of lymph ?

A

One way flap valves.

105
Q

Edema

A

when the volume of interstitial fluid is more than can be returned to venous from the lymph

106
Q

Autoregulation

A

BLOOD FLOW IS CONSTANT TO AN AREA DESPITE CHANGING ARTERIAL PRESSURES

107
Q

Active hyperemia

A

BLood flow to an organ is directly proportional to the its metabolic activity

108
Q

Reactive Hyperemia

A

Increased blood flow after an occlusive event . Can cause repercussion injuries.

109
Q

Myogenic Control

A

Smooth muscle tends to contract when stretched to a point.

110
Q

Metabolic Hypothesis

A

When O2 is low, ATP is low. Lack of ATP leads to build up of vasodilatory substances that causes SM to relax.

111
Q

What organ has the largest response to sympathetic innervation >

A

SKIN

112
Q

PGE’s are VASO….

A

dilatory

113
Q

PGF’s are VASO…

A

Constrictors

114
Q

Thromboxane A2 is ..

A

a vasoconstrictor

115
Q

What controls coronary circulation ?

A

Local Metabolic Factors (almost entirely)

116
Q

What are more innervated by sympathetics in SkMu: Arterioles or Venules ?

A

ARterioles

117
Q

Alpha I adrenergic stimulation in SkMu leads to ..

A

Vasoconstriction

118
Q

Beta 2 stimulation in SkMu leads to ..

A

Vasodilation.

119
Q

When does orthostatic hypotension occur ?

A

When a patients Carotid Barroreceptor reflex is impaired

120
Q

What occurs in the skin and peripheral tissues during exercise ?

A

Vasoconstriction so that (resistance increases) –> lowered blood flow to these organs

121
Q

What are some of the vasodilatory metabolites that are purported in the Metabolic Theory ?

A

Lactate, K+, Adenosine

122
Q

How does the Metabolic Theory Play into the Exercise physiology ?

A

As you exercise your vasodilatory metabolites build up leading to vasodilation in SkMu

Board Review: Physiology (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions