Brs Cardio Set

Front 1

Systemic blood flow

Back 1

Cardiac output from left side of the heart

Front 2

what is the stressed volume?

Back 2

the blood volume contained in the arteries

Front 3

Blood Vessel with Highest Pressure

Back 3

Arteries

Hint 3

arter-IES

(Intense pressure, Elastin, SM)

Front 4

stressed volume

definition?

Back 4

blood volume contained in systemic arteries

Front 5

What is the site of the highest resistance in the cardiovascular system?
What regulates this resistance?

Back 5

Arterioles, regulated by the autonomic nervous system.

Front 6

Pulmonary blood flow

Back 6

Cardiac output from right side of the heart

Front 7

what is the site of highest resistance of the cardiovascular system?

Back 7

arterioles

Front 8

Blood Vessel with Highest Resistance

Back 8

Arterioles

Hint 8

arteri-O-les

(O = Ohm's law = resistance)

Front 9

site of highest resistance in the cardiovascular system

Back 9

arterioles

Front 10

What type of receptors are found on the arterioles of the skin, splanchnic, and renal circulations?

Back 10

α1-Adrenergic recptors

Front 11

Deliver oxygenated blood to the tissues

Back 11

Arteries

Front 12

what ANS receptors are found in the arterioles of the skin, splanchnic and renal circulations?

Back 12

alpha-1 adrenergic receptors

Front 13

Blood Vessel with Largest Cross Sectional Area & Surface Area

Back 13

Capillaries

Hint 13

CA-pillaries

(Cross-sectional & surface Area)

Front 14

vessels with largest total cross sectional and surface area of circulation

Back 14

capillaries

Front 15

Where are the β receptors found in the circulation system? What type of β receptors are they?

Back 15

β2-Adrenergic receptors are found on arterioles of skeletal muscle.

Front 16

are the smalles branches of the arteris

Back 16

Arterioles

Front 17

what ANS receptors are found in the arterioles of skeletal muscle?

Back 17

Beta-2 adrenergic receptors

Front 18

Blood Vessel with Highest Proportion of Blood

Back 18

Veins

Hint 18

V-eins

(Volume of blood proportionally)

Front 19

vessels regulated by the autonomic system

Back 19

arterioles and venules

Front 20

What part of the circulatory system has the largest total cross-sectional and surface area?

Back 20

Capillaries

Front 21

Are formed from merged capillaries

Back 21

Venules

Front 22

Which vessels have the lowest vascular resistance? Why?

Back 22

capillaries, due to their parallel arrangement (highest cross-sectional area).

Front 23

Blood Vessel with extensive amounts of Elastic Tissue & Smooth muscle

Back 23

Arteries

Hint 23

arter-IES

(Intense pressure, Elastin, SM)

Front 24

vessels with highest proportion of the blood

Back 24

veins

Front 25

What part of the circulatory system contains the highest proportion of the blood?
What type of receptors are found here?

Back 25

Veins
α1-adrenergic receptors

Front 26

Are thick-walled with extensive elastic tissue and smooth muslce

Back 26

Arteries

Front 27

Describe the histology of large arteries

Back 27

thick-walled, with extensive elastic tissue and smooth muscle

Front 28

Arterioles have Alpha1 receptors where?

Back 28

Skin, Splanchnics, & Renal arterioles

Front 29

unstressed blood volume

definition?

Back 29

blood volume in the veins

Front 30

Is velocity of blood flow proportional to Q (blood flow)? A (Cross-sectional area)?

Back 30

Velocity is directly proportional to blood flow, inversely proportional to the cross-sectional area at any level of the cardiovascular system.

Front 31

Under high pressure

Back 31

Arteries

Front 32

describe the histology of arterioles

Back 32

smooth muscle wall that is highly innervated by ANS

Front 33

Skeletal muscle arterioles have what receptors?

Back 33

Beta 2 receptors

Front 34

relationship between:

blood velocity
blood flow
cross sectional area

Back 34

v = Q/A

Front 35

Is Cardiac Output (blood flow/Q) proportional to pressure gradient (ΔP)? Resistance?

Back 35

Blood flow is directly proportional to ΔP (blood flows from high pressure to low pressure), inversely proportional to the resistance of the blood vessels.

Front 36

Highest resistance in the cardiovascular system

Back 36

Arterioles

Front 37

describe teh histology of capillaries

Back 37

consist of a single layer of endothelial cells surrounded by basal lamina. thin-walled

Front 38

Alpha 1 receptors are found on Arterioles and ..... ?

Back 38

Veins

Front 39

relationship between:

blood flow
pressure gradient
resistance

Back 39

Q = dP/R

Front 40

What is the relationship between Resistance (R) and viscosity of blood, length of blood vessel, and the radius of blood vessels (to the fourth power)?

Back 40

Resistance is directly proportional to the viscosity of the blood and length of the vessel, and inversely proportional to the fourth power of the vessel radius.

Front 41

the blood volume contained in the arteries is called the stressed volume

Back 41

Arteries

Front 42

where is the majority of the blood stored in the body?

Back 42

veins

Front 43

Blood Vessel with the Lowest pressure?

Back 43

Veins

Front 44

relationship between :

Resistance
viscosity
length of vessel
radius of blood vessel

Back 44

R = (8n*l)/(pi*r^4)

R = resistance
n = viscosity
l = length
r^4 = radius to fourth power

Front 45

How would increasing the hematocrit change the viscosity of the blood, and the resistance?

Back 45

Increasing hematocrit will increase viscosity, and will thus increase the resistance and decrease the blood flow.

Front 46

Are teh site of exchange of nutrients water and gases

Back 46

capillaries

Front 47

what is the unstressed volume?

Back 47

the blood volume contained in the veins

Front 48

Velocity of blood flow is highest in?

Velocity of blood flow is lowest in?

Back 48

Aorta

Capillaries

Front 49

if blood vessel radius decreases by factor of 2, what change in resistance?

Back 49

increased by 16 (2^4)

Front 50

What is Reynolds number?
What increases Reynolds number?

Back 50

Reynolds number predicts whether blood flow will be laminar or turbulent.
When Reynolds number is increased, there is a greater tendency for turbulence, which causes audible vibrations called bruits.

Reynolds number (and therefore turbulence) is increased by:
Decreased blood viscosity (e.g. decreased hematocrit, anemia)
Increased blood velocity (e.g. narrowing of a vessel)

Front 51

Have a smooth muslce wall that is extensively innervated by autonomic nerve fiber

Back 51

Arterioles

Front 52

what ANS receptors are present in veins?

Back 52

alpha-1 adrenergic receptors

Front 53

Velocity (v) of Blood flow equation?

Back 53

V = Q / A

(where Q = blood flow / CO)
(where A = cross sectional area)

Hint 53

Think Velocity = Length / Distance

Front 54

Reynold's number

Back 54

predicts whether blood flow will be laminal or turbulent

Front 55

What is the site of the highest resistance in the cardiovascular system?
What regulates this resistance?

Back 55

Arterioles, regulated by the autonomic nervous system.

Front 56

B2-adrenergic receptors in arteriols are found on?

Back 56

are found on arterioles of skeletal muslce

Front 57

What is the formula for calculating Cardiac Output?

Back 57

Cardiac Output = (mean arterial pressure - right atrial pressure) / Total peripheral resistance

Front 58

Blood Flow (Q) equation?

Back 58

Q = dP / R

(where dP = change in pressure)
(where R = resistance)

Hint 58

Think of Ohm's law ==> P = QR

Front 59

anemia:
effect on reynold's number

Back 59

increased (decreased viscosity)

Front 60

What type of receptors are found on the arterioles of the skin, splanchnic, and renal circulations?

Back 60

α1-Adrenergic recptors

Front 61

*1- adrenergic receptors are found on the arterioles

Back 61

of the skin, splanchic, and renal circulations

Front 62

what happens to the total resistance if an artery is added in parallel?

Back 62

resistance decreases.
(you increase the surface area
through which the blood can flow)

Front 63

Blood Flow (Q) in Inversely proportional to?

Back 63

BV Resistance

Front 64

capacitance (compliance), defining equation

Back 64

C = V/P

V= volumr
P = pressure

Front 65

Where are the β receptors found in the circulation system? What type of β receptors are they?

Back 65

β2-Adrenergic receptors are found on arterioles of skeletal muscle.

Front 66

Arteriolar resistance is regulated by the?

Back 66

autonomic nervous system

Front 67

if the radius of an artery is doubled what happens to the resistance to flow through that artery?

Back 67

resistance is decreased by a factor of 16

Front 68

Based on Blood flow equation, what is another equation for CO (which is Q)?

Back 68

CO = (MAP - RAP) / TPR

(where MAP = Mean Arterial Pressure)
(where RAP = Right ATRIAL Pressure)
(where TPR = Total Peripheral Resistance)

Front 69

vessels across which the greatest pressure decrease occures

Back 69

arterioles (because site of highest resistance)

Front 70

What part of the circulatory system has the largest total cross-sectional and surface area?

Back 70

Capillaries

Front 71

what have the largest total cross sectional and surface area

Back 71

Capillaries

Front 72

what factor causes the reynold's number of blood to increase?

Back 72

decreased viscosity
(low hematocrit, anemia)
and increased blood velocity (narrowing of a vessel)

Front 73

Resistance equation (Poiseuille's law)

Back 73

R =
(8 x viscosity x length) / (Pi x radius^4)

Front 74

most important determinant of pulse pressure

Back 74

stroke volume

Front 75

What part of the circulatory system contains the highest proportion of the blood?
What type of receptors are found here?

Back 75

Veins
α1-adrenergic receptors

Front 76

are thin walled

Back 76

Capillaries

Front 77

what is the result of a high reynold's number in the blood?

Back 77

greater tendency for turbulence,
causes audible bruits.
Turbulent flow may result in clot formation.

Front 78

Resistance is proportional to?

Back 78

Viscosity and Length

Front 79

atrial depolarization on EKG

Back 79

P wave

Front 80

Is velocity of blood flow proportional to Q (blood flow)? A (Cross-sectional area)?

Back 80

Velocity is directly proportional to blood flow, inversely proportional to the cross-sectional area at any level of the cardiovascular system.

Front 81

Capillaries are consist of single layer of_______ cells surrounded by________.

Back 81

endothelial cells surrounded by basal lamina

Front 82

what is capacitance?

Back 82

ability of a blood vessel to distend. inversely related to elastance

Front 83

Resistance is inversely proportional to?

Back 83

4th power of radius

Front 84

interval from atrial depolarization to ventricular depolarization

Back 84

PR interval

Front 85

Is Cardiac Output (blood flow/Q) proportional to pressure gradient (ΔP)? Resistance?

Back 85

Blood flow is directly proportional to ΔP (blood flows from high pressure to low pressure), inversely proportional to the resistance of the blood vessels.

Front 86

Veins have __adrenergic receptors

Back 86

*1

Front 87

which has greater capacitance, arteries or veins?

Back 87

veins

Front 88

If BV radius decreases by half (a factor of 2), then the resistance change will be what?

- thus the change to blood flow will be?

Back 88

Resistance increases by 16

BF decreases by 16

Front 89

represents depolarization of ventricle on EKG

Back 89

QRS complex

Front 90

What is the relationship between Resistance (R) and viscosity of blood, length of blood vessel, and the radius of blood vessels (to the fourth power)?

Back 90

Resistance is directly proportional to the viscosity of the blood and length of the vessel, and inversely proportional to the fourth power of the vessel radius.

Front 91

Largest vein is the

Back 91

vena cava

Front 92

where in the vascular system would one find the greatest decrease in pressure? why?

Back 92

across the arterioles due to it being the greatest site of resistance

Front 93

When an artery is added in parallel, what changes?

(as in systemic circulation)

Back 93

Total Resistance is decreased

Front 94

interval representing entire period of depolarization and repolarization of ventricle

Back 94

QT interval

Front 95

How would increasing the hematocrit change the viscosity of the blood, and the resistance?

Back 95

Increasing hematocrit will increase viscosity, and will thus increase the resistance and decrease the blood flow.

Front 96

Vena cava return

Back 96

blood to the heart

Front 97

what is the mean arterial pressure of the aorta?

Back 97

100 mmHg

Front 98

When an artery is added in series, what changes?

(as in BV arrangements INSIDE organ)

Back 98

Pressure decreases

Front 99

isoelectric segment when entire ventricle is deplarized

Back 99

ST segment

Front 100

What is Reynolds number?
What increases Reynolds number?

Back 100

Reynolds number predicts whether blood flow will be laminar or turbulent.
When Reynolds number is increased, there is a greater tendency for turbulence, which causes audible vibrations called bruits.

Reynolds number (and therefore turbulence) is increased by:
Decreased blood viscosity (e.g. decreased hematocrit, anemia)
Increased blood velocity (e.g. narrowing of a vessel)

Front 101

Veins have what kind of wall?

Back 101

thin

Front 102

what is the mean arterial pressure of the arterioles?

Back 102

50 mmHg

Front 103

Most contributions of Resistance in SERIES can be attributed to what vessel?

Back 103

Arterioles

Hint 103

again, arteri-O-les, think Ohms

Front 104

represents ventricular repolarization on EKG

Back 104

T wave

Front 105

What is a chronotropic effect? What is a dromotropic effect?

Back 105

Chronotropic effects produce changes in heart rate.
Dromotropic effects produce changes in
conduction velocity, primarily the AV node.

Front 106

veins are under waht kind of pressure

Back 106

low

Front 107

what is the mean arterial pressure of the capillaries?

Back 107

20 mmHg

Front 108

An increase in Reynold's #, will increase the likelihood of what flow?

Back 108

Turbulent flow

(non-straight flow)

Front 109

normally is the pacemaker of heart

Back 109

SA node

Front 110

How does the parasympathetic system decrease heart rate?

Back 110

Parasympathetic innervation causes a negative chronotropic effect (decreases heart rate) by decreasing If, and therefore decreasing the rate of phase 4 depolarization.

Front 111

what contains the highes porportion of bloood in the cardi system

Back 111

veins

Front 112

what is the mean pressure of the Vena Cava?

Back 112

4 mmHg

Front 113

Reynolds # can be increased with an ...

- increase in what property (give example)
- decrease in what property (give example)

Back 113

Increase in VELOCITY
(narrowing BV radius)

Decrease in VISCOSITY
(anemia, or decreased Hct)

Front 114

SA nodal action potential phases (#'s)

Back 114

0 (Ca++)
3 (K+)
4 (Na+ current, I*f*)

Front 115

What is the mechanism of the parasympathetic system’s negative dromotropic effect?

Back 115

Decreased inward Ca2+ current and increased outward K+ current causes a decreased conduction velocity through the AV node.

Front 116

the blood volume contained in the veins is called the

Back 116

unstressed volume

Front 117

what is the pulse pressure?

Back 117

the difference between the systolic and diastolic pressures

Front 118

Capacitance is also known as?

Back 118

Compliance
or
Distensibility

Front 119

Bowditch staircase

Back 119

increased heart rate
increases strength of contraction
in a stepwise fashion
b/c as intracellular Ca++ increases over several beats

Front 120

Are mitochondria more numerous in cardiac muscle or in skeletal muscle?

Back 120

Cardiac muscle.

Front 121

velocity is directly peoportional to ____and inversily to______

Back 121

blood flow
cross sec area

Front 122

what is the most important determinant of pulse pressure?

Back 122

stroke volume

Front 123

Capacitance equation?

Back 123

C = V / P

(where V = volume)
(where P = pressure)

Front 124

post extrasystolic potentiation

Back 124

the beat *following* an extrasystolic beat has increased strength of contraction

***increased intracellular Ca++

Front 125

What structure of the myocardial cells are more developed in the ventricles than in the atria? What do they form?

Back 125

T tubules, which invaginate the cells at the Z lines and carry action potentials into the cell interior.
T tubules form dyads with the sarcoplasmic reticulum.

Front 126

Flow is analogous to?

Back 126

current

Front 127

how does one measure the left atrial pressure?

Back 127

pulmonary wedge pressure

Front 128

Capacitance is inversely related to?

Back 128

Elastance

Front 129

mechanisms by which beta receptors increase strength of contraction

Back 129

increased Ca++ into cell during plateau

increased activity of Ca++ of SR (phospholambam, therefore more Ca++ accumulated)

Front 130

During excitation-contraction coupling, what does Ca2+ bind to, and what happens after?

Back 130

Ca2+ binds to troponin C, and tropomyosin is moved out of the way, removing the inhibition of actin and myosin binding.
Actin and myosin bind, the thick and thin filaments slide past each other, and the myocardial cell contracts.

Front 131

Pressure is analogous to?

Back 131

voltage

Front 132

how does one calculate the mean arterial pressure?

Back 132

diastolic pressure plus 1/3 pulse pressure

Front 133

Capacitance is greater in which?

- arteries or veins? (why?)

Back 133

Veins

(b/c arteries have lots of elastic tissue, thus more elastance, so less capacitance)

Front 134

preload

Back 134

end diastolic volume/venous filling presure

Front 135

What determines the magnitude of the tension during excitation-contraction coupling?

Back 135

The intracellular [Ca2+]

Front 136

What is ejection fraction? What is its normal value?

Back 136

Ejection fraction = stroke volume/end-diastolic volume
Normally 0.55 (55%)

Front 137

what drives blood flow

Back 137

pressure gradient

Front 138

What is the PR interval and what is its significance?

Back 138

It is the interval between the beginning of the P wave to the beginning of the Q wave. It is a measure of the conduction velocity through the AV node

Front 139

Pressure drops the most at?

Back 139

Arterioles

(b/c site of highest resistance)

Front 140

afterload

Back 140

aortic pressure

Front 141

What is inotropism?

Back 141

The contractility, or the intrinsic ability of cardiac muscle to develop force at a given muscle length.

Front 142

Resistance is directly proportional to the

Back 142

viscosity of the blood

Front 143

what does an increased PR interval signify?

Back 143

AV nodal heart block

Front 144

What type of pressure is pulsatile?

Back 144

Arterial pressure

Front 145

y intercept of venous return curve

Back 145

mean systemic pressure

Front 146

What are some factors that increase contractility?

Back 146

1) Increased heart rate: more Ca2+ enters the myocardial cells -> more Ca2+ released from the SR -> greater tension produced
2) Sympathetic stimulation (catecholamines) via β1 receptors: increases inward Ca2+ current during plateau of each action potential; increases the activity of the Ca2+ pump of the SR (by phosphorylation of phospholamban) -> more Ca is accumulated and available for release
3) Cardiac glycosides (digitalis)

Front 147

Resistance is inversily proportional to?

Back 147

blood flow

Front 148

What is the QT interval and what is its significance?

Back 148

QT interval is measured from the beginning of the Q wave to the end of the T wave. It represents the entire period of depolarization and repolarization of the ventricles

Front 149

AGING causes a DECREASE in?

Thus causes an INCREASE in?

Back 149

Decrease in Capacitance,

so an Increase in Pulse Pressure

Front 150

clockwise rotation of venous return curve

Back 150

decrease total peripheral resistance

Front 151

How do cardiac glycosides (digitalis) work?

Back 151

Cardiac glycosides increase the force of contraction by inhibiting Na+, K+-ATPase in the myocardial cell membrane. As a result, the intracellular [Na] increases, diminishing the Na gradient across the cell membrane. Na-Ca exchange (which extrudes Ca from the cell) depends on the size of the Na gradient and thus is diminished, producing an increase in intracellular [Ca].

Front 152

resistance is directly pro to 2 things

Back 152

viscosity of the blood
lenght of the vessel

Front 153

What is the ST segment?

Back 153

the segment from the end of the S wave to the beginning of the T wave; it is isoelectric period of ventricular depolarization

Front 154

Pulse Pressure equation

Back 154

PP = SBP - DBP

Front 155

Type I hyperlipidemia

Back 155

high chylomicrons

Front 156

What are factors that decrease contractility?

Back 156

Parasympathetic stimulation (ACh) via muscarinic receptors decreases the force of contraction in the atria by decreasing the inward Ca-current during the plateau of the cardiac action potential.

Front 157

resistance is inversily pro to the?

Back 157

fourth power of the vessel radius

Front 158

What determines the resting membrane potential?

Back 158

conductance to K+

Front 159

Stroke Volume is the Primary Determinant of what?

Back 159

PP

Front 160

Type IIa hyperlipidemia

Back 160

high LDL

Front 161

What is preload? What is afterload?

Back 161

Preload: End-diastolic volume, which is related to right atrial pressure.
Afterload: Aortic pressure (for the left ventricle)

Front 162

Parallel resistance is illustrated by the

Back 162

systemic circulation

Front 163

what is resting membrane potential of myocardial cells?

Back 163

-90 mV

Front 164

Mean Arterial Pressure equation?

Back 164

= 1/3 PP + DBP

Front 165

Type IIb hyperlipidemia

Back 165

high LDL and VLDL

Front 166

What is the equation for Cardiac Output?

Back 166

Cardiac output = stroke volume x heart rate

Front 167

When an artery is added in parallel the total resistance dec or inc

Back 167

dec

Front 168

Describe Phase 0 of the cardiac action potential?

Back 168

upstroke of action potential; It is marked by a transient increase in Na conductance that has inward flow of ions depolarizing membrane

Front 169

Veins can hold more blood because of High ______ & Low _______.

Back 169

High Capacitance

Low Pressure

Front 170

Type III hyperlipidemia

Back 170

high chylomicrons and IDL (intermediate density lipoprotein)

Front 171

What is stroke work? What is the equation?

Back 171

Stroke work is the work the heart performs on each beat.
Stroke work = Aortic pressure x stroke volume

Front 172

Series resistance is illustrated by the?

Back 172

arrangement of blood vessels within a given organ

Front 173

Describe Phase 1 of the cardiac action potential

Back 173

initial repolarization caused by outward flow of K ions

Front 174

Left Atrial Pressure (LAP) is slightly lower than?

Back 174

Venous pressure

Front 175

Type IV hyperlipidemia

Back 175

high triglycerides

Front 176

What increases cardiac oxygen consumption?

Back 176

1. Increased afterload
2. Increased size of the heart
3. Increased contractility
4. Increased heart rate

Front 177

Largest proportion of resistance in series is contributed by

Back 177

arterioles

Front 178

Describe Phase 2 of the cardiac action potential

Back 178

plateau of AP; transient increase in Ca conductance that results in an inward flow of Ca along with a balanced outward flow of K

Front 179

Left Atrial Pressure (LAP) is measured as what pressure?

Back 179

Pulmonary Wedge Pressure

Front 180

Type V hyperlipidemia

Back 180

very similar to Type I (high cholymicrons), but with high VLDL

Front 181

How do you measure the pulmonary vein [O2] and pulmonary artery [O2]?

Back 181

Pulmonary vein [O2] is measured in a peripheral artery.
Pulmonary artery [O2] is measured in systemic mixed venous blood.

Front 182

What happens to the pressure when blood flows through the series of blood vessels

Back 182

dec

Front 183

Describe Phase 3 of the cardiac AP

Back 183

Repolarization; Ca conductance decreases, K conductance increases; large outward flow of K toward Vm(K), hyperpolarizing the membrane

Front 184

Pulmonary Wedge Pressure (PWP) is taken by placing a catheter where?

Back 184

smallest branch of Pulmonary artery

(almost directly on Pulmonary capillaries)

Front 185

stroke work equation

Back 185

stroke work = stroke volume * aortic pressure

Front 186

What is the a wave on the venous pulse curve?

Back 186

The increase in atrial pressure (venous pressure) casued by atrial systole.

Front 187

reynolds number?

Back 187

perdicts whether blood flow is laminar or tur

Front 188

Describe Phase 4 of the cardiac AP

Back 188

resting membrane potential; inward adn outward currents are equal and Vm approaches K equilibrium potential

Front 189

ECG representation of Atrial Depolarization

Back 189

P wave

(does not include atrial Repolarization buried in the QRS complex)

Front 190

coronary vasoactive metabolite control of circulation

Back 190

Adenosine
Hypoxia

Front 191

What causes the fourth heart sound?

Back 191

Filling of the ventricle by atrial systole.

Front 192

Reynolds number and therefore tur is increased by the following factors

Back 192

dec blood viscosity
inc blood velocity

Front 193

Where is the pacemaker of the heart?

Back 193

SA node

Front 194

ECG representation of Ventricle Depolarization

Back 194

QRS complex

Front 195

cerebral vasoactive metabolite control of circulation

Back 195

CO2
H+

Front 196

What causes the first heart sound?

Back 196

Closing of the AV valves (mitral and then tricuspid).

Front 197

example of dec blood viscosity

Back 197

anemia, hematocrit

Front 198

How is Phase 4 of the SA nodal AP different from the other cardiac APs?

Back 198

It undergoes phase 4 depolarization. Phase 4 is unstable and derives automaticity from slow inward Na current depolarizing the cell

Front 199

PR interval is the interval between ______ & ________.

Back 199

Beginning of P wave (atrial depolar.)
to
Beginning of Q wave (initial Vent. dep.)

Front 200

muscular vasoactive metabolite control of circulation

Back 200

Lactate
K+
Adenosine

Front 201

In which phases of the cardiac cycle does atrial filling occur?

Back 201

Atrial filling begins during the rapid ventricular ejection and continues during the reduced ventricular ejection.

Front 202

Higher the elastance is the lower the?

Back 202

compliance is

Front 203

How is Phase 0 or the SA nodal AP different from the other cardiac APs?

Back 203

Membrane depolarization is due to influx of Ca in SA node, where the atrial, ventricular and purkinje APs are a result of Na currents

Front 204

Sympathetic stimulation affects PR interval how?

(why?)

Back 204

Decreases PR interval

(by increasing AV CV)

Front 205

pulmonary vasoactive metabolite control of circulation

Back 205

hypoxia constricts

Front 206

What is the “blip” in the aortic pressure tracing that occurs after closure of the aortic valve?

Back 206

Dicrotic notch, or incisura

Front 207

cmpliance is directly proportional to? and inversily?

Back 207

volume
pressure

Front 208

How are phases 1 and 2 different in the SA nodal AP different from the other cardiac APs

Back 208

Phases 1 and 2 do not exist in the SA nodal AP

Front 209

Parasympathetic stimulation affects PR interval how?

(why?)

Back 209

Increases PR interval

(by decreasing AV CV)

Front 210

vascular effects of histamine

Back 210

arteriolar vasodilation
venous vasoconstriction

**effect of increasing capillary pressure->edema

Front 211

What causes the third heart sound?

Back 211

Rapid flow of blood from the atria into the ventricles causes the third heart sound.

Front 212

Compliance is much greater for_____ than for _____

Back 212

veins than for arteries

Front 213

What determines the speed of the conduction velocity?

Back 213

size of inward current during phase 0 of the AP

Front 214

PR interval varies with heart property?

Back 214

CV through the AV node

Front 215

vascular effects of bradykinin

Back 215

arteriolar vasodilation
venous vasoconstriction

**increased capillary pressure -> edema

Front 216

What are the two most important mechanisms for regulating arterial pressure?

Back 216

Baroreceptor: Fast, neurally mediated
Renin-Angiotensin-Aldosterone: slower, hormonally regulated

Front 217

Capacitance of the arteries decreases with

Back 217

age

Front 218

Where is the conductance velocity fastest? Slowest?

Back 218

Fastest in the purkinje system and slowest in the AV node (to allow time for ventricular filling)

Front 219

ECG representation of the entire period of Ventricle Depolarization & Repolarization?

Back 219

QT interval

Front 220

serotonin vascular effects

Back 220

arteriolar vasoconstriction in response to blood vessel damage

Front 221

Where are the baroreceptors located?

Back 221

Baroreceptors are stretch receptors located within the walls of the carotid sinus near the bifurcation of the common carotid arteries.

Front 222

What are chronotropic effects?

Back 222

changes in heart rate

Front 223

QT interval is the interval from ______ to _______.

Back 223

Beginning of Q wave
to
End of the T wave

Front 224

What is Hering’s nerve? What cranial nerve is it a branch of?

Back 224

Hering’s nerve carries information from the baroreceptors of the carotid sinus to the vasomotor center in the brain stem. It is a branch of the glossopharyngeal nerve (CN IX).

Front 225

How are chronotropic effects elicited?

Back 225

by affecting the firing rate of the SA node

Front 226

ECG representation of the period when Ventricles are depolarization

Back 226

ST segment

Front 227

What are the four effects that attempt to increase the arterial pressure to normal (i.e. after acute hemorrhage?)

Back 227

1) Increased heart rate: resulting from decreased parasympathetic and increased sympathetic tone to the SA node of the heart
2) Increased contractility and stroke volume
3) Increased vasocontriction of arterioles
4) Increased vasocontriction of veins
Note: All effects result from increased sympathetic tone

Front 228

What are Dromotropic effects?

Back 228

changes in conduction velocity, primarily in AV node.

Front 229

ECG representation of Ventricle repolarization

Back 229

T wave

Front 230

How can you test the baroreceptor mechanism?

Back 230

Valsalva maneuver. Expiring against a closed glottis causes an increase in intrathoracic pressure, which decreases venous return -> decreased cardiac output and arterial pressure (Pa).
If the baroreceptor is intact, the decrease in Pa is sensed and leads to an increase in sympathetic outflow to the heart and blood vessels. In the test, an increase in heart rate would be noted.

Front 231

How do dromotropic changes affect ECG readings?

Back 231

negative dromotropic effects, slow AV conduction and increase PR interval; positive dromotropic effects are the opposite.

Front 232

ST segment is the period from ______ to ______.

Back 232

END of the S wave
to
Beginning of T wave

Front 233

What causes the secretion of renin? What secretes renin?

Back 233

A decrease in renal perfusion pressure causes the juxtaglomerular cells of the afferent arteriole to secrete renin.

Front 234

Which parts of the heart have parasympathetic vagal innervation?

Back 234

SA node, atria, AV node.

Front 235

ECG representation that is ISOELECTRIC.

Back 235

ST segment

Front 236

What happens during cerebral ischemia?

Back 236

Partial pressure of CO2 (PCO2) in brain tissue increases -> Chemoreceptors in the vasomotor center respond by increasing sympathetic outflow to the heart and blood vessels -> constriction of arterioles causes intense peripheral vasoconstriction and increased TPR.

Front 237

What receptors does ACh affect in the heart and what are the effects?

Back 237

Muscarinic receptors; causes decrease in HR, decreased conduction velocity through AV node, decreases contractility of atria

Front 238

What kind of current movement DEPOLARIZES?

Back 238

Inward current

(brings positive charges inward)

Front 239

Besides baroreceptors and chemoreceptors, what else regulates arterial blood pressure? What are they in response to? What is their mechanism?

Back 239

Vasopressin:
released from posterior pituitary
in response to hemorrhage;
is a potent vasoconstrictor
that increases TPR by activating
V1 receptors on arterioles; increases
water reabsorption by the renal distal
tubule and collecting ducts by activating V2 receptors.

Atrial natriuretic peptide (ANP):
released from atria in response to increase in blood volume and atrial pressure; causes relaxation of vascular smooth muscle, dilation of arterioles, and decreased TPR; causes increased excretion of Na and water by the kidney; inhibits renin secretion.

Front 240

what is the mechanism of decreased dromotropic effect?

Back 240

decreased inward Ca current and increased relative outward K current causing longer APs

Front 241

What kind of current movement HYPERPOLARIZES/REPOLARIZES?

Back 241

Outward current

(brings positive current outward)

Front 242

What is blood flow through the capillaries regulated by?

Back 242

Contraction and relaxation of the arterioles and the precapillary sphincters (smooth muscle bands at the arteriole-capillary junctions).

Front 243

These receptors cause constriction of skin, splanchnic, and skeletal vascular smooth muscle

Back 243

alpha-1 adrenergic receptors

Front 244

Resting Membrane Potential in Cardiac AP is determined by?

Vm approaches what potential?

Back 244

K+ conductance

K+ equilibrium potential
(approx. - 90mV)

Front 245

When does edema occur?

Back 245

Edema occurs when the volume of interstitial fluid exceeds the capacity of the lymphatics to return it to the circulation. This can be caused by excess filtration or blocked lymphatics.

Front 246

these receptors cause relaxation of skeletal muscle

Back 246

Beta-2 adrenergic receptors

Front 247

What maintains the ionic gradient across cell membranes in the Cardiac AP?

Back 247

Na+/K+ ATPase

(Na+/K+ Adenosine Phosphatase)

Front 248

What effect does Histamine have on the blood flow?

Back 248

Histamine causes arteriolar dilation and venous constriction. The combined effects cause increased Pc and increased filtration out of the capillaries, resulting in local edema. Histamine is released in response to tissue trauma.

Front 249

What is the mechanism of the positive chronotropic effect?

Back 249

increased inward Na current during phase 4 depolarization in SA node

Front 250

VENTRICLES, ATRIA, PURKINJE SYSTEM

- Phase 0 character?

- Phase 0 is caused by?

Back 250

Upstroke

Increased Na+ conductance
(inward current)

Front 251

What effect does Bradykinin have on the blood flow?

Back 251

Bradykinin causes arteriolar dilation and venous constriction, and produces increased filtration out of the capillaries (similar to histamine). It also causes local edema.

Front 252

how do cardiac muscles communicate?

Back 252

through gap junctions

Front 253

VENTRICLES, ATRIA, PURKINJE SYSTEM

- Phase 1 character?

- Phase 1 is caused by?

Back 253

Initial Repolarization

1.) Increased K+ conductance
(outward)
2.) Decreased Na+ conductance
(inward)

Front 254

What effect does Serotonin (5-hydroxytryptamine) have on the blood flow?

Back 254

Serotonin causes arteriolar constriction and is released in response to blood vessel damage to help prevent blood loss. Serotonin has also been implicated in the vascular spasms of migraine headaches.

Front 255

where is Ca stored for excitation-contraction coupling?

Back 255

in the Sarcoplasmic Reticulum

Front 256

VENTRICLES, ATRIA, PURKINJE SYSTEM

- Phase 2 character?

- Phase 2 is caused by?

Back 256

Plateau

Increased Calcium conductance
(inward current)

(which equals increased K+ conductance outward)

Front 257

What effect do Prostaglandins have on the blood flow?

Back 257

Prostacyclin (PGI2) is a vasodilator in several vascular beds.
E-series prostaglandins are vasodilators
F-series prostaglandins are vasoconstrictors
Thromboxane A2 is a vasoconstrictor

Front 258

how does an influx of Ca cause muscle contraction?

Back 258

Ca binds to troponin C, causing tropomyosin to cease the inhibition of actin and myosin binding.

Front 259

VENTRICLES, ATRIA, PURKINJE SYSTEM

- Phase 3 character?

- Phase 3 is caused by?

Back 259

Repolarization

Increased K+ current outward (I k)

Front 260

What is the difference between active and reactive hyperemia?

Back 260

Active hyperemia is an increased blood flow that is proportional to its increased metabolic activity (i.e. skeletal muscles)
Reactive hyperemia is an increase in blood flow to an organ that occurs after a period of occlusion of flow. The longer the period of occlusion is, the greater the increase in blood flow is above preocclusion levels.

Front 261

How does one estimate cardiac contractility?

Back 261

Ejection Fraction (stroke volume / end-diastolic volume)

Front 262

VENTRICLES, ATRIA, PURKINJE SYSTEM

- Phase 4 character?

- Phase 4 is caused by?

Back 262

Resting membrane potential

Increased K+ conductance ( I k1)

Front 263

W1. hat special circulations are controlled almost entirely by local metabolic factors? What are those vasoactive metabolites/metabolic factors?

Back 263

Coronary circulation: Hypoxia, Adenosine
Cerebral circulation: CO2, H+
Muscle (during exercise): Lactate, K+, Adenosine
Pulmonary: Hypoxia vasoconstricts

Front 264

What is the normal EF?

Back 264

0.55

Front 265

SA > AV > His-Purkinje system

describes what intrinsic rate?

Back 265

Phase 4 Depolarization

(aka - Automaticity)

Front 266

What special circulations are controlled almost entirely by sympathetic control?

Back 266

Muscle (at rest): α1 receptor causes vasoconstriction; β2 receptor causes vasodilation.
Skin (temperature regulation)

Front 267

What are three factors that increase contractility?

Back 267

increased heart rate, sympathetic stimulation (catecholamines) via Beta-1 receptors, and cardiac glycosides (digitalis)

Front 268

SA / AV / HIS-PURKINJE SYSTEM

- Phase 0 character?

- Phase 0 is caused by?

Back 268

Upstroke

Increased Calcium current (inward)

Front 269

What are the changes that occur when an individual moves from a supine position to a standing position?

Back 269

1) When a person stands, a significant amount of blood pools in the lower extremities because of the high compliance of the veins.
2) Pc in the legs increases and fluid is filtered into the interstitium. If net filtration exceeds the ability of the lymphatics to return it to circulation, edema occurs.
3) Blood volume and venous return decrease, resulting in both stroke volume and cardiac output decreasing
4) Arterial pressure decreases because of the reduction of cardiac output. If cerebral blood pressure is low enough, fainting may occur
5) Compensatory mechanisms attempt to increase blood pressure to normal. Carotid sinus baroreceptors decrease firing -> increased sympathetic outflow

Front 270

By what mechanism does digitalis increase the force of contraction?

Back 270

inhibiting Na,K-ATPase in the myocardial cell membrane

Front 271

SA / AV / HIS-PURKINJE SYSTEM

- Phase 1 character?

- Phase 1 is caused by?

Back 271

does not exist
in the SA/AV/His-Purkinje system

Front 272

What is orthostatic hypotension?

Back 272

Fainting or lightheadedness on standing, may occur in individuals whose baroreceptor reflex mechanism is impaired (e.g. individuals treated with sympatholytic agents)

Front 273

What factors decrease contractility?

Back 273

parasympathetic ACh stimulation in the atria

Front 274

SA / AV / HIS-PURKINJE SYSTEM

- Phase 2 character?

- Phase 2 is caused by?

Back 274

does not exist
in the SA/AV/His-Purkinje system

Front 275

What are the changes that occur with exercise?

Back 275

A) The central command (anticipation of exercise)
-sympathetic outflow to the heart and blood vessels is increased, parasympathetic outflow is decreased -> heart rate and contractility increased
-cardiac output is increased
-venous return is increased
-arteriolar resistance in skin, splanchnic regions, kidneys, and inactive muscles is increased
B) Increased metabolic activity of skeletal muscle
-vasodilator metabolites (lactate, K+, adenosine) accumulate because of increased metabolism of muscle
-these metabolites cause arteriolar dilation in the active skeletal muscle, increasing muscle blood flow (active hyperemia)
-as a result of increased blood flow, O2 delivery is increased
-vasodilation accounts for the overall decrease in TPR that occurs with exercise.

Front 276

What is preload?

Back 276

it is equivalent to end-diastolic volume, which is related to right atrial pressure

Front 277

SA / AV / HIS-PURKINJE SYSTEM

- Phase 3 character?

- Phase 3 is caused by?

Back 277

Repolarization

Increase K+ conductance (outward)

Front 278

What are the compensatory responses to acute blood loss?

Back 278

1) A decrease in blood volume produces a decrease in mean systemic pressure -> decreased cardiac output and arterial pressure
2) Carotid sinus baroreceptors detect decreased arterial pressure -> increased sympathetic outflow to heart and blood vessels and decreased parasympathetic outflow to the heart -> increased heart rate, increased contractility, increased TPR (arteriolar constriction, except in coronary and cerebral vessels)
3) Chemoreceptors in the carotid and aortic bodies sense hypoxia -> increase sympathetic outflow
4) Cerebral ischemia (If present) causes an increase in PCO2 -> increases sympathetic outflow
5) Arteriolar vasoconstriction causes a decrease in Pc -> capillary absorption is favored
6) Adrenal medulla releases epinephrine and NE
7) Renin-angiotensin-aldosterone system is activated
8) ADH is released when atrial receptors detect decreased blood volume.

Front 279

What is afterload?

Back 279

determined in the LV by aortic pressure, and in the RV by pulmonary artery pressure

Front 280

SA / AV / HIS-PURKINJE SYSTEM

- Phase 4 character?

- Phase 4 is caused by?

Back 280

SLOW Depolarization

Increase Na+ conductance (inward)
(I f)

Front 281

What are the changes that occur when an individual moves from a supine position to a standing position?

Back 281

1) When a person stands, a significant amount of blood pools in the lower extremities because of the high compliance of the veins.
2) Pc in the legs increases and fluid is filtered into the interstitium. If net filtration exceeds the ability of the lymphatics to return it to circulation, edema occurs.
3) Blood volume and venous return decrease, resulting in both stroke volume and cardiac output decreasing
4) Arterial pressure decreases because of the reduction of cardiac output. If cerebral blood pressure is low enough, fainting may occur
5) Compensatory mechanisms attempt to increase blood pressure to normal. Carotid sinus baroreceptors decrease firing -> increased sympathetic outflow

Front 282

What is the Frank-Starling relationship?

Back 282

an increase in preload results in stretching of the sarcomere, and a resulting increase in developed tension (and increase in SV).

Front 283

SA / AV / HIS-PURKINJE SYSTEM

- I (subscript f) is what kind of current?

- I (subscript f) occurs in which phase of what type?

Back 283

Inward Na+ current

Phase 4 (slow depolarization)
of
SA/AV/His-Purkinje system

Front 284

What is orthostatic hypotension?

Back 284

Fainting or lightheadedness on standing, may occur in individuals whose baroreceptor reflex mechanism is impaired (e.g. individuals treated with sympatholytic agents)

Front 285

what is the mechanism that matches cardiac output to venous return?

Back 285

Frank-Starling relationship

Front 286

SA / AV / HIS-PURKINJE SYSTEM

- I (subscript f) is turned on by what?

Back 286

Repolarization of the preceding AP

Front 287

What are the changes that occur with exercise?

Back 287

A) The central command (anticipation of exercise)
-sympathetic outflow to the heart and blood vessels is increased, parasympathetic outflow is decreased -> heart rate and contractility increased
-cardiac output is increased
-venous return is increased
-arteriolar resistance in skin, splanchnic regions, kidneys, and inactive muscles is increased
B) Increased metabolic activity of skeletal muscle
-vasodilator metabolites (lactate, K+, adenosine) accumulate because of increased metabolism of muscle
-these metabolites cause arteriolar dilation in the active skeletal muscle, increasing muscle blood flow (active hyperemia)
-as a result of increased blood flow, O2 delivery is increased
-vasodilation accounts for the overall decrease in TPR that occurs with exercise.

Front 288

What phase of the pressure-volume ventricular diagram is altered by an increase in preload?

Back 288

end-diastolic volume is increased, so the isovolumetric contraction phase is shifted to the right and increases stroke volume

Front 289

What phases are seen in atria/verntricle/purkinje system, but NOT seen in SA/AV/His-purkinje system?

Back 289

Phase 1 & 2

Front 290

What are the compensatory responses to acute blood loss?

Back 290

1) A decrease in blood volume produces a decrease in mean systemic pressure -> decreased cardiac output and arterial pressure
2) Carotid sinus baroreceptors detect decreased arterial pressure -> increased sympathetic outflow to heart and blood vessels and decreased parasympathetic outflow to the heart -> increased heart rate, increased contractility, increased TPR (arteriolar constriction, except in coronary and cerebral vessels)
3) Chemoreceptors in the carotid and aortic bodies sense hypoxia -> increase sympathetic outflow
4) Cerebral ischemia (If present) causes an increase in PCO2 -> increases sympathetic outflow
5) Arteriolar vasoconstriction causes a decrease in Pc -> capillary absorption is favored
6) Adrenal medulla releases epinephrine and NE
7) Renin-angiotensin-aldosterone system is activated
8) ADH is released when atrial receptors detect decreased blood volume.

Front 291

What phase of the pressure-volume ventricular diagram is altered by an increase in afterload?

Back 291

an increase in aortic pressure will create more resistance to LV contraction. The end-systolic volume will shift right (increase), causing a decrease in stroke volume

Front 292

I (subscript k1) is what kind of current?

I (subscript k1) is seen in which phase of what type?

Back 292

Outward K+ current

Phase 4 of Atria/Ventricle/Purkinje system

Front 293

What phase of the pressure-volume ventricular diagram is altered by an increase in contractility?

Back 293

this results in an increase in LV pressure during systole, reducing the end-systolic LV volume and increasing stroke volume

Front 294

Conduction Velocity depends on what?

Back 294

SIZE of the Inward current during Upstroke

(thus Size of the Calcium current)

Front 295

What factors increase Mean systemic pressure?

Back 295

increase in blood volume or decrease in venous compliance

Front 296

Conduction Velocity is Fastest where?

CV is slowest where?

Back 296

Purkinje system

AV node

Front 297

an increase in blood volume has what effect on cardiac output and right atrial pressure?

Back 297

both are increased

Front 298

Why is it beneficial for AV node to have a slow CV?

Back 298

allows time for ventricles to fill before contraction

Front 299

What effect does an increase in TPR have on CO, venous return, and right arterial pressure?

Back 299

CO and venous return are decreased but RA pressure is unchanged

Front 300

Changes in cardiac AP Excitability are described by?

Back 300

Refractory periods

Front 301

how is the stroke volume calculated?

Back 301

end-diastolic volume - end-systolic volume

Front 302

Absolute Refractory Period (ARP) begins when?

ARP ends when?

Back 302

Begins @ the Upstroke

Ends after Plateau

Front 303

calculation for cardiac output?

Back 303

CO = stroke volume x heart rate

Front 304

Which is slightly longer than the ARP?

Back 304

Effective Refractory Period (ERP)

Front 305

what is the primary energy source for cardiac stroke work?

Back 305

fatty acids

Front 306

What period occurs immediately after the ARP?

Back 306

Relative Refractory Period (RRP)

Front 307

Cardiac oxygen consumption is increased by what?

Back 307

afterload, size of heart, contractility, heart rate

Front 308

Which refractory period can there be NO action potential initiated?

Back 308

ARP

Front 309

what is the cardiac output in terms of O2 consumption?

Back 309

CO = O2 consumption / (PaO2 - PvO2)

Front 310

Which refractory period can CONDUCTED action potential be NOT elicited?

Back 310

ERP

Front 311

during what phase of the cardiac cycle do you hear the first heart sound? what causes the sound?

Back 311

heard during isovolumetric contraction. caused by closure of the mitral and tricuspid valves

Front 312

Which refractory period can AP be elicited BUT more than usual INWARD current is required?

Back 312

RRP

Front 313

Define Chronotropic (specify locale)

Back 313

ANS effects on HR for the SA node

Front 314

during what phase of the cardiac cycle do you hear the second heart sound? what causes the sound?

Back 314

heard during isovolumetric relaxation. caused by closure of the aortic and pulmonic valves

Front 315

Define Dromotropic (specify locale)

Back 315

ANS effects on CV for the AV node

Front 316

what and where are baroreceptors?

Back 316

stretch receptors found within the walls of the carotid sinus

Front 317

ANS can exert positive/negative Chronotropic effects by doing what to the SA node??

Back 317

By increasing/decreasing
the
FIRING RATE of the SA node

Front 318

What happens to the baroreceptors when there is a decrease in arterial pressure?

Back 318

reduced stretch in baroreceptors --> reduced firing of APs in baroreceptors --> decreased sympathetic outflow to heart and blood vessels by vasomotor center

Front 319

ANS can exert positive/negative Dromotropic effects by doing what to the AV node?

Back 319

By increasing/decreasing
the
CONDUCTION VELOCITY of the AV node

Front 320

what are the end effects of an attempt to increase arterial pressure from baroreceptor activation?

Back 320

increased heart rate, increased contractility and stroke volume, increased vasoconstriction of arterioles, increased vasoconstriction of veins

Front 321

Conduction Velocity of the AV node is INVERSELY proportional to what ECG finding?

Back 321

PR interval

(thus Increase AV CV will decrease PR)

Front 322

What causes the release of Renin?

Back 322

decrease in renal perfusion pressure causes juxtaglomerular cells of the afferent arteriole to secrete renin

Front 323

Sympathetic effects on chronotropy and dromotropy via what NT?

- which acts on what receptor?

Back 323

NE

Beta 1 receptors

Front 324

What is the function of renin?

Back 324

converts angiotensinogen to angiotensin I

Front 325

Parasympathetic effects on chronotropy and dromotropy via what NT?

- which acts on what receptor?

Back 325

Acetylcholine

Muscarinic receptors

Front 326

What are the effects of angiotensin II?

Back 326

stimulates secretion of aldosterone by adrenal cortex (increases Na reabsorption in by renal distal tubule) and causes vasoconstriction of efferent arterioles, increasing TPR and MAP

Front 327

Sympathetic effects on Chronotropy?

- what is the MOA?
(include current, phase & locale)

Back 327

Positive (increase HR)

Increase inward Na+ current (If)
@ phase 4 slow depolarization of SA node

Front 328

What is the cushing reaction?

Back 328

increases in intracranial pressure cause compression of cerebral blood flow --> cerebral ischemia --> increase in sympathetic outflow to heart and blood vessels to correct for cerebral ischemia --> profound increase in arterial pressure

Front 329

Sympathetic effects on Dromotropy?

- what is the MOA?
(include current, phase & locale)

Back 329

Positive (increase AV CV)

Increase inward Ca+ current (Ica)
@ phase 0 upstroke of AV node

Front 330

ADH acts on which receptors to cause vasoconstriction?

Back 330

V1 receptors

Front 331

Parasympathetic effects on Chronotropy?

- what is the MOA?
(include current, phase & locale)

Back 331

Negative (decreases HR)

Decreases Inward Na+ current (If)
@ Phase 4 Depolarization of SA node

Front 332

ADH acts on what receptors in the renal distal tubule and collecting ducts to increase water reabsorption?

Back 332

V2 receptors

Front 333

Parasympathetic effects on Dromotropy?

- what is the MOA?
(include current, phase & locale)

Back 333

Negative (decrease AV CV)

Decreases Inward Ca+ current (Ica)
@ phase 0 Upstroke of AV

Front 334

What is the function of ANP?

Back 334

released from RA due to increased atrial pressure --> causes relaxation of vascular smooth muscle, decreasing TPR --> also causes increased excretion of Na and water by kidney to reduce blood volume --> inhibits renin secretion

Front 335

Sympathetic effects on Heart

(also include receptors)

Back 335

Increase HR, AV CV, & Contractility

(all via Beta1 receptor with NE)

Front 336

What factors increase filtration out of the capillary?

Back 336

increased capillary hydrostatic pressure and interstitial osmotic pressure and decreased interstitial hydrostatic pressure and capillary osmotic pressure

Front 337

Parasympathetic effects on Heart

(also include receptors)

Back 337

Decrease HR, AV CV

Decrease Contractility @ ATRIA only!

(all via Muscarinic receptor with ACh)

Front 338

what is the mechanism and function of NO?

Back 338

causes relaxation of smooth muscle by stimulating guanylate cyclase, which produces cGMP.

Front 339

Sympathetic effects on Blood Vessel (in other words, the vascular SM)

(also include receptors)

Back 339

@ Alpha 1 receptor, Constriction
of
Skin, Splanchnic, & Skeletal muscle BV

@ Beta2 receptor, Relaxation
of
Skeletal muscle BV

Front 340

what products of metabolic activity will cause a local increase in perfusion?

Back 340

CO2, H, K, lactate, adenosine

Front 341

Parasympathetic effects on Blood Vessel
(in other words, the vascular SM)

(also include receptors)

Back 341

Parasympathetics have NO effects on the blood vessels

Front 342

histamine does what to blood vessels?

Back 342

arteriolar dilation and venous constriction, resulting in increased capillary hydrostatic pressure and increased filtration

Front 343

What is unique about the ANS effects on Contractility in terms of locale?

Back 343

Sympathetics increase Contractility

Parasympathetics decrease Contractility @ the Atria ONLY!

Front 344

bradykinin does what to blood vessels?

Back 344

arteriolar dilation and venous constriction, resulting in increased capillary hydrostatic pressure and increased filtration

Front 345

Upstroke is which phase of the cardiac AP cycle?

Back 345

Phase 0

Front 346

By what mechanism does edema occur?

Back 346

filtration through capillary beds exceeds lymph drainage capacity.

Front 347

Upstroke is due to what for:

- Non-automaticity cells?

- Automaticity cells?

Back 347

Non-automaticity cells
= Na+ conductance (inward)

Automaticity cells
= Ca+ conductance (inward)

Front 348

serotonin does what to blood vessels?

Back 348

it causes arteriolar constriction and is releasedin response to blood vessel damage to help prevent blood loss. it has been implicated in vascular spasms of migraine headaches

Front 349

Increased Calcium conductance occurs in which phase for

- Non-automaticity cells?

- for Automaticity cells?

Back 349

Phase 2 (Plateau)

Phase 0 (upstroke)

Front 350

which prostaglandins cause vasoconstriction?

Back 350

F-series prostaglandins and Thromboxane A2

Front 351

Slow Depolarization of Automaticity cells is in which phase?

This is due to what current?

Back 351

Phase 4

Na+ conductance (I subscript f)

Front 352

which prostaglandins cause vasodilation?

Back 352

DIE-AE prostaglandin D, I, E1 and E2 and A2

Front 353

K+ conductance (I subscript k) occurs in which phases for non-automaticity cells and automaticity cells?

Back 353

Phase 3 for both

Front 354

what are the most important local metabolic factors in the coronary circulation?

Back 354

hypoxia and adenosine

Front 355

I (subscript f) is what & occurs when?

Back 355

Na+ conductance (inward)
& Phase 4 of Automaticity cells

Front 356

what controls the cerebral circulation?

Back 356

metabolic factors almost exclusively

Front 357

I (subscript k1) is what & occurs when?

Back 357

K+ conductance (outward)
& Phase 4 of Non-automaticity cells

Front 358

what factor causes cerebral artery vasodilation?

Back 358

CO2

Front 359

What type of current is always Outward (thus hyperpolarizing/repolarizing)?

Back 359

K+ current conductance

Front 360

what are the effects on the CV system during exercise?

Back 360

increased sympathetic outflow; increased CO; increased venous return; arteriolar resistance in skin, splanchnic regions, kidneys and inactive muscles is increased

Front 361

Plateau phase occurs in which cells?

Plateau phase is due to what current?

Plateau phase is which phase?

Back 361

Non-automaticity cells

Calcium conductance (inward)

Phase 2

Front 362

ANS control of Chronotropy occurs by affecting ......
- what current?
- of what phase?
- in which cells?

Back 362

I (subscript f) - Na+ conductance inward

Phase 4 (Slow Depolarization)

Automaticity cells (SA node)

Front 363

ANS control of Dromotropy occurs by affecting ......
- what current?
- of what phase?
- in which cells?

Back 363

Ica (Calcium conductance inward)

Phase 0 (Upstroke)

Automaticity cells (AV node)