Xx - Cv Physiology Uw

Front 1

Cardiac muscle gets venous drainage via what vessel? (located where?)

Back 1

Coronary Sinus (@ Right Atrium)

(remaining venous blood will drain directly into the heart chambers)

Front 2

Cardiac muscle is mostly perfused during what period?

Back 2

Diastole

Front 3

Characteristics of LV Perfusion

Back 3

10% of total perfusion @ Systole

(occurs thru LV capillaries)

Front 4

Coronary Blood Flow reduction is Highest in which cells?

Occurs during what period?

Why?

Back 4

LV Subendocardium myocytes

Systole

Greatest contraction occurs at the LV subendocardium, thus causing greatest compression of coronary vessels.
(thus reduction in coronary BF)

Front 5

Cardiac Blood Flow Perfusion consumes what percentage of Cardiac Output?

Back 5

5% of CO

Front 6

Cardiac Myocytes have the highest consumption of?

Back 6

O2

Front 7

Coronary Perfusion Regulation is primarily controlled via what process?

What are the primary factors involved?

Other vasodilator effectors?
Other vasoconstrictor effectors?

Back 7

Local Factors

Hypoxia & Adenosine (Vasodilators)

VD ==> NO & Alpha-adrenergics
VC ==> Beta-adrenergics

Front 8

Vascular Blood Flow is proportional to?

Vascular Blood Flow is Inversely Proportional to?

Back 8

(proportional to) ==> radius^4

(inversely proportional to) ==> Resistance

Front 9

Decreased pH, Bicarb, & pCO2

(which one is compensatory)

Back 9

Metabolic Acidosis

(pCO2 decrease is compensatory)

Front 10

Increased pH, Bicarb, & pCO2

(which one is compensatory)

Back 10

Metabolic Alkalosis

(pCO2 increase is compensatory)

Front 11

Decreased pH
Increased Bicarb & pCO2

(which is compensatory)

Back 11

Respiratory Acidosis

(Increased Bicarb)

Front 12

Increased pH
Decreased Bicarb & pCO2

(which is compensatory)

Back 12

Respiratory Alkalosis

(Decreased Bicarb)

Front 13

DKA signs & symptoms

Back 13

Metabolic Acidosis (ketoacidosis)

(DATA)
Dehydration
Altered Mental Status (confusion)
Tachypnea
Abdominal pain

Front 14

Primary Tx for DKA

Back 14

Insulin & Fluids

Front 15

In treating DKA, Insulin increases & decreases what?

Back 15

Increases Bicarb
(glucose uptake decreases lipolysis, thus decreasing ketones, which causes Bicarb increase)

Decreased Glucose
Decreased Potassium
(insulin causes Intracellular Shift of K+)

Front 16

In treating DKA, Fluid hydration increases and decreases what?

Back 16

Increase Sodium (Na+)

Decrease Osmolarity

Front 17

Insulin causes intracellular shift of what ions?

Back 17

Potassium

Front 18

Opioid OD causes what respiratory change?

What pathology does this cause?

Back 18

Hypoventilation

Respiratory Acidosis

Front 19

Mineralocorticoids retains what?

Mineralocorticoids waste what?

Back 19

(retains) Na+ & Water

(wastes) Postissum

Front 20

Thyroxine causes what osmolar changes?

Thyroxine causes what fluid change?

Back 20

Decreased Na+ & H2O

ECF expansion

Front 21

What process has properties of NO Carrier Proteins & NO Saturation?

Back 21

Simple Diffusion

Front 22

What process has properties of Carrier Proteins & Saturation?

Back 22

Facilitated Diffusion

Front 23

Max & Min Pressures of:

- Right Atria
- Right Ventricle
- Pulmonary Artery

Back 23

10 / 0

25 / 4

25 / 10

Front 24

Max & Min Pressures of:

- Left Atria
- Left Ventricle
- Aorta

Back 24

12 / 2

130 / 10

130 / 70

Front 25

Which heart side has greater pressure?

Back 25

Left side > Right side

Front 26

ANP is produced by?

ANP released in response to?

Back 26

Atrial myocytes

Hypertension & Hypervolemia

Front 27

ANP functions?


Overall effect of ANP on CV properties

Back 27

(ANP)

Arteriolar vasoDilation
Natretic/Diuretic
Prevents Renin

Decreased TPR

Front 28

Resting membrane potential in Heart?

Resting membrane potential in Skeletal muscle?

Why difference important?

Back 28

- 90 mV

-75 mV

Higher Negative Vm in cardiocytes means larger stimulus required to excite cells, thus preventing arrythmias

Front 29

Phase 2 Plateau stage involves what kind of channels?

Back 29

L-Type Calcium Voltage-gated channels

Front 30

MCC of Palpitations is?

Back 30

Anxiety

Front 31

Atrial Fibrillation signs & symptoms

Back 31

(CIITA)

Conscious w/
Irregularly Irregular Tachy-Arrythmia

Front 32

Atrial Fibrillation is the Most Common what?

Back 32

Chronic Arrythmia

Front 33

Acute, isolated episodes of Atrial Fibrillation can be seen with what conditions?

Back 33

Alcohol Binging ("Holiday Heart Syndrome")
Increased Sympathetic tone
Pericarditis

Front 34

Atrial Fibrillation has what EKG findings?

Back 34

(ATRI-al fibrillation)

Absent P wave
Tachycardia
R-R variability
Irregularly irregular QRS

Front 35

Prolonged-QT is associated with what marked property?

Prolonged-QT predisposes to what condition?

Back 35

Markedly increased HR

Torsade De Pointes
(unique V-tachy)

Front 36

Prolonged-QRS has a normal what?

Back 36

Normal HR

Front 37

MCC of Prolonged-QRS?

Back 37

BBB

Front 38

High-QRS-Voltage
(aka - High Voltage of Precordial Leads)
- has what QRS characters

Back 38

No irregularities

Front 39

High-QRS-Voltage
(aka - High Voltage of Precordial Leads)
- indicates what condition?
- usually due to what condition?

Back 39

Ventricular Hypertrophy

Prolonged, Untreated HTN

Front 40

Absent P-wave
Tachycardia
R-R variability
Irregularly irregular QRS

Back 40

Atrial Fibrillation

Front 41

Absent P-wave
Bradycardia
Normal QRS

Back 41

3rd degree AV block

(aka - Complete AV Block)

Front 42

Absent P-wave
Bradycardia
Abnormal QRS
(prolonged, abnormal shaped QRS)

Back 42

Pacemaker @ Below AV (purkinje)

Front 43

Inspiration causes what pressure change?

Back 43

Decreased Intrathoracic Pressure

Front 44

Cardiac Failure stimulates what compensatory physiological mechanisms?

Back 44

Sympathetics
&
RAAS

Front 45

Renin is made by what cells?

Cells are located where vascularly?

Back 45

JGA cells

Afferent arteriole (of renals)

Front 46

Angiotensinogen is made where?

Back 46

Liver

Front 47

ACE is made by what cells?

Back 47

Pulmonary Vascular ENDOThelium

Front 48

ACE functions? x2

Back 48

Converts Angiotensin I to Angiotensin II

Breaks down Bradykinin

Front 49

Aldosterone is made by cells where?

Back 49

Zona Glomerulosa
(of adrenal cortex)

Front 50

Aldosterone is produced in response to what signals?

Back 50

Angiotensin II
&
Hyperkalemia

Front 51

PV LOOP

How does Infusion of Normal Saline change the vascular volume?

How does this affect SV?

How does this affect the PV Loop?

What other pathologies cause same events to PV LOOP?

Back 51

Increases PRELOAD

Increase SV

Increases Width to the right

Any fluid overload scenario
(i.e. - Renal Failure, HF, NS infusion)

Front 52

PV LOOP

Loss of myocardial cells cause what changes in terms of CV function?

How does this affect the SV?

How does this affect the PV Loop?

Is this a systolic or diastolic dysf(x)?

Back 52

Decrease Contractility
(b/c less myocytes to contract)

Decrease SV (thus less EF)

Decreases Width from left

Systolic
(systolic is cardiac contraction)
(diastolic is cardiac innervation)

Front 53

Upon entering cells via voltage-gated L-type Calcium channels, Ca2+ will bind to what receptor on the SR?

Back 53

Ryanodine receptors

Front 54

Cardiomyocyte relaxation occurs by Ca2+ efflux via what 2 transporters?

Back 54

1.) Ca2+ ATPase

2.) Na+/Ca++ Exchanger
(does not require ATP)

Front 55

What molecule acts as an INDIRECT contributor for Ca2+ efflux in cardiomyocyte relaxation?

This molecule binds what?

What is the effect of this binding?

Back 55

Calmodulin

Binds Ca2+ ATPase

Removes intracellular Ca++ by hydrolyzing ATP

Front 56

During normal Diastole, when the Mitral Valve is open, what 2 pressures are nearly equal?

Back 56

LAP ~ LVP
(or LAEDP ~ LVEDP)

(due to minimal resistance btw LA & LV)

Front 57

What variable can used in the measurement of LAEDP (LAP)

Back 57

PCWP

(Pulmonary Capillary Wedge Pressure)

Front 58

Under what pathology would PCWP (or LAEDP) be significantly elevated relative to LVEDP?

(PCWP or LAEDP >> LVEDP)

Back 58

Mitral Stenosis

(thus marked increased resistance btw LA & LV, with LAP being much greater)

Front 59

Short Acting BALANCED Vasodilator?

Back 59

Nitroprusside

Front 60

Nitroprusside affects Preload how?

Nitroprusside affects Afterload how?

Nitroprusside affects SV how?

Back 60

Decreases

Decreases
(to same extent as Preload b/c Balanced)

No change in stroke volume
(b/c equal decreases btw preload & afterload)

Front 61

In acute hemorrhage, what is the initial compensatory physiological response once the blood loss is significant (~ >10%)

If the hemorrhage persists Massively and Chronically, then what can it lead to?

Back 61

Sympathetics

Hypovolemic shock

Front 62

In what pathology is the Sympathetic response stimulation MAXED out?

Why clinically relevant?

Back 62

HYPOVolemic SHOCK!

Vasopressors are of little & temporary benefit.

Front 63

In Hypovolemic Shock, what is the primary treatment?

Back 63

Crystalloid FLUIDS

(i.e. - Normal Saline)

Front 64

Infusion of crystaloid fluids (i.e. NS) in treating Hypovolemic Shock, causes what volume changes?

This volume change causes what change in cardiomyoctes?

Thus causing what change in CV properties?

Back 64

Increased PRELOAD
(due to incr. intravascular volume)

Increases ventricular
END-DIASTOLIC
SARCOMERE LENGTH

Thus, increased CO & SV

Front 65

Aortic Arch Baroreceptors have what afferent nerve?

Baroreceptors at the Bifurcation of the Common Carotid Artery (@ Carotid Sinus) have what afferents?

Back 65

Vagus (CN X)

Glossopharyngeal (CN IX)
(aka: Hering nerve, Carotid sinus nerve)

Front 66

What CN nucleus does the afferents of the Baroreceptors @ Aortic Arch & Carotid Sinus travel to?

(what part of brain is that?)

Back 66

Solitary Nucleus

(of Medulla)

Front 67

External Pressure on the Carotid Sinus (Carotid massage) stimulate the baroreceptor afferents how?

How does this affect vascular radius?

Back 67

Increase it's Firing rate
(baroreceptors act as if Systemic BP increased)

VasoDILATION

Front 68

External Pressure on the Carotid Sinus (Carotid massage) manifest on to the patient with what signs?

Back 68

Bradycardia
HYPOTension
Syncope (possibly)

Front 69

What is the most important mediator of Coronary vasoDILATION of LARGE Arteries?

Back 69

Nitric Oxide (NO)

Front 70

What is the most important mediator of Coronary vasoDILATION of SMALL Arteries?

Back 70

Adenosine
(byproduct of ATP metabolism)

Front 71

Nitric Oxide (NO) is synthesized by what cells?

NO is synthesized from compounds?

Via what enzyme?

Back 71

Endothelial cellls

Arginine & O2

endothelial NO Synthase (eNOS)

Front 72

NO vasodilates large vessel coronary by relaxing SM via what Secondary messenger system?

Back 72

G-Protein --> cGMP

messenger system

Front 73

What is the significance of the Autonomic Nervous system on Coronary Blood flow?

Back 73

Very Little Effect (teeny tiny effect)

(alpha-adrenergics = vasodilates)
(beta-adrenergics = vasoconstricts)

Front 74

Conservation of Mass equations x2

Back 74

Qin = Qout : for Q = V x A
(V=Velocity & A = XS area)

Mass(in) = Mass(out) : for M = VD
(V= Volume & D=Density)

Front 75

Coronary BF occurs primarily at what period?

Back 75

Diastole

(b/c @ systole, open Aortic Valve partially blocks coronary & contracting myocytes compress coronary)

Front 76

What is the most important factor when considering Coronary BF?

Back 76

Duration of Diastole

Front 77

During Exercise, what happens to the Diastolic Duration?

What compensatory event occurs to preserve the metabolic needs of the heart?

Back 77

Decreases
(and w/ increased HR cause hypoxia)

Adenosine (vasodilator released)

Front 78

During Diastole with Exercise, Adenosine has what effects on BF & Resistance of coronary arteries?

Back 78

(vasodilator, so)

Increase coronary BF
Decrease coronary Resistance

Front 79

During Exercise, what is the Limiting Factor for coronary BF?

Back 79

Diastolic Duration

Front 80

EXCITATION-COUPLING

- depends on what electrolyte properties for Skeletal muscle

- depends on what electrolyte properties for Smooth muscle

Back 80

INTRACellular Pool of Ca2+ (in SR)

EXTRACellular Influx of Ca2+

Front 81

EXCITATION-COUPLING

- Extracellular Calcium enters muscle in which muscle type?

- Enters cells via what receptor?

Back 81

Smooth muscle & Cardiac muscle

Voltage Gated Ca++ Channels
(skeletal muscles don't have this)

Front 82

EXCITATION-COUPLING

- For Skeletal muscles, what event initiates AP?

- For Smooth muscles, what event initiates AP?

Back 82

Release of ACh

Influx of Ca2+
(via voltage-gated Ca++ channels)

Front 83

EXCITATION-COUPLING

Can skeletal muscle cells self-depolarize?

Can smooth muscle cells self-depolarize?

Back 83

No

Some can
(i.e. - GI, uterus, bladder, etc.)

Front 84

EXCITATION-COUPLING

- what causes Ca2+ release in skeletal muscle cells?

- what causes Ca2+ release in smooth muscle cells?

Back 84

ACh release & widespread depolarization

Ca2+-dependent-Ca2+-channel (of SR)

Front 85

EXCITATION-COUPLING

- In skeletal muscle cells, intracellular calcium binds to what?

- In smooth muscle cells, intracellular calcium binds to what?

Back 85

- Troponin C

- Calmodulin

Front 86

EXCITATION-COUPLING

- Are T-tubules found in either skeletal muscle or smooth muscle cells?

Back 86

only in skeletal muscle cells

Front 87

EXCITATION-COUPLING

- what induces contraction in skeletal muscle cells?

- what induces contraction in smooth muscle cells?

Back 87

- Calcium binding Troponin C

- Calcium binding Calmodulin

Front 88

EXCITATION-COUPLING

- Calcium-TroponinC complex found in which muscle cells?

- what does it do to induce contraction?

Back 88

- Skeletal muscle cells

- displaces tropomyosin so that Actin can bind Myosin

Front 89

EXCITATION-COUPLING

- Calcium-Calmodulin complex found in which muscle cells?

- what does it do to induce contraction?

Back 89

- Smooth muscle cells

- activates Myosin Light Chain Kinase

Front 90

EXCITATION-COUPLING

- Myosin-Light-Chain Kinase is found in which muscle cell type?

- is activated by what?

- once activated, will do what?

Back 90

- Smooth muscle cells

- Calcium-Calmodulin complex

- Phosphorylate Myosin
(allowing it to bind to Actin)

Front 91

EXCITATION-COUPLING

- in order for contraction to occur after Myosin and Actin bind, what additional reaction must occur?

Back 91

ATP hydrolysis

(of the ATP on Myosin)

Front 92

EXCITATION-COUPLING

- Verapamil is what class drug?

- Verapamil can affect what muscles?

Back 92

- CCB

- Cardiac & Smooth muscles

Front 93

EXCITATION-COUPLING

- Verapamil MOA

- which muscle can it not effect?

- why?

Back 93

- Blocks Voltage Gated Calcium channels
(so Ca2+ can not enter cell)

- can NOT affect skeletal muscles

- b/c skeletal muscle is not dependent on extracellular calcium
(its dependent on intracellular pool of Ca2+)

Front 94

EXCITATION-COUPLING

- Verapamil has what effects on the vasculature radius?

Back 94

Vasodilates

(by relaxing vascular smooth muscles)

Front 95

Heart Failure (with repeated bouts of MI) will affect which cardiac property?

Back 95

Decreased EF

(due to ischemic loss of myocytes)

Front 96

S3 heart sounds are normal in?

S3 heart sounds are pathological in?

S3 heart sounds are associated with what heart pathology?

Back 96

children

adults

LVHF

Front 97

Describe S3 frequency.

Thus, should be auscultated how?

Back 97

Low frequency (unlike S1 & S2)

Bell

Front 98

S3 immediately follows what heart sound?

What PV Loop phase is this in?

Back 98

S2

Rapid Ventricular filling
(soon after Mitral Valve Opens)

Front 99

What pathophysiological process causes the S3 to be audible?

Back 99

Blood rapidly rushing into
PARTIALLY-FILLED ventricles
or
STIFF ventricles

Front 100

S3 is best heard at what location?

What conditions could enhance the audible nature of S3?

Back 100

Apex

1.) Left Lateral Decubitus position
2.) Complete exhalation by pt
(to bring heart closer to wall)

Front 101

What maneuvers would increase VR?

(thus increasing LV volume & pressure)

Back 101

Valsalva RELEASE

Squatting

Front 102

What maneuvers would decrease VR?

(thus decreasing LV volume & pressure)

Back 102

Valsalva MANEUVER

Standing

Front 103

Valsalva maneuver (or standing) is good for enhancing the audible sounds of what murmurs?

But also decreases audible murmurs of?

Back 103

1.) Hypertropic Cardiomyopathy
2.) MVP

- Aortic Stenosis

Front 104

Furosemide causes brisk diuresis, thus it will affect what heart sound and how?

Back 104

S3 gets less audible

Front 105

Amyl Nitrate Inhalation causes vasodilation and decreased BP, thus it will affect what heart sounds and how?

Back 105

(same as valsalva maneuver)

Enhances murmurs of
- Hypertropic cardiomyopathy
- MVP

Decreases audible for:
- Aortic Stenosis

Front 106

Verapamil is what drug class?

Back 106

CCB
&
Class 4 Antiarrhythmic

Front 107

Verapamil is used as Tx in what conditions?

Back 107

(ASH)
Angina
SVT
HTN

Front 108

Verapamil MOA for the heart

(include specific cells affected)

Back 108

Blocks Voltage-gated Ca2+ channels

(at the SA & AV node)

Front 109

Verapamil causes what changes in on the cardiac AP? (specify which AP phase)

Back 109

Slows down
Phase 0 Diastolic Depolarization

Front 110

Verapamil causes what physical changes in cardiac property?

Back 110

Decrease HR (by decr. SA firing rate)

Decrease AV CV (by decr. AV firing rate)

Front 111

Impulse conduction going from SA --> AV --> Ventricular myocardium occurs during what period?

Back 111

Diastole

(myocyte contraction occurs @ systole)

Front 112

Verapamil causes what physical changes in muscles & BV?

Back 112

Smooth muscle relaxation
(thus vasodilation)

Front 113

Which Antiarrythmic drugs INCREASE THRESHOLD POTENTIAL (the amt of depolarization needed to initiate AP)

Back 113

Class IA
Class IB
Class IC

Front 114

Which Antiarrythmic drugs SHORTENS AP
(via Na+ channel blockade)

Back 114

Class IB

Front 115

Which Antiarrythmic drugs PROLONG REPOLARIZATION?

Back 115

Class IA
Class IC

Class III

Front 116

Acutely, AV Fistulas cause what vascular effect?

Back 116

Decrease TPR

(b/c it shunts blood from arteries to veins)

Front 117

Over time, Chronic AV Fistulas compensate for decreased TPR by what 2 mechanisms?

Back 117

1.) Sympathetic stimulation

2.) Renal Retention of Fluids

Front 118

In Chronic AV Fistulas, the sympathetics stimulate what CV changes?

Back 118

Increased CO, thus Increased VR

Front 119

How does Acute AV Fistula cause a right shift on the VR curve?

Back 119

It does not.

(Right shift on VR curve happens later on with Chronic AV Fistula)

Front 120

In Chronic AV Fistula, how does the Sympathetics promote Right shift in VR curve?

Back 120

Increase VR

Front 121

In Chronic AV Fistula, how does the Renals promote Right shift in VR curve?

Back 121

Renal Retention of Fluids

==> Increased Blood Volume

Front 122

Chronic AV Fistula has what changes in:
- CO?
- MSP?
- TPR?

Back 122

Increase
Increase

Decrease

Front 123

CO & VR CURVES

- changes seen with Chronic AV Fistula

Back 123

CO curve shifted Upward
(b/c increased CO)

VR curve shifted Right
(b/c increased MSP)

Slopes of both curves Increase
(b/c of decreased TPR)

Front 124

CO & VR CURVES

- affects from Acute GI Bleed

Back 124

loss of blood volume, so

Left shift of VR curve

Front 125

CO & VR CURVES

- affects from Phenylephrine infusion

Back 125

increases sympathetics, so vasoconstriction causing Increased TPR, thus

Downshift CO curve
Decreased Slope (CCW rotation) of VR curve

Front 126

CO & VR CURVES

- what changes are seen with Anaphylaxis?

Back 126

causes widespread vasodilation, so

Massively Decreased VR

Front 127

CO & VR CURVES

- what changes are seen with MI

Back 127

less myocytes, so decreased contractility, thus decrease EF, so decreased CO, so

Decrease in CO curve
WITHOUT Changes in VR Curve

Front 128

CO & VR CURVES

- affects seen with Chronic Anemia

Back 128

CO is increased to meet metabolic needs, so

Increased CO Curve Slope

Front 129

CO & VR CURVES

- Isolated decrease in CO curve ONLY implies what conditions?

Back 129

- Negative Ionotropic drugs
or
- Heart injury inhibiting contraction
(i.e. Myocardial Infarction)

Front 130

CO & VR CURVES

- which curve illustrates Frank-Starling effect?

Back 130

CO curve

Front 131

CO & VR CURVES

- what is the value at the point when VR curve intersects the X-axis?

Back 131

MSP

Front 132

CO & VR CURVES

- TPR is presented by what on the curves?

Back 132

VR curve Slope

(thus when TPR increases, slope decreases)

Front 133

PV LOOP

- Right shift of Isovolumetric Contraction line (1-->2) implies what CV change?

Back 133

Increased Preload

(increased EDV means increased EDP)

Front 134

PV LOOP

- Left shift of Isovolumetric Relaxation line (3-->4) implies what?

Back 134

Increased Contractility

(thus increases in EF & SV)
(decrease in ESV)

Front 135

For Fick's CO equation, the Venous concentration of O2 is obtained from what vessel?

Back 135

Pulmonary artery

Front 136

Acutely, AV Fistulas cause what vascular effect?

Back 136

Decrease TPR

(b/c it shunts blood from arteries to veins)

Front 137

Over time, Chronic AV Fistulas compensate for decreased TPR by what 2 mechanisms?

Back 137

1.) Sympathetic stimulation

2.) Renal Retention of Fluids

Front 138

In Chronic AV Fistulas, the sympathetics stimulate what CV changes?

Back 138

Increased CO, thus Increased VR

Front 139

How does Acute AV Fistula cause a right shift on the VR curve?

Back 139

It does not.

(Right shift on VR curve happens later on with Chronic AV Fistula)

Front 140

In Chronic AV Fistula, how does the Sympathetics promote Right shift in VR curve?

Back 140

Increase VR

Front 141

In Chronic AV Fistula, how does the Renals promote Right shift in VR curve?

Back 141

Renal Retention of Fluids

==> Increased Blood Volume

Front 142

Chronic AV Fistula has what changes in:
- CO?
- MSP?
- TPR?

Back 142

Increase
Increase

Decrease

Front 143

CO & VR CURVES

- changes seen with Chronic AV Fistula

Back 143

CO curve shifted Upward
(b/c increased CO)

VR curve shifted Right
(b/c increased MSP)

Slopes of both curves Increase
(b/c of decreased TPR)

Front 144

CO & VR CURVES

- affects from Acute GI Bleed

Back 144

loss of blood volume, so

Left shift of VR curve

Front 145

CO & VR CURVES

- affects from Phenylephrine infusion

Back 145

increases sympathetics, so vasoconstriction causing Increased TPR, thus

Downshift CO curve
Decreased Slope (CCW rotation) of VR curve

Front 146

Verapamil is what drug class?

Back 146

CCB
&
Class 4 Antiarrhythmic

Front 147

Verapamil is used as Tx in what conditions?

Back 147

(ASH)
Angina
SVT
HTN

Front 148

Verapamil MOA for the heart

(include specific cells affected)

Back 148

Blocks Voltage-gated Ca2+ channels

(at the SA & AV node)

Front 149

Verapamil causes what changes in on the cardiac AP? (specify which AP phase)

Back 149

Slows down
Phase 0 Diastolic Depolarization

Front 150

Verapamil causes what physical changes in cardiac property?

Back 150

Decrease HR (by decr. SA firing rate)

Decrease AV CV (by decr. AV firing rate)

Front 151

Impulse conduction going from SA --> AV --> Ventricular myocardium occurs during what period?

Back 151

Diastole

(myocyte contraction occurs @ systole)

Front 152

Verapamil causes what physical changes in muscles & BV?

Back 152

Smooth muscle relaxation
(thus vasodilation)

Front 153

Which Antiarrythmic drugs INCREASE THRESHOLD POTENTIAL (the amt of depolarization needed to initiate AP)

Back 153

Class IA
Class IB
Class IC

Front 154

Which Antiarrythmic drugs SHORTENS AP
(via Na+ channel blockade)

Back 154

Class IB

Front 155

Which Antiarrythmic drugs PROLONG REPOLARIZATION?

Back 155

Class IA
Class IC

Class III

Front 156

Verapamil is what drug class?

Back 156

CCB
&
Class 4 Antiarrhythmic

Front 157

Verapamil is used as Tx in what conditions?

Back 157

(ASH)
Angina
SVT
HTN

Front 158

Verapamil MOA for the heart

(include specific cells affected)

Back 158

Blocks Voltage-gated Ca2+ channels

(at the SA & AV node)

Front 159

Verapamil causes what changes in on the cardiac AP? (specify which AP phase)

Back 159

Slows down
Phase 0 Diastolic Depolarization

Front 160

Verapamil causes what physical changes in cardiac property?

Back 160

Decrease HR (by decr. SA firing rate)

Decrease AV CV (by decr. AV firing rate)

Front 161

Impulse conduction going from SA --> AV --> Ventricular myocardium occurs during what period?

Back 161

Diastole

(myocyte contraction occurs @ systole)

Front 162

Verapamil causes what physical changes in muscles & BV?

Back 162

Smooth muscle relaxation
(thus vasodilation)

Front 163

Which Antiarrythmic drugs INCREASE THRESHOLD POTENTIAL (the amt of depolarization needed to initiate AP)

Back 163

Class IA
Class IB
Class IC

Front 164

Which Antiarrythmic drugs SHORTENS AP
(via Na+ channel blockade)

Back 164

Class IB

Front 165

Which Antiarrythmic drugs PROLONG REPOLARIZATION?

Back 165

Class IA
Class IC

Class III