Physiology Unit 2 Ekg Flashcards

Front 1

What does the following ECG Waves/Intervals represent?
P wave

Back 1

the sequential activation (depolarization) of the right and left atria
duration =conduction time through atria

Front 2

What does the following ECG Waves/Intervals represent?
QRS complex

Back 2

right and left ventricular depolarization (normally the ventricles are activated simultaneously)

Front 3

What does the following ECG Waves/Intervals represent?
ST-T wave:

Back 3

ventricular repolarization

Front 4

What does the following ECG Waves/Intervals represent? U wave:

Back 4

origin for this wave is not clear - but probably represents "afterdepolarizations" in the ventricles

Front 5

What does the following ECG Waves/Intervals represent?
PR interval:

Back 5

time interval from onset of atrial depolarization (P wave) to onset of ventricular depolarization (QRS complex)
↑ conduction velocity through AV node → ↓ PR interval
↓ conduction velocity through AV node → ↑ PR interval

Front 6

What does the following ECG Waves/Intervals represent?
QRS duration:

Back 6

duration of ventricular muscle depolarization

Front 7

What does the following ECG Waves/Intervals represent?
QT interval:

Back 7

duration of ventricular depolarization and repolarization

Front 8

What does the following ECG Waves/Intervals represent?
RR interval:

Back 8

duration of ventricular cardiac cycle (an indicator of ventricular rate)

Front 9

What does the following ECG Waves/Intervals represent?
PP interval:

Back 9

duration of atrial cycle (an indicator of atrial rate)

Front 10

What are the bipolar limb leads and what plane are they in?

Back 10

Frontal Plane
Lead I
Lead II
Lead III

Front 11

Where is Lead I and what are the charges?

Back 11

RA (-) to LA (+) (Right Left, or lateral)

Front 12

Where is Lead II and what are the charges?

Back 12

RA (-) to LF (+) (Superior Inferior)

Front 13

Where is Lead III and what are the charges?

Back 13

LA (-) to LF (+) (Superior Inferior)

Front 14

Which are the Augmented unipolar limb leads? What plane?

Back 14

Frontal plane
aVR
aVL
aVF

Front 15

Where is lead aVR placement, charge and direction?

Back 15

Lead aVR: RA (+) to [LA & LF] (-) (Rightward)

Front 16

Where is lead aVL placement, charge and direction?

Back 16

Lead aVL: LA (+) to [RA & LF] (-) (Leftward)

Front 17

Where is lead aVF placement, charge and direction?

Back 17

Lead aVF: LF (+) to [RA & LA] (-) (Inferior)

Front 18

What are the Unipolar (+) chest leads and in what plane? What direction?

Back 18

(Transverse plane):
Leads V1, V2, V3: (Posterior Anterior)
Leads V4, V5, V6:(Right Left, or lateral)

Front 19

The 6 major sections in the "method" of reading an ECG (per extra info, not slides).

Back 19

1. Measurements
2. Rhythm Analysis
3. Conduction Analysis
4. Waveform Description
5. Ecg Interpretation
6. Comparison with Previous ECG (if any)

Front 20

What is the resultant cardiac vector?

Back 20

The vector sum of all cardiac electrical activity (at any time).

Front 21

Depolarization moving towards a Positive electrode produces what type of deflection?

Back 21

Upward

Front 22

Depolarization moving towards a negative electrode produces what type of deflection?

Back 22

downward

Front 23

What is Einthoven’s law?

Back 23

States that the net QRS magnitude in
leads I & III = Lead II

Front 24

How are the Augmented Limb Leads
different than the bipolar limb leads?

Back 24

They are 50% larger

Front 25

what does the aVR lead show?

Back 25

Sees the cavities of the ventricles. Atrial & ventricular depolarization and ventricular repolarization move away from the electrode: P-wave, QRS, T-wave are all negative.

Front 26

what does the aVL and aVF lead show?

Back 26

looks at the ventricles. Deflections are predominantly positive.

Front 27

Leads V1 & V2 are mainly where?
What is their QRS wave typically?

Back 27

the Right side of the heart
mainly NEGATIVE QRS wave...

Front 28

Lead V3 is mainly where?
What is their QRS wave typically?

Back 28

Over interventricular septum
measuring the right bundle branch
QRS is "net" Neutral

Front 29

Lead V4 is mainly where?
What is their QRS wave typically?

Back 29

Over interventricular septum
measuring the left bundle branch
{QRS is "net" Neutral-more positive]

Front 30

Lead V5 & V6 are mainly where?
What is their QRS wave typically?

Back 30

the Left side of the heart
mainly POSITIVE QRS wave...

Front 31

How will hypertrophy affect the EKG?

Back 31

Hypertrophy: ↑ depolarization activity and displaces mean QRS vector towards hypertrophied side for a right or left axis deviation

Front 32

What is the arrhythmia?

Back 32

First Degree Heart block:
Long PR interval

Front 33

Back 33

Asystole

Front 34

Back 34

Digitalis Effect
Scooping ST segment

Front 35

Back 35

Bradycardia
Normal P, QRS, T, rate < 60

Front 36

Back 36

Hypercalcemia
Short/absent ST segment

Front 37

Back 37

Tent-shaped Twave
hyperkalemia

Front 38

Back 38

Idioventricular Rhythm (IVR)
No Pwave, bizarre QRS, rate 20-40

Front 39

Back 39

Normal

Front 40

Back 40

Premature Atrial Contraction (PAC)
Premature Pwave, irregular P-P interval

Front 41

Back 41

Premature Ventricular Contraction (PVC)
Wide QRS, unrelated to Pwave

Front 42

Back 42

Normal P, QRS, T, rate > 100
Tachycardia, Sinus Rhythm

Front 43

Back 43

Ventricular Fibrillation (VFIB)
Chaotic waves

Front 44

Back 44

Bizarre, wide QRS, no Pwav, rate > 100
Ventricular Tachycardia (VTAC)

Front 45

Elevation of the ST segment my be caused by:

Back 45

Angina w/o exertion
Pericarditis

Front 46

Depression of the ST segment my be caused by:

Back 46

digitalis

Front 47

What is the sequence of electrical events in the heart? (Pathway)

Back 47

Cardiac Depolarization at the SA node ->AV node ->Bundle of His->
Bundle branches (L & R) ->
Purkinje fibers

Front 48

Where is the the fastest conduction in the heart?

Back 48

Purkinje fibers @ 4.0 m/s

Front 49

What are the 4 main pathways of the atrial conduction system?

Back 49

Anterior, Middle and Posterior Internodal Track and Bachmans bundle to left atrium

Front 50

The rate of the SA node varies with what factor?

Back 50

Inspiration causea and Increase
while expiration causes a decrease

Front 51

Name the three automaticity foci

Back 51

Atrial automaticity foci
Juntional automaticity foci
Ventricular automaticity foci

Front 52

Where is the Juntional automaticity
foci located?

Back 52

middle & distal regions of AV node

Front 53

Where is the Ventricular
automaticity foci located?

Back 53

His bundle & Bundle branches

Front 54

What is the highest rate of automaticity for the SA node?

Back 54

72/min

Front 55

What is the rate of automaticity for the atrial foci?

Back 55

60-80 per minute

Front 56

What is the rate of automaticity for the AV junction foci?

Back 56

40-60 per minute

Front 57

What is the rate of automaticity for the ventricle foci?

Back 57

20-40 per minute

Front 58

What is the term for the faster more superior foci taking control/lead?

Back 58

Overdrive supression

Front 59

The ventricles are completely depolarized during
which isoelectric part of the EKG recording?

Back 59

ST Segment

Front 60

How long is a typical P wave and what does the time/length represent?

Back 60

0.1 sec
conduction time through atria

Front 61

How long is a normal PR interval?
What does it represent?

Back 61

0.12-0.20
Time from initial atrial depolarization to time of initial depolarization of ventricles. It is the filling time for the ventricles.

Front 62

↑ conduction velocity through AV node shows how in an EKG?

Back 62

↓ PR interval

Front 63

↓ conduction velocity through AV node shows how on an EK?

Back 63

↑ PR interval

Front 64

How long should the T wave be and what does it represent? What plase of the cardiac cycle?

Back 64

0.16 sec
Later repolarization of ventricles
( Reduced ejection phase)

Front 65

What direction does Repolarization occur?

Back 65

epicardial surfaces to endocardium. OUTSIDE→IN

Front 66

What direction does depolarization occur?

Back 66

endocardium.surfaces to epicardial INSIDE→OUT

Front 67

The QT interval Represents?
What does it include?

Back 67

First ventricular depolarization to last ventricular ventricular
repolarization or Duration of Ventricular systole
• Includes:
– QRS complex
– ST segment
– T wave.

Front 68

How long should a QT interval be?

Back 68

QT interval is normal if it is ½ the R-R interval.

Front 69

What is the relationship between heart rate, QT interval and RR Interval?

Back 69

If HR increases, RR & QT decrease and visa versa

Front 70

What does the U wave reperesent?

Back 70

repolarization of papillary muscle.
(Not always visible)

Front 71

Changes in Duration & Amplitude of EKG waves & intervals waves & intervals indicate what?

Back 71

depict changes in Muscle mass
(hypertrophy)or conduction issues

Front 72

↑ HR & ↓ cycle length have what affect on duration of AP, refractory periods and excitability?

Back 72

They decrease

Front 73

How do you calculate heart rate?

Back 73

HR = 1/cycle length (or r-r time)

Front 74

What are the time measurements of the x-axis on dark (large) and light gridmarks on EKG paper?

Back 74

dark lines on grid are 0 2 sec apart; light lines are 0 04 sec apart.

Front 75

What does the y axis of the ekg paper reperesent?

Back 75

Voltage gain = 1 mV/cm

Front 76

What is the pattern for counting big squares (from Dubin)?

Back 76

300,150, 100, 75,60,50

Front 77

What steps per physiology to analyze EKG?

Back 77

1. Calculate –ventricular and atrial rate:
2. Calculate – P-R interval
3. Calculate – QRS duration:

Front 78

how do you Calculate the mean axis of ventricular depolarization?

Back 78

take the net from Leads I,II, & III and plot on triangle. Intersection is correlating quadrant. (each space 2 ticks)

Front 79

What does the The amplitude (voltage) of and EKG tell us?

Back 79

The size of the chamber or The mass (number) of active cells

Front 80

How do Arrhythmias generally present on an EKG?

Back 80

P-P interval will lengthen or decrease

P, QRS, T waves = normal
↑ or ↓ HR: Cardiac cycle duration
changes

Front 81

What would cause a short P-P interval?

Back 81

SNS/ flight/fight
>100 bpm is sinus tachycardia

Front 82

Under what influence/stimulation would cause a longer P-P interval?
What is a long p-p generally named/diagnosed?

Back 82

PNS (athletes)
< 60 cycles/min sinus bradycardia

Front 83

What are the characteristics of a 1° Atrioventricular conduction blocks?

Back 83

Electrical transmission through the AV node is impeded. Delay is located ABOVE the His bundle

PR interval is lengthened > 0.2s
Rate = variable
P wave = normal
Rhythm = regular

Look for the start of a Pwave to the tip of an R wave to be bigger than 1 large box (.2sec)

Front 84

What could cause a a 1° Atrioventricular conduction block?

Back 84

Digitalis toxicity

Front 85

What are the characteristics of a Mobitz type I - Wenckebach conduction block?

Back 85

Second Degree AV block occurs IN the AV node
P-R interval is progressively longer until one P wave is blocked; the cycle begins again following the blocked P wave.
Not all P waves are followed by QRS complexes.
Rate = variable
Failure of impulses to reach ventricles.
P wave = normal with constant P-P interval
Rhythm = irregular

Front 86

What could cause a a 2° Type I conduction block?

Back 86

Mobitz type I - Wenckebach
Digoxin toxicity, calcium channel blockers

Front 87

Whats the Wenckebach ratio?

Back 87

Wenckebach series has a
consistent P:QRS ratio; 3:2, 4:3, 5:4
(1 less QRS than P)

Front 88

What's the tx for Type 1 Mobitz 2* AV block?

Back 88

Tx : not indicated since rhythm produces no symptoms

Front 89

What are the characteristics of a Second Degree AV Type II block?

Back 89

Second Degree AV block occurs below the Bundle of His.
Dropped beats that are NOT preceded in a change in PR interval.
Rate = variable

P wave = normal with constant P-P interval
QRS = often widened
Rhythm = regular

Front 90

Whats the Mobitz Type II ratio?

Back 90

Each repeating Mobitz series has a
consistent P:QRS ratio; 3:1, 4:1, 5:1

Front 91

What are the potential causes of a Second Degree AV Mobitz Type II block?

Back 91

After acute anterior MI – due to damage in bundle branches.

Front 92

What is the treatment of a a Second Degree AV Mobitz Type II block?

Back 92

artificial pacing

Front 93

What would a Mobitz 2:1 block look like? 3:1?

Back 93

2 P-waves to 1 QRS; 3 P-waves to 1 QRS

Front 94

What are the characteristics of a 3° Atrioventricular conduction block?

Back 94

Atrial & ventricular activities are unrelated due to complete block of atrial impulses to ventricles. Complete block at AV junction, common bundle or bundle branches.
Rate = atrial rate is normal, ventricular rate < 70bpm.
P wave = normal with constant P-P interval (not “married” to QRS complexes)

Another automaticity focus will pick up ventricle pacing QRS = widened or normal
Rhythm = irregular

Front 95

What are the potential causes of a 3° Atrioventricular conduction block?

Back 95

Older pt with degeneration of conductive tissue

Front 96

What are the tx of a 3° Atrioventricular conduction block?

Back 96

external pacing

Front 97

In First degree A-V block the PR interval is?

Back 97

Greater than 0.2s.

Front 98

Describe the relationship between velocity of blood flow, pressure and the cross-sectional area of the vascular bed.

Back 98

Velocity and pressure are inversely related to area.

High velocity, higher pressure, smaller area

Front 99

Describe the relationship between blood flow, pressure and resistance in a typical vascular bed.

Back 99

Blood flow rate is constant
Velocity of flow is decreased as
blood is ejected smaller vessels.

Velocity of flow inversely proportional to the total X-
sectional area
Velocity of flow is slowest in the
capillaries, which have the
largest X-sectional area
Cardiac output is in parallel series to organs with different % of blood to different organs)

Front 100

What does the pressure at the beginning of systemic circulation equal?

Back 100

mean arterial pressure? (Average 93 mmHg)

Front 101

What is the pressure at the end of systemic circulation?

Back 101

0 mmHg

Front 102

increasing pressure does what to flow?

Back 102

increases it

Front 103

if absolute pressure stays the same, what will happen to flow?

Back 103

It will remain the same

Front 104

What is Vascular resistance?

Back 104

is a measure of hindrance to blood flow caused by friction between moving blood and the vessel wall

Front 105

What is the most important factor in Poiseuille’s Equation?

Back 105

Most important factor is radius.
Decreasing the radius by ½ does not increase the resistance 2-fold. It increases it 16-fold.

Front 106

flow rate depends on what 2 main factors?

Back 106

Pressure gradients (delta-P between two points along the vascular system) & Vascular resistance

Front 107

What is laminar flow?

Back 107

Energy efficient flow where the velocity touching the wall of the vessel is 0 and the blood that is most center is the fastest (parabola in between)

Front 108

How might flow become turbulent?

Back 108

with clot, thrombi, aneurysm, anemia, atherosclerosis, valvular defects

Front 109

What are the criteria of laminar and turbulent flow?

Back 109

N R less than 2000, flow is laminar
N R greater than 3000, flow is turbulent
N R between 2000 and 3000:
-flow is transitional between laminar and turbulent

Front 110

Which vessles are most compliant?

Back 110

Veins/Venous structures

Front 111

What is an unstressed volume?

Back 111

Large Volume, low Pressure (veins)

Front 112

What is an stressed volume?

Back 112

Low Volume, high Pressure (arteries)

Front 113

When do arteries become arterioles?

Back 113

In the organ: can adjust flow within

Front 114

Arteries contain more of what type of fibers?

Back 114

smooth muscle and elastic fibers to serve as PRESSURE reservoir

Front 115

Veins contain more of what type of fibers?

Back 115

more collagen fibers to serve as a BLOOD reservoir

Front 116

What is cardiac inootropy?

Back 116

the same thing as Contractility

Front 117

What is Trepp?

Back 117

It is the increasing HR that causes Ca 2+ accumulation which increases
contractility

Front 118

When afterload increases what happends to the ESV and stroke volume?

Back 118

there is an increase in end-systolic volume and a decrease in stroke volume.
(Preload changes secondarily to changes in afterload)

Front 119

Afterload is increased when...

Back 119

aortic pressure and systemic vascular resistance are increased, by aortic valve stenosis, and by ventricular dilation.

Front 120

What is Contractility?

Back 120

the intrinsic ability of the heart to contract independent of preload and afterload at any given fiber length

Front 121

what factors affect contractility?

Back 121

– ANS activity
– circulating hormones (i.e.,epinephrine)
– Ca 2+ influx and availability

Front 122

What is preload?

Back 122

Preload can be defined as the initial stretching of the cardiac myocytes prior to contraction. It is "measured" by the end-diastolic volume (EDV) which will indicate how stretched the sarcomeres are.

Front 123

What factors affect preload? (5)

Back 123

- filling time
- compliance
- filling pressure
- atrial systole
- pericardial constraint

Front 124

What is afterload?

Back 124

Afterload can be thought of as the "load" or pressure that the heart must eject blood against.

Front 125

What factors affect afterload?

Back 125

- arterial pressure
 peripheral resistance
 arterial compliance
- viscosity of blood
- valve function

Front 126

What is the effect of Norepinepherine on contractility?

Back 126

– increases the velocity of shortening
– increases ejection velocity
– increases stroke volume
– decreases ESV

Front 127

What happens to the rate of relaxation under SNS stimulation?

Back 127

it is also enhanced to allow for the increased heart rate (needs filling time still)

Front 128

A decrease in contractility causes what changes in ESV and SV?

Back 128

increase in ESV and a decrease in stroke volume

Front 129

What is the ratio of SV to EDV?
What is abnormal?

Back 129

– normal 50-75%
– abnormal < 40

Front 130

What is the The Effect of Heart Rate on Cardiac Output in the following senario:
stroke volumes declines as heart rate encroaches on the rapid filling phase

Back 130

There is a peak output and then a
decrease. At too high of a SV, the cardiac output would be too drastically affected due to the decrease in filling time

Front 131

What is the The Effect of Heart Rate on Cardiac Output in the following senario:
stroke volume increases due to compensatory mechanisms, such as increased contractility

Back 131

then cardiac output will reach a higher peak before diastolic filling time becomes limiting

Front 132

What does Ventricular minute work measure?

Back 132

Contractile work per minute rather than per beat.

Front 133

What is the “Resting” metabolic rate of the heart?

Back 133

4.8 - 6 ml / gm / h.

Front 134

How is the RMR of the heart divided?

Back 134

25% to basal metabolism, the rest for contraction

Front 135

How does left ventricle work compare to right ventricle work?

Back 135

left ventricle does 6 to 7X the work of the right ventricle

Front 136

What are the Metabolic substrates of the heart and their percentages?

Back 136

35 to 40% of energy requirement from carbohydrate oxidation under basal conditions
Balance from Fatty Acid Oxidation

Front 137

What is Cardiac Efficiency?

Back 137

Ratio of the work performed to the energy consumed

Front 138

What is the Efficiency of myocardium usually? How does it change during exercise?

Back 138

Efficiency of myocardium is usually from 5 to 15 %
Efficiency improves during exercise

Front 139

A . ↑↑HR (>150) will have what effect?

Back 139

SV decreases, can't fill
CO decreases

Front 140

Where is the atrial kick represented on the EKG

Back 140

P wave

Front 141

What are the exogenous sources of fuel for the heart?

Back 141

BLOOD
» glucose, lactate
» fatty acids, ketone bodies

Front 142

What are the endogenous sources of fuel for the heart?

Back 142

(intracellular stores):
» glycogen, triglycerides

Front 143

Uptake of fuels by the heart is
dependent on what factors?

Back 143

Workload
fed/fasted metabolic state
changes in concentrations of fuel in the circulation

Front 144

4 Sources of ATP from carbohydrate metabolism

Back 144

– glycolysis
– glucose oxidation
– lactate oxidation
– glycogen stores

Front 145

3 Sources of ATP from fatty acid metabolism

Back 145

– triglyceride lipolysis and oxidation of the fatty acid
– lipoprotein and chylomicron oxidation
– ketone body oxidation

Front 146

What is the Randle Cycle?

Back 146

The Randle cycle is a metabolic process involving the competition of glucose and fatty acids for substrates in the fed (favoring CHO) or fasted state (favoring FFA.

High levels of lipids are oxidized in
preference to glucose

Front 147

Whats generally going on during a fasted state?

Back 147

Low levels of insulin; causes
– adipose tissue lipolysis is stimulated
– blood FFA are high
– FFA uptake by the heart
– As FFA are oxidized, glucose use is inhibited

Front 148

What are the effects of low insulin?

Back 148

– adipose tissue lipolysis is stimulated
– blood FFA are high
– FFA uptake by the heart
– As FFA are oxidized, glucose use is inhibited

Front 149

What happens when insulin levels are high?

Back 149

– inhibits adipose tissue lipolysis
– increases glucose uptake in heart
– increases glucose use by the heart

Increase in glucose use overcomes the effects of FFA.

Front 150

What is the relationship between fat oxidation and glucose oxidation

Back 150

inverse

Front 151

Increased mitochondrial b-oxidation results in what enzymatic changes?

Back 151

Cirtate and Acetly-CoA increase
– Citrate inhibits phosphofructokinase activity
– Acetyl CoA inhibits pyruvate dehydrogenase

This increases G-6-P, inhibiting
hexokinase and resulting in a decrease in glucose uptake.

Front 152

when fat metabolism is decreased what two enzymes are no longer inhibited?

Back 152

Inhibition on PDH and PFK is removed

Front 153

As the level of fatty acid increases, oxidation of what increases?

Back 153

palmitate oxidation

Front 154

What is the effect of inhibiting glucose oxidation on the heart?

Back 154

Inhibiting glucose
oxidation contributes
to LV failure

Front 155

What conditions are associated
with excessively high rates of fatty
acid oxidation?

Back 155

angina, infarct, diabetes, and post cardiac surgery

Front 156

Why are high rates of fatty
acid metabolism detrimental?

Back 156

 Induce cardiac arrhythmias
 Increase oxygen consumption
 Promotes oxygen wasting yg g
 Reduces cardiac performance
 Leads to heart failure

Front 157

FAs inhibit key enzyme functions in what systems/mechanisms? (5)

Back 157

»Na + -K + -ATPase, Ca 2+ ATPase
»ETS and Krebs cycle
»Adenine nucleotide translocase
»Pyruvate dehydrogenase Pyruvate dehydrogenase
»Suppress glucose oxidation

Front 158

What is the metabolic breakdown of a heart with uncontrolled DM?

Back 158

The heart relies exclusively on fatty acid metabolism

Front 159

Infarct and cardiac surgery release what hormone with what effect on the heart?

Back 159

epinephrine which increases plasma FFA (free fatty acids)

Front 160

What enzyme is pharomocologically targeted to inhibit B-Oxidation?

Back 160

ketoacyl CoA thiolase

Front 161

What (2) drugs can block ketoacyl CoA thiolase?

Back 161

Ranolazine, trimetazidine

Front 162

How is FA uptake into the mitochondira inhibited pharmocologically?

Back 162

by inhibiting carnitine palmitoyl transferase

Front 163

What two drugs can inhibit carnitine palmitoyl transferase?

Back 163

etomoxir, oxfenicine

Front 164

Stimulation of pyruvate dehydrogenase will do what? What drug assists with this?

Back 164

» dichloroacetate
pyruvate dehydrogenase is an enzyme for glucose metabolism, it will stimulate those cycles

Front 165

How can mitochondrial acetyl CoA levels be modulated with L-carnitine?

Back 165

Use it to make acetylcarnitine reducing its ACoA's levles in the mitochondria which will Removes inhibition on pyruvate dehydrogenase
an enzyme in glucose metabolism pathways

Front 166

carnitine palmitoyltransferase I can be inhibited by what 2 drugs?

Back 166

Oxfenicine
Etomoxir
decreases FA oxidation

Front 167

What two drugs angian drugs can inhibit the oxidation of Fatty Acids?

Back 167

Trimetazidine
Ranolazine

Front 168

What drug can inhibit inhibit the enzyme pyruvate dehydrogenase kinase?

Back 168

Dichloroacetate

Front 169

What pathways does lactate belong to?

Back 169

Glucose oxidation pathway

Front 170

What are the cnductile cells and why are they special

Back 170

Bundle of His, Purkinje fibers, Sinoatrial (SA) node and
Atrioventricular (AV) node.
they can generate spontaneous action potentials.

Front 171

What are the contractile cells of the heart called?

Back 171

cardiac myocytes

Front 172

Generally describe the Spread of Excitation in the heart

Back 172

1. SA node: initiates action potential
2. Spread to the atria and to AV node
3. AV node: slow conduction
4. Bundle of His and Purkinje system: fast conduction

Front 173

What is conduction velocity?

Back 173

speed of AP propagation through heart
fasest in the purkinjies
slowest in the AV nodes

Front 174

What affects Conduction velocity?

Back 174

1) rate of change in membrane potential as a function of time (i.e.
upstroke phase of action potential).
2) resistance

Front 175

What is a syncytium.?

What acts like this?

Back 175

A multinucleated mass of cytoplasm that is not separated into individual cells'
Cardiac cells

Front 176

Within intercalated discs, what two kinds of membrane junctions?

Back 176

– Desmosomes: Mechanical junctions
– Gap junctions: Electrical junctions

Front 177

How does the legnth of cardiac AP compare to skeletal AP?

Back 177

Long duration comparatively

Front 178

Fast action potentials occur in what cell types?

Back 178

contractile cells

Front 179

Slow action potentials occur in what cell types?

Back 179

pacemaker cells

Front 180

What is Phase 0 of the Fast AP?
What Ionic influence?

Back 180

upstroke, rapid depolarization
– due to fast inward Na + current.

Front 181

What is Phase 1 of the Fast AP?
What Ionic influence?

Back 181

Phase 1: early repolarization
– electrochemical gradient favors K + movement out of the cell
– inactivation gates on Na + channels close

Front 182

What is Phase 2 of the Fast AP?
What Ionic influence?

Back 182

Phase 2: plateau phase
–cause by balance between Ca 2+ (L-type channel; inward) current and K + (outward) currents

Front 183

What is Phase 3 of the Fast AP?
What Ionic influence?

Back 183

repolarization
Caused by turn-off of Ca 2+ current and further increase in K + currents.

Front 184

What is Phase 4 of the Fast AP?
What Ionic influence?

Back 184

resting potential
– Caused by large background K + outward current. (different channels than in Phase 3)
– balanced by inward Na + and Ca 2+ current

Front 185

How can Phase 2 be inhibited?

Back 185

can be inhibited by Ca 2+ channel blockers

Front 186

Which phase of the fast AP is responsible for the very long AP?

Back 186

Phase 2

Front 187

What are the kinetics of Na+, Ca+, and K+?

Back 187

Fast In
Slow In
Fast Out

Front 188

What makes summation and tetanus of cardiac muscle is unlikely?

Back 188

The fact that the long refractory period occurs in conjunction with
prolonged plateau phase,

Front 189

What are the key differences b/w fast and slow Aps?

Back 189

1. automaticity
2. unstable resting membrane
potential
3. no sustained plateau
4. No phases 1 & 2

Front 190

What is happening in Phase 0 of the Slow Action Potentials?
What Ionic Influences?

Back 190

upstroke
– Slow due to inward long-lasting Ca 2+ current (L-type)

Front 191

What is happening in Phase 1 of the Slow Action Potentials?
What Ionic Influences?

Back 191

There isn't a phase 1

Front 192

What is happening in Phase 2 of the Slow Action Potentials?
What Ionic Influences?

Back 192

There isn't a phase 2

Front 193

What is happening in Phase 3 of the Slow Action Potentials?
What Ionic Influences?

Back 193

repolarization
– Caused by turn-off of Ca 2+ current
and further increase in K + current.

Front 194

What is happening in Phase 4 of the Slow Action Potentials?
What Ionic Influences?

Back 194

pacemaker potential
(spontaneous depolarization)

1) repolarization from preceding AP turns on If (funny) current causing inward Na +
2)if threshold is reached a transient Ca 2+ current (T-type channel; inward) is turned on
3)AP peaks and K+ moves out of the cell

Front 195

Maximum diastolic potential in slow AP?

Back 195

-65mV

Front 196

What are the three criteria for "Normal" sinus rhythm?

Back 196

AP must originate from the SA node
SA impulses must be regular and 60-100 per minute
normal conduction

Front 197

When do Latent pacemakers appear?

Back 197

If conduction is blocked or superior pacemaker isn't working

Front 198

What is the Source of initiating calcium for cardiac muscle?

Back 198

Extracellular

Front 199

Whats the role of tropomyosin?

Back 199

inhibits binding of myosin to actin

Front 200

What is the role of troponin?

Back 200

Ca 2+ -sensitive molecular switch, changes conformation so binding site for myosin can be exposed

Front 201

What are the three parts of troponin?

Back 201

TnC: “calcium sensor”, calcium binding produces a conformational change in TnI
TnT: links Tn complex to Tm, appears to control the position of Tm on the thin filament
TnI: binds to actin and inhibits myosin ATPase

Front 202

how are myofilaments arranged?

Back 202

into sarcomeres like skeletal muscle

Front 203

Whats the legnth of a sarcomere?

Back 203

z to z band

Front 204

What's the A band?

Back 204

the legnth of the myofilaments

Front 205

Which bands shorten in a cross bridge cycling? Which stays the same?

Back 205

I-bands and the H-zone shorten, Z bands come closer together,

A-bands do not change their length

Front 206

What are the steps of Excitation-Contraction Coupling in Cardiac
Contractile Cells?

Back 206

1. Excitation - AP causes the
depolarization of the membrane.
2. Ca 2+ channels open (during plateau of AP).
3. Ca 2+ enters cell (“trigger” Ca 2+ )
• Ca 2+ -induced Ca 2+ release from SR via ryanodine receptor.
4. Ca 2+ binds to troponin.
5. Crossbridge cycling.

Front 207

When are Ca++ channels opening in a long AP?

Back 207

During phase 2 plateau phase

Front 208

What is SERCA?
What does it do?

Back 208

Sarco(Endo)plasmic Reticulum Ca++-ATPase
It is a Ca2+ ATPase that transfers Ca2+ from the cytosol of the cell to the lumen of the SR at the expense of ATP hydrolysis during muscle relaxation.

Front 209

What effect does inhibiting the Na + /K + ATPase have on the cardiac muscle cell?

Back 209

Blocking na/katpase exchanger will cause intracellular Na+ to stay high. If Na+ is high, the Na+/Ca2+ will want to get rid of Na+ and hang on to Ca+. Higer intracellular Ca+
will Enhances force of contraction as tension development proportional to Ca 2+

Front 210

What drugs inhibit Na/K-ATPase exchanger?

Back 210

Digitalis, Digoxin

Front 211

T h e f o r c e d e v e l o p e d b y
contraction of cardiac muscle
depends on...

Back 211

Initial fiber legnth

Front 212

Describe Length-Tension Relationship & Starling’s Law of the Heart

Back 212

the greater the volume of blood entering the heart during diastole (end-diastolic volume), the greater the volume of blood ejected during systolic contraction (stroke volume) and vice-versa, such that Initial length of myocardial fibers determines the initial work done during the cardiac cycle.

Front 213

Increasing cardiac muscle length has what impact on Ca+:
(3)

Back 213

• increases the Ca 2+ sensitivity of troponin C
• increases Ca 2+ release from the SR
• Produce large changes in tension

Front 214

Positive inotropic effect

Back 214

increase in contractility and rate
of tension development at a given
fiber length.

Front 215

Negative inotropic effect

Back 215

decrease in contractility and a
decrease in the rate of tension
development at a given fiber
length.

Front 216

What factors have a - negative inotropic effect?

Back 216

parasympathetic stimuation
heart failure

Front 217

What factors have a + positive inotropic effect?

Back 217

Sympathetic NS stimulation
Catecholamines
Heart Rate

Front 218

Nuclei of cardiac muscle are...

Back 218

usually single, central

Front 219

What is contraction of cardiac muscle like (compared to smooth and skeletal)

Back 219

slower onset, cannot be tetanized

Front 220

What is the significance of the only slightly curved line on the volume/pressure graph during diastole?

Back 220

It indicates that the ventricle is easy to fill and that the heart is difficult to "overfill"

Front 221

On a Pressure-Volume loop what point would indicate where the mitral valve opens?

Back 221

lower left "corner"

Front 222

On a Pressure-Volume loop what point would indicate where the mitral valve closes?

Back 222

lower right "corner"

Front 223

On a Pressure-Volume loop what point would indicate where the aortic valve opens?

Back 223

upper right "corner"

Front 224

On a Pressure-Volume loop what point would indicate where the aortic valve closes?

Back 224

upper left "corner"

Front 225

Where is the EDV indicated on a PV Loop?

Back 225

lower right "corner" on the X axis... Mital valve is closing, so at end volume for the ventricle

Front 226

How do you find the stroke volume in the PV loop?

Back 226

It is the measure of the horozontal line inside the loop (the equivialent of measuring 0 volume to EDV and subtracting 0-start of the loop on the x axis which is equivialent to the ESV

Front 227

Where is the end systolic point on the PV loop?

Back 227

Top left corner b4 isov relaxation

Front 228

If you added 2nd loop to the PV loop with the preload increased and the afterload and contractility remained the same how would it look?

Back 228

The EDV for loop 2 would be at a higher volume on the x axis and the pressure at this point is higer than that of loop1. The slope for the end systolic pressure/volume line is the same and the afterload lines are parallel, so they are considered the same. The stroke volume of loop 2 is larger.

Front 229

If you added 2nd loop to the PV loop with the afterload increased and the preload and contractility remained the same how would it look?

Back 229

The EDV point would be the same for both loops
loop 2 would have a greater angle/slope on the line from the end systolic point to the x axis indicating the afterload was increased. The stroke volume would decrease

Front 230

How do you find preload on the PV loop?

Back 230

Its the EDV or lower right "point"

Front 231

How do you find afterload on the PV loop?

Back 231

Its the line from the top left "corner" to the EDV on the x axis. The greater the angle (more upright the line) the greater the afterload

Front 232

What would cause the endsystolic PV line to have an increased slope?

Back 232

if contractiltiy was increased, like with and adrenaline rush

Front 233

着る

Kiru

Back 233

To be wearing

Hint 233

きる

Front 234

Factors that determine preload

Back 234

Ventricular filling time
Ventricular compliance
Filling pressure
Contribution of atrial systole to filling
Pericardial constraint

Front 235

Preload in absence of sympathetic stimulation has what effect on cardiac output?

Back 235

– CO usually not affected since decreased SV compensated for by increased HR.
– CO adversely affected at HR > 150 to 180 BPM.

Front 236

Preload With sympathetic stimulation has what effect on cardiac output?

Back 236

With sympathetic stimulation:
– SV preserved due to increased contractility
– CO can increase dramatically.
(associate with exercise)

Front 237

Decreasing intrathoracic pressure (inspiration) will have what affect on stroke volume and preload?

Back 237

Increase RIGHT ventricular SV & Preload, which increase

Front 238

Increasing central venous pressure will have what affect on stroke volume and preload?

Back 238

Increase RIGHT ventricular SV & Preload

Front 239

How much does atrial kick contribute to EDV?

Back 239

20-30% but has greater impact when filling times are reduced

Front 240

Effect of cardiac tamponade on cardiac cycle...

Back 240

reduces ventricular compliance, reduces EDV, reduces SV

Front 241

Factors that affect Afterload

Back 241

– arterial pressure
– peripheral vascular resistance (PVR)
– arterial wall compliance
– mass of the column of blood in the aorta
– viscosity of the blood

Front 242

How is afterload measured?

Back 242

Estimated by mean arterial pressure (= DP + 1/3 PP)

Front 243

What is the reelationship between the afterload and SV and maximum velocity of ejection?

Back 243

Inverse
if afterload is bigger (greater resistance) it will decrease volume and velocity

Front 244

An increased afterload w/ a constant EDV will cause what changes in the PV loop?

Back 244

– increased ESV
– reduction in SV

Front 245

Clinically, afterload is increased by what pathologies.factors?

Back 245

– aortic stenosis
– elevated arterial pressure
– ↑ PVR
– ↑ blood viscosity
– ↓ arterial compliance

Front 246

What is Systole?

Back 246

contraction of a chamber and blood is being ejected (contraction and emptying)

Front 247

What is Diastole?

Back 247

period of relaxation during which the chamber is filling (relaxation and filling) and coronary arteries are perfused

Front 248

When are the coronary arteries perfused?

Back 248

During relaxation/diastole.
Coronary blood flow (70%) Diastole and 30% during systole.

Front 249

What are the phases of the cardiac cycle?

Back 249

„ A: Atrial systole
„ B: Isovolumetric contraction
„ C: Rapid ejection
„ D: Reduced ejection
E: Isovolumetric relaxation
„ F: Rapid filling
„ G: Reduced filling

Front 250

For the given phase, what are the valves doing and what phase is the left ventricle in?
„ A: Atrial systole

Back 250

AV Valves Open
Diastole

Front 251

For the given phase, what are the valves doing and what phase is the left ventricle in?
B: Isovolumetric contraction

Back 251

Closing of AV valves (all 4)
Systole

Front 252

For the given phase, what are the valves doing and what phase is the left ventricle in?
„ C: Rapid ejection

Back 252

Opening of SL valves
Systole

Front 253

For the given phase, what are the valves doing and what phase is the left ventricle in?
„ D: Reduced ejection

Back 253

Opening of SL valves
Systole

Front 254

For the given phase, what are the valves doing and what phase is the left ventricle in?
E: Isovolumetric relaxation

Back 254

Closing of SL valves (all 4)
Diastole

Front 255

For the given phase, what are the valves doing and what phase is the left ventricle in?
„ F: Rapid filling & G: Reduced Filling

Back 255

Diastole
Opening of AV valves

Front 256

At what phase might a 4th heart sound be heard?

Back 256

‹ During Atrial Systole
caused by vibration of ventricular walls
‹ noted when ventricular compliance is reduced, as in LV hypertrophy, MI, or ischemic heart disesase

Front 257

What are the values for EDV for normal, atheletic and heart failure patients?

Back 257

) Normal: ~120 ml
) Endurance athletes: ~180-240 ml
) Heart failure: ~180-240 ml

Front 258

When does the mitral valve close on the cardiac cycle chart? What else does this point signify?

Back 258

at end of atrial systole (part a)
Also the point of EDV (can't fill anymore, valves closed)

Front 259

What phase is the S1 sound heard? What causes it?

Back 259

During Isovolumetric contraction causes Rise in pressure causes the AV valves to close,

Front 260

What's happening During Isovolumetric contraction?

Back 260

depolarization leads to a rapid
increase in LV pressure
Pressure rises without a
change in blood volume

Front 261

What phase of the EKG corrosponds with Isovolumetric contraction?

Back 261

QRS

Front 262

What phase of the EKG corrosponds with atrial systole?

Back 262

P wave

Front 263

What happens to Isovolumetric contraction and relaxation under sympathetic control?

Back 263

rates of pressure development
and dissipation are increase

Front 264

What happens in the rapid ejection phase?

Back 264

When intraventricular pressures
exceeds pressures within the great vessels, pulonic/aortic valves open and blood is ejected
Maximal LV systolic and RV systolic pressure is achieved
Atrial filling begins

Front 265

the rapid ejection phase corrosponds to what on the ekg?

Back 265

End of this phase coincides with the end of the ST segment

Front 266

What happens in the reduced ejection phase?

Back 266

Ventricles begin to repolarize
Blood continues to be ejected due to inertial energy of blood
Atrial pressure continue to rise due to venous return

Front 267

What part of the EKG corrosponds to the reduced ejection phase?

Back 267

T wave

Front 268

When is the S2 sound heard?

Back 268

Isovolumetric relaxation when LV pressure drops below vessel pressure and aortic and pulmonic valves to close

Front 269

In what phase is the ESV found? What is it approximatly?

Back 269

Isovolumetric relaxation
(ESV) is ~ 50 ml

Front 270

What causes splitting of S2 sound?

Back 270

Inspiration causes splitting of S 2 (A 2 P 2 ) „„ During the isovolumetric relaxation, the aortic valve closes before the pulmonary valve

Front 271

What happens during rapid filling phase?

Back 271

Ventricular pressures fall below
atrial pressures; AV valves open; LV filling begins

Front 272

When might you hear a 3rd sound?

Back 272

Durong rapid ventricular filling phase

indicates recoil of blood against LV wall--sudden deceleration of flow

Front 273

What is the longest phase of the cardiac cycle?

Back 273

Reduced ventricular filling

Front 274

What happens in the Reduced ventricular filling phase?

Back 274

„ Final portion of the passive ventricular filling
„„ As ventricles continue to fill with blood and expand, compliance decreases
„„ This reduces the pressure gradient across the AV valves
rate of filling therefore falls
„„ Increase in heart rate decreases the time available for this phase

Front 275

What phase of the cardiac cycle might get shortened in an increase HR situation

Back 275

Reduced ventricular filling phase

Front 276

What are peaks a,c,v?

Back 276

venous pulses that occur in the right atrium that are transmitted as peaks in the large veins

Front 277

What/when occuring:
a wave

Back 277

Occurs during atriol systole:
atrial contraction increase right atrial pressure and reflected back to the veins

Front 278

What/when occuring:
c wave

Back 278

Rapid ejecting phase
Caused by bulging of the tricuspid valve into the right atrium during ventricular systole

Front 279

What/when occuring:
v wave

Back 279

(isovolumic relaxation)
filling of central veins and right
atrium behind a closed tricuspid

Front 280

Which opens first, pulmonary or aortic valve?

Back 280

Pulmonary
(less pressure to overcome?)

Front 281

Which closes first, pulmonary or aortic valve?

Back 281

aortic
greater pressure
pulmonary

Front 282

Which opens first, tricuspid or mitral?

Back 282

tricuspid

Front 283

Which measurement is an indicator of contractiltiy?

Back 283

Ejection fraction

Front 284

When might S4 be heard?

Back 284

heard during atrial systole where ventricular compliance is decreased as in ventricular hypertrophy

Front 285

What pathological conditions can widen S 2?

Back 285

pulmonic stenosis
right ventricular failure
‹right bundle branch block

Front 286

What Pathology can cause S2 split to narrow or disappear?

Back 286

Left bundle branch block
Delayed depolarization of left ventricle
Aortic stenosis

Front 287

Whats a pradoxical split?

Back 287

When P2 is heard before A2 i
>severe aortic stenosis

Front 288

What are most common causes of
turbulence?

Back 288

Valve dysfunctions
‹stenotic valve
‹insufficient (regurgitant) valve

Front 289

Whats a stenotic valve?

Back 289

stiff narrow valve that‹‹ does not open completely
‹‹ turbulence created when blood must be forced through

Front 290

What's an insufficient valve?

Back 290

One that does not completly close
blood flows backwards and collides with incoming blood

Front 291

Whats a systolic murmur?

Back 291

heard during systole or after S1

Front 292

What are possible causes of systolic murmurs?

Back 292

aortic or pulmonary valve stenosis
mitral or tricuspid regurg

Front 293

Whats a midsystolic murmur?

Back 293

‹ crescendo decrescendo character
‹‹ caused by aortic or pulmonary valve stenosis

Front 294

Whats a holostolic murmur?

Back 294

caused by AV valve regurgitation or ventricular septal defect

Front 295

Whats a diastolic Murmur?

Back 295

murmur heard after S2

Front 296

What are causes of diastolic murmurs?

Back 296

atrial and pulmonary regurg
tricuspid or mitral stenosis

Front 297

What causes mitral stenosis?

Back 297

rheumatic heart disease.
congenital lesions, calcium depositions, and myxoma

Front 298

What are the effects of aortic stenosis on the heart?

Back 298

narrowing of vessel makes LV have to contract harder increasing LVP and causing hypertophy of the heart and eventual failure

Front 299

What are the effects of mitral valve stenosis on the cardiac cycle?

Back 299

LAP is greater than LVP during filling
atrial have to contract harder, and left ventricles fill less.
increase in pressure leads to pulmonary congestion

Front 300

What are the effects of aortic regurgitation on the cardiac cycle?

Back 300

blood flow back iont left ventricle increasing preload which increase stroke volume
atria get back up as ventricles get backed up

Front 301

What causes a widening pulse pressure/

Back 301

aortic regurge

Front 302

What are the effects of mitral regurge on the cardiac cycle?

Back 302

Regurgitant flow from left ventrical goes back int left atrium.
This decreases LVSV and causes enlargement of the atrial chamber
„„Can lead to venous congestion

Front 303

What is main feature of Atrial Flutter?

Back 303

P wave rate greater than 250 bpm

Front 304

What are the features of Atrial Fibrillation?

Back 304

•No discrete P-waves

Front 305

What are the features Ventricular Fibrillation?

Back 305

• random waveforms
• unidentifiable QRS

Front 306

What are the features Long QT Syndrome?

Back 306

Prolonged interval between QRS &
T-wave.

Front 307

Ribbon looking EKG characterized by rapid ventricular rhythm.

Back 307

Tosades de Pointes

Front 308

Main characteristic of atrial tacycardia

Back 308

rapid atrial rate (150-250)
P waves uniform
Narrow QRS

Front 309

Main characteristic of Atrial Fibrilation?

Back 309

Always irregular R-R

Front 310

Main characteristic of junctional rhythms

Back 310

Absent or inverted p waves

Front 311

Main characteristic of ventricular rhythms

Back 311

WIDE QRS (>.10 s)

Front 312

Main characteristic of 1* AV block

Back 312

Prolonged P-R interval (>.20s)
P:QRS 1:1

Front 313

Main characteristic of Mobitz I

Back 313

PR increasingly longer
P:QRS ratio variable

Front 314

Main characteristic of Mobitz II

Back 314

PR fixed
P:QRS ratio variable, not all P's married to QRA

Front 315

Main characteristic 3* block

Back 315

Reg PP
Reg RR
Changing PR