Heart Cards Two

Front 4

Cardiac Muscles Cells

Back 4

Intercalated Discs

1. interconnect cardiac muscle cells

2. secured by Desmosomes

a. linked by gap junctions

3. Convey force of Contraction

a. propagate action potentials

Front 5

Characteristics of Cardiac Muscle Cells

Back 5

1. Small size

2. Single, central nucleus

3. Branching interconnections between cells

4. Intercalated discs

Front 6

Structure of Cardiac Tissue

Back 6

Striated with light and dark bandings

a. A bands-dark

b. I bands -light

Front 7

Characteristics of Cardiocytes

Back 7

1. Extensive system of short,wide T tubules which are filled with extracellular rich fluid.

2. Rely on Extracellular Ca2 for contraction

3. Individual Muscle Cells

a. no triads b. Has SR- no terminal cisternae

c. aerobic - high in myoglobin, mitochondria

d. limited capacity for regeneration

Front 8

Intercalated Discs

Back 8

1. Specialized contact points between cardiocytes.

Front 9

Functions of Intercalated Discs

Back 9

1. Join cell membrane of adjacent cardiocytes using gap junctions and desmosomes

2. Maintain Structure

3. Enhance molecular and electrical connections

4. conduct action potentials

Front 10

Coordination of Cardiocytes

Back 10

1. From Functional Syncytia

a. fused mass of cells

2. Are mechanically, chemically, electronically connected

3. All pull together for max efficiency

4. 2 Syncytia

a. atrial syncytium

b. ventricular syncytium

5. Separated by Fibrous Skeleton

Front 11

Energy Source for Cardiocytes

Back 11

1. At rest ---Fatty Acids(60%)

2. (35%) glucose

3. Small amounts of lactic acid burned aerobically

4. ATP used to sustain power stroking

5. Cardiocites use creatine kinase to produce ATP

6. During exercise cardiocytes use more lactic acid then converted to Pyruvic acid by enzyme

Lactate Dehydrogenase.

Front 12

The Heart Beat

Back 12

single contraction of heart

1. Atria first -------> Then Ventricles

Front 13

Types of Cardiac Muscle cells

Back 13

1. Conducting system

a. controls and coordinates heartbeat

2. Contractile cells

a. produces contractions

Front 14

Conducting System

Back 14

Cardiac Cycle-------->Action Potential at SA Node

1. Produces action potentials in cardiac muscle cells (contractile cells)

2. System of specialized cardiac muscle cells

a. initiates and distributes electrical impulses that stimulate contraction

Front 15

Automaticity (Conducting System)

Back 15

Cardiac muscle tissue contracts automatically (no outside stimuli needed)

Front 16

Structure of the Conducting System

Back 16

1. Sinoatrial Node(SA)

2. Atrioventricular Node (AV)

3. Conducting Cells

Front 17

Conducting Cells

Back 17

Interconnect SA and AV nodes

1. Distribute stimulus through gap junctions in intercalated discs in myocardium.

2. In the Atrium

a. internodal pathways

3. In the ventricles

a. AV bundle and bundle branches

Front 18

Pacemaker (Autorhythmic) Cells

Back 18

Pacemaker Potential #1

a. unstable resting membrane potentials due to slow unstable opening of slow NA+ channels

b. Continuously depolarize, never flat line

Depolarization #2

1. At threshold CA2 channels open

2. Explosive Ca2 influx produces the rising phase of action potential.

Front 19

Repolarization in Pacemaker cells

Back 19

Results from inactivation of Ca2 channels and opening of Voltage Gated K+ channels

Front 20

Heart Rate

Back 20

SA - 80-100 action potentials per minute

Parasympathetic stimulation slows heart rate

AV - 40-60 Action potentials per minute

Subendocardial conducting network of Purkinje Fibers and AV bundle generates 20-40 AP/min

Front 21

Sinoatrial Node ( Impulse Conduction through heart)

Back 21

In Posterior wall of right atrium

1. Contains pacemaker cells

2. Primary pacemaker of the heart

3. Connected to AV Node by Internodal pathways

4. Begins Atrial activation (Step 1)

5. Responsible for Normal Sinus Rhythm 75beats per minutes

Front 22

Atrioventricular Node (AV) (Impulse Conduction through the heart)

Back 22

In floor of right atrium

1. Is the secondary pacemaker of the heart

2. Receives impulse from SA node (Step 2)

3. Delays impulse because of the cell allows time for the Atria to contract first.

5. Atrial contraction begins

Front 23

The AV Bundle (of HIS)

Back 23

In the Septum

1. Forms an electrical bridge from the otherwise separated atrium and ventricles

2. Carries impulse to left and right bundle branches

a. which conduct to the Purkinje fibers (step 4)

3. And to the moderator band

a. conducts to papillary muscles

Front 24

Subendocardial conducting network

or

Purkinje Fibers

Back 24

1. Distribute impulse through ventricles(Step 5)

2. Atrial connection is completed

3. Ventricular contraction begins

4. Also have ability to contract 20-40 action potentials per minute

Front 25

Bradycardia

Back 25

abnormally slow heart rate

Front 26

Tachycardia

Back 26

abnormally fast heart rate

Front 27

Junctional Rhythm

Back 27

Defective SA Node: AV node takes over , sets slower heart rate (40-60 beats/min)

Front 28

Ectopic Pacemaker (outside)

Back 28

Abnormal cells

Generate a high rate of action potentials

Bypass conducting cells

Disrupts ventricular contractions

Front 29

CNS Input to SA Node

Back 29

Receives stimulation from the Cardiac Center in the Medulla via the cardiac plexus.

Front 30

Cardiac Center

1. Cardio Acceleratory Center (CAC)

Back 30

Sympathetic- uses NE to stimulate Beta 1 receptors to increase rate and strength of contraction

Front 31

Cardiac Center

2. Cardioinhibitory Center (CIC)

Back 31

Parasympathetic - uses ACh to stimulate muscarinic M2 receptors to decrease hear rate.

Heart is under Parasympathetic domination

Front 32

Electrocardiogram (ECG)or (EKG)

Back 32

A recording of electrical events in the heart.

Obtained by electrodes at specific body locations

Abnormal patterns diagnose damage

Front 33

Features of ECG

Back 33

1. Series of waves or deflection repeated 72/minute.

2. Each set of deflections correspond to 1 heartbeat or cardiac cycle.

3. Requires .8 sec to complete

Front 34

P wave of ECG

Back 34

SA node firing to atrial depolarization

.8 sec duration

Front 35

ORS complex of ECG

Back 35

AV node firing to ventricular depolarization

.8 sec duration

atrial repolarization also occurs (really small)

Front 36

T Wave of ECG

Back 36

Ventricles repolarize

Time is less important than its shape and or location.

Front 37

Time Intervals

Back 37

S-T segment - Entire Ventricular myocardium depolarized.

QT interval- beginning of ventricular depolarization through ventricular repolarization

PR Interval - From start of Atrial Depolarization(SA Node firing) to start of QRS complex

Normal is approx .16

Front 38

Cardiac Arrhythmias

Back 38

Abnormal patterns of cardiac electrical activity

1. Can be diagnosed by observing ECG

Front 39

Abnormal Time Intervals

Back 39

1. P-R wave greater than .18 = First Degree Heart Block --- Slow Transit through AV Node

2. If more than 1 P wave is seen before AV node firing = Second Degree Heart Block -very slow

3. P-R interval very long - no relationship between P wave and QRS complex= Third Degree Heart Block or Complete Heart Block = Need for real Pacemaker

Front 40

Contractile Cells

Back 40

Perkinje fibers distribute the stimulus to the contractile cells, which make up most of the muscle cells in the heart.

All connected by gap junction

Front 41

Action Potentials in Skeletal and Cardiac Muscle

Resting Potential

Back 41

Ventricle Cell negative 90 mv ( RMP)

Atrial Cell negative 80 mv

Front 42

1st Step of Cardiac Action Potential

Back 42

1. Rapid Depolarization(Stimulus)

a. Voltage regulated sodium channels (fast channels) open

b. As NA channels close, Voltage regulated Calcium channels (slow channels) open

c. balance Sodium ions pumped out

d. Hold membrane at 0mV plateau

Front 43

2nd Step of Cardiac Action Potential

Back 43

2. Repolarization:

a. Plateau continues

b. slow calcium channels close

c. slow potassium channels open

d. rapid repolarization restores resting potential

Front 44

Refractory Periods

Back 44

Absolute Refractory Period:

1. long

2. cardiac muscles cannot respond

Relative Refractory Period:

1. Short

2. Response depends on degree of stimulus

Front 45

Timing of Refractory Periods

Back 45

Length of Cardiac Action Potential in Ventricular Cell: 250-300 mseconds

30 times longer than skeletal muscle fiber

long refractory period prevents summation and tetany

Front 46

Contraction of Cardiac Muscle

Back 46

Produced by increase in calcium ion concentration around myofibrils.

Front 47

2 Steps of Calcium Ion Concentration

Back 47

1. 20% of calcium ions required for a contraction

a. Enter Cell membrane during plateau phase

2. Arrival of Extracellular Ca2

b. from calcium reserves in Sarcoplasm Reticulum

Front 48

Intracellular and Extracellular Calcium

Back 48

1. Slow calcium channels close - intracellular Ca2 absorbed by SR or pumped out of cell.

Front 49

Cardiac Cycle

Back 49

Period between start of 1 heart beat and the beginning of the next.

Both contraction and relaxation

Front 50

2 Phases of Cardiac Cycle

Back 50

Within any one chamber.

1. Systole (Contraction)

2. Diastole (Relaxation)

Front 51

Blood Pressure

Back 51

1. Rises during Systole

2. Falls during Diastole

Blood flows from high to low pressure

a. controls by timing of contractions

b. directed by one way valves

Front 52

4 Phases of the Cardiac Cycle

Back 52

1. Atrial Systole

2. Atrial Diastole

3. Ventricular Systole

4. Ventricular Diastole

Front 53

Cardiac Cycle and Heart Rate

Back 53

75bpms, 800msecs

When heart rate increases, all phases of cardiac cycle shorten. Especially diastole.

Front 54

STEP 1 in Cardiac Cycle

Back 54

1. Atrial Systole begins.

a. right and left AV valves are open

Front 55

STEP 2 in Cardiac Cycle

Back 55

2. Atria eject blood into ventricles:

a.Filling Ventricles

Front 56

STEP 3 in Cardiac Cycle

Back 56

3. Atrial Systole Ends:

a. AV valves close

b. ventricles contain maximum volume

c. end-diastolic volume (EDV)

Front 57

Step 4 in Cardiac Cycle

Back 57

4. Ventricular Systole

a. isovolemic ventricular contraction

b. pressure in ventricles rise

c. AV valves stay shut

Front 58

Step 5 in Cardiac Cycle

Back 58

5. Ventricular ejection

a. Semilunar valves open

b. blood flows into pulmonary and aortic trunks

c. Stroke Volume (SV) = 60% of end diastolic volume

Front 59

Step 6 in Cardiac Cycle

Back 59

6. Ventricular pressure falls:

a. semilunar valves close

b. ventricles contain end-systolic volume (ESV), about 40% of end-diastolic volume

Front 60

Step 7 in Cardiac Cycle

Back 60

7. Ventricular Diastole

a. ventricular pressure is higher than atrial pressure

b. all heart valves are closed

c. ventricles relax (isovolumetric relaxation)

Front 61

Step 8 in Cardiac Cycle

Back 61

8. Atrial pressure is higher than ventricular pressure

a. passive atrial filling

b. AV valves open

c. passive ventricular filling

More than 80% of ventricular filling is passive

Cardiac cycle ends.

Front 62

Heart Failure

Back 62

Lack of adequate blood flow to peripheral tissues and organs due to ventricular damage.

1.Usually starts with left ventricle

2. Left Ventricle fails.

a. causing blood to back up in the pulmonary circuit.

b. right ventricle eventually fails b/c of increased workload

Front 63

Heart Sounds

Back 63

S1 -closure of AV valves - "lubb"

S2 - closure of semilunar valves "Dupp" (quick snap)

S3, S4 - soft sounds, blood flow into ventricles and atrial constriction

Front 64

Heart Murmur

Back 64

1. Extra heart sounds

2. benign - innocent

a. Turbulence of blood flow during extreme physical activity in cardiac reserve

3. pathologic- disease process

a. Aortic Stenosis (narrowing) of aortic valve

b. can be congenital, Rheumatic fever, calcium deposits

c. generates a hissing sound

Front 65

Cardiodynamics

Back 65

The movement and force generated by cardiac contractions

Front 66

End Diastolic Volume (EDV)

Back 66

Volume in heart at end of relaxation (completely filled heart)

Front 67

End-Systolic Volume (ESV)

Back 67

Volume left in heart at end of contraction ( only residual volume left in the heart)

Front 68

Stroke Volume - Volume of blood ejected from heart in one single heart beat

Back 68

SV = EDV - ESV

EXAMPLE 100(EDV) - 40(ESV) = 60SV

Front 69

Ejection Fraction

Back 69

The % of EDV represented by SV.

From example in previous card it would be 60%

Front 70

Cardiac Output

Back 70

The volume pumped by each ventricle in 1 minute.

Example continued. 100bpm x 60SV = 6,000ml/per minute

Front 71

Control of Cardiac Output

Adjusting to Conditions

Back 71

Cardiac Output

a. adjusted by changes in heart rate or stroke volume.

b. heart rate - autonomic nervous system or

hormones.

c. stroke volume - adjusted by changing EDV or ESV

Front 72

Autonomic Innervation

Back 72

1. Cardiac Plexuses - innervate heart

2. Vagus nerves - parasympathetic fibers to cardiac plexus

3. Cardiac Centers of Medulla Oblongata

Front 73

Cardioacceleratory Center

Back 73

Controls sympathetic neurons

Uses NE to stimulate B1 receptors to increase rate.

Front 74

Cardiac Inhibitory Center

Back 74

Control Parasympathetic output

a. uses ACh to stimulate muscarinic to decrease heart rate.

Healthy heart is under Parasympathetic

domination

Front 75

Cardiac Centers monitor :

Back 75

1. baroreceptors(blood pressure)

2. Chemoreceptors (arterial oxygen and CO2

levels

Front 76

Autonomic Tone

Back 76

Dual innervation maintain resting tone by releasing Ach and NE

a. fine adjustments meet needs of other systems

Front 77

Vasomotor Center in Medulla

Back 77

Controls Blood Pressure

Exclusively Sympathetic

Uses NE to stimulate Alpha 1 receptors on smooth muscle of arteries/arterioles to contract.

Responsible for regulating vasoconstriction and blood pressure

Decrease in NE = Vasodialation = less contraction and more relaxation

Front 78

Autonomic Pacemaker Regulation

Back 78

1.Sympathetic and Parasympathetic

a. greatest at SA Node

2.Rate of Spontaneous Depolarization

a. RMP

b. Rate of Depolarization

3. Ach - (para)

a. slows heart - hyperpolarization of nodal cells

b. increases time for spontaneous depolarization to occur

4. NE (symp)

a. speeds heart, decreases time for spontaneous depolarization

Front 79

Hormonal Effects on Heart Rate

Back 79

Sympathetic stimulation increases HR

a. Epinephrine

b. norepinephrine

c. thyroid hormone

Front 80

2 Factors Affecting EDV (Filling up of Heart)

Back 80

1. Filling time

a. duration of ventricular diastole

2. Venous Return

a. rate of blood flow during ventricular diastole

Front 81

Preload in EDV

Back 81

Degree of Ventricular Stretching during ventricular diastole

a. Directly proportional to EDV

b. affects ability of muscle cells to produce tension

Front 82

EDV, Preload, Stroke Volume

Back 82

1. At Rest

a. EDV low, Myocardial stretches less, stroke volume is low

2. With Exercise

a. EDV increases, myocardial stretches more,

stroke volume increases

Front 83

Frank-Starling Principle

Back 83

As EDV increases, Volume Increases

1. greater stretch, greater the recoil

2. Length Tension Relationship

a. forcefulness of muscle contraction depends on length of sarcomeres

b. Increased Stretch increases amount of tension produces in the sarcomeres

Law true for healthy heart

Front 84

Frank- Starling Principe - Not obeyed in these conditions

Back 84

1.Cardiac Tamponade - fluid buildup in pericardial cavity

2. History of repeated Myocardial Infractions (scar tissue buildup)

3. Valvular insuffiency

4. Cardiomyopathy - inflamed & working poorly

5. CHF - failure of a heart as a pump

Front 85

Physical Limits of Ventricular Expansion

Back 85

Keeps from getting overstretched

1. Myocardial CT

2. Fibrous Skeleton

3. Pericardial Sac

Front 86

End Systolic Volume (ESV)

Back 86

The amount of blood that remains in the

ventricle at the end of ventricular systole is ESV

Front 87

3 Factors that Affect ESV

Back 87

1. Preload

a. ventricular stretching during diastole

2. Contractility

a. force produced during contraction at a

given preload

3. Afterload

a. Tension the ventricle produces to open the semilunar valve and eject blood.

Front 88

Contractility

Back 88

Affected by:

1. Autonomic Activity

2. Hormones

Front 89

Inotropic effects on the heart

Back 89

Factors that increase contractility = positive

Factors that decrease contractility = negative

Front 90

Autonomic Activity

Sympathetic stimulation

Back 90

1. NE released by postganglionic fibers

2. Epinephrine & NE released by adrenal

medullae

3. Stimulates b1 receptors causing ventricles to contract with more force

4. Increases ejection fraction and decreases ESV

5. Positive Inotropic action

Front 91

Autonomic Activity

Parasympathetic

Back 91

1. Ach released by Vagus nerves

2. Stimulates muscarinic, M1 receptors

3. Reduces force of Cardiac contractions to a small extent

4. Small negative inotropic action compared to sympathetic stimulation

Front 92

Hormones and Contractility

Back 92

Many Hormones can Affect Heart Contraction

1. Thyroxin and Glucagon - increase contractility

2. Beta blockers -stimulate of block beta

receptors

3. Digitalis - given to heart failure patients for its positive inotropic effects

4. Calcium channel blockers - affect calcium ions

Front 93

Afterload of ESV

Back 93

It is increased by any factor that:

1. Increases resistance to arterial blood flow

2. Or restricts arterial blood flow

After afterload increases, stroke volume decreases

Front 94

Heart Rate Control Factors

Back 94

1.Autonomic nervous system

a. sympathetic and parasympathetic

2. Circulating Hormones

3. Venous Return and Stretch Receptors

Front 95

Stroke Volume Control Factors

Back 95

EDV - Filling time and Rate of Venous Return

ESV - Preload, Contractility, Afterload

Front 96

Cardiac Reserve

Back 96

Difference between resting and max cardio output.

It can be pumped if needed.

Average = 300-400% or 20-25L/m

Athletes 500-600% or 30-35L/min

Necessary for fight or flight responses

Front 97

Heart and Cardiovascular Regulation

Back 97

Ensures adequate circulation to body tissues

Front 98

Cardiovascular Centers

Back 98

Control Heart and peripheral blood vessels

Front 99

Cardiovascular system

Back 99

1.Responds to changing activity patterns

2. Circulatory Emergencies

Front 100

Autonomic Reflexes

Back 100

Homeostatic and work on negative feedback principles.

Cartoid Reflex

Aortic Reflex

Right Heart (Bainbridge) Reflex

Front 101

Cartoid Reflex

Back 101

Increased blood pressure in the carotid artery causes increased firing of baroreceptors with increased afferent stimuli to :

1. Vasomotor center - Decrease NE to Increase vasodilation.

2. Cardiac Center CAC- decrease Sympathetic Stimulation to slow heart and decrease strength of contraction

3. Cardiac Center CIC- Increase parasympathetic stimulation ( Increase Ach) to slow heart

4. Brain Natriurectic Peptide - activates dumping of Na into urine

Results in Decrease in Blood volume and BP

Front 102

Aortic Reflex

Back 102

Engaged when BP in Aorta increases. baroreceptors fire

1. Same steps of Cartoid Reflex

Front 103

Right Heart or Atrial Reflex

Back 103

Adjust heart rate in response to venous return.

1. Increased blood pressure in vena cava and right atrium cause increased firing of baroreceptors.

2. CAC - increase sympathetic stimulation( (NE) to increase heart rate and increase strength of contraction.

3. CIC - Decrease parasympathetic to increase stimulation of heart.

4. Atrial Natriuretic Peptide - dumps NA

5. Decrease in Blood Volume, and BP

6. Slowing heart would increase atrial pressure and create a dangerous feedback

Front 104

Hyperkalemia

Back 104

Too much K in blood

Heart becomes depolarized and repolarization is inhibited.

Contractions become weak and irregular

Heart can stop I diastole

Front 105

Hypokalemia

Back 105

Not enough blood in K

Cells become hyperpolarized(less responsive)

Hyperpolarization at nodes slow heart rate

Front 106

Hypercalcemia

Back 106

Too much calcium

Cells become extremely excitable

Powerful prolonged contractions, Tetany

Front 107

Hypocalcemia

Back 107

Low calcium

Contraction becomes weak and can cease completely

Front 108

Abnormal body Temperature

Back 108

Low body temp slows hr

High body temp speeds up hr