Physio 2B Ch. 19 Heart

Front 1

The heartbeat is coordinated by:

Back 1

the Cardiac Conduction System

Front 2

1st in the Cardiac Conduction System

Back 2

SA node

Front 3

a patch of modified cardiocytes in the right atrium, just under the epicardium near the superior vena cava.

Back 3

SA node

Front 4

the pacemaker that initiates each heartbeat and determines the heart rate.

Back 4

SA node

Front 5

node located near the right AV valve at the lower end of the interatrial septum; acts as an electrical gateway to the ventricles.

Back 5

AV node

Front 6

acts as an insulator to prevent currents from getting to the ventricles by any other route.

Back 6

fibrous skeleton

Front 7

Sympathetic stimulation can raise the heart rate to as high as ____ bpm.

Back 7

230bpm

Front 8

parasympathetic stimulation can slow the heart rate down to as low as ____ bpm

Back 8

20bpm or even stop the heart for a few seconds

Front 9

the sympathetic pathway to the heart originates:

Back 9

in the lower cervical to upper thoracic segments of the spinal cord.

Front 10

sympathetic stimulation increases the heart rate and contraction strength but dilates these:

Back 10

the coronary arteries to increase myocardial blood flow.

Front 11

the parasympathetic pathway begins with nuclei of the _____ nerves in the __________.

Back 11

begins with nuclei of the VAGUS NERVES in the MEDULLA OBLONGATA.

Front 12

Postganglionic fibers from the right vagus nerve lead mainly to the ___ node and those from the left vagus lead mainly to the ___ node.

Back 12

Postganglionic fibers from the right vagus nerve lead mainly to the SA node and those from the left vagus lead mainly to the AV node.

Front 13

the normal heartbeat triggered by the SA node is called:

Back 13

sinus rhythm

Front 14

at rest, the typical adult heartbeat is:

Back 14

70-80 bpm

Front 15

when stimulants cause other parts of the cardiac conduction system to fire before the SA node does, the extra heartbeat is called:

Back 15

premature ventricular contraction (PVC) or extrasystole

Front 16

if the SA node is damaged, the AV node produces a heartbeat of ____bpm, called:

Back 16

40-50bpm, called Nodal Rhythm

Front 17

parasympathetic stimulation ________ the heart rate.

Back 17

reduces

Front 18

a pathway by which signals leave the AV node:

Back 18

AV bundle of His

Front 19

forks that develop from the AV bundle of His which enter the interventricular septum and descend toward the apex

Back 19

right & left bundle branches

Front 20

nervelike processes that arise from the lower end of the bundle branches and turn upward to spread throughout the ventricular myocardium.

Back 20

Purkinje fibers

Front 21

the potential of the SA node is called:

Back 21

pacemaker potential

Front 22

the pacemaker potential starts at ___mv and reaches threshold at:

Back 22

-60mv and gradually depolarizes until reaching threshold at -40mv

Front 23

what causes the slow depolarization of the pacemaker potential?

Back 23

a slow inflow of sodium without a compensating outflow of potassium.

Front 24

when the pacemaker potential reaches threshold, whats the name of the gates that open? And what rushes into the cell?

Back 24

when the pacemaker potential reaches threshold, fast calcium-sodium channels open and both calcium and sodium flow in from the extracellular fluid.

Front 25

after the depolarizing phase of the pacemaker potential, what channels open and what leaves to repolarize the cells?

Back 25

after the depolarizing phase of the pacemaker potential, potassium channels open and potassium leaves the cell, repolarising the cytosol.

Front 26

each depolarization of the SA node sets off ___ heartbeat(s)

Back 26

1

Front 27

at rest, the SA node fires every ___ sec., creating a heart rate of ___bpm.

Back 27

at rest, the SA node fires every 0.8 sec., creating a heart rate of about 75 bpm.

Front 28

do pacemaker cells contract?

Back 28

no, they don't have actin or myosin.

Front 29

describe the pacemaker potential and action potential of the SA node:

Back 29

-pacemaker potential starts at -60mv
-slowly depolarizes due to a slow inflow of Na+ (pacemaker potential)
-when the pacemaker potential reaches threshold (-40mv), voltage-regulated Fast Calcium-Sodium Channels open and both calcium and sodium flow in. This produces the depolarization phase of the pacemaker potential, which peaks just above zero.
- at about zero, potassium channels open and potassium leaves the cell, repolarizing it.
-when repolarization is complete, the potassium channels close and the pacemaker potential starts over.

Front 30

describe the myocardial action potential:

Back 30

-resting membrane potential = -90mv
-stimulus opens voltage-gated sodium channels
-sodium flows in and depolarizes the cell to threshold.
-threshold voltage rapidly open additional sodium gates.
-the action potential peaks at 30mv.
-the sodium gates close quickly
-as the action potentials spread over the cell membrane, they open slow calcium channels
-a small amount of calcium enters and binds to ligand regulated calcium channels on the sarcoplasmic reticulum which causes the SR to release even more calcium into the cytosol.
-the second wave of calcium binds to troponin and triggers contraction.
-at the end of plateau, calcium channels close and potassium channels open.
-potassium leaves the cell rapidly and calcium is transported back to the SR and extracellular fluid.

Front 31

How long is the absolute refractory period in cardiac muscle compared to skeletal muscle?

Back 31

the absolute refractory period in cardiac muscle is 250 msec., compared with 1 to 2 msec. in skeletal muscle.

Front 32

a composite recording of all the action potentials produced by the nodal and myocardial cells

Back 32

ECG or EKG

Front 33

electrical activity proceeding contraction =

Back 33

waves

Front 34

P wave =

Back 34

signal from SA node that depolarizes the atria.

Front 35

PQ segment =

Back 35

atrial systole 100msec. after P wave begins.

Front 36

PQR complex =

Back 36

AV node signal depolarizing ventricles & atrial repolarization and diastole.

Front 37

ST segment =

Back 37

ventricular systole

Front 38

T wave =

Back 38

ventricular repolarization just before diastole.

Front 39

List the features of the ECG:

Back 39

-P wave
-PQ segment
-QRS complex
-ST segment
-T wave

Front 40

One complete contraction and relaxation of all 4 heart chambers:

Back 40

a Cardiac Cycle

Front 41

Fluid dynamics: Flow is governed by these two main variables:

Back 41

Pressure: which impels a fluid to move, &
Resistance: which opposes flow.

Front 42

Blood pressure is measured with a:

Back 42

sphygmomanometer

Front 43

A fluid flows only if:

Back 43

it is subjected to more pressure at one point in space than at another.

Front 44

The difference in pressure that allows movement of fluids is called:

Back 44

a Pressure Gradient

Front 45

Fluids always flow ________ their pressure gradient, from ________ pressure to ________ pressure.

Back 45

Fluids always flow DOWN their pressure gradient, from HIGH pressure to LOW pressure.

Front 46

Pressure is _________ proportional to the volume of a container.

Back 46

Pressure is INVERSELY proportional to the volume of a container.

Front 47

If P₂ > P₁ then pressure gradient is:
If P₁ > P₂ then pressure gradient is:

Back 47

If P₂ > P₁ → pressure gradient
If P₁ > P₂ → pressure gradient

Front 48

Do the heart valves exert effort to open & close?

Back 48

No, they are passively pushed open and closed by the changes in blood pressure.

Front 49

The first heart sound =
The second heart sound =

Back 49

The first heart sound =S₁ "lubb"
The second heart sound = S₂ "dupp"

Front 50

Which heart sound is louder & longer?
Which one is softer and sharper?

Back 50

S₁ is louder & longer.
S₂ is softer and sharper.

Front 51

The third heart sound, S₃ is only heard in:

Back 51

Children & adolescents and is rarely heard in those older than 30.

Front 52

What are the 4 phases of the cardiac cycle?

Back 52

-Ventricular filling
-Isovolumetric contraction
-Ventricular ejection
-Isovolumetric relaxation

Front 53

What are the 3 phases of Ventricular filling?

Back 53

-rapid ventricular filling: 1st. 1/3rd; blood enters quickly
-diastasis: 2nd 1/3rd; slower filling
-atrial systole: last 1/3rd; completion of filling

Front 54

The P wave of the electrocardiogram occurs at which phase of ventricular filling?

Back 54

diastasis

Front 55

At the end of ventricular filling, each ventrical contains an End-diastolic volume (EDV) of:

Back 55

about 130mL of blood

Front 56

Phase where contraction of the ventricles takes place but there is no blood pumped out of the heart. S1 is heard at this phase:

Back 56

Isovolumetric contraction

Front 57

The amount of blood ejected during ventricular ejection is ___ mL and is called:

Back 57

70mL and is called the stroke volume. (% of EDV ejected = 54%, called ejection fraction)

Front 58

The blood that remains behind in the ventricles is called:

Back 58

End-systolic volume (ESV)

Front 59

EDV-SV=ESV therefore:

Back 59

130mL - 70mL = 60mL

Front 60

Isovolumetric relaxation =

Back 60

early ventricular diastole

Front 61

The amount of blood ejected by each ventricle in 1min. is called:

Back 61

cardiac output (CO)

Front 62

CO =

Back 62

HR x SV
CO= 75bpm x 70ml/beat = 5,250mL/min
CO= 5.25L/min.

Front 63

Tachycardia =
Bradycardia =

Back 63

persistent resting adult heart rate ↑ 100bpm
persistent resting adult heart rate ↓ 60bpm

Front 64

Factors that raise the heart rate:
Factors that lower the heart rate:

Back 64

positive chronotropic agents
negative chronotropic agents

Front 65

The nervous system doesn't initiate the heartbeat but it does modulate its:

Back 65

rhythm & force

Front 66

autonomic output to the heart is initiated by the:

Back 66

cardiac centers of the medulla oblongata

Front 67

S₁ = (sound) & occurs because of:
S₂ = (sound) & occurs because of:
S₃ = (sound) & occurs because of:

Back 67

S₁ = "Lubb" & occurs mainly becuase of the L. ventrical blood turbulance/ hitting wall and valves.
S₂ = "Dupp & occurs mainly because of blood hitting semilunar valves
S₃ = occurs because of blood filling the ventricles.

Front 68

When auscultating the heart, the sound heard are made by:

Back 68

turbulence of the blood

Front 69

the heart is under _________ nervous system control.

Back 69

autonomic

Front 70

The two stimulatory effects of the neurons in the cardiac centers are:

Back 70

cardiostimulatory &
cardioinhibitory

Front 71

the cardiostimulatory effects of the cardiac centers are transmitted via the _________ pathway; the cardioinhibitory effects are transmitted via the __________.

Back 71

SYMPATHETIC PATHWAY; VAGUS NERVES

Front 72

Cardiostimulatory center:
The sympathetic postganglionic fibers are adrenergic and release ___________ which then:

Back 72

norepinephrine which then binds to beta-adrenergic fibers in the heart. This activates the cAMP second messenger system in the cardiocytes and nodal cells. cAMP activates an enzyme that opens up calcium channels in the plasma membrane. The inflow of calcium accelerates depolarization of the SA node and contraction of the cardiocytes, speeding up the heart. cAMP also accelerates the uptake of Ca2+ by the SR which enables cardiocytes to relax more quickly. Thus, norepinephrine and cAMP accelerate both the contraction and relaxation, increasing the heart rate.

Front 73

hormones produced by the adrenal glands that also serve as neurotransmitters, aka catecholamines:

Back 73

epinephrine, norepinephrine, & dopamine.

Front 74

What do beta-blocker do then?

Back 74

they would prevent the increase of the heart rate from sympathetic stim.

Front 75

What are the two types of adrenergic receptors:

Describe them and their subtypes:

Back 75

Alpha α & Beta β

Alpha: all are innervated and respond to norepinephrine
-α1: causes muscle contraction & glandular secretion
-α2: causes muscle relaxation & inhibits glandular secretion

Beta:
β1: causes muscle contraction; innervated= responds to norepinephrine
β2: causes muscle relaxation; uninnervated= responds to epinephrine more

Front 76

What are the two types of ACH receptor types:

Back 76

Nicotinic = on skeletal muscle NMJs, stimulation causes action potential and contraction (Na+ rushes in)
Muscarinic = inhibits cardiac muscle action potentials, ∴ Slows ♥ rate

Front 77

Cardioinhibitory center:
The Vagus nerves release ______ which:

Back 77

ACh, which have an inhibitory effect on the SA & AV nodes. ACh binds to muscarinic receptors and opens K+ gates in the nodal cells. As K+ exits the cells, they become hyperpolarized and less likely to fire, so the heart rate ↓.

Front 78

Which have a faster-acting effect on the heart, the vagus nerves or sympathetic nerves?

Back 78

the vagus nerves because ACh acts directly on ion channels in the plasma membrane, whereas the sympathetic effects are delayed by the 2nd messenger system that acts on the ion channels.

Front 79

List some positive & negative chronotropic agents?

Back 79

Positive chronotropic agents:
-Sympathetic stim.
-catecholamines
-Digitalis
-hypocalcemia
-hypercapnia & acidosis


Negative chronotropic agents:
-Parasympathetic stim.
-ACh
-Hyperkalemia
-Hypokalemia
-Hypercalcemia
-Hypoxia

Front 80

Chronotropic agents influence:
Inotropic agents influence:

Back 80

Chronotropic agents influence: Heart Rate
Inotropic agents influence: Contraction Strength

Front 81

List some positive & negative Inotropic agents?

Back 81

Positive Inonotropic agents:
-Sympathetic stim.
-catecholamines
-Digitalis
-hypercalcemia
-Glucagon

Negative Inonotropic agents:
-Hyperkalemia
-Hypokalemia
-Myocardial hypoxia
-Myocardial hypercapnia

Front 82

When catecholamines act on β1 receptors, they cause muscle to constrict. When they act on β2 receptors it causes muscle to dialate, so which receptors do coronary arteries have?

Back 82

coronary arteries have β2 receptors, thus when catecholamines are affecting β1 receptors causing the rate & force of contraction to ↑, they act on the β2 receptors to relax and dilate the coronary arteries, increasing blood to the heart muscles.

Front 83

The intrinsic rate of the SA node is:

Back 83

100bpm

Front 84

The resting heart rate is held back from the intrinsic rate of the SA node by:

Back 84

Vagal tone: a steady background firing rate of the vagus nerves, about 70-80bpm.

Front 85

The cardiac centers receive input and integrate signals from:

Back 85

-Proprioceptors
-Baroreceptors (carotid sinus & aortic arch)
-Chemoreceptors (carotid & aortic bodies & medulla)

Front 86

Describe the proprioceptors:

Back 86

Proprioceptors in the muscles and joints provide information on changes in physical activity. Thus the heart can increase its output even before the metabolic demands of the muscles rise.

Front 87

Describe the baroreceptors:

Back 87

the Baroreceptors are pressure sensors found in the aorta and internal carotid arteries. They send signals to the medulla which may increase or decrease heart rate & pressure depending on circumstance.

Front 88

Describe chemoreceptors:

Back 88

The chemoreceptors occur in the aortic arch, carotid arteries, and the medulla itself. They are sensitive to blood pH, CO₂, & O₂. Hypercapnia and acidosis stimulate the cardiac centers of the medulla to ↑ the heart rate.
The chemoreceptors also respond to hypoxemia by ↓ heart rate.

Front 89

Such responses to fluctuations in blood chemistry & blood pressure are called:

Back 89

Chemoreflexes & Baroreflexes respectively, and are good examples of Negative feedback loops.

Front 90

The electrolyte with the greatest chronotropic effect is:

Back 90

potassium

Front 91

Hyperkalemia:
Describe the effects of a quick onset of potassium:

Back 91

Sudden increase in extracellular potassium makes cells more excitable. Outward diffusion of K+ is reduced, more K+ remains in the cell, and is closer to threshold. Can quickly lead to cardiac arrest. Used for euthanasia.

Front 92

Hyperkalemia:
Describe the effects of a slow onset of potassium:

Back 92

nerve and muscle fibers become LESS excitable. Inactivation of sodium gates, the heart rate becomes slow and irregular and the heart may arrest in diastole.

Front 93

What can cause a Fast onset of Hyperkalemia?

Back 93

When a crushing injury, rapid hemolysis, or old transfused blood releases large amounts of K+ from ruptured cells.

Front 94

What can cause a Slow onset of Hyperkalemia?

Back 94

renal failure & acidosis

Front 95

Describe the process of Hypokalemia:

Back 95

As ECF potassium concentration falls, more potassium moves from the ICF to the ECF and the cells become hyperpolarized and harder to stimulate.

Front 96

The electrolyte with the most important Inotropic effects:

Back 96

Calcium

Front 97

Hypercalcemia produces ________________ contractions and _____ heart rate; may lead to:

Back 97

Hypercalcemia produces STRONG PROLONGED contractions and SLOWS heart rate; may lead to: ARREST IN SYSTOLE

Front 98

Hypocalcemia produces ________________ contractions and _____ heart rate; may lead to:

Back 98

Hypocalcemia produces WEAK, IRREGULAR contractions and RAPID heart rate; may lead to: TETANY

Front 99

3 factors that affect stroke volume:

Back 99

-preload
-contractility
-afterload

Front 100

The amount of tension in the ventricular myocardium immediately before it begins to contract:

Back 100

preload

Front 101

factor that affects stroke volume:
=strength of contraction

Back 101

contractility

Front 102

-the more the heart fills with blood during diastole, the greater the force of contraction during systole (or “the ventricles eject as much blood as they receive”)

Back 102

the Frank-Starling law of the heart.
SV ∝ EDV

Front 103

Factors that increase contractility:
Factors that decrease contractility:

Back 103

Factors that increase contractility: Positive Inotropic agents
Factors that decrease contractility: Negative Inotropic agents

Front 104

The blood pressure in the aorta and pulmonary trunk immediately distal to the semilunar valves; opposes the opening of these valves and thus limits stroke volume:

Back 104

Afterload

Front 105

↑ afterload = __ stroke volume.

Back 105

↑ afterload = ↓ stroke volume

Front 106

___________ and __________ increase afterload.

Back 106

Hypertension and atherosclerosis increase afterload.

Front 107

Right ventricular failure due to obstructed pulmonary circulation is called:

Back 107

Cor pulmonale; a common complication of emphysema, chronic bronchitis, and black lung disease.

Front 108

Explain how exercise affects proprioceptors and blood flow:

Back 108

Proprioceptors in the muscles and joints transmit to the cardiac centers signalling the need for increased blood flow to muscles → Muscular activity increases venous return → This ↑ preload on R. Ventricle → ↑ preload in L. ventricle as more blood flows through the pulmonary circuit → stroke volume to body ↑ to match ↑ venous return.

Front 109

Training → ventricle hypertrophy which:

Back 109

→ ↑ SV and allows the heart to beat more slowly and still maintain the same cardiac output.

Front 110

Solution of these is used for the emergency treatment of heart attacks:

Back 110

calcium chloride & glucagon

Front 111

cardiac stimulant from the foxglove plant that raises the intracellular calcium level and contraction strength; used to treat congestive heart failure:

Back 111

Digitalis