Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Anat/Phys > Chapter 17: The Heart -Lecture > Flashcards

Chapter 17: The Heart -Lecture Flashcards

1
Q

pacemaker potentials

A

spontaneously changing membrane potentials that will initiate action potentials that will then spread throughout the heart to trigger contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

autorythmic cells

A

make up the intrinsic conduction system and do not maintain a stable resting potential (*unlike skeletal muscle fiber and other contractile heart cells)
- unstable resting potential continuously depolarizes, drifting slowly towards threshold

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

electrocardiograph

A

-used to detect electrical currents generated in the heart, the electrical currents that then spread throughout the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

electrocardiogram (ECG or EKG)

A
  • record of heart activity is a composite of all the action potentials generated by both your modal and nodal and contractile cells at a given time
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

heart murmur

A
  • abnormal heart sounds
    1. swishing sound(insufficient or incomplete): the valves are not closing properly
    2. High pitched sound or click (stenotic): valves don’t open all the way
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

systole

A

-contractions of the heart that force blood from the chambers of the heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

diastole

A

-relaxation where the heart is filling with blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

cardiac output(CO)

A
  • amount of blood pumped by each ventricle in one minute

- ~ 5.25 L/min - how fast its moving

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

stroke volume

A

-volume of blood pumped out by one ventricle with each beat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

vagal tone

A

-in resting conditions, the dominant impulses sent to the SA node by autonomic system are inhibitory, causing the heart to beat at around 75 bpm instead of the 100 bpm the SA node would normally dictate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

pericarditis

A
  • inflammation of the pericardium, roughens the serous membrane surfaces
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

cardiac tamponade

A
  • “heart plug”
  • condition in which the heart is compressed by fluid
  • Physicians treat it by inserting a syringe into the pericardial cavity and draining off the excess fluid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

angina pectoris

A
  • “choked chest”
  • thoracic pain caused by a fleeting deficiency in blood delivery to the myocardium
  • it may result from stress-induced spasms of coronary arteries or from increased physical demands on the heart
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

myocardial infarction (MI)

A
  • AKA Heart Attack
  • serious prolonged coronary blockage
  • whether or not a person survives depends on the extent & location of damage
  • damage to the left ventricle(systemic pump) is MOST serious
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Arrythmia

A

-uncoordinated atrial & ventricular contractions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Fibrillation

A

-rapid & irregular or out-of-phase contractions where rapid activity in other regions of the heart take control away from the SA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Ectopic Focus

A
  • abnormal pacemaker takes over the heart

- ex. AV node sets rhythm rather than SA

18
Q

Junctional Rhythm

A

-pace set by AV node- 40-60 beats/min

19
Q

Extrasystole

A
  • (premature ventricular beat -PVB)
  • small region of the heart creates impulses more quickly than the SA node, so you get premature contraction
  • they are often felt as “skipped beats” or palpitations
20
Q

Heart Block

A
  • impulses are blocked between the atria and ventricles

- if this blockage is total , an artificial pacemaker may be needed

21
Q

Hypocalcemia

A
  • low calcium blood levels

- slows heart’s response to electrical signals

22
Q

Hypercalcemia

A
  • too high calcium blood levels

- increases heart responses; leads to spastic heart contractions that permit the heart a little rest

23
Q

Hypokalemia

A
  • too low potassium blood levels
  • the heart beats feebly and arrythmically
  • life threatening
24
Q

Hyperkalemia

A
  • too high potassium blood levels
  • interferes with depolarization by lowering the resting potential
  • leads to heart block & cardiac arrest
25
Q

Tachycardia

A
  • abnormally fast heart rate- >100beats/min

- can be caused by changes in body temp, stress, drugs or heart disease

26
Q

Bradycardia

A
  • heart rate < 60beats/min
  • can be caused by drugs, low body temp, parasympathetic activation
  • in trained athletes: the HR is often as low as 40bpm because the heart has hypertrophied and SV has increased, allowing resting HR to be lower and still provide the same CO
27
Q

Congestive heart failure(CHF)

A
  • heart can’t pump efficiently enough to meet the demands of the tissue
  • can be caused by : coronary athersclerosis(clogged artery vessels), persistent high blood pressure, multiple myocardial infarctions, dilated cardiomyopathy, DCM(ventricles stretch and become flabby and myocardium deteriorates)
28
Q

edema

A

-excess of watery fluid collecting in cavity or tissues of body

29
Q

Pulmonary congestion

A
  • failure of the LEFT side of the heart; fluid builds up in the lungs(pulmonary edema)
  • right side keeps sending blood
30
Q

Peripheral congestion

A

-failure of right side of the heart; blood stagnates in organs and edema occurs in extremities

31
Q

Mechanism of Contraction of Contractile Cardiac Muscle Fibers

A
  1. Na+ influx from extracellular space, causes positive feedback opening of voltage-gated Na+ channels; membrane potential quickly depolarizes (-90 to +30 mV); Na+ channels close within 3 ms of opening.
  2. Depolarization causes release of Ca++ from sarcoplasmic reticulum (as in skeletal muscle), allowing sliding actin and myosin to proceed.
  3. Depolarization ALSO causes opening of slow Ca++ channels on the membrane (special to cardiac muscle), further increasing Ca++ influx and activation of filaments. This causes more prolonged depolarization than in skeletal muscle, resulting in a plateau action potential, rather than a “spiked” action potential (as in skeletal muscle cells).
32
Q

Differences Between Skeletal & Cardiac MUSCLE Contraction

A
  1. All-or-None Law - Gap junctions allow all cardiac muscle cells to be linked electrochemically, so that activation of a small group of cells spreads like a wave throughout the entire heart. This is essential for “synchronistic” contraction of the heart as opposed to skeletal muscle.
  2. Automicity (Autorhythmicity) - some cardiac muscle cells are “self-excitable” allowing for rhythmic waves of contraction to adjacent cells throughout the heart. Skeletal muscle cells must be stimulated by independent motor neurons as part of a motor unit.
  3. Length of Absolute Refractory Period - The absolute refractory period of cardiac muscle cells is much longer than skeletal muscle cells (250 ms vs. 2-3 ms), preventing wave summation and tetanic contractions which would cause the heart to stop pumping rhythmically.
33
Q

*plateau in contractile cardiac muscle cells

A
  • slow Ca2+ channels open allowing Ca2+ from the EXTRACELLULAR SPACE.
  • this triggers Ca2+ channels in SR to be opened; allowing more into the cell, this keeps cell depolarized because few K+ channels are open, then creates plateau
  • this allows for the sustained contraction necessary to eject blood from heart
34
Q

Sequence of cardiac intrinsic conduction system

A
  1. SINOTRIAL(SA) NODE- in right atrium- The heart’s main pacemaker; sets heart rate by generating impulses at about 75bpm; called sinus rhythm.
  2. ATRIOVENTRICULAR NODE(AV)-in R.atrium- Impulse is delayed here for about 0.1 s to allow atria to complete their contraction before the ventricle contracts, slows down signal.
  3. ATRIOVENTRICULAR(AV) BUNDLE OF HIS- in Atrialventricular septum- Only electrical connection between the atria and ventricles.
  4. RIGHT&LEFT BUNDLE OF BRANCHES-conducts impulses through the Interventricular septum.
  5. PURKINJE FIBERS-in Ventricular Walls-Depolarize the contractile cells of the ventricles(both)
35
Q

sympathetic nervous system & HR

A
  • the SNS releases NOREPINEPHRINE which results in increased HR.
  • also speeds up Ca2+ movement to cells, which increases contractility and speeds relaxation. SV(stroke volume) is increased
36
Q

Parasympathetic nervous system

A
  • the PNS uses ACETYLCHOLINE Ach, will reduce heart rate, but does not affect contractlity. Ach opens up channels to start AP.
37
Q

what causes “lub dup” heart sounds?

A

closing of the heart valves

38
Q

Mechanical events of Cardiac Cycle

A
  1. VENTRICULAR FILLING:MID-TO-LATE DIASTOLE: ventricles fill and contract; AV valves open, your semilunar valves are closed
  2. VENTRICULAR SYSTOLE-atria relax, ventricles begin to contract; ventricular blood pressure forces AV valves closed, leading to ISOVOLUMETRIC CONTRACTION
    - when the pressure in the ventricles rises above that in the large vessels leaving them; the SL valves open and blood is expelled into the aorta and pulmonary trunk during the VENTRICULAR EJECTION PHASE
  3. ISOVOLUMETRIC RELAXATION: EARLY DIASTOLE-ventricles relax, ventricular pressure drops rapidly and blood in the aorta & pulmonary trunk flows back toward the heart; closing the SL valves. *during isovolumetric contraction and isovolumetric relaxation both AV and SL valves are closed
39
Q

Why is pulmonary arterial pressure so much lower than aortic?

A

Blood is just going to the lungs , Vs. the aorta that goes to the whole body

40
Q

What is Cardiac Reserve? How does it different between athletes and nonathletes?

A
  • CR is the difference between resting and maximal cardiac input
  • NONATHLETE- 20-25L/min(4-5X resting CO)
  • ATHLETE-up to 35L/min (7X resting CO)
    • CO is variable & increases to special demands-ex.running to catch bus
41
Q

3 factors that affect regulation of stroke volume

A
  1. PRELOAD(degree of stretch of heart muscle before contraction)- Cardiac muscles are normally shorter than optimal length, so stretching can increase contractile force.
    - Venous Return- amount of blood returning to the heart can affect muscle stretch- slow HR &exercise increase volume or speed of venous return and this increase EDV and SV
  2. CONTRACTILITY-contractile strength achieved at a given muscle length
    - this depends on the amount of Ca2+ entering the cytoplasm
    - increased contractile strength can be caused by:hormones, drugs, sympathetic stimulation>positive inotropic agents
    - decreased contractile strength can be caused by: acidosis, high extracellular potassium, some drugs> negative inotropic agents
  3. AFTERLOAD-back pressure exerted on atrial blood. In people w/ hypertension(high BP) afterload can reduce the ability of ventricles to eject blood, increasing ESV & decreasing SV.
42
Q

What is normal heart rate for fetus, women, men?

A

Fetus- fastest (140-160 beats/min)
Women- (72-80 beats/min)
Men- (64-72 beats/min)

Anat/Phys (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions