Brainscape's Knowledge GenomeTM

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


See full index

Physiology Unit 3 > Cardiovascular Physiology (heart) > Flashcards

Cardiovascular Physiology (heart) Flashcards

1
Q

ECG Diagnostic issues

A
  1. Heart rate,
  2. heart rhythm: irregularities arrhythmia, atrial fibrillation
  3. Are all waves present P, R, T?
  4. For each P-wave is there a QRS complex? - heart block if no P-wave present
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Cardiac cycle systole & diastole

A
  1. Late diastole
  2. Atrial systole
  3. Isovolumetric ventricular contraction (1st sound)
  4. Ventricular ejection
  5. Isovolumetric relaxation (2nd sound)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Late diastole

A

Step one:
superior and inferior vena cava & pulmonary veins Fill atria in heart, causing high pressure, and by gravity and pressure starts to fill ventricles (about 80%)
*AV valves open

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

Atrial systole

A

Step 2: atria contracts last 20% of blood goes into ventricle.

(End diastolic volume) : volume of blood in ventricles at the end of diastolic phase

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

Isovolumetric ventricular contraction

A

Step 3: increase of ventricular pressure causes, AV valve to shut (AV and SL are both shut) * s1, 1st heart sound (Lup)
High pressure is create volume is same
[when the av node delays the signal in the conduction cycle]
atrial repolarization before QRS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Ventricular ejection

A

Step 4 : Increases in ventricular pressure causes SL valves to open, blood goes into aorta and pulmonary arteries
( end systolic volume ) : blood remaining in ventricles after contraction
* ventricular contraction

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

Isovolumetric relaxation

A

Step 5: ventricular diastole begins; high pressure in aorta and pulmonary arteries close the SL valves (causing the s2 heart sound ‘dub’)

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

Pwave

A

Atria depolarization

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

QRS complex

A

Ventricular depolarization and contraction. (Ventricular systole and atrial repolarization)

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

T wave

A

Ventricular repolarization (relaxation of ventricles)

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

EDV

A 
End diastolic volume is the maximum amount of blood in the ventricles before contraction 
*during atrial systole
End (finished)
Diastolic (relaxation)
[low pressure high volume]
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

ESV

A

End systolic volume: blood remaining in ventricles after contraction. During the ventricular ejection phase of the cardiac cycle
[high pressure low volume]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Pressure volume curve

A

X axis : left ventricle volume (ml)
Y axis : left ventricle pressure (mmhg)
A= (late diastole) (ESV) ~65ml
1. A-A1: passive filling ventricle
2. A1-B: aorta contracts (EDV) ~135ml
3. B-C: isovolumetric ventricular contraction (pressure building)
4. C-D: ventricular ejection (stroke volume)
5. D-A: isovolumetric ventricular relaxation. (ESV)

Stroke volume = EDV-ESV
135ml-65ml= 70 ml

  • practice on whiteboard
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Ways to modulate heart variables

A 
Heart rate (BPM) x 
stroke volume (ml/beat) [EDV-ESV] 
= cardiac out put (ml/min)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

To meet metabolic needs

A

Increase or decrease HR and/or increase or decrease in stroke volume is controlled by ANS control and neurohormones (epi/ne)

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

Modulating stroke volume

A
  1. Length of sarcomere cells at beginning of contraction (effects preload) [starlings curve]
  2. Contractility of cells (more calcium = stronger HB)
  3. After load (refers to resistance of arterial system)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Stroke volume

A

Stroke volume= force of contraction

^force=^stroke volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Starlings curve

A

*length of sarcomere
As stretch^ [preload EDV{ml}]= ^force [rubber band] = ^ stroke volume.

More blood in heart = more blood pumped out “Frank’s starling law of the heart”

Stretch is a function of EDV and function of venous return.

  • white board
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Modulating stroke volume:

Contractility of cells ca2+

A

^ca2+= ^ force of contraction
Altered by Structures:
•altered by ECF entry ; SR release / reuptake/ storage

• chemicals that have an effect of contractility:

  1. Inotropic agents : positive (E,NE) & negative
  2. Phospholambin: protein that ^ ca2+atpase activity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Epi/NE catecholamines increase of cardiac contraction

A

Epi/NE bind to B1 (adrenergic) receptors>
activates cAMP 2nd messenger system>
1.Voltage gated Ca2+ channels: open time increases> ^ca2+ entry from ECF> *on both ^ ca2+ stores in SR, ^ ca2+ released[more forceful contraction]

  1. phospholamban> ^ ca2+ atpase on SR: ca2+ removed from cytosol faster > shortens ca-troponin binding time [ shorter duration of contraction]
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Afterload

A

The resistance or pressure exerted of the arterial system.
^ afterload resistance = less stroke volume

Lower compliance = ^ afterload (heart must work harder)
^ work= ^ muscle hypertrophy = enlarged heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Explain mechanistic level how sympathetic nervous system influences EDV and cardiac output

A

** 20 point question **

23
Q

Cardiac output : HRxSV

A

..

24
Q

Sympathetic nervous system on EDV

A

Sympathetic(Epi) ^ causes venous construction = greater venous return = ^EDV = ^ force of contraction = larger stroke volume (ml/beat)
[which affects cardiac output]

25
Q

How does the sympathetic nervous system affect HR, therefore cardiac output?

A

ANS (sympathetic) controls rate of depolarization of autorythmic cells NE
Increases HR and cardiac output

26
Q

Where does blood go after aorta

A

To arteries, arterials, capillaries
>
Venules, Veins, vena cava

27
Q

Heart circulation

A

Superior and inferior vena cava to R atrium, R ventricle, pulmonary vein , into lungs (gas exchange co2-o2) left atrium through pulmonary vein , left ventricle, aorta and pulmonary artery

28
Q

What are the three pathways Of blood?

A

Systemic circuit, pulmonary circuit, portal system(bypasses the systemic circuit example hepatic, renal nephron)

29
Q

Cardiac muscle

A

Called Myocardium, is made of myocytes cells. The two types are contractile Cells and autorythmic cell

30
Q

Perfusion carries

A

Oxygen, carbon dioxide, proteins, ions, nutrients, waste to tissues and organs from the transportation of blood.

31
Q

Differences of contractile myocytes from skeleton muscle fibers

A
  1. Smaller/shorter,
  2. mono nuclear/one nucleus per myocyte,
  3. branched structure connected to one another via intercalated discs
32
Q

Intercalated discs

A

Forms coordinated network of cells that share their cytoplasm through gap Junction and Desmosomes

33
Q

Name 4 similarities in the process of contraction in cardiac muscles as skeleton muscles

A
  1. Calcium is primarily ion involved
  2. Calcium Stored SR
  3. Action potential influx of sodium travels down the t tubules to initiate the calcium signal ( not same mech.)
  4. Sodium potassium ATPase pump maintains RMP
34
Q

Name the four differences in the contraction process of cardiac muscle in comparison to skeleton myself

A
  1. Voltage gated Calcium L type channels in t tube initiate the ligand gated a calcium spark from the SR ( calcium inducible, Calcium release)
  2.  calcium Sparks Summit intracellularly to build a strong enough calcium signal to cause contraction (graded contraction)
  3.  calcium is removed from cytoplasm by two pumps NCX and ca atpase pump
  4. Cardiac muscles do not have motor units because Intercalated discs act as one big motor unit
    (variation of tension comes from altering the calcium signal strength) 
35
Q

How does calcium concentration affect force of contraction

A

More calcium causes more cross bridges which causes higher tension

36
Q

What are the different types of channels involved in cardiac contraction compared to skeletal

A
  1. Fast and slow K+ channels (contractile cells)
    - ca2+ channels (plateau)
  2. Na & K+ If (funny) leak channels (auto rhythmic) (cause pacemaker potential)
    - ca2+ channels (depolarization)
37
Q

Name the steps of contractile cell action potential

A
  1. Cell is at resting potential -90 mV
  2. Depolarization occurs when signal received from a neighboring myocyte.
    - Na channel open (influx) reaches +20mV. Na close, fast K begin open.
  3. Initial repolarization begins as fast K channels are fully open (k efflux)
  4. Repolarization Plateau occurs as Calcium channels open (ca influx) and fast k close.
  5. Rapid repolarization occurs as calcium channels close and slow potassium channels open (K efflux)
38
Q

What are the unique characteristics of a contractile cell action potential’s

A
  1. Resting membrane potential is -90mv
  2. Action potential are triggered by auto rhythmic cells
  3. Action potential plateaus during repolarization (caused by Ca)
  4. Action potential lasts about 200 ms due to plateau
39
Q

Why is the plateau important in contractile cell action potential

A

It prevents tetanus in myocardium which would be fatal. Because the action potential lasts about as long as the contraction, the longer refractory period prevents summation

40
Q

List the steps of auto rhythmic cell action potential‘s

A
  1. pacemaker potential around -60 mV
  2. Open IF channels allow Na influx mainly and Drift potential towards threshold -40mv
  3. As membrane potential nears threshold if channels close and some calcium channels open CA influx pushing membrane toward threshold
  4. At threshold many channels Ca open causing depolarization (ca influx) -20mV
  5. Rapid repolarization begins when CA channels close and K channels open (K efflux) bringing membrane potential back down to pacemaker potential -60mv
41
Q

Autorythmic cell action potential unique characteristics

A
  1. Resting membrane potential is unstable and fluctuating (pacemaker potential )
  2. Action potential‘s initiate on their own through iF channels and then opening of calcium channels
  3. Rising phase of depolarization is caused by influx of calcium (compared to contractile and skeletal are Na )
  4. Action potential duration is variable generally 150 ms
42
Q

How can heart rate the modulated

A

By altering ion permeability of auto rhythmic cells through autonomic nervous system and or hormonal imput

43
Q

HR modulation in autorythmic cells example

A

Increase or decrease duration of pacemaker potential
causes
increase or decrease rate of action potential
which causes
increased or decreased rate of contractions
which causes
increased or decreased heart rate

44
Q

How do the 2 ANS divisions control heart rate

A

*antagonistic
Parasympathetic signal decrease heart rate.
Sympathetic signal increases heart rate


45
Q

The signal to increase or decrease heart rate initiates where

A

In the cardiovascular center in the medulla oblongata

46
Q

How does the parasympathetic signal continuously and put tonic control on the heart rate

A

SA node (hearts pacemaker) Autorythmic cells have a basal rate at 90 to 100 bpm. Average heart rate is 70 bpm, meaning that parasympathetic signals normally have a continuous input and allow fine-tuning to decrease or increase heart rate

47
Q

Mechanisms of parasympathetic control

A
  1. ACh released by parasympathetic neurons from ANS in the CVCC medulla oblangata
  2. Stimulation of auto rhythmic cell muscarinic cholinergics receptor
  3. ^ k+ efflux, decrease ca influx
  4. Lowers depolarization (hyperpolarization )
  5. Decreases HR
48
Q

What sets the pace for contractile cell contraction

A

The depolarization of auto rhythmic cells, that are normally led by the cells in the SA node

49
Q

Trace the pathway through the heart of the cardiac conduction system

A
  1. Sa node ( right atrium, initiate the pace of depolarization)
  2. Internodal pathway (conducting non contractile)
  3. Av node (slows down signal)
  4. Av septum (AV bundle and RL bundle branches)
  5. Purkinje fibers (smaller branches ) contract ventricles
50
Q

What are two important functional characteristics of the conduction Pathway

A
  1. Atria contracts first and the ventricles due to AV node delay. If this didn’t happen the atria and ventricles were to contract at the same time and blood wouldn’t flow properly
  2. Ventricles contract from Apex to base direction due to location of fibers and direction of signal conduction. This allows blood to be pushed down from the atria to the ventricles and up from the ventricles into the aorta/pulmonary trunk
51
Q

ECG waves, segments, and intervals

A

Waves: departure from baseline
Segments: regions between waves
Intervals: consisting of both waves and segments

52
Q

What does the cardiac cycle describe

A

The mechanical events of the heart namely diastole (relaxation of cardiac muscles) and systole (contraction of cardiac muscles)

53
Q

How does blood flow

A

From areas of high pressure to low pressure

54
Q

Contractility

A

The hearts ability of cardiac fibers to contract at any given length and is affected by calcium levels (determines force some contraction)

Physiology Unit 3 (4 decks)

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