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BIOL 432 > ECG, Cardiac Cycle, Cardiac output > Flashcards

ECG, Cardiac Cycle, Cardiac output Flashcards

1
Q

What does an ECG measure?

A

difference btw the skin and the electrical changes which accompany the cardiac cycle

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2
Q

What happens during the P wave?

A

movement of depolarization from the SA node through the atria
- atrial contraction begins shortly after onset of P wave

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3
Q

What happens during the PQ interval?

A

measured from beginning of atrial depolarization to beginning of ventricular depolarization
- beginning of P wave right before Q wave
- includes atrial depolarization, passage of DP wave through AV node, AV bundle, bundle branches, conduction myofibers

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4
Q

What happens during the QRS wave?

A

movement of depolarization through the ventricles
complicated shape is due to the different sizes of ventricles
- moves through apex to semilunar valves

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5
Q

What happens during the T wave?

A

movement of repolarization wave through the ventricles
- depolarization of the atria masked by QRS

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6
Q

What is the TP interval?

A

measured from the end of the T wave to the beginning of atrial depolarization
- period of ventricular filling
- both atria and ventricle are in diastole

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7
Q

What is an AV nodal block?

A

damage to autorhytmic cells of AV node
- increased time btw P wave and QRS
- can see another P wave prior to QRS

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8
Q

What is premature ventricular contraction?

A

ectopic place in atria or ventricle that initiates an addition QRS
- prolonged QRS interval
- inverted T wave

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9
Q

What is a myocardial infarction?

A

tissue damage due to ischemia - lack of O2 to myocardial muscle
- elevated ST segment
- enlarged R wave
- prolonged PR segment

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10
Q

What is mitral stenosis?

A

Narrowing of the L AV valve with insufficient closure
- back flow of blood/enlargement of L atrium
- enlargement of the P wave
- sharp P wave peak

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11
Q

What is diastole? What do the AV and semilunar valves look like?

A

diastole - heart at rest - atria and ventricle both at rest
- blood flows into atria via VC
- ventricular filling - AV valves open bc P atria > P ventricles
- semilunar valves closed bc P pulmonary trunk > P ventricle

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12
Q

What is isovolumetric contraction? What do the AV and SL valves look like?

A

ventricle increases in pressure
ALL 4 VALVES CLOSED - no change in volume but pressure in ventricle increases

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13
Q

What is ventricular ejection? What do the AV and SL valves look like?

A

ventricular ejection - P ventricles > P pulmonary trunk/aorta
- semilunar valves open
- AV nodes closed

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14
Q

What is isovolumentric relaxation? What do the AV and SL valves look like?

A

ventricles relax and decrease in P
- semilunar valves close, back flow of blood in aorta and pulmonary trunk
- AV valves still closed bc P ventricle > P atria
ALL 4 VALVES CLOSED

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15
Q

What is the diacrotic notch and what causes it?

A

After semilunar valves close, there is a small pressure blurb in aorta

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16
Q

Describe ventricular filling

A

TP interval - both A/V are in diastole
- AV valves open, SL closed
- ventricles almost completely fill b4 atria contract
- atrial and ventricular P gradually rise

17
Q

Describe atrial systole (ventricular diastole)

A

shortly after onset of P wave
- AV valves remain open, SL closed
- atrial contraction sharply increases P atria
- short rise and fall of P ventricle

18
Q

Describe ventricular systole (continuation of atrial diastole)

A

shortly after onset of QRS wave
- AV closes right after the R wave - beginning is-volumetric contraction
- P atrial increases sharply before falling in response of ventricular blood, begins to slowly rise
- P ventricle rises until > P aorta: SL valves open and ends isovolumetric contraction
- V ventricle decreases

19
Q

Describe ventricular diastole (and continuation of atrial diastole)

A

shortly after onset of T wave, continues through TP interval
- P ventricle falls as contraction stops
- SL valves close - isovolumetric relaxation begins
- AV valves open as P ventricle continues to decrease and fall believe P atria - end of isovolumetric relaxation

20
Q

What are the heart sounds lubb dupp cause by?

A

Lubb - closure of AV valves - long and booming

Dupp - closure of SL valves - short and sharp

21
Q

What is end diastolic volume?

A

greater amount of blood in ventricles
- end of resting period/ventricular filing
- AV valves closed

22
Q

What is end systolic volume?

A

at the end of ventricular contraction, the volume of blood left over in the heart
- lowest volume

23
Q

What is stroke volume?

A

End Diastolic volume - End systolic volume
= volume moved out of ONE ventricle

24
Q

What is cardiac output and what is it determined by?

A

cardiac output is the heart rate x stroke volume

typically around 5 mL/min

25
Q

How does the parasympathetic nervous system have an effect on heart rate?

A

cardiac center located in medulla oblongata - connects to vagus nerve and slows HR
- preganglionic neural axons of vagus nerve enter SA and AV nodes
- SA nodal depolarization rate inhibited
- decreased synthesis of cAMP, less transient Ca open
- B/G subunits open K channels

26
Q

How does the sympathetic nervous system have an effect on heart rate?

A

Beta 1 receptors bind NE/EPI on SA and AV nodes
- activated the alpha 1 subunits to activate adenylate cyclase = increase cAMP
- cAMP opens more funny channels ad P enzymes that open transient Ca channels = faster heart rate

27
Q

What effect foes the sympathetic nervous system have on the following structures:
ventricular conduction pathway
ventricular muscle
atrial muscle
adrenal medulla
veins

A

ventricular conduction pathway: increases excitability and conduction though AV bundle/bundle fibers

atrial AND ventricular muscle - increases contractility

adrenal medulla - promotes EPI secretion

veins - increases venous return

28
Q

What effect does the parasympathetic nervous system have on the following structures:
ventricular conduction pathway
atrial muscle
ventricular muscle
adrenal medulla
veins

A

atrial muscle - decreases contractility

ventricular conduction pathway, ventricular muscle, adrenal medulla, veins - no effect

29
Q

What is stoke volume and what is it dependent on?

A

volume ejected by one ventricle
- each ventricle ejects the same amount of blood
- average stoke volume = 70 mL

affected by:
preload
contractility
after load

30
Q

What is preload and how does it affect stroke volume? What is starlings law?

A

preload - the amount of blood which stretches the ventricles as AV valve closes (end diastolic volume)
- dependent on myofiber length

increased by:
increasing filling time (slower HR)
increasing venous return:
- exercise (contracting deep veins)
- inspiration (decreased intrathoracic pressure)
- increased blood volume (ADH, aldosterone)

Starlings law: the more the heart is filled and stretched, the grease the force in which the heart contracts

31
Q

What is contractility and how does it affect stroke volume?

A

cardiac fiber contractile force - independent of myofiber length

increase Ca influx from extracellular fluid and SR
- enhanced by hormones (glucagon, thyroxin, epi)
- enhanced by low extracellular [K]
- enhanced by drugs - digitalis

depressed by
- acidosis (increased level of H ions)
- excess extracellular [K]
- Ca-channel blocking drugs ( verapamil, cadizem, procardia)

32
Q

How does epi effect contractility?

A

epinephrine - adrenal glands
- same effect as ANS
- binds to GPCR on ventricular contractile cells to activate protein kinase A - phosphorylates PM and SR Ca channels and increases Ca in cytosol

33
Q

How does thyroxin affect contractility intranuclearly and extranuclearly?

A

Thyroxin - thyroid gland
- produces slower but more sustained increase in HR
- enhances epi and NE from adrenal gland

  • intranuclear - binds to genes that increase transcription of gene that increases velocity of contraction btw myosin and actin
  • increases level of transcription mRNA = increased number of SR Ca ATPase pumps
  • extranuclear - increased transport of AA, Ca and sugars across plasma membrane
34
Q

What influence does Na have on the heart?

A

excess Na inhibits Ca entry into cardiac muscle
- blocks heart contraction

35
Q

What influence does K have on the heart?

A

excess K lowers resting potential and inhibits depolarization
- leads to heart block and cardiac arrest
- decreased HR and force

Low K - decreases heart rate and leads to arrhythmia

36
Q

What effect does Ca have on the heart?

A

excess Ca - prolongs plateau phase of AP
- increases heart irritability
- leads to spastic heart contractions = higher HR
- increased contractility

low Ca - depresses heart activity

37
Q

What is after load and what affects it?

A

after load - the pressure pushing against the SL valves by the aorta and pulmonary trunk
- increased pressure = harder to pump blood out

increased after load
- aortic stenosis/insufficiency
- pulmonary stenosis
- HTN
- high blood viscosity
- increased intrathoracic pressure

decreased for individuals with mitral valve prolapse

BIOL 432 (25 decks)

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