ECG, Cardiac Cycle, Cardiac output Flashcards by Jerica Golez

What does an ECG measure?

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

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What happens during the P wave?

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

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What happens during the PQ interval?

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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What happens during the QRS wave?

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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What happens during the T wave?

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

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What is the TP interval?

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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What is an AV nodal block?

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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What is premature ventricular contraction?

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

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What is a myocardial infarction?

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

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What is mitral stenosis?

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

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

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

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

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

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

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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What is the diacrotic notch and what causes it?

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

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Describe ventricular filling

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

Describe atrial systole (ventricular diastole)

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

Describe ventricular systole (continuation of atrial diastole)

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

Describe ventricular diastole (and continuation of atrial diastole)

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

What are the heart sounds lubb dupp cause by?

Lubb - closure of AV valves - long and booming

Dupp - closure of SL valves - short and sharp

What is end diastolic volume?

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

What is end systolic volume?

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

What is stroke volume?

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

What is cardiac output and what is it determined by?

cardiac output is the heart rate x stroke volume

typically around 5 mL/min

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

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

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

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

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

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

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

atrial muscle - decreases contractility ventricular conduction pathway, ventricular muscle, adrenal medulla, veins - no effect

What is stoke volume and what is it dependent on?

volume ejected by one ventricle - each ventricle ejects the same amount of blood - average stoke volume = 70 mL affected by: preload contractility after load

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

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

What is contractility and how does it affect stroke volume?

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)

How does epi effect contractility?

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

How does thyroxin affect contractility intranuclearly and extranuclearly?

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

What influence does Na have on the heart?

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

What influence does K have on the heart?

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

What effect does Ca have on the heart?

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

What is after load and what affects it?

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