ECG, Cardiac Cycle, Cardiac output Flashcards
What does an ECG measure?
difference btw the skin and the electrical changes which accompany the cardiac cycle
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
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
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
What happens during the T wave?
movement of repolarization wave through the ventricles
- depolarization of the atria masked by QRS
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
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
What is premature ventricular contraction?
ectopic place in atria or ventricle that initiates an addition QRS
- prolonged QRS interval
- inverted T wave
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
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
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
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
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
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
What is the diacrotic notch and what causes it?
After semilunar valves close, there is a small pressure blurb in aorta
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
