Test 4 Flashcards
5 phases of the cardiac Cycle
1) Isovolumetric Ventricular Contraction
2) Ventricular Ejection
3) Isovolumetric Relaxation
4) Ventricular Filling
5) Atrial Systole
Isovolumetric (putting out effort but not moving) Ventricular Contraction
- wall tension of the ventricles increases
- intraventricular pressures increase
- mitral and tricuspid vavles close
- pulmonic and aortic vavles remain closed (R of the QRS complex) until there is a certain amount of pressure in the ventricles
- volume stays the same
Mitral valve closes when
LV pressure exceeds LA pressure
Ventricular ejection
- Pressure = flow x resistance
- intraventricular pressure has risen and eventually the pressure exceeds the pressure in the pulmonary artery and aorta which results in the valves opening.
- LV achieved maximum volume
Ventricular ejection fraction
- about 40-60% of blood in the ventricles is ejected
- EF=SV/EDV
T wave created by
Ventricular repolarization toward the end of ventricular systole
Isovolumetric relaxation
- Toward the end of ventricular systole, the pressure inside the ventricles fall below that of aorta and pulmonary artery
- AV and PV valves slam closed and the MV and TV already closed
- blood continues to fill the atria
Dicrotic notch
- Reflective pressure wave as the aortic valve slams closed after ventricular systole
- important for intra-aortic balloon pump (IABP)
Rapid Ventricular Filling
- Atrial pressure greater than ventricular pressure
- MV and TV open
- Blood flows passively from the pressurized atria into the ventricles
- 70% of the ventricular filling takes place by PASSIVE PROCESS
Atrial Systole (Atrial Kick)
- Coincides with late ventricular diastole
- ventricles receive a 30% boost from the atrial kick for more effective diastolic filling
P wave
atrial depolarization
Cardiac Output
CO= Heart rate x stroke volume
Factors affecting stroke volume
- Preload
- afterload
- contractility (inotropy)
Preload
- Passive stretching of the ventricular walls
- caused by the blood volume in the ventricles at the end of diastole (EDV)
- Valvular insufficiency may allow backflow altering the EDV
Afterload
- Resistance
- pressure the the LV must overcome to eject blood
Contractility (inotropy)
- Capability of the heart walls to contract after depolarization
- ability to contract depends on how much fiber gets stretched at EDV and health of the fibers
Doplarization
- electrical change of cell membrane potential making it less negative
- Na+ coming in
Repolarization
- electrical change of cell membrane potential making it more negative to its resting state after depolarization
- K+ leaving
Nernst equation
EMF= (+or-61.5/valence)(log([inside]/[outside])
-Na, K, Ca, Cl
SA node as the pacemaker
- it does not require a stimulus to fire like most nerve cells
- self-firing
SA node ion potentials
- SA node slowly leaks K+ out of the cell and slowly leaks Na+ into the cells (funny current)
- when the leaks reduce the membrane potential to -40mV it hits the excitation threshold
- once excitation occurs, you just can’t stop it
Cardiac conduction
Heart cannot contract and pump unless and until there’s electrical stimuli
automaticity
cell’s ability to spontaneously initiate an impulse
excitability
cell’s responsiveness to an electrical stimuli
conductivity
cell’s ability to transmit electrical stimulus to another cell
contractility
how well a cell contracts after exposure to a stimulus
conduction
-electrical stimuli created by pacemakers cells usually travels through the heart via the CONDUCTION SYSTEM
Conduction system pathway
SA node-> internodal tracts-> AV node-> Bundle of His-> right and left bundle branches-> purkinje fibers
Conduction rate of SA node (affected by sympathetic or parasympathetic inervation)
SA node: 100 bpm
-not from an upstream source with a faster inherent rate
Conduction rate of AV node (affected by sympathetic or parasympathetic inervation)
AV node: 40-60 bpm
-not from an upstream source with a faster inherent rate
Conduction rate of purkinje fibers (affected by sympathetic or parasympathetic inervation)
Purkinje fibers: 20-40 bpm
-not from an upstream source with a faster inherent rate
how electrical signals captured
- via electrodes
- amplified
- then sent to a monitor producing an ECG
ECG
- voltage graph
- 5 large blocks is a second
- one large box is .20 seconds and .5 mV
- each smaller box in the large box is .04 sec and each small box is .1 mV
one ECG wave =
one cardiac cycle
p wave
- atrial depolarization
- first wave on ECG
Q wave
first negative deflection (below isoelectric line)
R wave
-first upward or positive deflection
S wave
first negative deflection after the R wave
T wave
- ventricular repolarization/ recovery
- usually rounded upward immediately after QRS complex
U wave
- purkinje fiber repolarization (often not seen)
- usually only seen in slow heart rhythms
PR interval
- atrial impulse extending from the SA node through the AV node, bundle of his, and Right and Left branches
- Starts at the beginning of the P wave and ends at the beginning of the QRS complex
- normally .12-.20 seconds
- greater than .20 seconds= conduction delay through the atria or AV junction
- less than .12= the impulse started somewhere other than the SA node
QRS interval/ QRS Complex
- Follows P wave
- measured from beginning of Q wave to End of S wave
- REPRESENTS THE INTRAVENTRICULAR CONDUCTION TIME
- Wide QRS may be due to MI or conduction delay (AV block)
- “Notched” may be due to bundle branch block
ST Segment (very important)
- Represents the end of ventricular depolarization and the beginning of repolarization
- VERY IMPORTANT in open heart Sx
- Should be isoelectric (flat and at baseline)
- depression may suggest acute MI or ischemia
- elevation may suggest injury to the myocardium
- OBSERVE BOTH PRE-OP AND POST-OP!
QT interval
- represents ventricular depolarization and repolarization
- measured from beginning of QRS to end of T wave
- length varies with rate (increased HR= short QT interval)
- Normal: .36-0.44
- prolonged QT= longer relative refractory period
- short QT= hypercalcemia, digoxin toxicity
Elusive U wave
- purkinje/ ventricular recovery/ repolarization
- not on every strip
- upright and round
8 easy steps to evaluating ECG’s
1) Are the atria and ventricles “regular”?
2) What’s the rate?
3) Evaluate the P waves
4) What’s the P-R interval duration?
5) What’s the QRS complex duration?
6) Evaluate the T waves
7) What’s the Q-T interval?
8) “Other” (ectopic beats, abnormal rhythms, unique rate characteristics)
Are the Atria and Ventricles regular?
What to look at
- measure P to P interval (atrial regularity)
- measure R to R interval (ventricular regularity)
Whats the rate?
- the 10x method
- 1500 method (# of small squares between P-P and divide 1500 by that #)
- Bradycardia= 100bpm
Evaluate the P waves
- Are they present?
- is there one P wave for every QRS complex
- normal size and shape?
What is the P-R interval duration
- Should be .12-.20 seconds
- is the interval constant
- is there QRS complex for every P wave
What is the QRS complex duration
- Normal .06-.12
- Prolonged suggests a conduction delay through ventricles (ischemia, electrolyte abnormalities, drugs)
- Is the shape normal for that lead
Evaluate T waves
-are they present?
-normal shape?
-if peaked= hyperkalemia
-inversion is normal in peds and yound females
-other causes of T wave inversion = ischemia, pulmonary emboli,
cardiomyopathy, electrolyte abnormalities
What is the Q-T interval
- Normal: .36-.44 seconds
- # of small boxes from beginning of the QRS Complex to the end of the T wave and returning to baseline and multiply by .04
PR interval >.20 suggests
-Conduction delay through atria or AV junction
PR interval
-impulse started somewhere other than SA node
QRS interval Wide may be due to
-MI or conduction delay (AV block)
QRS interval “notched” may be due to
bundle branch block (RBBB or LBBB)
ST segment depression may suggest
-acute MI or ischemia
ST segment elevation may suggest
-injury to the myocardium
QT interval prolonged
-longer relative refractory period
QT interval short
hyercalcemia
Elusive U wave seen prominently in
hypercalcemia and hypokalemia
