P: Cardiac cycle Flashcards
What generates 1st heart sound?
Closure of AV valves
What generates 2nd heart sound?
Closure of semilunar valves
What is the order of cells generating contraction?
Spontaneous depolarizations generated in SA node by autorhythmic cells pass into surrounding myocardial cells and generate contraction as follows:
- atrial myocardial cells
- pause (fibrous layer)
- ventricular myocardial cells
What happens just before atrial systole?
- Both atria and ventricles are in diastole (relaxed)
- Atrial pressure slightly higher than ventricular –> semilunar valves closed, AV valves open –> blood leaks from atria to ventricle –> fills up 80-100% of ventricle
- Wave of depolorization spreads through both atria (P wave) generates atrial systole
What happens at atrial systole and at which second does it occur?
- t = 0 sec
- Pressure in atria increases –> ventricles are full (remaining 0-20%) –> End Dialostic Volume (EDV)
What is the End Dialostic Volume (EDV) at rest?
135 mL
(or 120-135 mL)
What happens at isovolumetric contraction phase of ventricular systole and at which second does it occur?
- t = 100 msec
- Slow rate of conduction at AV node
- Depolarization wave spreads into ventricles –> QRS wave (onset of ventricular contraction)
- Ventricle pressure > atrial pressure –> AV valves close (1st heart sound)
- Ventricular volume is constant
What pressure is required to open semilunar valves into aorta?
Minimum 80 mmHg (left ventricle)
What pressure is required to open semilunar valves into pulmonary artery?
Minimum 8 mmHg (right ventricle)
How long does isovolumetric contraction phase of ventricular systole last?
30 msec
What happens to atrial pressure during isovolumetric contraction phase of ventricular systole and why?
Rises slightly: pressure of ventricle causes AV valves to bulge into atria
What happens at ventricular systole and at which second does it occur?
- t = 130 msec
- Pressure LV > 80 mmHg > pressure aorta
- Pressure RV > 8 mmHg > pressure pulmonary artery
- Semilunar valves open
- Sharp increase in ventricular + aortic pressure to 120 mmHg
- Abrupt drop in ventricular volume –> rapid ejection
- Pressure falls as blood leaves ventricle –> reduced ejection
What is the End Systolic Volume (ESV) at rest?
60 mL
(or 50-65 mL)
What is stroke volume and how can you calculate it + what is its normal value?
Total volume of blood ejected
Stroke volume = EDV - ESV = 75 mL (or 70 mL)
To what pressure do the atria fall to during ventricular systole?
0 mmHg
What happens at isovolumetric relaxation phase of ventricular diastole and at what which second does it occur?
- t = 300 msec : repolarization of ventricles begin (T wave)
- t = 350 msec: LV pressure (100 mmHg) < aortic pressure ; RV pressure (10 mmHg) < pulmonary arterial pressure ; semilunar valves close (2nd heart sound)
- AV valves remain closed –> ventricular volume constant
What happens to ventricular, atrial and aortic pressures during isovolumetric relaxation phase of ventricular diastole?
- Ventricular pressure falls
- Atrial pressure increases (filling)
- Aortic pressure falls back to 80 mmHg
How long does isovolumetric relaxation phase of ventricular diastole last?
60 msec
What happens at ventricular diastole, at what which second does it occur and at which second does it end?
- t = 450 msec
- Atrial pressure > ventricular pressure –> AV valves open
- Rapid filling phase: blood flows abruptly into ventricles
- Diastasis (slow ventricular filling): blood entering atria from veins continue into ventricles
- Ends at 800 msec
How long does systole last in total?
0.3 sec
How long does diastole last in total?
0.5 sec
Does the rise in atrial pressure curve happen before or after P wave?
Immediately after
Does the ventricular pressure begin to rise before or after QRS complex?
After
Does the end of ventricular contraction happen before or after T wave?
Slightly after (pressure is already falling due to ejection of blood)
Explain the importance of atria contraction in slow heart rate vs tachycardia
- Slow heart rate: ventricles are full at diastasis –> atria contraction not so important
- Tachycardia: diastasis is shortened –> atria contraction is important
What can happen if inadequate ventricular filling occurs?
Syncope (fainting)
Explain A, C and V waves in atrial pressure
- A wave: atrial contraction causes rise in pressure (increase of 7-8 mmHg in LA and 4-6 mmHg in RA)
- C wave: increase of ventricular pressure causes AV valves to bulge into atria
- V wave: atrial filling
Where is the right atrium pressure change transmitted?
Into right jugular vein (jugular venous pulse)
Explain atrial fibrillation
- Arrhythmia which causes uncoordinated contractions of atrial fibres –> uncoordinated rippling motion
- AV node activation is irregular –> ventricular contractions irregular
- No P wave on ECG
- Irregular fluctuations: f waves
- Not usually life threatening, but clots can form in atria
What is the normal interval between successive ventricular contractions?
0.8 sec (0.35 - 0.95 sec)
What causes the characteristic notch in the aortic pressure curve and what is it called?
Incisura or dicrotic notch caused by short period of backward flow of blood into ventricle immediately before closure of aortic valve
What values does aortic pressure range from during systole and diastole?
- Pressure increases to 120 mmHg (systolic pressure) –> blood from LV stretches walls of arteries
- Falls slowly to 80 mmHg (diastolic pressure) –> elastic recoil “pushes” blood continually into peripheral vessels
Give a detailed explanation of what causes S1
- Upon systole, AV valves close and bulge into atria until chordae tendineae stop the back bulging
- Tautness of valves/chordae causes blood to bounce forward again into each ventricle
- Vibrations of valves and turbulent blood transmitted to ventricle walls and blood vessels
Is S1 or S2 louder? Give duration of each
S1 is louder and longer
S1 = 0.14 sec
S2 = 0.11 sec
Give a detailed explanation of what causes S2
- Upon diastole, semilunar valves close and bulge back into ventricles
- Elastic stretch recoils blood back into arteries
- Reverberation of blood between arterial walls and valves, and between valves and ventricular walls
When do S1 and S2 happen in relation to ECG waves?
- S1 happens right after QRS complex because contraction of ventricles causes closure of AV valves
- S2 happens after T wave because ventricular relaxation causes closure of semiliunar valves
What is a sign of pulmonary hypertension?
Sound of aortic valve < pulmonic valve
Describe S3 and S4
2 additional sounds that can be detected with a microphone
- S3: inrushing blood from atria during middle third of diastole, low rumbling sound, normal <40 years, abnormal >40 years (hole in septum)
- S4: inflow of blood into ventricles following atrial contraction, very weak sound
Describe events at each step of left ventricle pressure-volume loop
- A: opening of mitral valve and beginning of filling
- A-B: pressure falls as diastole progresses, blood volume increasing (rapid filling)
- B-C: pressure and volume increase as filling progresses (diastasis), small pressure increase before C = atrial contraction
- C: mitral valves close, EDV
- C-D: systole begins, isovolumetric contraction
- D: aortic valve opens (80 mmHg)
- D-E: pressure rises (120 mmHg), volume falls, rapid ejection
- E-F: pressure and volume fall, reduced ejection
- D-F: stroke volume
- F: aortic valve closes, ESV
- F-A: Diastole begins, isovolumetric contraction
What’s preload and what point does it represent on the pressure-volume loop?
- Degree of tension on the muscle when it begins to contract
- Point C: magnitude of EDV and corresponding end diastolic pressure
What’s afterload and what point does it represent on the pressure-volume loop?
- Force against which muscle is acting
- Blood pressure in aorta which ventricle must exceed to open aortic valve
- Point D: aortic blood pressure
What is contractility and what’s another word for it? What is the index of contractility? What can increase/reduce contractility?
- Strength of contraction at a given preload and afterload (inotropy)
- Index of contractility (A) = maximum dP/dt (slope of ventricular pressure curve)
- Drugs like adrenaline can increase it (B), cardiac failure reduces it (C)
Describe the diastolic pressure curve
Pressure generated by progressively larger EDVs right before ventricular contraction (preload)
Describe the systolic pressure curve
- During ventricular contraction with increasing EDV
- It increases linearly with EDV (Frank-Starling law)
What happens at large EDVs in systolic pressure curve?
Pressures generated fall due to overstretch of actin and myosin filaments in cardiac muscle fibres
What does the area of pressure-volume loop represent and what happens to it when heart pumps larger quantities of blood?
- External work (EW) output of the ventricle during contraction cycle
- EW becomes larger
What happens during ventricular fibrilation?
- In normal heart: depolarization waves spread rapidly to myocardial cells, all cells become simultaneously refractory, impulse fades
- Here, re-entry occurs if cells become excitable again –> generates 2nd wave of depolarization
- During re-entry, some fibres still refractory, other fully excitable and others can conduct impulses at low rates: abnormal cardiac rhythm/patterns of cardiac contraction ignore pace-setting effects of sinus node
- Most serious arrhythmia, fatal within 1-3 mins
What can cause re-entry?
- Increase in tissue mass causing a “long pathway” for impulses
- Decreased rate in conduction caused by: blockage of Purkinje system, ischemia of the muscle or high blood K+ levels
- Shorter refractory period in response to various drugs
What is the most serious cardiac arrhythmia?
Ventricular fibrilation (fatal within 1-3 min)
Explain what a defibrillator does
- Passes high-voltage alternating electrical current through ventricles
- Stops fibrilation by simultaneously placing myocardium into a refractory state
- Autorhythmic cells regain pacemaker control
