Cardiac Cycle Flashcards
Outline the features of diastole and systole.
DIASTOLE
- aortic semilunar valves CLOSE & atrioventricular valves OPEN
- walls of aorta recoil, pushing blood towards the smaller vessels (auxiliary pump)
- ~70-80mmHg
SYSTOLE
- aortic semilunar valves OPEN and atrioventricular valves CLOSE
- left ventricular contraction
- walls of elastic arteries stretch (pressure reservoirs)
- ~120mmHg
Outline the movement of blood in a single heartbeat.
Superior & Inferior Vena Cavae and pulmonary veins ————–> ———–> Passive filling ———————————————>
(AV valves open)
DIASTOLE --------> Atrial contraction ----> AV valves close ------------------->
(AV valves open)
(SYSTOLE) ----------> Ventricular contraction ----> blood enters aorta and pulmonary arteries
(Semilunar valves open)
Define diastole and systole.
DIASTOLE = period of relaxation between contractions
SYSTOLE = period when myocardium is contracting
What does a pacemaker do?
Generates on action potential at regular intervals
How long is a single contraction? How long is diastole at rest?
Ventricular systole: 280ms
Diastole: 700ms (shortens with exercise)
What is the myocardium?
Individual cells joined by low resistance electrical connections
Outline the electrical conduction that occurs during a contraction.
SAN ———> AVN ———–> delayed by 120ms ———> Bundle of His ———-> bundle branches ————> Purkinjie fibres
Ventricular myocardium: Endocardial —–> Epicardial on helical pattern (wrings blood out of heart from apex up)
Describe the different heart sounds that may be heard.
1st (“lup”): AV valves close, oscillations induced in surrounding structures produces sound (onset of ventricular systole)
2nd (“dup”): semilunar valves close, oscillations induced in surrounding structures produces sound (end of ventricular systole)
3rd (skinny people & children): rapid filling of heart (rumbling sound)
4th (skinny people & children): atrial contraction (rattling sound) - PATHOLOGICAL
What is stroke volume? How do you calculate cardiac output?
STROKE VOLUME = volume of blood pumped out of heart each beat (~80ml at rest)
CARDIAC OUTPUT = STROKE VOLUME X HEART RATE = ~ 5l/min at rest
Detail the different stages within a heartbeat.
ISOVOLUMETRIC RELAXATION (early ventricular diastole): Reduced intraventricular pressure but no change in volume (some blood left in ventricle) Backflow closes outflow valves (all valves CLOSED)
Atrial pressure increases until atrial pressure>intraventricular pressure
—> AV valves OPEN
VENTRICULAR FILLING (late ventricular diastole):
Majority of filling of ventricles happens in this phase (200-300ms)
The higher the venous pressure, the more the heart fills
Intraventricular pressure increases as ventricular walls stretch. Slow filling until intraventricular pressure=atrial pressure
ATRIAL CONTRACTION:
Tops up atria with same amount as backflow.
Small amount of extra blood forced into ventricles
ISOVOLUMETRIC CONTRACTION:
Intraventricular pressure increases until intraventricular pressure>atrial pressure —-> backflow causes AV valves to CLOSE (all valves CLOSED)
VENTRICULAR EJECTION (rapid ejection phase):
Intraventricular pressure>atrial pressure so outflow valves OPEN
Arterial pressure increases (arteries increase in diameter to resist pressure)
What is Starling’s Law (of ventricular filling)?
The more the heart fills, the harder it contracts (to a point) and the bigger the stroke volume
Therefore increased venous pressure -> increased stroke volume
Limiting due to pericardium restricting the heart/vessels being compressed/muscle overstretching so that filaments do not overlap
(CHECK)
Define contractility. What is it affected by?
CONTRACTILITY = the extent to which a given increase in venous pressure leads to an increase in stroke volume (at a given fibre length)
NOT THE FORCE OF CONTRACTION!!!!!!
Affected by:
- force of contraction (determined by end-diastolic volume)
- difficulty ejecting blood (aortic impedance, which depends on total peripheral resistance)
- stroke volume (depends on venous pressure)
How is the heart rate controlled by the ANS?
ANS outflow to the heart controlled by baroreceptors & arterial pressure sensed by carotid sinus (-> medulla)
Reduced arterial pressure -> increased sympathetic activity -> increased contractility & increased heart rate -> increased cardiac output
note: temporary increase in flow resistance in skin & gut -> increases total peripheral resistance -> increases arterial pressure again
Increased venous pressure (sensed by right atrium & baroreceptors in great veins) -> reduced parasympathetic activity -> increases heart rate
(Bainbridge reflex)
Why do we not get pulmonary oedema whenever we exercise?
Exercise increases demand —> muscles pumping & pre-capillary sphincters open —-> increased venous return
Venous pressure & arterial pressure increase
No other change: increased venous pressure overfills heart, causing pulmonary oedema
This is prevented by an anticipatory increase in heart rate which reduces the stroke volume required by the brain
How is postural hypotension usually prevented?
On standing, blood pools in superficial veins of legs (reduced pressure as they are surrounded by air, not fluid)
Pooled blood not returned to heart —> reduced stroke volume & reduced central venous pressure —> reduced cardiac output —> reduced arterial pressure —> increased heart rate & reduced blood flow to skin and gut —> increases arterial pressure
