Lecture 21 Cardiovascular system 2: Cardiac Function Flashcards
(22 cards)
Systole
contraction phase
ventricular systole 1/3 of cycle
Diastole
relaxation phase
ventricular diastole 2/3 of cycle
5 specific phases of cardiac cycle
ventricular filling atrial systole isovolumic contraction ventricular ejection isovolumic relaxation
Ventricular Filling
mid to late diastole low Pressure in ventricle AV valves open, semilunar valves closed ventricular volume increased this is the P wave
Atrial systole
end of ventricular diastole
atrial contraction “tops off” ventricles after passive phase of ventricular filling
AV valves are still open
Isovolumic Contraction
beginning of ventricular systole
pressure rapidly increases as ventricles contract
AV valves close -> 1st hear sound “LUB”
semilunar valves still closed, so volume stays constant as Pressure increases
Volume is maximal
QRS phase
Ventricular Ejection
mid to late systole Pressure increase to maximal semilunar valves open blood ejected to arteries and ventricular volume decreases S-T segment (Plateau)
isovolumic relaxation
beginning of diastole P rapidly decrease AV valves stay closed until ventricular Pressure < atrial Pressure volume is the lowest T wave
Pressure in LV ranges
from about 0 during diastole to 120 mm Hg at peak of systole
Atrial BP in aorta and large arteries ranges
from 80 (diastolic) to 120 mm Hg (systolic) BP is sustained in diastole by closure of semilunar valves and elastic recoil of arteries
Volume in ventricles
is highest at end of diastole
lowest at end of systole
Wiggers cardiac output diagram correlates
electrical events (ECG) pressure changes in atria, ventricles, and aorta, volume and heart volume changes in ventricles heart sounds
Cardiac Output
total blood flow per minute from one ventricle
RV and LV have the same output
CO is totaly blood flow to all tissues of the body (systemic circuit)
increased demand for O2 and nutrients is accommodated by increase in CO
Cardiac output (CO) =
hear rate (HR) X stroke volume (SV)
Stroke Volume
amount of blood ejected from each ventricle
end-diastolic volume (EDV) - end-systolic volume (ESV) = SV
resting values: 130 mL 60mL 70mL
Control of Cardiac output
Modulation of heart rate
Modulation of stroke volume
Modulation of heart rate
Sympathetic (ANS)
sympathetic cardiac nerve (NE) -> B1 adrenergic receptors
->increased heart rate of peacemaker depolarization at SA node -> increases HR
E & NE secreted by the adrenal medulla also bind to B1 receptors to increase HR
Modulation of heart rate
Parasympathetic (ANS)
vagus nerve (ACh) -> muscarinic receptors -> decreases HR at SA node
parasympathetic control dominates at rest ("vagal tone")Modulation of Stroke Volume
Intrinsic control
Starling’s law of the heart (shows the relationship between SV and EDV)
increase in EDV -> Increase in force of contraction -> increase in SV
results from the length-tension relationship of cardiac muscle: increased filling stretches sarcomeres to a more optimal part of the L-T curve
EDV increases due to increased venous return to the heart
HOW YOU INCREASE STROKE VOLUME
Modulation of Stroke Volume
Extrinsic control
sympathetic NS -> NE ->increase in contractility of the heart
adrenal medulla -> E & NE (neural & hormonal)
INCREASE STOKE VOLUME
Contractility
beats stronger
builds up force more rapidly
greater SV
Signal transduction pathway
- E and NE bind to B1 adrenergic receptors
- GPCR activates the cAMP second messenger system -> phosphorylation of proteins
- increase Ca2+ entry from the ECF and increase Ca2+ release from the SR
- increase actin-myosin crossbridge formation -> increase force and speed of contraction
