Flashcards in Pathophys Deck (52)
What is occuring during systole? Diastole?
systole: heart is contracting
diastole: heart is relaxing
Describe the phase of ventricular filling?
- takes place mid to late diastole
- AV valves are open, 80% of blood passively flows into ventricles
- atrial systole occurs, delivering the remaining 20%
- EDV: volume of blood in each ventricle at the end of ventricular diastole
Describe ventricular systole?
- atria relax and ventricles begin to contract
- rising ventricular pressure results in closing of AV valves
- isovolumetric contraction phase (all valves are closed)
- in ejection phase: ventricular pressure exceeds pressure in large arteries forcing SL valves open
- ESV: volume of blood remaining in each ventricle at the end of systole
Describe isovolumetric relaxation that occurs in early diastole?
- ventricles relax
- backflow of blood in aorta and pulmonary trunk closes SL vlaves and causes dicrotic notch (brief rise in aortic pressure)
- closing of SL valves: Dupp
What is CO?
-volume of blood pumped by each ventricle in one minute
SV = volume of blood pumped out by a ventricle with each beat
- normal = 75x 70 m/beat = 5.25 L/min
What is the cardiac reserve?
difference between resting and max CO
What 3 main factors affect SV?
What is the ejection fraction?
- measurement of ventriculat systolic function
normal is 60%
get exact # with echo or cardiac catheterization
What is the preload?
- degree of stretch of cardiac muscle cells before the contract (frank-starling law of the heart)
- cardiac muscle exhibits a length tension relationship
- at rest, cardiac muscle cells are shorter than optimal length
- a slow heartbeat and exercise increase venous return
- increased venous return distends ventricles and increases contraction force
- increase preload = increase in SV
- increase after load= decrease in SV
- increasing contractile state shifts isovolemic pressure volume relationship leftward (decreasing ESV) increasing SV
What factors regulate contractility?
- contractility: contractile strength at a given muscle length, independent of muscle stretch and EDV
- positive inotropic agents increase contractility: increased Ca2+ influx due o sympathetic stimulation, hormones = thyroxine, glucagon and epi
- negative inotropic agents decrease contractility: acidosis, increased extracellular K+, and Ca Channel blockers
What is the after load and what affects this?
- pressure that must overcome for ventricles to eject blood
- HTN increases afterload, resulting in increased ESV and reduced SV
- positive chronotropic factors: increase HR
- negative decrease HR
Sympathetic effect on heart?
- activated by emotional or physical stressors
- NE causes pacemaker to fire more rapidly and also increase contractility
- NE is released and this causes increased sinus node discharge, and increases rate of conduction of impulse and also increases force of contraction in atria and ventricles
- it increases pacemaker rate by decreasing K+ perm and increasing slow inward Ca2+ and Na+
Parasympathetic effect on heart?
- opposes sympathetic effects,
Acetylcholine hyperpolarizes pacemaker cells by opening K+ channels
- heart at rest exhibits vagal tone (parasympathetic)
- doesn't affect contractility though
- Vagal nerves release acetylcholine at their endings, innervate SA node and AV juntional fibers prox to VA node. This causes hyperpolarization becuase of increased K+ perm in response to acetylcholine, this causes decreased transmission of impulses maybe temporarily stopping heart rate, ventricular escape occurs
What is the atrial (bainbridge) reflex?
- a sympathetic reflex initiated by increased venous return
- stretch of atrial walls stimulates SA node and also stimulates atrial stretch receptors activating sympathetic reflexes
- fast heart rate (tachycardia) can decrease C.O. because there isn't enough time for heart to fill during diastole
Explain how exercising can increase SV?
- exercise increases venous return, will have decreased heart rate to begin with so ventricles have more time to fill - this increases venous return and increases EDV which in turn increases SV, also producing Epi, thyroxine and excess Ca2+ which increases contractility and decreases ESV which increases SV
Explain how exercising or having anxiety can increase HR?
- increases sympathetic activity which increases HR and also contractility and decreases parasympathetic activity hence increasing HR
- increasing SV and HR = increase CO
How is the heart chemically regulated?
- Epi from adrenal medulla enhances HR and contractility
- thyroxine increases HR and enhances the effects of NE and E
- intra and extracellular ion concentrations (Ca and K) must be maintained for normal heart function
What other big factors influence heart rate?
- gender (females have faster heart rate)
- body temp
What is tachycardia?
- abnorm fast heart rate (greater than 100 bpm)
if this is persistent, it may lead to fibrillation
What is bradycardia?
- HR slower than 60
- may result in grossly inadequate blood circulation
- may be desirable result of endurance training