chapter 18.5 Flashcards
Systole
period of heart contraction
Diastole:
period of heart relaxation
Cardiac cycle
blood flow through heart during one complete heartbeat
Atrial systole and diastole are followed by
cardiac Cycle represents series of
Mechanical events follow
ventricular systole and diastole
pressure and blood volume changes
electrical events seen on ECG
___ phases of the cardiac cycle
3
Ventricular filling: mid-to-late diastole
Ventricular systole
Isovolumetric relaxation (early diastole)
Ventricular filling: mid-to-late diastole
End diastolic volume (EDV)
(QRS wave)
-Atria finish contracting and return to diastole
- Pressure is low; 80% of blood passively flows from atria through open AV valves into ventricles from atria (SL valves closed)
- Atrial depolarization triggers atrial systole (P wave), atria contract, pushing remaining 20% of blood into ventricle
- —End diastolic volume (EDV): volume of blood in each ventricle at end of ventricular diastole
- Depolarization spreads to ventricles (QRS wave)
- Atria finish contracting and return to diastole while ventricles begin systole
Ventricular systole End systolic volume (ESV): Rising ventricular pressure causes closing of what valves Pressure in aorta around -End systolic volume (ESV):
- Atria relax; ventricles begin to contract
- Rising ventricular pressure causes closing of AV valves
- Two phases
- —-2a: Isovolumetric contraction phase: all valves are closed
- —-2b: Ejection phase: ventricular pressure exceeds pressure in large arteries, forcing SL valves open
- -Pressure in aorta around 120 mm Hg
-End systolic volume (ESV): volume of blood remaining in each ventricle after systole
Isovolumetric relaxation: early diastole Causes Following Backflow of blood in aorta and pulmonary trunk Ventricles are totally
- Following ventricular repolarization (T wave), ventricles are relaxed; atria are relaxed and filling
- Backflow of blood in aorta and pulmonary trunk closes SL valves
- -Causes dicrotic notch (brief rise in aortic pressure as blood rebounds off closed valve)
- –Ventricles are totally closed chambers (isovolumetric)
- When atrial pressure exceeds ventricular pressure, AV valves open; cycle begins again
Heart Sounds
two sounds
Pause between lub-dups indicates
- Two sounds (lub-dup) associated with closing of heart valves
- First sound is closing of AV valves at beginning of ventricular systole
- Second sound is closing of SL valves at beginning of ventricular diastole
- Pause between lub-dups indicates heart relaxation
Bicuspid valve closes
Differences allow
slightly before tricuspid, and aortic closes slightly before pulmonary valve
Differences allow auscultation of each valve when stethoscope is placed in four different regions
Heart murmurs:
abnormal heart sounds heard when blood hits obstructions
Usually indicate valve problems
Incompetent (or insufficient) valve:
fails to close completely, allowing backflow of blood
Causes swishing sound as blood regurgitates backward from ventricle into atria
Stenotic valve
fails to open completely, restricting blood flow through valve
Causes high-pitched sound or clicking as blood is forced through narrow valve
Cardiac Output (CO) normal=
Volume of blood pumped by each ventricle in 1 minute
CO = heart rate (HR) × stroke volume (SV)
HR = number of beats per minute
SV = volume of blood pumped out by one ventricle with each beat
Normal: 5.25 L/min
Regulation of Pumping
Maximal CO is
Maximal CO may reach
CO changes (increases/decreases) if either or both
4–5 times resting CO in nonathletic people (20–25 L/min)
35L/min in trained athletes
SV or HR is changed
Cardiac reserve
difference between resting and maximal CO
CO is affected by factors leading to:
Regulation of stroke volume
Regulation of heart rates
Mathematically: SV =
EDV is affected by length of
ESV is affected by
Normal SV =
EDV − ESV
ventricular diastole and venous pressure (~120 ml/beat)
arterial BP and force of ventricular contraction (~50 ml/beat)
120 ml − 50 ml = 70 ml/beat
Three main factors that affect SV:
Preload
Contractility
Afterload
Preload Changes in preload cause changes in Affects Relationship between preload and SV called Cardiac muscle exhibits a
degree of stretch of heart muscle
Preload: degree to which cardiac muscle cells are stretched just before they contract
-Changes in preload cause changes in SV
Affects EDV
Relationship between preload and SV called
Frank-Starling law of the heart
Cardiac muscle exhibits a length-tension relationship
At rest, cardiac muscle cells are shorter than optimal length; leads to dramatic increase in contractile force
Most important factor in preload stretching of cardiac muscle is
venous return—amount of blood returning to heart
- Slow heartbeat and exercise increase venous return
- Increased venous return distends (stretches) ventricles and increases contraction force
Contractility Independent of Increased contractility \_\_\_\_ ESV Positive inotropic agents negative inotropic agents
-Contractile strength at given muscle length
-Independent of muscle stretch and EDV
-Increased contractility lowers ESV; caused by:
Sympathetic epinephrine release stimulates increased Ca 2+ influx, leading to more cross bridge formations
Positive inotropic agents
increase contractility
Thyroxine, glucagon, epinephrine, digitalis, high extracellular
negative inotropic agents
Acidosis
Afterload -Aortic pressure is around -Pulmonary trunk pressure is around -Hypertension\_\_\_\_\_\_afterload resulting in \_\_\_\_\_\_\_ESV and \_\_\_\_\_\_ SV
back pressure exerted by arterial blood
Afterload is pressure that ventricles must overcome to eject blood
-Back pressure from arterial blood pushing on SL valves is major pressure
-Aortic pressure is around 80 mm Hg
-Pulmonary trunk pressure is around 10 mm Hg
-Hypertension increases afterload, resulting in increased ESV and reduced SV
Regulation of Heart Rate
If SV decreases as a result of decreased blood volume or weakened heart, CO can be maintained by
-factors that increase and decrease heart rate
If SV decreases as a result of decreased blood volume or weakened heart, CO can be maintained by increasing HR and contractility
Positive chronotropic factors increase heart rate
Negative chronotropic factors decrease heart rate
