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
Heart rate can be regulated by:
Autonomic nervous system
Chemicals
Other factors
Autonomic nervous system regulation of heart rate
_______ nervous system can be activated by
is released and binds to
causing:
- Sympathetic nervous system can be activated by emotional or physical stressors
- Norepinephrine is released and binds to β1-adrenergic receptors on heart, causing:
- -Pacemaker to fire more rapidly, increasing HR
- –EDV decreased because of decreased fill time
- -Increased contractility
- –ESV decreased because of increased volume of ejected blood
Autonomic nervous system
Because both EDV and ESV decrease,
SV can remain unchanged
Parasympathetic nervous system opposes sympathetic effects
Acetylcholine hyperpolarizes pacemaker cells by opening
Autonomic nervous system regulation of heart rate
Heart at rest exhibits
vagal tone
- Parasympathetic is dominant influence on heart rate
- Decreases rate about 25 beats/min
- Cutting vagal nerve leads to HR of ∼100
When sympathetic is activated, parasympathetic is
inhibited, and vice-versa
Atrial (Bainbridge) reflex
- sympathetic reflex initiated by increased venous return, hence increased atrial filling
- Atrial walls are stretched with increased volume
- Stimulates SAnode, which increases HR
- Also stimulates atrial stretch receptors that activate sympathetic reflexes
Chemical regulation of heart rate
Hormones
- Epinephrine from adrenal medulla increases heart rate and contractility
- Thyroxine increases heart rate; enhances effects of norepinephrine and epinephrine
Ions
Intra- and extracellular ion concentrations must be maintained for normal heart function
Imbalances are very dangerous to heart
Hypocalcemia
depresses heart
Hypercalcemia:
increases HR and contractility
Hyperkalemia:
alters electrical activity, which can lead to heart block and cardiac arrest, death
Hypokalemia
results in feeble heartbeat; arrhythmias
Other factors that influence heart rate
Age
Fetus has fastest HR; declines with age
Gender
Females have faster HR than males
Exercise
Increases HR
Trained atheles can have slow HR
Body temperature
HR increases with increased body temperature
Tachycardia
abnormally fast heart rate (>100beats/min)
If persistent, may lead to fibrillation
Bradycardia
heart rate slower than 60beats/min
May result in grossly inadequate blood circulation in nonathletes
May be desirable result of endurance training
Congestive heart failure (CHF)
Progressive condition; CO is so low that blood circulation is inadequate to meet tissue needs
Reflects weakened myocardium caused by:
Coronary atherosclerosis: clogged arteries caused by fat buildup; impairs oxygen delivery to cardiac cells
–Heart becomes hypoxic, contracts inefficiently
Congestive heart failure (CHF)
Persistent high blood pressure:
Multiple myocardial infarcts: Dilated cardiomyopathy (DCM):
aortic pressure >90 mmHg causes myocardium to exert more force
Chronic increased ESV causes myocardium hypertrophy and weakness
Multiple myocardial infarcts: heart becomes weak as contractile cells are replaced with scar tissue
Dilated cardiomyopathy (DCM): ventricles stretch and become flabby, and myocardium deteriorates
Drug toxicity or chronic inflammation may play a role
Congestive heart failure (CHF)
Either side of heart can be
Failure of either side ultimately
-Left-sided failure results in pulmonary congestion
Blood backs up in lungs
-Right-sided failure results in peripheral congestion
Blood pools in body organs, causing edema
-Failure of either side ultimately weakens other side
Leads to decompensated, seriously weakened heart
Treatment: removal of fluid, drugs to reduce afterload and increase contractility
Frank starling
preload and SV
chonotropic
heart rate
inotropic
contractility
