0-1 Chapter 19 the heart Flashcards
cardiology
the scientific study of the heart and the treatment of its disorders
cardiovascular system
heart and blood vessels
circulatory system
heart, blood vessels, and the blood
major divisions of circulatory system
pulmonary circuit
systemic circuit
pulmonary circuit
right side of heart
•carries blood to lungs for gas exchange and back to hear
–lesser oxygenated blood arrives from inferior and superior vena cava
–blood sent to lungs via pulmonary trunk
systemic circuit
left side of heart
•supplies oxygenated blood to all tissues of the body and returns it to the heart
–fully oxygenated blood arrives from lungs via pulmonary veins
–blood sent to all organs of the body via aorta
Heart
heart located in mediastinum, between lungs
tilted to the left
base
wide, superior portion of heart, blood vessels attach here
apex
inferior end, tilts to the left, tapers to point
pericardium
double-walled sac (pericardial sac) that encloses the heart
–allows heart to beat without friction, provides room to expand, yet resists excessive expansion
–anchored to diaphragm inferiorly and sternum anteriorly
parietal pericardium
outer wall of sac
–superficial fibrous layer of connective tissue
–a deep, thin serous layer
visceral pericardium
(epicardium) –heart covering
–serous lining of sac turns inward at base of heart to cover the heart surface
pericardial cavity
space inside the pericardial sac filled with 5 -30 mL of pericardial fluid
pericarditis
inflammation of the membranes
–painful friction rub with each heartbeat
epicardium
(visceral pericardium)
–serous membrane covering heart
–adipose in thick layer in some places
–coronary blood vessels travel through this layer
endocardium
–smooth inner lining of heart and blood vessels
–covers the valve surfaces and continuous with endothelium of blood vessels
myocardium
layer of cardiac muscle proportional to work load
•muscle spirals around heart which produces wringing motion
fibrous skeleton of the heart
-framework of collagenous and elastic fibers
•provides structural support and attachment for cardiac muscle and anchor for valve tissue
•electrical insulation between atria and ventricles important in timing and coordination of contractile activity
four chambers
right and left atria
right and left ventricles
right and left atria
- two superior chambers
- receive blood returning to heart
- auricles (seen on surface) enlarge chamber
right and left ventricles
two inferior chambers
•pump blood into arteries
atrioventricular sulcus
- separates atria and ventricles
- sulci contain coronary arteries
interventricular sulcus
- overlies the interventricular septum that divides the right ventricle from the left
- sulci contain coronary arteries
interatrial septum
–wall that separates atria
pectinate muscles
internal ridges of myocardium in right atrium
interventricular septum
muscular wall that separates ventricles
trabeculae carneae
internal ridges in both ventricles
Heart Valves
valves ensure a one-way flow of blood through the heart
atrioventricular (AV) valves
controls blood flow between atria and ventricles
–right AV valve has 3 cusps (tricuspid valve)
–left AV valve has 2 cusps (mitral or bicuspid valve)
chordae tendineae
cords connect AV valves to papillary muscles on floor of ventricles
•prevent AV valves from flipping inside out or bulging into the atria when the ventricles contract
tricuspid valve
right AV valve has 3 cusps (tricuspid valve)
bicuspid valve
left AV valve has 2 cusps (mitral or bicuspid valve)
semilunar valves
control flow into great arteries –open and close because of blood flow and pressure
pulmonary semilunar valve
in opening between right ventricle and pulmonary trunk
aortic semilunar valve
in opening between left ventricle and aorta
AV Valve Mechanics
ventricles relax
–pressure drops inside the ventricles
–semilunar valves close as blood attempts to back up into the ventricles from the vessels
–AV valves open
–blood flows from atria to ventricles
AV Valve Mechanics
ventricles contract
–AV valves close as blood attempts to back up into the atria
–pressure rises inside of the ventricles
–semilunar valves open and blood flows into great vessels
Blood Flow Through Heart
part 1
- Blood enters right atrium from superior and inferior venae cavae
- Blood in right atrium flows through right AV valve into right ventricle
- Contraction of right ventricle forces pulmonary valve open
- Blood flows through pulmonary valve into pulmonary trunk
- Blood is distributed by right and left pulmonary arteries to the lungs, where it unloads CO2 and loads O2.
Blood Flow Through Heart
part 2
- Blood returns from lungs via pulmonary veins to left atrium
- Blood in left atrium flows through left AV valve into left ventricle
- Contraction of left ventricle (simultaneous with step 3 ) forces aortic valve open
- Blood flows through aortic valve into ascending aorta
- Blood in aorta is distributed to every organ in the body, where it unloads O2and loads CO2
- Blood returns to heart via venae cavae
Coronary Circulation
5% of blood pumped by heart is pumped to the heart itself through the coronary circulation to sustain its strenuous workload
–250 ml of blood per minute
–needs abundant O2and nutrients
left coronary artery
(LCA) branch off the ascending aorta
- anterior interventricular branch
- circumflex branch
anterior interventricular branch
•supplies blood to both ventricles and anterior two-thirds of the interventricular septum
circumflex branch
- passes around left side of heart in coronary sulcus
- gives off left marginal branch and then ends on the posterior side of the heart
- supplies left atrium and posterior wall of left ventricle
right coronary artery
RCA) branch off the ascending aorta
–supplies right atrium and sinoatrial node (pacemaker)
right marginal branch
•supplies lateral aspect of right atrium and ventricle
posterior interventricular branch
supplies posterior walls of ventricles
myocardial infarction
MI) (heart attack)
–interruption of blood supply to the heart from a blood clot or fatty deposit (atheroma) can cause death of cardiac cells within minutes
–some protection from MI is provided by arterial anastomoses which provides an alternative route of blood flow (collateral circulation) within the myocardium
blood flow to the heart muscle during ventricular contraction is
slowed, unlike the rest of the body
three reasons:
–contraction of the myocardium compresses the coronary arteries and obstructs blood flow
–opening of the aortic valve flap during ventricular systole covers the openings to the coronary arteries blocking blood flow into them
–during ventricular diastole, blood in the aorta surges back toward the heart and into the openings of the coronary arteries
•blood flow to the myocardium increases during ventricular relaxation
angina pectoris
chest pain from partial obstruction of coronary blood flow
–pain caused by ischemia of cardiac muscle
–obstruction partially blocks blood flow
–myocardium shifts to anaerobic fermentation producing lactic acid stimulating pain
myocardial infarction
sudden death of a patch of myocardium resulting from long-term obstruction of coronary circulation
–MI responsible for about half of all deaths in the United States
Venous Drainage of Heart
5 -10% drains directly into heart chambers, right atrium and right ventricle, by way of the thebesian veins
the rest returns to right atrium by the following routes:
great cardiac vein
middle cardiac vein
left marginal vein
great cardiac vein
- travels along side of anterior interventricular artery
- collects blood from anterior portion of heart
- empties into coronary sinus
middle cardiac vein
(posterior interventricular)
•found in posterior sulcus
•collects blood from posterior portion of heart
•drains into coronary sinus
left marginal vein
•empties into coronary sinus
coronary sinus
- large transverse vein in coronary sulcus on posterior side of heart
- collects blood and empties into right atrium
cardiocytes
striated, short, thick, branched cells, one central nucleus surrounded by light staining mass of glycogen
intercalated discs
join cardiocytes end to end
interdigitating folds
folds interlock with each other, and increase surface area of contact
mechanical junctions
tightly join cardiocytes
fascia adherens
broad band in which the actin of the thin myofilaments is anchored to the plasma membrane
–each cell is linked to the next via transmembrane proteins
desmosomes
weldlike mechanical junctions between cells
–prevents cardiocytes from being pulled apart
electrical junctions
gap junctions allow ions to flow between cells –can stimulate neighbors
•entire myocardium of either two atria or two ventricles acts like single unified cell
repair of damage of cardiac muscle is almost entirely by
fibrosis (scarring)
cardiac muscle depends almost exclusively on
aerobic respiration used to make ATP
–rich in myoglobin and glycogen
–huge mitochondria –fill 25% of cell
adaptable to organic fuels used
fatty acids (60%), glucose (35%), ketones, lactic acid and amino acids (5%) –more vulnerable to oxygen deficiency than lack of a specific fuel PREFERS FAT
fatigue resistant
since makes little use of anaerobic fermentation or oxygen debt mechanisms
–does not fatigue for a lifetime
Cardiac Conduction System
coordinates the heartbeat
–composed of an internal pacemaker and nervelike conduction pathways through myocardium
–generates and conducts rhythmic electrical signals in the following order:
Cardiac Conduction System
Order
sinoatrial (SA) node
atrioventricular (AV) node
atrioventricular (AV) bundle (bundle of His)
Purkinje fibers
sinoatrial (SA) node
modified cardiocytes
–initiates each heartbeat and determines heart rate
–signals spread throughout atria
–pacemaker in right atrium near base of superior vena cava
atrioventricular (AV) node
–located near the right AV valve at lower end of interatrial septum
–electrical gateway to the ventricles
–fibrous skeleton acts as an insulator to prevent currents from getting to the ventricles from any other route
atrioventricular (AV) bundle (bundle of His)
–bundle forks into right and left bundle branches
–these branches pass through interventricular septum toward apex
Purkinje fibers
–nervelike processes spread throughout ventricular myocardium
•signal pass from cell to cell through gap junctions
Cardiac Conduction System
sequence
- SA node fires
- Excitation spreads through atrial myocardium
- .AV node fires
- Excitation spreads down AV bundle
- Purkinje fibers distribute excitation through ventricular myocardium.
sympathetic nerves
(raise heart rate)
•increase heart rate and contraction strength
•dilates coronary arteries to increase myocardial blood flow
sympathetic nerves
path
–sympathetic pathway to the heart originates in the upper thoracic segments of the spinal cord
–continues to adjacent sympathetic chain ganglia
–some pass through cardiac plexus in mediastinum
–continue as cardiac nerves to the heart
–fibers terminate in SA and AV nodes, in atrial and ventricular myocardium, as well as the aorta, pulmonary trunk, and coronary arteries
parasympathetic nerves
(slows heart rate)
•parasympathetic stimulation reduces the heart rate
parasympathetic nerves
path
–pathway begins with nuclei of the vagus nerves in the medulla oblongata
–extend to cardiac plexus and continue to the heart by way of the cardiac nerves
–fibers of right vagus nerve lead to the SA node
–fibers of left vagus nerve lead to the AV node
–little or no vagal stimulation of the myocardium
systole
atrial or ventricular contraction
diastole
atrial or ventricular relaxation
sinus rhythm
normal heartbeat triggered by the SA node
–set by SA node at 60 –100 bpm
–adult at rest is 70 to 80 bpm (vagal tone)
ectopic focus
another parts of heart fires before SA node
–caused by hypoxia, electrolyte imbalance, or caffeine, nicotine, and other drugs
Abnormal Heart Rhythms
spontaneous firing from some part of heart not the SA node
ectopic foci
region of spontaneous firing
nodal rhythm
if SA node is damaged, heart rate is set by AV node, 40 to 50 bpm
intrinsic ventricular rhythm
if both SA and AV nodes are not functioning, rate set at 20 to 40 bpm
–this requires pacemaker to sustain life
arrhythmia
any abnormal cardiac rhythm
–failure of conduction system to transmit signals (heart block)
•bundle branch block
•total heart block (damage to AV node)
Cardiac Arrhythmias
atrial flutter
premature ventricular contractions
ventricular fibrillation
atrial flutter
ectopic foci in atria
–atrial fibrillation
–atria beat 200 -400 times per minute
premature ventricular contractions
–caused by stimulants, stress or lack of sleep
ventricular fibrillation
–serious arrhythmia caused by electrical signals reaching different regions at widely different times
•heart can‟t pump blood and no coronary perfusion
–kills quickly if not stopped
defibrillation
strong electrical shock whose intent is to depolarize the entire myocardium, stop the fibrillation, and reset SA nodes to sinus rhythm
SA node
•SA node is the system‟s pacemaker
SA node does not have a stable resting membrane potential
–starts at -60 mV and drifts upward from a slow inflow of Na+
•gradual depolarization is called pacemaker potential
–slow inflow of Na+ without a compensating outflow of K+
–when reaches threshold of -40 mV, voltage-gated fast Ca2+and Na+ channels open
•faster depolarization occurs peaking at 0 mV
•K+ channels then open and K+ leaves the cell
–causing repolarization
–once K+ channels close, pacemaker potential starts over
each depolarization of the SA node sets off one heartbeat
one heartbeat
-at rest, fires every 0.8 seconds or 75 bpm
Impulse Conduction to Myocardium
- signal from SA node stimulates two atria to contract almost simultaneously
- signal slows down through AV node
- signals travel very quickly through AV bundle and Purkinje fibers
- ventricular systole progresses up from the apex of the heart
Electrical Behavior of Myocardium
- cardiocytes have a stable resting potential of -90 mV
* depolarize only when stimulated
depolarization phase
(very brief)
•stimulus opens voltage regulated Na+ gates, (Na+ rushes in) membrane depolarizes rapidly
•action potential peaks at +30 mV
•Na+ gates close quickly
plateau phase
lasts 200 to 250 msec, sustains contraction for expulsion of blood from heart
•Ca2+ channels are slow to close and SR is slow to remove Ca2+ from the cytosol
repolarization phase
Ca2+channels close, K+ channels open, rapid diffusion of K+ out of cell returns it to resting potential
has a long absolute refractory period of
250 msec compared to 1 –2 msec in skeletal muscle
–prevents wave summation and tetanus which would stop the pumping action of the heart
Action Potential of a Cardiocyte
1) Na+ gates open
2) Rapid depolarization
3) Na+ gates close, K+ channels begin to open
4) Slow Ca2+ channels open
5) Ca2+channels close, K+ channels fully open (repolarization)
Electrocardiogram
(ECG or EKG)
•composite of all action potentials of nodal and myocardial cells detected, amplified and recorded by electrodes on arms, legs and chest
ECG Deflections
P wave
QRS complex
ST segment -ventricular systole
T wave
P wave
–SA node fires, atria depolarize and contract
–atrial systole begins 100 msec after SA signal
QRS complex
–ventricular depolarization
–complex shape of spike due to different thickness and shape of the two ventricles
ST segment -ventricular systole
–plateau in myocardial action potential
T wave
–ventricular repolarization and relaxation
Electrical Activity of Myocardium
1) atrial depolarization begins
2) atrial depolarization complete (atria contracted)
3) ventricles begin to depolarize at apex; atria repolarize (atria relaxed)
4) ventricular depolarization complete (ventricles contracted)
5) ventricles begin to repolarize at apex
6) ventricular repolarization complete (ventricles relaxed)
Diagnostic Value of ECG
- abnormalities in conduction pathways
- myocardial infarction
- nodal damage
- heart enlargement
- electrolyte and hormone imbalances
cardiac cycle
one complete contraction and relaxation of all four chambers of the heart
atrial systole
(contraction) occurs while ventricles are in diastole(relaxation)
atrial diastole
occurs while ventricles in systole
quiescent period
all four chambers relaxed at same time
two main variables that govern fluid movement:
pressure
resistance
pressure
causes a fluid to flow (fluid dynamics)
–pressure gradient -pressure difference between two points
–measured in mm Hg with a manometer or sphygmomanometer
resistance
opposes fluid flow
–great vessels have positive blood pressure
–ventricular pressure must rise above this resistance for blood to flow into great vessels
Pressure Gradients and Flow
fluid flows only if it is subjected to more pressure at one point than another which creates a pressure gradient
–fluid flows down its pressure gradient from high pressure to low pressure
events occurring on left side of heart
–when ventricle relaxes and expands, its internal pressure falls
–if bicuspid valve is open, blood flows into left ventricle
–when ventricle contracts, internal pressure rises
–AV valves close and the aortic valve is pushed open and blood flows into aorta from left ventricle
opening and closing of valves are governed
by these pressure changes
–AV valves limp when ventricles relaxed
–semilunar valves under pressure from blood in vessels when ventricles relaxed
valvular insufficiency
(incompetence) -any failure of a valve to prevent reflux (regurgitation) the backward flow of blood
valvular stenosis
cusps are stiffened and opening is constricted by scar tissue
•result of rheumatic fever autoimmune attack on the mitral and aortic valves
•heart overworks and may become enlarged
heart murmur
–abnormal heart sound produced by regurgitation of blood through incompetent valves
mitral valve prolapse
insufficiency in which one or both mitral valve cusps bulge into atria during ventricular contraction
•hereditary in 1 out of 40 people
•may cause chest pain and shortness of breath
auscultation
listening to sounds made by body
first heart sound
(S1), louder and longer “lubb”, occurs with closure of AV valves, turbulence in the bloodstream, and movements of the heart wall
second heart sound
(S2), softer and sharper “dupp” occurs with closure of semilunar valves, turbulence in the bloodstream, and movements of the heart wall
Phases of Cardiac Cycle
- ventricular filling
- isovolumetric contraction
- ventricular ejection
- isovolumetric relaxation
Ventricular Filling
during diastole, ventricles expand
–their pressure drops below that of the atria
–AV valves open and blood flows into the ventricles
ventricular filling occurs in three phases:
rapid ventricular filling
diastasis
atrial systole
rapid ventricular filling
first one-third
•blood enters very quickly
diastasis
second one-third
•marked by slower filling
•P wave occurs at the end of diastasis
atrial systole
final one-third
•atria contract
end-diastolic volume
(EDV) –amount of blood contained in each ventricle at the end of ventricular filling
–130 mL of blood
Isovolumetric Contraction
atria repolarize and relax
ventricles depolarize
AV valves close
heart sound S1
atria repolarize and relax
–remain in diastole for the rest of the cardiac cycle
ventricles depolarize
create the QRS complex, and begin to contract
AV valves close
as ventricular blood surges back against the cusps
heart sound S1
occurs at the beginning of this phase
isovolumetric‟
because even though the ventricles contract, they do not eject blood
–because pressure in the aorta (80 mm Hg) and in pulmonary trunk (10 mm Hg) is still greater than in the ventricles
cardiocytes exert force, but
but with all four valves closed, the blood cannot go anywhere
Ventricular Ejection
•ejection of blood begins when the ventricular pressure exceeds arterial pressure and forces semilunar valves open
–pressure peaks in left ventricle at about 120 mm Hg and 25 mm Hg in the right
rapid ejection
blood spurts out of each ventricle rapidly at first
reduced ejection
then more slowly under reduced pressure
ventricular ejections last
about 200 –250 msec
–corresponds to the plateau phase of the cardiac action potential
T wave occurs
late in this phase
stroke volume (SV)
of about 70 mL of blood is ejected of the 130 mL in each ventricle
ejection fraction
of about 54%
–as high as 90% in vigorous exercise
end-systolic volume (ESV
the 60 mL of blood left behind
Isovolumetric Relaxation
early ventricular diastole
–when T wave ends and the ventricles begin to expand
elastic recoil and expansion would cause pressure to drop rapidly and suck blood into the ventricles
–blood from the aorta and pulmonary artery briefly flows backwards
–filling the semilunar valves and closing the cusps
–creates a slight pressure rebound that appears as the dicrotic notch of the aortic pressure curve
–heart sound S2occurs as blood rebounds from the closed semilunar valves and the ventricle expands
–„isovolumetric‟ because semilunar valves are closed and AV valves have not yet opened
•ventricles are therefore taking in no blood
when AV valves open
ventricular filling begins again
Timing of Cardiac Cycle
in a resting person
–atrial systole last about 0.1 sec
–ventricular systole about 0.3 sec
–quiescent period, when all four chambers are in diastole, 0.4 sec
total duration of the cardiac cycle is
therefore 0.8 sec in a heart beating 75 bpm
Overview of Volume Changes
end-systolic volume (ESV)60 ml
-passively added to ventricle during atrial diastole+30 ml
-added by atrial systole+40 ml
total: end-diastolic volume (EDV) 130 ml
stroke volume (SV) ejected by ventricular systole-70 ml
leaves: end-systolic volume (ESV)60 ml
both ventricles must eject same amount of blood
Unbalanced Ventricular Output
pulmonary edema
-Right ventricular output exceeds left ventricular output. -Pressure backs up -Fluid accumulates in pulmonary tissue
Unbalanced Ventricular Output
peripheral edema
-Left ventricular output exceeds right ventricular output. -Pressure backs up -Fluid accumulates in systemic tissue
congestive heart failure
(CHF) -results from the failure of either ventricle to eject blood effectively
–usually due to a heart weakened by myocardial infarction, chronic hypertension, valvular insufficiency, or congenital defects in heart structure.
-eventually leads to total heart failure
left ventricular failure
blood backs up into the lungs causing pulmonary edema
–shortness of breath or sense of suffocation
right ventricular failure
blood backs up in the vena cava causing systemic or generalized edema
–enlargement of the liver, ascites (pooling of fluid in abdominal cavity), distension of jugular veins, swelling of the fingers, ankles, and feet
cardiac output
(CO) –the amount ejected by ventricle in 1 minute
cardiac output =
cardiac output = heart rate x stroke volume
–about 4 to 6 L/min at rest
–a RBC leaving the left ventricle will arrive back at the left ventricle in about 1 minute
–vigorous exercise increases CO to 21 L/min for fit person and up to 35 L/min for world class athlete
cardiac reserve
the difference between a person‟s maximum and resting CO
–increases with fitness, decreases with disease
pulse
surge of pressure produced by each heart beat that can be felt by palpating a superficial artery with the fingertips
pulse rates
–infants have HR of 120 bpm or more
–young adult females avg. 72 -80 bpm
–young adult males avg. 64 to 72 bpm
–heart rate rises again in the elderly
tachycardia
resting adult heart rate above 100 bpm
–stress, anxiety, drugs, heart disease, or fever
–loss of blood or damage to myocardium
bradycardia
resting adult heart rate of less than 60 bpm
–in sleep, low body temperature, and endurance trained athletes
positive chronotropic agents
factors that raise the heart rate
negative chronotropic agents
factors that lower heart rate
Chronotropic Effects of the Autonomic Nervous System
- autonomic nervous system does not initiate the heartbeat, it modulates rhythm and force
- cardiac centers in the reticular formation of the medulla oblongata initiate autonomic output to the heart
cardiostimulatory effect
some neurons of the cardiac center transmit signals to the heart by way of sympathetic pathway
cardioinhibitory effect
others transmit parasympathetic signals by way of the vagus nerve
sympathetic postganglionic fibers are adrenergic
–they release norepinephrine
–binds to β-adrenergic fibers in the heart
–activates c-AMP second-messenger system in cardiocytes and nodal cells
–leads to opening of Ca2+ channels in plasma membrane
–increased Ca2+ inflow accelerated depolarization of SA node
–cAMP accelerates the uptake of Ca2+ by the sarcoplasmic reticulum allowing the cardiocytes to relax more quickly
–by accelerating both contraction and relaxation, norepinephrine and cAMP increase the heart rate as high as 230 bpm
–diastole becomes too brief for adequate filling
–both stroke volume and cardiac output are reduced
parasympathetic vagus nerves have cholinergic, inhibitory effects on the SA and AV nodes
–acetylcholine (ACh) binds to muscarinic receptors
–opens K+ gates in the nodal cells
–as K+leaves the cells, they become hyperpolarized and fire less frequently
–heart slows down
–parasympathetics work on the heart faster than sympathetics
•parasympathetics do not need a second messenger system
without influence from the cardiac centers, the heart has a intrinsic ―natural‖ firing rate
of 100 bpm
vagal tone
holds down this heart rate to 70 –80 bpm at rest
–steady background firing rate of the vagus nerves
cardiac centers in the medulla
receive input from many sources and integrate it into the „decision‟ to speed or slow the heart
higher brain centers
affect heart rate
–cerebral cortex, limbic system, hypothalamus
•sensory or emotional stimuli
proprioceptors in the muscles and joints
inform cardiac center about changes in activity, HR increases before metabolic demands of muscle arise
baroreceptors signal cardiac center
- pressure sensors in aorta and internal carotid arteries
- blood pressure decreases, signal rate drops, cardiac center increases heart rate
- if blood pressure increases, signal rate rises, cardiac center decreases heart rate
chemoreceptors
•in aortic arch, carotid arteries and medulla oblongata
•sensitive to blood pH, CO2and O2levels
•more important in respiratory control than cardiac control
–if CO2accumulates in blood or CSF (hypercapnia), reacts with water and causes increase in H+levels
–H+lowers the pH of the blood possibly creating acidosis (pH < 7.35)
•hypercapnia and acidosis stimulate the cardiac center to increase heart rate
•also respond to hypoxemia –oxygen deficiency in the blood
–usually slows down the heart
chemoreflexes and baroreflexes, responses to fluctuation in blood chemistry, are
both negative feedback loops
Chronotropic Chemicals
chemicals affect heart rate as well as neurotransmitters from cardiac nerves
–blood-borne adrenal catecholamines (NE and epinephrine) are potent cardiac stimulants
drugs that stimulate heart
–nicotine stimulates catecholamine secretion
–thyroid hormone increases number adrenergic receptors on heart so more responsive to sympathetic stimulation
–caffeine nhibits cAMP breakdown prolonging adrenergic effect
electrolytes
–K+ has greatest chronotropic effect
–calcium
hyperkalemia
excess K+diffuses into cardiocytes
–myocardium less excitable, heart rate slows and becomes irregular (inhibition of repolarization)
hypokalemia
K+diffuses out of cardiocytes
–cells hyperpolarized, require increased stimulation
hypercalcemia
excess of Ca2+
–decreases heart rate
hypocalcemia
deficiency of Ca2+
–increases heart rate
stroke volume
the other factor that in cardiac output, besides heart rate, is stroke volume
three variables govern stroke volume:
- preload
- contractility
- afterload
preload
the amount of tension in ventricular myocardium immediately before it begins to contract
–increased preload causes increased force of contraction
–exercise increases venous return and stretches myocardium
–cardiocytes generate more tension during contraction
–increased cardiac output matches increased venous return
Frank-Sterling law of heart
SV inversely proportional to EDV
–stroke volume is proportional to the end diastolic volume
–ventricles eject as much blood as they receive
–the more they are stretched, the harder they contract
contractility
refers to how hard the myocardium contracts for a given preload
positive inotropic agents
increase contractility
–hypercalcemia can cause strong, prolonged contractions and even cardiac arrest in systole
–catecholamines increase calcium levels
–glucagon stimulates cAMP production
–digitalis raises intracellular calcium levels and contraction strength
negative inotropic agents reduce contractility
–hypocalcemia can cause weak, irregular heartbeat and cardiac arrest in diastole
–hyperkalemiar educes strength of myocardial action potentials and the release of Ca2+ into the sarcoplasm
–vagus nerves have effect on atria but too few nerves to ventricles for a significant effect
afterload
the blood pressure in the aorta and pulmonary trunk immediately distal to the semilunar valves
–opposes the opening of these valves
–limits stroke volume
hypertension
increases afterload and opposes ventricular ejection
anything that impedes arterial circulation can also increase afterload
–lung diseases that restrict pulmonary circulation
cor pulmonale
right ventricular failure due to obstructed pulmonary circulation
80Exercise and Cardiac Output
exercise makes the heart work harder and increases cardiac output
exercise produces
ventricular hypertrophy
–increased stroke volume allows heart to beat more slowly at rest
–athletes with increased cardiac reserve can tolerate more exertion than a sedentary person
coronary artery disease
(CAD) –a constriction of the coronary arteries
–usually the result of atherosclerosis–accumulation of lipid deposits that degrade the arterial wall and obstruct the lumen
–endothelium damaged by hypertension, virus, diabetes or other causes (e.g. free radicals!)
–monocytes penetrate walls of damaged vessels and transform into macrophages
Effects of Atheromas
causes angina pectoris, intermittent chest pain, by obstructing 75% or more of the blood flow
arteriosclerosis
hardened complicated plaque
major risk factor for atherosclerosis is
excess of low-density lipoprotein (LDL) in the blood combined with defective LDL receptors in the arterial walls
unavoidable risk factors
heredity, aging, being male
avoidable risk factors
obesity, smoking, lack of exercise, anxious personality, stress, aggression, and diet
coronary artery disease
treatment
–coronary bypass surgery
•great saphenous vein
–balloon angioplasty
–laser angioplasty
