• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/127

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

127 Cards in this Set

  • Front
  • Back
MEDIASTINUM
Contains heart, anatomical region extends from sternum to vertebral column.

average mass 250 g in adult females, 300 g adult males
APEX
Formed by tip of left ventricle and rests on the diaphragm.
BASE
Posterior surface, formed atria (upper chambers) of the heart, mostly left atrium.
ANTERIOR SURFACE
Deep to the sternum and ribs
INFERIOR SURFACE
Between apex and right border, rests mostly on diaphragm
RIGHT BORDER
Faces right lung and extends from inferior surface to the base
LEFT (PULMONARY) BORDER
Faces left lung and extends from base to apex
PERICARDIUM
Membrane surrounds and protects heats.

Confines heart to position in mediastinum, allowing freedom of movement for rapid contraction
FIBROUS PERICARDIUM
Superficial, composed of tough, inelastic, dense irregular connective tissue.

Prevents overstretching of heart, protection, anchors heart in mediastinum.
SEROUS PERICARDIUM
Deeper, thin delicate membrane that forms double layer around heart.
PARIETAL LAYER OF SEROUS PERICARDIUM
Outer layer, fused to fibrous pericardium
VISCERAL LAYER OF SEROUS PERICARDIUM
Inner layer, part of heart wall, adheres tightly to surface of heart.
PERICARDIAL FLUID
Thin film of lubricating serous fluid between parietal and visceral layer

Reduces friction between layers of serous pericardium as heart moves
PERICARDIAL CAVITY
Space that contains pericardial fluid
LAYERS OF HEART WALL:
EPICARDIUM
outermost visceral layer of serous pericardium & thin transparent outer layer composed of mesothelium.

Between mesothelium layer delicate fibroelastic tissue and adipose tissue. Adipose tissue thickest over ventricular surfaces, where houses major coronary and cardiac vessels of the heart.

contains BV, lymphatics, vessels that supply the myocardium.
LAYERS OF HEART WALL:
MYOCARDIUM
pumping action of heart, composed of cardiac muscle tissue. Approx. 95% of heart wall.

Muscle fibers (cells) wrapped with connective tissue sheaths composed of endomysium and perimysium.

cardiac muscle fibers organized in bundles that swirl diagonally around heart.
LAYERS OF HEART WALL:
ENDOCARDIUM
thin layer of endothelium overlying thin layer of connective tissue.

Provides smooth lining for chambers of heart and covers valves, minimizes surface friction as blood passes through heart.
CHAMBERS OF THE HEART
consists of 4 chambers:
2 superior chambers, atria
2 inferior chambers, ventricles.
ATRIA
receive blood from blood vessels returning blood to heart, called veins
VENTRICLES
eject blood from the heart into blood vessels called arteries.
AURICLE
Wrinkled pouch-like structure located on anterior surface of each atrium.

increases capacity of atrium so it can hold greater volumes of blood.
SULCI
series of grooves on surface of the heart, contain coronary blood vessels and variable amount of fat.

marks external boundary bw 2 chambers of heart.
CORONARY SULCUS
encircles most of the heart and marks external boundary between superior atria and inferior ventricles.
ANTERIOR INTERVENTRICULAR SULCUS
shallow groove on anterior surface of heart, marks external boundary between right and left ventricles.
POSTERIOR INTERVENTRICULAR SULCUS
posterior surface of heart, marks external boundary between ventricles on posterior aspect heart.
RIGHT ATRIUM
forms right border of the heart and receives blood from 3 veins: superior vena cava, inferior vena cava, and coronary sinus.
PECTINATE MUSCLES
Muscular ridges present on inside of anterior wall of right atrium.
INTERATRIAL SEPTUM
thin partition between right atrium and left atrium
FOSSA OVALIS
Oval depression on interatrial septum, opening in fetal heart that normally closes soon after birth.
TRICUSPID VALVE / RIGHT ATRIOVENTRICULAR VALVE
blood passes from right atrium into the right ventricle through valve.

composed of dense connective tissue covered by endocardium.
RIGHT VENTRICLE
forms most of anterior surface of heart.
TRABECULAE CARNEAE
raised bundles of cardiac muscle fibers, inside right ventricle.

Some contribute to conduction system of the heart.
CHORDAE TENDINEAE
tendonlike cords that connect cusps of tricuspid valve
PAPILLARY MUSCLES
cone-shaped trabeculae carneae that connect chordae tendineae
INTERVENTRICULAR SEPTUM
partition that separates right and left ventricle internally.
PULMONARY VALVE
blood first passes through right ventricle, proceeds into large artery (pulmonary trunk), divides into right and left pulmonary arteries that carry blood to lungs.
LEFT ATRIUM
forms most of base of heart. Receives blood from lungs through 4 pulmonary veins.
BICUSPID (MITRAL) VALVE / LEFT ATRIOVENTRICULAR VALVE
blood first passes from left atrium into left ventricle through this valve.
LEFT VENTRICLE
thickest chamber of the heart, forms the apex of the heart.

contains trabeculae carneae and has chordae tendineae that anchor cusps of bicuspid valve to papillary muscles.
AORTIC VALVE
blood first passes from left ventricle through this valve into ascending aorta.

some blood flows into coronary arteries, which branch from ascending aorta, carry blood to heart wall.

remainder passes into arch of aorta, spread throughout body.
MYOCARDIAL THICKNESS / FUNCTION
thickness of 4 chambers varies according to each chamber’s function.

ventricles pump blood under higher pressure over greater distances, their walls are thicker.

Left ventricle also works harder than right ventricle, considerably thicker wall.
FIBROUS SKELETON OF THE HEART
4 dense connective tissue rings surround valves of heart, fuse with one another, and merge with interventricular septum.

prevents outstretching of valves as blood passes through them, serves as a point of insertion for bundles of cardiac muscle fibers, act as electrical insulator between atria and ventricles.
ATRIOVENTRICULAR (AV) VALVES
tricuspid & bicuspid valves

AV valves open, rounded ends of cusps project into ventricle.

Ventricles relaxed, papillary muscles relaxed, chordae tendineae slack, blood moves from higher pressure in atria to lower pressure in ventricles through open AV valves.

Ventricles contract, pressure of blood drives cusps upward until edges meet and close opening.

Same time, papillary muscles contract, pulls on and tightens chordae tendineae. Prevents valve cusps from everting (opening into atria) in response to high ventricular pressure.
SEMILUNAR (SL) VALVES
aortic & pulmonary valves

Each cusp attaches to arterial wall by convex outer margin. SL valves allow ejection of blood from heart into arteries but prevent backflow of blood into ventricles.

Free borders of cusps project into lumen of artery.

Ventricles contract, pressure builds up within chambers. Semilunar valves open when pressure in ventricles exceeds pressure of arteries, permitting ejection of blood from ventricles into pulmonary trunk and aorta.

Ventricles relax, blood starts to flow back toward heart. Backflowing blood fills valve cusps, causes free edges of semilunar valves to contract each other tightly and close opening between ventricle and artery.
SYSTEMATIC CIRCULATION
left side of heart, receives bright red oxygenated blood from lungs

Left ventricle ejects blood into aorta.

From aorta, blood divides into separate streams, entering into smaller systematic arteries that carry it to all organs throughout body.

Systematic tissue, arteries give rise to smaller diameter arterioles, which lead into extensive beds of systematic capillaries.

Exchange of nutrients/gases occur across thin capillary walls; blood unloads O2 and picks up CO2.

Blood flows through 1 capillary, enters systematic venule; venule carries deoxygenated blood away from tissues and merge to form larger systematic veins.

Ultimately blood flows back to right atrium.
PULMONARY CIRCULATION
right side of heart, receives dark red deoxygenated blood returning from systematic circ

Blood ejected from right ventricle flows into pulmonary trunk, branches into pulmonary arteries that carry blood to right and left lungs.

Pulmonary capillaries, blood unloads CO2, which is exhaled, and picks up O2 from inhaled air. Freshly oxygenated blood then flows into pulmonary veins and returns to left atrium.
CORONARY (CARDIAC) CIRCULATION
right and left coronary arteries branch from ascending aorta and supply oxygenated blood to the myocardium.
LEFT CORONARY ARTERY
passes inferior to left auricle and divides into anterior interventricular and circumflex branches.
ANTERIOR INTERVENTRICULAR BRANCH
is in anterior interventricular sulcus and supplies oxygenated blood to the walls of both ventricles.
CIRCUMFLEX BRANCH
lies in coronary sulcus and distributes oxygenated blood to the walls of left ventricle and left atrium.
RIGHT CORONARY ARTERY
supplies small branches (atrial branches) to right atrium. Continues inferior to right auricle, ultimately divides into posterior interventricular and marginal branches.
POSTERIOR INTERVENTRICULAR BRANCH
follows posterior interventricular sulcus and supplies the walls of the 2 ventricles with oxygenated blood.
MARGINAL BRANCH
beyond coronary sulcus runs along right margin of heart and transports oxygenated blood to myocardium of right ventricle.
CORONARY SINUS
found on posterior surface of heart, most deoxygenated blood from myocardium drains into large vascular sinus in coronary sulcus
CORONARY VEINS
deoxygenated blood in coronary sinus empties into right atrium. Principal veins carry blood into coronary sinus
GREAT CARDIAC VEIN
drains the areas supplied by left coronary artery
MIDDLE CARDIAC VEIN
drains areas supplied by posterior interventricular branch of right coronary artery.
SMALL CARDIAC VEIN
drains the right atrium and right ventricle.
ANTERIOR CARDIAC VEIN
drain right ventricle and open directly into right atrium.
CARDIAC MUSCLE TISSUE
muscle fibers short in length and less circular in transverse section.

one centrally located nucleus
INTERCALATED DISCS
irregular transverse thickenings of sarcolemma, connect ends of cardiac muscle fibers
DESMOSOMES
contained within intercalated discs, hold fibers together.
GAP JUNCTIONS
allow muscle APs to conduct from one muscle fibers to its neighbours.

allow entire myocardium of atria or ventricles to contract as a single, coordinated unit.
AUTORHYTHMIC FIBERS
network of specialized cardiac muscle fibers that are self-excitable, repeatedly generate APs that trigger heart contractions.
PACEMAKER
autorhythmic fibers set rhythm of electrical excitable that causes contraction of the heart.
CARDIAC CONDUCTION SYSTEM
formed by autorhythmic fibers, provide path for each cycle of cardiac excitation to progress through heart. Ensures cardiac chambers become stimulated to contract in coordinated manner, makes heart effective pump.
SINOATRIAL (SA) NODE
cardiac excitation begins, located in right atrial wall.

cells repeatedly depolarize to threshold spontaneously.
PACEMAKER POTENTIAL
Spontaneous depolarization; reaches threshold, triggers AP.
ATRIOVENTRICULAR (AV) NODE
Each AP from SA node propagates throughout both atria via gap junctions in intercalated discs of atrial muscle fibers. Following AP 2 atria contract at same time

AP reach node, located in interatrial septum. AP slows considerably as result of various differences in cell structure. Delay provides time for atria to empty their blood into ventricles.
ATRIOVENTRICULAR (AV) BUNDLE / BUNDLE OF HIS
AP enters from AV node.

only site where AP can conduct from atria to ventricles.
RIGHT & LEFT BUNDLE BRANCHES
After propagating along AV bundle, AP enters here.

branches extend through interventricular septum toward apex of heart.
PURKINJE FIBERS
Large diameter, rapidly conduct AP beginning at apex of heart upward to remainder of ventricular myocardium.

Ventricles contract, pushing blood upward toward semilunar valves.
CONTRACTILE FIBERS
atrial and ventricular muscle fibers, AP initiated by SA node travels along conduction system and spreads out to excite fibers.
ACTION POTENTIAL: DEPOLARIZATION
contractile fibers have stable resting membrane potential close to -90 mV.

Brought to threshold when voltage gated fast Na+ channels open. Opening allows Na+ inflow, inflow down electrochemical gradient produces rapid depolarization.

Within few milliseconds, channels automatically inactivate and Na+ inflow decreases.
ACTION POTENTIAL: PLATEAU
period of maintained depolarization.

opening of voltage gated slow Ca+ channels in sarcolemma. Calcium ions move from interstitial fluid into cytosol.

Inflow of calcium causes even more Ca+ to pour out of sarcoplasmic reticulum into cytosol through additional Ca+ channels in SR membrane.

Increased calcium concentration in cytosol ultimately triggers contraction.

just before plateau phase begins, some K+ channels open, allowing potassium ions to leave contractile fiber. Depolarization sustained as Ca+ inflow balances K+ outflow. Membrane potential of contractile fiber close to 0 mV.
ACTION POTENTIAL: REPOLARIZATION
after delay (prolonged in cardiac muscle) additional voltage gated K+ channels open. Outflow of K+ restores negative resting membrane potential (-90 mV); same time calcium channels in sarcolemma and SR are closing.
REFRACTORY PERIOD
time interval during which second contraction cannot be triggered.

lasts longer than contraction itself; another contraction cannot begin until relaxation is well under way.
ELECTROCARDIOGRAM (ECG)
recording of electrical signals. composite record of APs produced by all heart muscle fibers during each heartbeat.

Electrocardiograph used to record.

can determine if conducting pathway is abnormal, heart is enlarged, certain regions of heart are damaged, and cause of chest pain.
P WAVE
small upward deflection on ECG.

represents atrial depolarization, which spreads from SA node through contractile fibers in both atria.
QRS COMPLEX
begins as downward deflection, continues as large, upright, triangular wave, ends as downward wave; represents rapid ventricular depolarization, as AP spreads through ventricular contractile fibers.
T WAVE
dome shaped upward deflection, indicates ventricular repolarization and occur just as ventricles start to relax.
CARDIAC CYCLE: SYSTOLE
phase of contraction
CARDIAC CYCLE: DIASTOLE
phase of relaxation
CARDIAC CYCLE
atria and ventricles alternately contract and relax, forcing blood from areas of higher pressure to areas of lower pressure. As chamber of heart contracts, blood pressure within increases.
ATRIAL SYSTOLE
lasts about 0.1 sec, atria are contracting, same time ventricles are relaxing:

depolarization of SA node causes atrial depolarization, marked by P wave

depolarization cause atrial systole; atria contract, exert pressure on blood within, forces blood through open AV valves into ventricles.
END DIASTOLIC VOLUME (EDV)
Atrial systole contributes 25 mL of blood to vol already in each ventricle. End of atrial systole also end of ventricular diastole; each ventricular contains about 130 mL at end of relaxation period

QRS complex marks onset of ventricular depolarization.
VENTRICULAR SYSTOLE
lasts about 0.3 sec, ventricles are contracting, at same time atria are relaxed in atrial diastole.

Ventricular depolarization causes ventricular systole. Systole begins, pressure rises inside ventricles and pushes blood up against atrioventricular (AV) valves, forcing them shut.
ISOVOLUMETRIC CONTRACTION
About 0.05 secs both SL and AV valves are closed. Cardiac muscle fibers are contracting and exerting force but are not yet shortening.
VENTRICULAR EJECTION
Continued contractions of ventricles cause pressure inside chambers to rise sharply. left ventricular pressure surpasses aortic pressure, and right ventricular pressure rises above pressure in pulmonary trunk, both SL valves open.

Ejection of blood from heart begins. Period when SL valves are open, lasts about 0.25 sec.
END SYSTOLIC VOLUME (ESV)
Left ventricle ejects about 70 mL of blood into aorta and right ventricle ejects same volume of blood into pulmonary trunk.

Volume remaining in each ventricle at end of systole, about 60 mL = ESV
STROKE VOLUME
volume ejected per beat from each ventricle, equals end diastolic volume – end systolic volume:

SV = EDV – ESV
RELAXATION PERIOD
lasts about 0.4 sec, atria and ventricles are both relaxed. As heart beats faster and faster, period becomes shorter and shorter.
VENTRICULAR DIASTOLE
caused by ventricular depolarization.

ventricles relax, pressure within chamber falls, and blood in aorta and pulmonary trunk beings to flow backward toward regions of lower pressure in ventricles. Backflowing blood catches in valve cusps and closes SL valves.
DICROTIC WAVE
Rebound of blood off closed cusps of aortic valve produces this on aortic pressure curve.
ISOVOLUMETRIC RELAXATION
After SL valve close, brief interval when ventricular blood vol does not change because all 4 valves are closed.
VENTRICULAR FILLING
ventricles continue to relax, pressure falls quickly. When ventricular pressure drops below atrial pressure, AV valves open, this begins. Major part occurs just after AV valves open.
LUBB SOUND
caused by blood turbulence associated with closure of AV valves soon after ventricular systole begins.
DUPP SOUND
caused by blood turbulence associated with closure of SL valves at the beginning of ventricular diastole.
HEART MURMUR
abnormal sound consisting of clicking, rushing or gurgling noise heard either before, between or after normal heart sounds, or may mask normal heart sounds. Can be common in children and do not cause an issue, but in adults often indicates valve disorder.
P-Q INTERVAL
represents conduction time from beginning of atrial excitation to beginning of ventricular excitation.
S-T SEGMENT
represents time when ventricular contractile fibers are depolarized during plateau phase of action potential.
Q-T INTERVAL
time from beginning of ventricular depolarization to end of ventricular repolarization.
CARDIAC OUTPUT (CO)
volume of blood ejected from left ventricle (or right ventricle) into aorta (or pulmonary trunk) each minute.

equals stroke volume (SV) multiplied by heart rate (HR:
CO = SV X HR

typical resting male, SV 70 mL/beat, and HR 75 beats/min:

CO = 70 mL/beat x 75 beats/min = 5250 mL/min = 5.25 L/min
CARDIAC RESERVE
difference between person’s maximum cardiac output and cardiac output at rest. Average person 4-5 x the resting value.
REGULATION OF STROKE VOLUME
preload, degree of stretch on the heart before it contracts.

contractility, the forcefulness of contraction of individual ventricular muscles fibers

afterload, pressure must be exceeded before ejection of blood from ventricles can occur
FRANK STARLING LAW OF THE HEART
more the heart fills with blood during diastole, the greater the force of contraction during systole.

Preload is proportional to end-diastolic volume (EDV); normally greater the EDV, more forceful next contraction.
2 FACTORS OF EDV
duration of ventricular diastole

venous return, volume of blood returning to right ventricle.
POSITIVE INOTROPIC AGENTS
substances increase contractility, promote calcium inflow during cardiac APs, which strengthens the force of the next contraction.
NEGATIVE INOTROPIC AGENTS
decrease contractility; increased K+ levels in the interstitial fluid, inhibition of the sympathetic division, anoxia will have negative effects.
AFTERLOAD
pressure must be overcome before semilunar valves can open
CARDIOVASCULAR CENTRE
found in medulla oblongata, nervous system regulation of the heart.

receives input from variety of sensory receptors and higher brain centers; centre then directs appropriate output by increasing or decreasing frequency of nerve impulses in both sympathetic and parasympathetic branches of ANS.
PROPRIOCEPTORS
monitoring position of limbs/muscles, send nerve impulses at an increased frequency to the cardiovascular centre once physical activity starts.
CHEMORECEPTORS / BARORECEPTORS
monitor chemical changes in blood

monitor stretching of major arteries and veins caused by pressure of the blood flowing through them.
CARDIAC ACCELERATOR NERVES
sympathetic neurons extend from medulla oblongata into spinal cord, from thoracic region these nerves extend out to the SA node, AV node, and most portions of the myocardium.

trigger release of norepinephrine, which binds to beta 1 receptors on cardiac muscle fibers. Interaction has 2 effects
EFFECTS OF CARDIAC ACCELERATOR NERVES
in SA and AV node fibers, norepinephrine speeds rate of spontaneous depolarization so pacemakers fire impulses more rapidly and HR increases

in contractile fibers throughout atria and ventricles, norepinephrine enhances calcium entry through the voltage gated slow calcium channels, thereby increasing contractility; as a result, greater volume of blood ejected during systole.
VAGUS (X) NERVE
parasympathetic nerve impulses reach heart via right and left ----- . axons terminate in SA node, AV node, and atrial myocardium. Release acetylcholine, which decrease HR by slowing rate of spontaneous depolarization in autorhythmic fibers.
CHEMICAL REGULATION OF HR: HORMONES
epinephrine and norepinephrine enhance heart’s pumping effectiveness; increase both HR and contractility. Exercise, stress and excitement cause adrenal medullae to release more hormones.

Thyroid hormones also enhance cardiac contractility and increase HR.
TACHYCARDIA
elevated resting HR.
CHEMICAL REGULATION OF HR: CATIONS
elevated blood levels of K+ or Na+ decrease HR and contractility

excess Na+ blocks Ca+ inflow during cardiac APs, thereby decreasing force of contraction, whereas excess K+ blocks generation of APs.

Moderate increase in interstitial fluid Ca+ levels speeds HR and strengthens heartbeat.
OTHER FACTORS THAT REGULATE HR
age, gender, physical fitness and body temperature

adult females have higher resting HRs than adult males, although regular exercise tends to bring resting HR down in both sexes.

increased body temp causes SA node to discharge impulses more quickly, = increasing HR.
BRADYCARDIA
physically fit person can exhibit resting HR under 50 beats/min.
EXERCISE & THE HEART
sustained exercise increases oxygen demand of muscles.

After several weeks of training, healthy person increases maximal cardio output, thereby increasing maximal rate of oxygen delivery to the tissues.

skeletal muscles develop more capillary networks in response to long term training.
ARTERIOSCLEROSIS
thickening of the walls of arteries and loss of elasticity are main characteristics

one form includes atherosclerosis, progressive disease characterized by formation in walls of large and medium sized arteries of lesions called atherosclerotic plaques.
VENTRICULAR FIBRILLATION
most deadly arrhythmia, contractions of ventricular fibers completely asynchronous so ventricles quiver rather than contract in coordinate way.

Result, ventricular pumping stops, blood ejection ceases, and circulatory failure and death occur unless
immediate medical intervention.

Most common cause inadequate blood flow to heart due to coronary artery disease, as occurs during myocardial infarction.

Causes unconsciousness in seconds and if untreated seizures and irreversible brain damage after 5 minutes.

Treatment involves CPR, defibrillation.
CARDIAC ARREST
cessation of an effective heartbeat. Heart may be completely stopped or in ventricular fibrillation.
PALPITATION
fluttering of the heart or an abnormal rate or rhythm of heat about which an individual is aware.
ARTIFICIAL PACEMAKER
device sends out small electrical currents to stimulate the heart to contract. Consists of a battery and impulse generator and usually implanted just inferior to clavicle. Wires threaded through superior vena cava and then passed into various chambers of the heart.