Cardiovascular I Flashcards
four chambers of the heart
-right atrium - recieve blood from systemic circuit
-right ventricle - pumps blood into pulmonary circuit
-left atrium-recieves blood from pulmonary circuit
-left ventircle - pumps blood into systemic circuit
valvular heart disease
-deterioation of valve function
-may develop after carditis
-may result from rheumatic fever
coronary circulation
-supplies blood to muscle of the heart
-coronary ateries originate at aortic sinuses
-elevated blood pressure and elastic rebound of aorta maintain blood flow through coronary arteries
right coronary artery supplies blood to
-right atirum
-portions of both ventircles
-portions of electrical conducting system of the heart
right coronary arter gives rise to
-marginal arteries
-posterior interventricular artery
left coronary artery supplies blood to
-left ventricle
-left atrium
-interventricular septim
-left coronary artery gives rise to
-circumflex artery
-anterior interventricular artery
cardiac veins
-great cardiac vein
-posterior vein of left ventricle
-middle cardiac vein
-small cardiac vein
-anterior cardiac veins
great cardiac vein drains blood from
-region supplied by anterior interventricular artery
-returns blood to coronary sinus
posterior vein of left ventricle, middle cardiac vein and small cardiac vein empty into
-empty into great cardiac vein or coronry sinus
where does the anterior cardiac veins empty into
-right atrium
photo of the great cardiac vein
coronary artery disease
-partial or complete blockage of coronary circulation
-reduction of cardiac performance due to lack of oxygen
-coronary ischemia = reduced circulatory supply from partial or complete blockage of cornary arteries
-usual cause is formation of fatty deposit or plauqe, reducing blood flow and spasms in smooth muscles of vessel wall can firther decrease or stop blood flow
angina pectoris
-one of first symptoms of CAD
-temporary ischemia develops when workload of heart increases
-individual may feel comfortable at rest
-exertion or emotional stress can produce sensations of pressure chest constriction and pain
pain may radiate from sternal area to arms and back
myocardial infarction
-part of coronary circulation becomes blocked
-death of cardiac muscles due to lack of oxygen
-death of affected tissue creates non-functional area known as infarct
-most commonly results from servere CAD
coronary thrombosis
-thrombus formation at a plaque
-most common cause of an MI
two types of cardiac muscle cells
-autorhytmic cells - control and coordinate heartbeat
-contractile cells - produce contractions that propel blood
conducting system
-consists of specialized cardiac muscle cells that initate and distribute electical impulses that stimulate contraction
-is autorhytmic
autorhytmicicty
-cardiac muscle tissue contracts without nueral or hormonal stimulation
components of conducting system
-pacemaker cells in SA node (RA) and AV node (AV junction)
-conducting cells fount in internodal pathways of atria, AV bunch, bundle branches, and purkinje fibers
pacemaker potential
-gradual depolarization of pacemaker cells
-pacemaker cells do not have stable RMP
rate of sponatneous depolarization of SA and AV node
-SA node: 60-100 AP/minute
-AV node: 40-60 AP/minute
which node depolarizes first-
-SA node, this establishes the sinus rhythym
-PSNS slows heart rate so that our heart rate avg iss not 80-100bpm
impulse conduction through the heart
- SA node activity and atrial activation begin
- stimulus spreads across atria and reaches AV node
- impulse is delayed for 100 msec at AV node and atrial contraction begin
Heart conduction systems accompanying ECG
disturbances in heart rhyhym
-bradycardia - slow
-tachycardia - fast
-ecotopic pacemaker - abnormal cells produce high rate of action potentials, disrupts timing of ventricular contractions
ECG
-recording of electrical events in the heart
-obtained by placing electrodes at specific locations on body surface
-abnormal patterns are used to diagnose famage
features of ECG
-P wave - depolarise atria
-QRS complex - depolarization of ventricles, ventricles begin contracting shortly after R wave
-T wave - repolarixation of ventricles
time intervals between ECG waves
-P-R intervals- from start of atrial depolarization to start of QRS complex
-Q-T interval - time required for ventircles to undergo a single cycle of depolarization and repolarization
cardiac contractile cells
-form bulk of atrial and ventricular walls
-recieve stimulus from purkinje fibers
-RMP of ventricular cell is -90, and atrial cell is -80
characteristics of cardiac contractile cells
-small size
-single, central nucleus
-branching interconnections between cells
-intercalated discs
intercalated discs
-interconnect cardiac contractile cells
-membranes of adjacent cells held together by desmosomes, and linked together by gap junctions
-transfer force of contraction from cell to cell
-propagate action potentials
action potential in cardiac contractile cells
-rapid depolarization - massive influx of Na+ through fast sodium channels
-plateau - extracellular Ca enters through slow calcium channels
-repolarazation - K rushes out of cell through slow potassium channels
refractory period of conducting cells
-absolute - cardiac contraction cells cannot respond
-relative refractory period - cells respond only to strong stimuli
action potential in ventricular contractile cell
-250-300msec
-30 times longer than that in skeletal muscle fiber
-prevents summation and tetany because absolute refractory period continues until relaxation is underway
calcium ions in cardiac contractions source
-extracellular ca crosses plasma membrane during plateau phase and provides 20% of calcium required for contraction
-extracellular caclicum triggers release fo additional calcium from SR
role of calcium ions in cardiac contractions
-cardiac muscle tissues are very sensitive to extracellular Calcium concentrations
-as slow calcium channels close, intracellular Calcium is pumped back into SR or out of cell
energy for cardiac contraction
-aerobic energy from mitochondrial break down of fatty acids and glucose
-oxygen delivered by circulation
-cardiac contractile cells store oxugen in myoglobin
diastole and systole
-diastole - relaxation
-systole - contraction
phases of the cardiac cycle
how long does cardiac cycle last
-800msec
what happens to cardiac cycle when heart rate increases
-all phases of cardiac cycle shorten, particularly diastole
atrial systole
- atrial contraction begins and right and left AV valves are open
- atria eject blood into ventricles
ventricular systole and atrial diastole
- atrial systole ends and atrial diastole begins, Ventricles contain max blood
- ventricles contract and build pressure closing AV vales and producing isovolumetric contracton
end diastolic volume
-max volume of ventricles
ventricular systole
- ventricular ejection, ventricular pressure exceeds arterial pressure, open semilunar vales and blood exits,
- semilunar valves close as ventricle pressure falls, ventricles containe nd systolic volume
stroke volume
-amount of blood ejected
ventricular diastole
-isovulmetric relaxation - all valves closed, ventricular pressure is higher than atrial pressure
-AV vales open and ventricles fill passibely
can individuals survive atrial damage
-yes they can survive atrial damage but not ventricular damage
first part of cardiac cycle photo
second part of cardiac cycle
heart sounds
-S1 - AV cvalves close
-S2- Semilunar valves close
-S3,S4 - blood flowing into ventricles and atrial contraction
heart murmur
-sounds produced by regurgiation through valves
cardiac output
-volume pumped by left ventricle in one minute
factors affecting CO
stroke volume equation
EDV-ESV
end diastolic volume
-amount of blood in each ventricle at end of ventricular diastole
end systolic volume
-amount of blood remaing in each ventricle at end of each ventricular systol
ejection fraction
-percentrage of EDV ejected during contraction
autonomic innervation of the heart
-cardiac plexus
-CN X carry parasympathetic fibers to small ganglia in cardiac plexus
-cardiac centers in medulla oblongata
-cardioaccelatory centers of MO controls sympathetic nuerons increase HR
-cardioinhibiotry centers controls parasympthatic nuerons that slow HR
cardiac reflexes
-cardiac centers monitor blood pressure, monitor arterial oxygen and CO2 levels, and adjust cardiac activity
autonomic tone of the heart
-maintaines by dual innervation and release of ACh and NE
-fine adjustments meet needs of other systems
effects on pacemaker cells of SA node
-membrane potentials of pacemaker cells are closer to threshold than those of cardiac contractile cells
-any factor that changes the rate of spontaneous depolarization or the duration of repolarization will alter HR by changing the time required to reach threshold
pacemaker cells spontaneous depolarization photo
parasympathetic stimulation of pacemaker cells
-
sympathetic stimulation of pacemaker cells
bainbridge reflex
-atrial reflex
-adjustments in HR in response to increase venous return
-stretch receptors in right atrium trigger increase in HR by stimulating sympathetic activity
factors affecting stroke volume
-changes in EDV or ESV affect stroke volume and thus cardiac output
two factors affect EDV
-filling time (duration of ventricular disastole)
-venous return
preload
-degree of ventricular stretching during ventricular diastole
-driectly proportional to EDV
-affect ability of muscle cells to produce tension
EDV and stroke volume at rest
-EDV is low
-mycocardium is stretched very little
-stroke volume is relatively low
EDV and stroke volume with excersize
-venous return increases
-EDV increases
-myocardium stretches more
-stroke volume increases
three factors affecting EDV
-preload (ventricular stretching furing diastole)
-contractility
-afterload
contractility
-force produced during contraction at given preload
-affected by autonomic activity and hormones
after load
tension that must be produced by ventricule to open semilunar valve and eject blood
sympathetic stimulation of heart
-NE released by cardiac nerves
-E and NE release by adrenal medullae
-causes ventricle to contract with more force
-increase ejection fraction and decreases ESV
parasympathetic stimulation
-ACH released by vagus nerves-reduces force of cardiac reduced force of cardiac contractions
hormones affecting heart
-pharmaceutical drigs mimic hormone actions by stimulate or block alpha or beta receptors
-block calcium channels
factors affecting stroke volume
summary of factors affecting cardiac output
