Cardiovascular system Flashcards
Anatomy of heart
-4 chambers
3 layers: endocardium, myocardium, epicardium
visceral and parietal pericardium
Left ventrical is 2-3x thicker than right
bloodflow through heart
SVC/IVC –> RA –> tricusp –> RV –> pulmonic valve –> pulmonary artery –> lungs –> pulmonary veins –> LA –> bicsup –> LV –> aortic valve –> systemic
chordae tendinae
anchored to papillary muscles –> keep mitral and tricuspid valve from going into atria during ventricular contraction
Coronary circulation
Left coronary artery
-Left anterior descending artery
-Left circumflex artery
-supply blood to LA, LV, interventricular septum, and part of RV
Right coronary artery
-supplies blood to RA, RV, part of posterior LV
-AV node and bundle of His –>imp for conduction
Coronary veins –> drain into coronary sinus
Conduction system
-specialized tissue creates and transports electrical impulses resulting in depolarization causing hear muscle contraction
SA node –> interatrial pathways –> atrial contraction –> AV node –> internodal pathways –> bundle of His –> left and right bundle branches –> Purkinje fibers –> ventricular contraction
Repolarization
Absolute refractory period
Relative refractory period
-contractile and conduction pathway cells regain resting polarized condition
-heart muscle doesn’t respond to any stimuli
-heart muscle gradually returns to normal
ECG waves and intervals
P wave = firing of SA node and depolarization of atria
QRS complex = depolarization from AV node throughout ventricles
T wave = repolarization of ventricles
U wave = repolarization of Purkinje fibers (big one= hypokalemia)
PR, QRS, QT intervals = travel time of signal from one area of heart to another
Mechanical system
Systole = contractin of heart muscles and ejection of blood from ventricles
Diastole = relaxation of heart muscles and ventricles fill with blood
Stroke volume = amt of blood ejected with each beat
Cardiac output and Cardiac index
CO = amt of blood pumped in a minute
-CO = SV x HR
-Normal = 4-8 L/min
Index = CO/BSA (body surface area)
-normal 2.8-4.2 L/min/m^2
Factors affecting CO
Stroke volume
-preload
-contractility
-afterload
Heart rate
-contolled by ANS
-sustained rapid HR = reduced diastolic filling and coronary artery perfusion
Preload
volume of blood stretching ventricles at end of diastole
-Frank starling law: increased stretch = increased force of contraction
**increased by HTN, aortic valve disease, and hypervolemia
Contractility
Increased with epinephrine and NE from SNS
Increased contractility raises SV by increasing ventricular emptying
Afterload
-peripheral resistance against which left ventricle must pump
*depends on size of ventricle, wall tension, and BP
*increased BP increases resistance = higher workload = hypertrophy (w/o change in chamber area or CO)
Cardiac Reserve
Ability of CV system to alter CO in response to situations like exercise, stress, and hypovolemia
Arteries
Arterioles
Endothelium
Arteries
-thick walls of elastic tissue to handle pressure; recoil propels blood forward
*large arteries (aorta/pulm art) also have smooth muscle
Arterioles = more smooth muscle
-major control of arterial BP and blood flow distribution through dilation and constriction
Endothelium = inner lining
-maintain homeostasis, promote blood flow, inhibits coagulation
-disruption results in coagulation and fibrin clot
Capillaries
Thin wall of endothelial cells –> no elastic or muscle
-connect arterioles and venules
-exchange nutrients and metabolic end products
Veins and Venules
Veins
-thin wall; large diameter
-low pressure; high volume
-intermittent valves move blood towards heart
-blood volume in venous sytem affected by: arterial flow, compression of veins by skeletal muscles, changes in thoracic and abdominal pressure, RA pressure (SVC=neck veins; IVC = liver engorgement)
Venules
-small muscle and CT
-collect blood from capillary beds to larger veins
ANS effect on CV syst
Effect on heart
-Sympathetic stimulation increases HR and speed of impulse thru AV node and force of contractions –> mediated by beta adrenergic receptors
-parasymp stimulation slows HR and impluse f/ SA to AV –> mediated by vagus nerve
Effects on blood vessels
-sympathetic stimulation of alpha adrenergic receptors causes vasoconstriction; decreased stimulation causes vasodilation
ANS: Baroreceptors
-Aortic arch and carotid sinus
-sensitive to stretch or pressure in arterial system
-stimulation sends message to vasomotor center in brainstem to inhibit SNS and enhance PNS to decrease HR and cause peripheral vasodilation
-decreased stretch/pressure does opposite
ANS: chemoreceptors
-aortic and carotid bodies and medulla
-increased CO2 = higher RR and changes in BP
Blood Pressure
Pressure exerted by blood on arterial walls
SBP = peak pressure during vent contraction –> under 120
DBP = residual pressure in arteries during vent relaxation –> under 80
Influencing factors: CO and SVR
-SVR = force opposing movement of blood
-BP = CO*SVR
Measurement of Bp
Invasive technique = catheter into artery –> attached to transducer
Noninvasive technique = sypygmomanometer and stethosope
-automated device
-doppler ultrasonic flowmeter
Pulse pressure and mean arterial pressure
Pulse pressure
-dif bt SBP and DBP
-Normally ab 1/3 of SBP
Mean arterial pressure
-average pressure w/in arterial system that’s felt by organs in body
-(SBP + 2DBP) / 3
-needs to be over 60 to perfuse vital organs
Gerontologic considerations
Risk for CVD increases with age
-CAD due to atherosclerosis is most common
CVD is leading cause of death in adults over 65
CV changes result of aging, disease, enviro, lifetime behaviors
Age related changes to CV system
composition
exercise
valves
pacemakers
beta adrenergic receptors
Increased collagen- decreased elastin
-myocardial hypertrophy
Decreased response to stress/exercise
-slower recovery HR, SV, CO
Heart valves become thick and stiff –> murmurs
Number of pacemaker cells decrease –> dysrhythmias; heart block
Decrease in number and func of beta adrenergic receptors –> decreased stress response and sensitivity to beta adrenergic agonists
Age related changes
blood vessels
venous valves
bp
spine
Blood vessels thicken and less elastic –> increase in SBP and decrease or no change in DBP
Incompetent venous valves –> dependent edema
Orthostatic hypotension and postprandial hypotension (fall risk)
kyphosis