How long does it take for all the blood to be pumped through?
one minute
Endocardium
a thin layer of endothelium in the heart
Myocardium
muscle layer (cardiac muscle)
Epicardium
thin external layer covering the heart
Sinoatrial node
SA node or pacemaker;located within the posterior wall of the right atrium; rhythmic impulses originate in the SA node and spread through the atria
Atrioventricular node
AV node; located within the lower right interatrial septum; an impulse is delayed there for about 1/10 of a second to allow the atria to contract before ventricular contraction
Atrioventricular bundle
AV bundle or bundle of HIS; originiates in the AV node, dividing into two bundle branches which extend down the two sides of the interventricualr septum
Purkinje fibers
originate from the right and left branches, extending to the papillary muscles and lateral walls of the ventricles
Factors that may alter the heartbeat rate
sympathetic and parasympathetic impulses, hormones, body temp., exercise, and emotions
the atria and ventricles are relaxed, the tricuspid and mitral valves are open, and the aortic and pulmonary valves are closed. Blood flows passively from the atria into the ventricles, with 65% to 85% of ventricular filling occurring before the end of t
atrial systole
atria contract ad pump the additional 20-30% of the blood into the ventricles. As the atria contract, the vena cava and pulmonary veins narrow; there is some regurgitation. There is about 135 ml of blood in each ventricle.
ventricular systole
pressure changes and the AV valves close “lub”. All 4 valves are closed (isovolumetric ventricular contraction phase). When the pressure on the right exceeds 10 mm Hg and the left exceeds 80 mm Hg the pulmonary and aortic valves open.
Isovolumetric ventricular contraction phase
the moment when all 4 valves are closed and no blood can enter or leave the ventricles.
Minimum diastolic pressure on both sides
10mm Hg and 80 mm Hg
Normal resting condition pressure
24 mm Hg and 120 mm Hg
Stroke volume
volume of blood ejected from either ventricle; 70 to 80 ml
End-systolic volume
Amount of blood remaining in either ventricle at the end of systole; 50 ml
Early diastole
as the ventricles relax, pressure drops; the pulmonary and aortic valves close, preventing backflow “dub”. The tricuspid and mutral valves open, and blod flows from the atria into the ventricles
Sphygmomanometer
the mercury manometer to take blood pressure
Auscultatory method
method to take blood pressure using atrial sounds
Sounds of Korotkoff
the turbulent flow of the blood with each beat creates vibrations that are heard in the stethoscope when taking blood pressure using the auscultatory method
Pulse pressure
the difference between the systolic and diastolic pressures; this pressure difference is what drives blood along the arteries to the capillaries.
the greater the filling during diastole, the greater the force of contractin during systole
catecholamines
epinephrine and norepinephrin
xanthines
caffeine, theophylline
digitalis
drug used for cardiac failure
factors that have a positive inotropic effect
frank starling, catecholamines, xanthines, digitalis
chronotropic
rate of contraction
dromotropic
rate of conduction of impulse
two ways nerves contrals the heart
chronotropic and inotropic
sympathetic control of heart
increase rate and force of contraction, uses norepinephrine to increase permeability to Na and Ca
max sympathetic stimulation
250 beats/min
parasympathetic control of heart
decrease rate and force of contraction, S.A node-right vagus, A.V. node- left vagus, uses acetylcholine to increase permeability to K+
max parasympathetic stimulation
20-30 beats/min
stroke volume
60-80 ml; amount of blood pumped out of each ventricle per beat
cardiac output
CO= stroke volume X heart rate
caradiac output of average person
5.76 Liters/minute
factors causing an increase in cardiac output
axiety, eating, exercies, increased body temperture, pregnancy
fick method
blood flow=cardiac output; the amount of oxygen consumed by the body in a perdod of time is divided by the AV difference
fick equation for cardiad output
CO=(oxygen consumed in ml/min)/(arterial O2-venous O2)
factors that may alter the heartbeat rate
sympathetic/parasympathetic impulses, hormones, body temperature, exercise, drugs, emotions, stimulation from exteroceptors
ectopic pacemakers
out of place pacemakers
einthoven's triangle
electrodes attached to the left shoulder, right shoulder, and left leg, forming a triangle to take ECGs
cardiac arrhythmia
deviations from nromal heart rate or from normal electrical activity of the conduction system
causes of ectopic pacemakers
ischemia, heart damage, dilation of heart, toxic irritants (nicotine, caffeine, alcohol), lack of sleep, anxiety, extremes in body temp, change in body pH
atrial premature beat
premature depolarization of SA node or ectopic pacemaker; some P waves are weird; little clinical significance
AV nodal premature beat
ectopic discharge of the AV node; normal QRS but no P wave before
Premature Ventricular Depolarization
PVD or PVC; ectopic pacemaker in ventricles; no P wave, wide QRS, high voltage, inverted T wave, pause afterwords like a skipped beat
bigeminy
one normal and one PVD
trigeminy
two normal and one PVD
SA block
pacemaker stops for at least one cycle and then resumes; all is identical before and after
first degree AV block (incomplete)
prolonged PR interval; caused by digitalis or vagal stimulation
second degree AV block type I (Wenckeback or Mobitz's type 1)
PR intervals lengthen progressively until a ventricle beat is dropped; can be caused by digitalis
second degree AV block type 2 (Mobitz's type 2)
takes 2 or more atrial impulses to stimulate the ventricles; usually 2:1, 3:1, or 4:1; caused by myocardial infarction or myocarditis; may lead to 3rd degree block
third degree AV block (complete)
none of the atrial impulses stimulate the AV node; ventricles are paced independently from the atria; ventricular rate is slower than the atrial rate of contraction; totally random ECG
atrial flutter
ectopic atrial pacemaker; p waves are very rapid and coordinated; 2:1, 3:1, 4:1; treatment-digitalis
Atrial fibrillation
many ectopic pacemakers in atria; irregular p waves; decrease in cardiac output; QRST look normal
Ventricular flutter
single ectopic pacemaker in ventricles; smooth sine wave; extremely dangerous; heart does not fill properly, decreased cardiac output, leads to fibrillation; decreased coronary flow
ventricular fibrillation
caused by many ventricular ectopic pacemakers, uncoordinated, chaotic twitching, bag of worms, blood pressure drops, unless stopped death will occur in short time
myocardial infarction
lack of blood flow to an area of the heart, may be caused by thrombus formation with blockage of vessels, spasms in the coronary arteries without total occlusion, narrowing caused by atherosclerosis; area is electrically dead
classical triad
3 phases of myocardial infarction 1)ischemia 2)injury 3)infarction
ischemia as a ecg
symmetrical inversion of the T wave; most obvious in chest leads; caused by delay in the recovery at the epicardial regions; altered repolarization; take nitroglycerin to correct
injury as a ecg
ST elevation means infarction is fresh (acute)
infarction as a ecg
significant Q wave-much wider than normal; Q may be 1/3 height of QRS; may last for years; some drugs can cause similar effects
symptoms of myocardial infarction
pain in neck, jaw, back, shoulder, and left arm; vomiting; catecholamines released, increased blood sugar; cardiac troponins in blood; released enzymes; amount of troponin and creatine kinase correlate with severity of infarction
flow is greater at the center of the vessel than along the outer edges
blood vessel diameter is mainly regulated by
autonomic nervous system
angiotensin II
causes vasoconstriction; produced as a result of secretion of renin from the kidneys, it may functiont o help maintain adequate filtration pressure in kidneys when systemic blood flow and pressure are reduced
ADH (vasopressin)
causes vasoconstriction
Histamine
causes vasodilation; promotes localized vasodilation during inflammation and allergic reactions
% circulation in systemic, pulmonary, and heart systems
79% systemic, 12% pulmonary, 9% max heart
percent breakdown of 79% of blood in systemic circulation
15% in arteries, 5% in capillaries, 59% in veins
blood pressure in different vessels
large arteries 100-95; small arteries 95-85; arterioles 85-30; capillaries 30-10; veins 10-0
where does most regulation of blood pressure occur
arterioles
precapillary sphincters
regulate blood flow to capillary. Use myogenic and metabolic mechanisms to regulate blood flow in relation to the local tissues need for oxygen called autoregulation
autoregulation
myogenic and metabolic mechanisms to regulate blood flow in relation to the local tissues need for oxygen
capillary hydrostatic pressure
CP; blood pressure in the capillary
osmotic force
usually stays the same in capillaries due to albumin
cardiac output, peripheral resistance, or total blood volume
long term regulation of blood pressure is regulated by
hormones
ADH (vasopressin) effects
decreases urine formation in kidneys which increases blood pressure
diuretic agent effecs
inhibit release of ADH, increase urine, decrease blood pressure
alcohol effect on ADH
inhibits ADH increasing urine to dump the alcohol
renin angiotensin system
releases aldosterone which raises blood pressure
aldosterone
hormone which raises blood pressure
steps of renin-angiotensin system up to angiotensin II formation
decrease in blood pressure->decrease in blood flow to kidney->juxtaglomerular apparatus in the kidney secretes renin->renin converts angiotensinogen to angiotensin I which is converted to angiotensin II
steps of renin-angiotensin system from angiotensin II to increased blood pressure
3 mxnsms;1)angiotensin II->increased ADH->water retention->higher bp 2)angiotensin II->adrenal cortex secretes aldosterone->salt and water retention->yep 3)angiotensin II->vasoconstriction of arterioles->increased resistance->higher bp
primary aldosteronism (Conn's syndrome)
results from hypersecretion of aldosterone from the adrenals->hypertension, increased exracellular fluid volume, hypernatremia and potassium depletion; mostly occurs because of an adrenal adenoma (tumor in adrenal cortex)
short term regulation of bp
nervous system controls to mechanism 1)baroreceptors 2)chemoreceptors; both are in medulla
baroreceptors
cardioinhibitory center->parasympathetic->HR down+CO down+vasodilation up->BP down
chemoreceptors
vasomoter center->sympathetic->HR up+CO up+vasocontriction=BP up
where are baroreceptors located
aortic arch, pulmonary veins, right and left atria, superior and inferior vena cava and in the carotid sinuses
how are baroreceptors stimulated
a change in pressure causes the walls of these arterial regions to stretch or relax and stimulate sensory receptors which stimulate or inhibit the cardioinhibitory center and the opposite to the vasomoter center
where are chemoreceptors located
aortic bodies and in the carotid bodies
how are chemoreceptors stimulated
decreased levels of oxygen and increased levels of CO2 and H+ in the blood; impulses sent through the same nerves as the baroreceptors where they stimulat the vasomoter center
what is circulatory shock
inadequate blood flow and/or oxygen delivered to the tissues
reduced blood volume as a result of hemorrhage, dehydration, or burns; symptoms: low blood pressure, rapid pulse, cold, clammy skin, little urine formation, increased respiration rate, and intense thirst
anaphylactic shock
rapid drop in bp from a severe allergic reaction causing an extreme release of histamine which causes vasodilation and a drop in bp
inadequate circulation of blood in body tissues due to cardiac failure
body's compensation for circulatory shock
vasoconstriction (except for heart and brain), venoconstriction, increased heart rate and respiration and thirst and hematopoiesis, secretion of epinephrine and norep and adh, spleen contracts, renin-angiotensin system activated
time frame the body restores homeostasis
plasma volume restored in hours, plasma proteins restored in days, blood cells restored in 3-4 weeks
hypertension
high bp; 1/5 people; 12% of all deaths by rupturing a vessel in a vital organ or by causing the heart or kidneys to fail; two types: primary (essential) and secondary
essential or primary hypertension facts
no cause;90% of all hypertensive patients; 25-50 years old; females more often; hereditory; blacks more often; from high salt intake; psycho emotional stress contributes
essentail or primary hypertenstion characteristics
asymptomatic (people don't know they have it); CO and extracellular fluid volumes are normal but total peripheral resistance is high; increased sensitivity to epi and norepi; many have left ventricular hypertrophy
secondary hypertension
definable causes; 10% of cases; renal artery disease, excess catecholamines (tumor of adrenal medulla), or excess aldosterone (Conn's syndrome)
mr. charles11
