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Bio 203 Heart


P wave atrial depolarization
SA to AV on EKG is straight line from p-q
QRS ventricle depolarization
T wave ventricle repolarization
P wave atrial contraction atrial depolarization
QRS ventricular contraction ventricle depolarization
coronary arteries bring what to heart oxygen, glucose
major coronary arteries (left side/right side) *left main coronary artery --> circumflex branch --> LAD left anterior descending *right coronary artery
if heart doesn't get enough 02, will switch to anaerobic metabolism which activates this rsn ADP + creatine (in presence of CK which indicates death of myocardium in that region)
ischemia decreased blood flow
infarction tissue death due to lack of 02 (blood supply)
complete occlusion usually results from a tear in endothelium/plaque that then clots
myocardial infarction heart attack
heart failure (congestive heart failure) decreased pumping ability
Right sided heart failure s/s failure of r ventricle --> can't get blood into pulmonary circuit. Blood pools in r ventricle *cyanosis *SOB *activates ANP/BNP markers for heart failure *blood backs up to R atria, vena cavae, backs up in venous system --> peripheral edema
Left sided heart failure s/s *oxy blood not reaching tissues (hypoxia, SOB) *pulmonary edema "crackles" bwo blood backing into L atrium and lungs
Tx of heart failure, want to increase pumping ability or tx symptoms *diuretics *02 therapy
cardiac output equals heart rate x stroke volume *volume ejected per minue
cardiac output is how many liters/minute 5.75 liters/minute
factors effecting stroke volume (3 -know) 1-preload 2-contractility 3-afterload
preload defn amount of blood entering ventricle during diastole (Frank Starling law)
Frank-Starling Law within limits, the greater the volume into heart during diastole, the greater the volume out during systole (not true during heart failure)
what increases preload? *increase SV *increase diastole (filling time) *exercise to increase venous return *elevate legs to increase venous return *increase blood volume (transfusion, IV fluids)
What decreases preload? *dehydration *hemorrhage *disease state that decreases venous return
contractility defn how strong ventricles contract
what increases contractility? *epi, norep binding Beta-1 in myocardium (not in SA which is rate related) *exercise training *other drugs, digoxin, digitalis (also increases AP to increase filing time), cocaine, amphetamines *T3, T4 bwo upregulated Beta-1s
what decreases contractility *decreased Ca *barbiturates *old age *MI which leaves scar tissue *heart failure
if i increase contractility, what happens to stroke volume increases sv
afterload defn resistance the ventricle has to overcome in order to eject its blood resistance ventricle has to overcome to eject its blood
if aorta/arterioles are compromised, sv will decreases, it has to push harder to eject same amount of blood
increased after load will do what to sv decrease sv
*Resistance in arterial system (severe HTN) *semilunar valves stenosis factors increasing after load
what decreases afterload? *vasodilating drugs will decrease resistance thereby decreasing afterload (which will lower bp)
factors effecting heart rate *NE at SA *T3/T4 to upregulate Beta-1s *exercise releases epi/ne
input to cardiovascular center from where? *higher brain centers: cerebral cortex, limbic system, hypothalamus *sensory receptors: proprioceptors, chemoreceptors and baroreceptors
output to heart *cardiac accelerator by symp nerves *cardiac decelerator by CN X vagus psymp
In addition to RAA, what regulates bp?
BP is related to . . . *cardiac output *peripheral resistance
BP equation BP=CO x PR
what effects periph resistance? 1. lumen diameter 2. viscosity of blood 3. vessel length bwo # of capillaries which actually create resistance (as in obese people have more capillaries, why theres increase pv, inc pv --> bp
mean arterial pressure, MAP equals CO x PR (cardiac output x periph resis)
MAP equation #2 1/3 systolic bp + 2/3 diastolic bp *must be >60 for adequate brain/tissue perfusion
Systolic bp is pressure on artery walls during ventricular systole
diastolic bp is pressure on walls of arteries during ventricular diastole (blood is perculating through systemic circ)
systolic bp indicates how much blood is out there
diastolic bp indicates how well blood is reaching systemic system
who controls bp? *medulla oblongata is location of basomotor center of medulla oblongata bwo glossopharyngeal and vagus nerves *also RAA, ADH involved
orthostatic decrease in bp temporarily decreases what? preload decreases, CO decreases
circulatory shock defn blood is not circulating, most concerned about brain
3 categories of circ shock 1. hypovolemic (low preload effects)bwo hemorrhage/dehydration 2. vascular shock - dilated bvessels 3. cardiogenic
types of vascular shock 1. anaphylactic (histamine binds to vasodil) 2. neurogenic (withdraw of symp ns, most likely in spinal cord injury of thoracolumbar where symp nerves are) 3. Toxic shock causes vasodil
cardiogenic shock is a really bad MI, decreases CO
Created by: lorrelaws