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Bio 203 Heart
Heart/hemodynamics/blood
| Question | Answer |
|---|---|
| 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
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