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 |