Heart/hemodynamics/blood
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| P wave | atrial depolarization
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| SA to AV on EKG is | straight line from p-q
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| QRS | ventricle depolarization
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| T wave | ventricle repolarization
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| P wave atrial contraction | atrial depolarization
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| QRS ventricular contraction | ventricle depolarization
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| coronary arteries bring what to heart | oxygen, glucose
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| major coronary arteries (left side/right side) | *left main coronary artery --> circumflex branch --> LAD left anterior descending
*right coronary artery
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| 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)
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| ischemia | decreased blood flow
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| infarction | tissue death due to lack of 02 (blood supply)
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| complete occlusion usually results from | a tear in endothelium/plaque that then clots
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| myocardial infarction | heart attack
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| heart failure (congestive heart failure) | decreased pumping ability
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| 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
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| Left sided heart failure s/s | *oxy blood not reaching tissues (hypoxia, SOB)
*pulmonary edema "crackles" bwo blood backing into L atrium and lungs
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| Tx of heart failure, want to increase pumping ability or tx symptoms | *diuretics
*02 therapy
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| cardiac output equals | heart rate x stroke volume
*volume ejected per minue
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| cardiac output is how many liters/minute | 5.75 liters/minute
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| factors effecting stroke volume (3 -know) | 1-preload
2-contractility
3-afterload
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| preload defn | amount of blood entering ventricle during diastole (Frank Starling law)
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| 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)
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| 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)
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| What decreases preload? | *dehydration
*hemorrhage
*disease state that decreases venous return
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| contractility defn | how strong ventricles contract
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| 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
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| what decreases contractility | *decreased Ca
*barbiturates
*old age
*MI which leaves scar tissue
*heart failure
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| if i increase contractility, what happens to stroke volume | increases sv
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| afterload defn | resistance the ventricle has to overcome in order to eject its blood
resistance ventricle has to overcome to eject its blood
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| if aorta/arterioles are compromised, sv will | decreases, it has to push harder to eject same amount of blood
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| increased after load will do what to sv | decrease sv
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| *Resistance in arterial system (severe HTN) *semilunar valves stenosis | factors increasing after load
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| what decreases afterload? | *vasodilating drugs will decrease resistance thereby decreasing afterload (which will lower bp)
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| factors effecting heart rate | *NE at SA
*T3/T4 to upregulate Beta-1s
*exercise releases epi/ne
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| input to cardiovascular center from where? | *higher brain centers: cerebral cortex, limbic system, hypothalamus
*sensory receptors: proprioceptors, chemoreceptors and baroreceptors
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| output to heart | *cardiac accelerator by symp nerves
*cardiac decelerator by CN X vagus psymp
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| In addition to RAA, what regulates bp? |
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| BP is related to . . . | *cardiac output
*peripheral resistance
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| BP equation | BP=CO x PR
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| 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
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| mean arterial pressure, MAP equals | CO x PR (cardiac output x periph resis)
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| MAP equation #2 | 1/3 systolic bp + 2/3 diastolic bp
*must be >60 for adequate brain/tissue perfusion
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| Systolic bp is | pressure on artery walls during ventricular systole
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| diastolic bp is | pressure on walls of arteries during ventricular diastole (blood is perculating through systemic circ)
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| systolic bp indicates | how much blood is out there
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| diastolic bp indicates | how well blood is reaching systemic system
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| who controls bp? | *medulla oblongata is location of basomotor center of medulla oblongata bwo
glossopharyngeal and vagus nerves
*also RAA, ADH involved
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| orthostatic decrease in bp temporarily decreases what? | preload decreases, CO decreases
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| circulatory shock defn | blood is not circulating, most concerned about brain
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| 3 categories of circ shock | 1. hypovolemic (low preload effects)bwo hemorrhage/dehydration
2. vascular shock - dilated bvessels
3. cardiogenic
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| 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
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| cardiogenic shock is a | really bad MI, decreases CO
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