Term
| The high speed gap junctions between electrical cells of the heart are known as |
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Definition
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Term
| What kind of Ca channels are in play during SA node depolarization |
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Definition
| T and L type calcium channels |
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Term
| The tracts leaving the SA node are high or low resistance? Why is this important |
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Definition
| The SA node contains cells with high speed gap junctions but is surrounded by higher resistance gap channels and tissue to prevent premature AP from spreading to the myocytes until enough of an impulse (collective depolarization of all SA nodes) occurs first. Then this stronger impulse is able to break through the higher resistance of surrounding the SA node and conduct along the tracts to the AV node and through to the Myocytes |
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Term
| What type of Ca channel is in the myocytes that is responsible for the plateau |
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Definition
| L-type Ca channels (L=Long) |
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Term
| what is the difference in force recruitment between skeletal muscle and heart muscle cells |
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Definition
| The heart myocytes are ALL in play every time they are illicited versus the skeletal muscle can be innervated in more areas and increase the # of myofibrils receiving action potentials in order to increase force during contraction. |
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Term
| What is the difference in the relationship of the Action potential and the ryanodine receptors of the skeletal muscle and cardiac muscle |
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Definition
Skeletal muscle has a DPH which is activated directly by Na binding and then the DPH physically opens the ryanodine receptor of the sarcoplasmic reticulum resulting in the outpouring of Ca and resultant contraction.
The cardiac muscle on the other hand is different. Na via the action potential causes the opening of a Ca L-type channel on the T tubule. The Ca now enters the cytosol and has to bind directly to the ryanodine receptor for it to open. This is much more time consuming. |
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Term
| increase inotropy means what is going on with actin and myosin |
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Definition
| increase inotropy = increase myosin and actin binding! MORE CROSS BRIDGING! |
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Term
| alcoholism negatively effects the heart in what ways |
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Definition
| dilates the heart causing dilated cardiomyopathy as a result of inflammatory mechanisms. |
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Term
| To increase CO in dilated cardiomyopathy patients you need to do what |
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Definition
|
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Term
| what physiological property of the AV node allows it to slow conduction from SA node to Ventricles |
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Definition
| AV node has low speed connexins which slows impulse since they are high resistance in nature |
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Term
| wolff parkinson white syndrome (WPW) is a type of ____ tachycardia |
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Definition
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Term
| What two characteristics of the conduction cycle contribute to reentry arrythmias |
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Definition
| 1. slow conductions 2. short refractory periods |
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Term
| what class of antiarrythmic cause prolonged hyperpolarization |
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Definition
|
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Term
| Four major causes of Afib |
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Definition
1. inflammation
2. scarring
3. drinking
4. diabetes |
|
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Term
| What is the physiology of propofol on the heart |
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Definition
| Acts as a type of Ca channel blocker and vasodilator. Action on Ca channels results in decrease vascular tone and decrease inotropy. It also effects response of the baroreflex. |
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Term
| how much pericardial fluid is there |
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Definition
|
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Term
| the subepicardium is the outer ___ layer |
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Definition
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Term
| THe left main is also known as |
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Definition
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Term
| the left main branches into what two arteries |
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Definition
|
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Term
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Definition
1. septal arteries
2. diagonal arteries |
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Term
| Off the RCA are what arteries |
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Definition
1. marginal descending artery
2. posterior descending artery |
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Term
| The SA nodal artery is usually off what? In some minor cases it is off? |
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Definition
| SA nodal artery is supplied by RCA in 60% of people. The other 40% the SA nodal artery comes from Left main |
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Term
| 85% of the hearts veins dump into the ____ via what three veins |
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Definition
| 85% of venous blood from heart is dumped into the coronary sinus. The small, middle and great cardiac veins dump into the coronary sinus. That all then dumps into the right atrium. |
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Term
| why in normal adults does some deoxygenated blood enter into the circulation? |
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Definition
| Due to thesbian veins which take deoxygenated blood from heart's muscles and dumps it directly into all four chambers resulting in a dilutional effect. |
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Term
| what part of the AP of cardiac myocytes helps prevent them from being early depolarized too soon |
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Definition
| The plateaus associated with the calcium channels result in a prolonged depolarization and absolute refractory period. |
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Term
| a healthy CO during exercise can be up to ___ Liters/min. Olympic athletes can get up to what CO |
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Definition
| 20L/min - exercise most adults. Olympic athletes can get up to 35L/min. |
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Term
| which reflex responds to volume |
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Definition
| Atrial stretch receptors associated with the bainbridge reflex. Increase volume = signal to brain to increase pumping! = increase HR. Also associated with ANP release which tells kidneys to secrete H20 and Na and also ANP vasodilates. ALL IN AN ATTEMPT TO DECREASE PRELOAD AND WORK OF HEART. |
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Term
| where are the atrial stretch receptors located |
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Definition
| right atrium at junction with vena cavae or at left atrium with junction to pulmonary veins. |
|
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Term
| how is bainbridge reflex and respirations related |
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Definition
| Bainbridge reflex describes how increase volume of blood to heart results in an increase in HR and release of ANP. Well when you breath in you also increase blood return to the heart as a indirect result of the diaphragm pressing down on the splenic, and other vascular beds in the abdomen. |
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Term
| an adult in excellent cardio health may have an arrythmia assoicated with breathing which is known as |
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Definition
|
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Term
| what is the troponin complex |
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Definition
| Made up of three troponin molecules. The key troponin is Troponin C which needs 4 Ca to bind to it so that it can trigger troponin I (inhibitory) to layoff the actin site for the myosin head to bind to it. Troponin T is the tether (T) to tropomyosin (T) |
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Term
| what is the sliding filament theory |
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Definition
| adding volume of preload to the mycardial cells results in a more ideal thin and thick filament alignment for greater # of myosin heads to link and crossbridge with actin. The result is a great force of contraction. |
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Term
| does preload or afterload affect tension more on the heart |
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Definition
| AFTERLOAD. the higher the afterload pressure then more the heart has to pump. To effectively pump that hard you reach HGIH tension |
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Term
| what is the biggest relationship of tension and the heart and why we care |
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Definition
| INCREASE TENSION = INCREASE Myocardial O2 use |
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Term
| increase afterload will shift frank starling curve where |
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Definition
| Down and to the right. So less stroke volume because have to generate so much pressure to get out of ventricle. But also higher LVEDP since not all blood can get out (like we said less stroke volume) therefore more blood left over in end diastole. |
|
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Term
| what factor must you alter to get increase SV and descrease end diastolic pressure/volume |
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Definition
| Decrease afterload, heart will more efficently pump blood out and have less blood left over after each stroke volume ejection. |
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Term
| is preload of afterload closely related to ventricular radius |
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Definition
| PRELOAD, the blood entering the ventricle during diastole will fill the ventricle like a ballon and it will enlarge/dilate. As this heart dilates it meets some resistance with the stretching of the myofibrils. This increases tension!!! Remember tension = dilation (radium) and Pressure |
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Term
| If high tension environment remains at the heart from let's say HTN what does the heart do to compensation |
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Definition
| Increase ventricular hypertorphy. Increase wall thickness means stronger and beefer heart to overcome the pathology of HTN. Remember thickness is inversely related to tension. So thicker the heart, lesser the tension. |
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Term
| what law can relate to aneurysm behavior and why |
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Definition
| LA Place's law can give credence to aneurysm behavior. The more an aneurysm on an artery ballons out (Which in other terms increases its radius) will result in a more unstable vessel since a higher radius means more tension on the vessel wall which is being stretched. So it increases the liklihood of rupturing. |
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Term
| what happens if left ventircular end diastolic pressure increases |
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Definition
| An increase in the LVEDP means higher pressure during diastole. That means higher pressure on the myocardium which depends on a lower pressure during diastole to supply the majority of blood to the heart's coronaries in the epicardium. So High LVEDP means compromise to hearts own blood supply |
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Term
| Since LA place's law states tension is related to the sum of intraventricular pressure and intraventricular radius what components of Stroke volume correlate with each of these values |
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Definition
Intraventricular pressure--> afterload
Increase afterload = increase IVP
Decrease Afterload = decrease IVP
Intraventricular Radius --> preload
increase preload=increased IVR (increase tension)
Decrease Preload = decrease IVR (decrease tension)
Decrease |
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Term
| what leads on an EKG are unipolar and what are bipolar |
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Definition
unipolar: precordial and augmented
bipolar: limb leads |
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Term
| what lead on the ecg is a reference point |
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Definition
|
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Term
| to set up a posterior EKG where would you place the leads |
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Definition
V7 goes to 5 intercostal posterior
V8 goes to tip of the scapula at 5th intercostal
V9 goes to 5th intercostal. |
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Term
| one cardiac cycle is how long |
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Definition
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Term
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Definition
|
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Term
| diastolic hf etiology/physiology... |
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Definition
| decreased compliance of the LV and abnormal relaxation of the LV during diastole. The EF and stroke volume is preserved. |
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Term
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Definition
1. MI or ischemia
2. ventricular remodeling.
3. chronic HTN
4. Aortic valvular disease
5. Pericardial disease |
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|
Term
| The CK biomarkers all rise in how much time |
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Definition
|
|
Term
| The troponin biomarkers all rise in how much time |
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Definition
|
|
Term
| the duration of CK biomarkers are |
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Definition
|
|
Term
| The duration of troponin is |
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Definition
Troponin T: (T=Two weeks) so 10-14 days
Troponin I: (I=one week) so 7-10 days |
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|
Term
| The peak of CK and troponin biomarkers is |
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Definition
|
|
Term
|
Definition
| is another name for cardiac MUSCLE (myocyte) relaxation. |
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Term
| What is the relationship of catecholamines and lusitropy? |
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Definition
| Catecholamines like dopamine will increase inotropy (increase contractility) and increase lusitropy (positive lusitropy). Ideally we give drugs like dopamine so that we can contractility for better cardiac output. Relaxation of the myocyte is also known as lusitropy. To get the myocyte to relax faster all the Ca in the cytosol needs to be put back in the sarcoplasmic reticulum so that the cell can relax and be ready for the next depolarization. Catecholamines work by increasing the action of the Ca pump on the SR (by phosphorylation) to get CA back into the SR FASTER. It also phosphorylates the troponin to cover the myosin binding sites quicker to break the cross bridging cycle. |
|
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Term
| what is the difference between how catecholamines affect lusitropy and how higher levels of extracellular Ca affect lusiptropy |
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Definition
High Extracellular Ca levels: Will enter cytosol and increase inotropy but decrease lusitropy b/c excess Ca in cystol will linger until the Ca pumps on the sarcoplasmic reticulum can catch up with all this extra workload. So the myocyte will have less time to relax b/c of the slower reuptake of Ca to the SR.
Catecholamine effect: Catecholamines phosphorylate the Ca pumps on the SR and troponin on the Actin. Thereby making them faster at getting the present Ca out of the cystol and back into SR. This means more relaxation time (positive lusitropy) and increase inotropy (b/c now we have a lot more Ca gathered in the SR for the next Action potential). |
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Term
| which ion channels are inhibited and results in long QT syndrome? Which drugs can do this? |
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Definition
| hERG Channels also known as rapid delayed rectifier IK channels. These are inhibited by drugs like zofran, haldol, and amiodarone and this results in prolonged QT syndrome. (takes longer to repolarization without the help of hERG channels) |
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Term
| Inhibition of hERG channels will result in what kind of arrythmia? Early afterdepolarization or delayed action depolarization? |
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Definition
| Early after depolarization. Since the myocyte is taking forever to fully repolarize the myocyte can be stimulate during its relative refractory period. |
|
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Term
| does digoxin contribute to delayed action depolarization or early afterdepolarization? |
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Definition
| Delayed action depolarization. Indirect consequence of excess Ca in myocyte from digoxin and effects of imbalance to Na levels. Remember Digoxin works directly on inhibiting Na/K exchanger. Results in extra Na inside cell. That then means a change in gradient. So now the Na/Ca exchanger will not work right since it wants to bring more Na into cell and remove Ca. So now we have more Ca as well. More CA and Na in cell means resting membrane potential will rise towards threshold and favor an action potential. |
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Term
| name three types of re=entry arrythmias |
|
Definition
1. Afib
2. Aflutter
3. atrial tachycardia
4. Wolf parkinson White syndrome |
|
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Term
| damaged myocytes are replaced with? Which is non-conductive tissue and increases risks for arrythmias |
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Definition
| fibroblasts will replaced dead cardiac myocytes with collagen. |
|
|
Term
| What is Wolf parkinson White syndrome |
|
Definition
| A type of re-entry arrythmia that results from fetal electrical pathways between atria and ventricles that did not close over. As a result AP can either leave the purkinjee fibers and travel back up to atria or they can leave atria and travel to ventricles directly and compete with normal pathway through AV node. |
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|
Term
| Is the S wave in II or III larger |
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Definition
| Lead III S wave is > Lead II |
|
|
Term
| does the SA node have a true resting membrane potential |
|
Definition
| NO. There are continuously open funny channels. The resting membrane is always shifting. |
|
|
Term
| does the nervous system directly affect the hearts intrinsic rate |
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Definition
| NO. IT modulates it through G protein coupled reactions via adenyl cyclase and cAMP to activate protein kinases to phosphorlate components of heart |
|
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Term
| Dilated cardiomyopathy can occur from what disease? In order to increase CO you need to |
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Definition
| Alcholism and increase CO via increase preload. |
|
|
Term
| what is the physiology for how SNS increases heart rate |
|
Definition
| Increase chronotropy via the SNS is down by G protein mechanisms which increases the permeability of funny current channels to raise phase 4 (depolarization) faster on a steeper incline towards threshold. This means the sooner the AP. Parrallel to this is SNS acting on getting CA back into the sarcoplasmic reticulum faster too so that the heart can relax and reset faster as well. |
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Term
| is torsades a early after or delay after depolarization |
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Definition
| Early after depolarization due to delay in full repolarization of the membrane (Ca still in the cytosol resulting in a raised resting membrane which is more prone to another AP) |
|
|
Term
| ventricular depolarization occuring during the relative refractory period of a cardiac myocyte will result in what |
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Definition
| Torsades R on T phenomenon |
|
|
Term
| what is the role of magnesium in the heart |
|
Definition
It acts as a major modulator and regulator of intracellular activity of the heart. It is a cation like potassium and is found almost exclusively intracellular. Does so by:
1. regulation of adenyl cyclase
2. acts as a antagonist to Ca binding at the ryanodine receptor to myocytes and Troponin C on actin.
3. increases parathyroid release of hormones that stimulate more Ca uptake to the body from diet.
4. endothelial muscle relaxation (competes with Ca thereby relaxing cell)
5. Membrane stabilization (hence why it can help with seizures by inhibiting NMDA)
6. may inhibit catecholamines
7. May help inhibit the increase Ca release from IgE hypersentivity reactions and subsequent histamine release.
6. Inhibits AcH release at the pre-synapse jucntion of skeletal muscles
7. |
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|
Term
| where on the left side of the heart are there some SA Node like cells |
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Definition
| Where the four pulmonary veins enter into the left atrium at this junction there are nodal like cells that can also illicit PACs. |
|
|
Term
| what are the two pathways in the AV node |
|
Definition
1. FAST conducting, slow recovering pathway
2. SLOW Conducting, fast recovering pathway. |
|
|
Term
| what findings on the EKG will you see with WPW |
|
Definition
| Since WPW involves an open accessory pathway between the Atrium and Ventricles it will result in Atria signal going to the AV node and through the accessory pathway at the same time. There are no slow conducting tissue in the accessory pathway therefore immediately after the P wave you start the R wave of the QRS. While at the same time the AV node is processing the normal conduction. This prolongs the R wave cause then the signal passes the AV node and also illicits the venttricle myocytes. So you get a wide R wave and very narrow PR interval. |
|
|
Term
| what is the difference between AV nodal re-entrant tachyarrythmias and AV reentry tachyarrythmias. |
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Definition
| AV Nodal reentry pathways have no accessory pathways!!! The issue is directly at the AV node where there is a slow and fast pathway. |
|
|
Term
| what drugs will help you treat arrhythmia in the sa or av node |
|
Definition
|
|
Term
| what class of antiarrythmics act the most on the IKr (Rapid Rectifiers K channels)..explain this process |
|
Definition
Class III Antiarrythmics
By inhibiting the Rapid iKr Rectifiers you don't get that fast repolarization. Instead you get this prolong period of being in between. That long period is contributes to a longer relative refractory periods. Therefore increasing your chance for a early after depolarization arrythmia like torsades. |
|
|
Term
| what do class I antiarrythmics act on the cardiac phases? |
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Definition
| Class I act primarily on The sodium upstroke (Phase 0) but also inhibit IKr like class III. |
|
|
Term
| name some diseases that predispose you to afib |
|
Definition
1. alcoholics
2. inflammation
3. scarring
4. diabetes |
|
|
Term
| explain digoxin toxicity and how it causes delayed after depolarization |
|
Definition
| Too much digoxin means excess effect on Na/K pumps. Which means excess Na intracellular. This indirectly effects the passive Na/Ca pump (exchanges 3 na from plasma for one Ca from intraceullar) Since already too much Na intracellular then this Ca/Na pump will not work. No we have extra Ca building up in the cell too. As more and more Ca builds up in the cell the Sarcoplasmic reticulum cant keep up with removing it all. So the extra Ca in the cytosol predisposes heart to a delayed action depolarization. |
|
|
Term
| explain pathophysiology behind propofol and its cardiac toxicity effect |
|
Definition
| Propofol acts by blocking calcium channels. In doing so it vasodilates the endothelial tissue (Hypotension) and decreases the inotropy of cardiac myocyctes. |
|
|
Term
| the adverse effects of propofol on the cardiac cells is most pronounced on what type of calcium channels |
|
Definition
| L-Type Calcium channels. IF you block those then you limit the time Ca can enter the mycocytes and open the most amount of ryanodine receptors. |
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