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220 Cards in this Set
- Front
- Back
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arrhythmias
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abnormal rhythms, pacemakers.
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detect from ECG, 5 things
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arrhythmias conduction abnormalities hypertrophy ischemia necrosis
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ECG
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a record of electrical changes within the heart as recorded from the surface of the body. Potential diffs, charge distribution on surface of heart. describes movement of AP from one end of cell to other end.
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ecg, first tissue excited
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atrial tissue.
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first wave in ecg
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p wave = atrial depolarization. Takes several 10s of ms. Atria become completely depolarized and signal goes back to baseline
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period at baseline, ecg
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conduction of excitation thru atrial ventricular node.
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way septum depolarizes
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depol of septum from left to ride, followed by ventricular depol of left then right walls
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QRS complex, ecg
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occurs when the ventricles deploarize
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Q wave
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septal depol. Wave moving away from lead.
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R wave
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majority of depol of l.eft and right ventricular walls. Toward lead one.
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S wave
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last stage of ventricular depol. Base (top) of heart where ventricles meet the atria. Points away from lead.
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ST segment
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tells you ventricle is uniformly depolarized. start at baseline. Can be elevated when ischemia in tissue. Look for elevation when someone comes in with chest pain. No potential difference.
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T wave
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large in area but amplitude not great. Ventricular repolarization. Goes from epicardium to epicardium
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p wave
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atrial depolarization.
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R wave
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conduction through AV node
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differential recording, ecg
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look at charge distribution of electrodes separated in space. Subtract one from another.
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positive electrode
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recording or active electrode
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negative electrode
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reference electrode
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lead comprised of
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positive and negative electrodes
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at rest what is diff btwn pos and neg electrodes
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zero for normal individual
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as record charge difference of cell surface potential when depol, what happens with AP?
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AP moves toward active electrode. sequentially reverse memb pot. Inside becomes more positive inside wrt outside (going from right to left). Ie right more positive first. Get large positive number when subtract positive minus negative electrode.
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after reach half of the depol wave, what does the recording electrode see?
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as time goes on, recording electrode sees less and less positivity. Start moving downward on graph. Get to point where entire cell is depolarized.
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when do you see the maximum difference between the two electrodes?
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Max diff between two when halfway through.
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When do you repolarize? Ie What does the surface of the heart look like?
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when the surface is all negative.
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as repol passes halfway through tissue what happens with polarization?
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reach max repol
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if depolarize toward lead , get + or - wave?
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get positive wave
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if repolarize toward lead, get + or - wave?
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get negative wave
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What kind of wave (positive or negative) would be produced in the ECG by a depolarizing wave away from the recording electrode?
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negative
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•What kind of wave (positive or negative) would be produced in the ECG by a repolarizing wave away from the recording electrode?
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positive
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•What would happen to the amplitude of a wave if the number of cells undergoing depolarization doubled?
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increase about double
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•What would happen to the amplitude of the wave if depolarization were perpendicular to the lead rather than parallel to the lead?
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get zero amplitutde bc even though charge distribution is changing, the same happens on both aspects of cell. So both electrodes record the same change and cancel each other out.
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•Where is the flow of current in the spread of activation?
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depol current is local circuit current from one segment to another along equivalent cell. But don’t measure this current. Measure the manifestation of this current. These local circuit currents move in same direction as depol.
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depol parallel to lead, what is amp?
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maximum
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wave goes from parallel to perpendiculr
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wave gets smaller and smaller until zero
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increase tissue mass give what amp
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increased amp
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When do you see zero recorded and does this mean you have all positive or negative on surface of the heart?
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At end have zero difference again. Before AP, record zero bc charge positive everywhere and when finish conducting all the way through we are at zero bc negative charge on surface of heart. so just because zero, dont know if positive or neg on heart..just that charge (of some kind) is everywhere.
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cell surface potential
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recorded as the difference between the recording electrode and the reference electrode
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potential measured on heart at rest
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is positive bc resting potential is negative inside so positive outside
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during the plateau what is potential measured by ekg
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potential is zero bc all cells depolarized (same either neg or zero)
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when do you see a positive wave?
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when you have a wave of depolarization moving toward a recording electrode and away from a reference electrode.
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lead
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any pair of points on the body surface where electrodes are placed to record the ekg. One assigned positive and one assigned negative
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potential diff, or pd =
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diff between positive electrode relative to negative electrode
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how many leads used in clinic
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12
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is ekg susceptible to interference? What kind?
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yes. 60 cycle AC current and muscular movements etc.
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lead one
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left arm (recording) and right arm (reference)
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lead two
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left leg (recording) and right arm (reference)
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lead three
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left leg (recording) and left arm (reference)
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einthoven's triangle
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on the wrists and the lower left leg
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limb leads record in a verticle or horizontal body plane and are bounded by what 2 things?
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vertical. Shoulder and hip joints
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limb leads detect activation in what direction(s)
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left right and top bottom
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precordial leads
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record electrical activity in a transverse plane from front to back, back to front. There are six of them. See spread of activation btwn the anterior and posterior surfaces.V1-V6.
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augmented limb leads
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used with standard limb leads to record activity from heart
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V1
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sees activity in right ventricle. Located to right of sternum
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V6
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sees activity in left ventricle. Over apex.
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ecg can determine ____ wrt pacemaker
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site of origin of the pacemaker
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ecg can determine sequence and time required for conduction through the heart. T or F.
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TRUE
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P-R interval
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conduction through the AV node
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why is a wave corresponding to atrial repolarization not seen?
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bc atrial potential diffs are small and masked by the large QRS complex arising from the ventricles.
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Why is T wave upright?
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bc the endocardial AP is lnoger in duration than the epicardial AP (repol passes from the epi to the endo).
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if vector is pointing toward the positive end of the lead and vector is parallel, max or min potential recorded?
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max
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Mean QRS axis
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when depol halfway through ventricular wall, endo cells are depolarized and have neg surface charge and epicardium cells are polarized at resting membpot and have positive surface charge. The sum of the instantaneous vectors is the mean wrs vector. Mean for young adults is 60.
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does left or right ventricle have greater muscle mass? What does this mean?
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left. Therefore potentials from left are greater than right and dominate parts of the ekg reporting ventricular depol (QRS) and repol (T wave).
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in disease of right ventricle what happens?
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e activity of right ventricle becomes evident in leads closest to right venticle (V1 and V2)
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leads of septum?
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V2,V3,V4
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electrical activity from back of heart to front, would leads record this?
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leads wouldn’t record this bc its perpendicular
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wilsons point
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Electrical average of three standard limb lead electrodes which is the average of all of limb leads. Limb leads form a triangle that pass through middle of heart. Middle of heart is the reference point.
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from six leads see what surfaces?
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anterior and lateral
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how do you see things on back of heart?
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instead of arraying V1-6 on front surface of body, arrange on back surface of body in same way.
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to see certain part of heart electrically what can you do?
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put a lead there
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when reach a peak in ekg. What does this mean for activation?
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activation has spread halfway between the tissue.
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atrai vs av node. How many cells?
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atrial have millions of cells. Av node have thousands of cells.
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time between P and Q wave is?
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delay in activation from AV node
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PR interval
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time it takes to initiate AP and get it through AV node. Really time between beginning of p wave and beginning of qrs
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septal depol from L to R or Vice Versa?
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left to right
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after septum what is activated?
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apex
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after apex what is activated?
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right and left sides
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why do you have swing up after septum depol on left?
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because left ventricular wall is bigger, takes more/longer to get it covered.
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where does net vector point? R or L?
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Left. Left side dominates bc left ventricular wall bigger.
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peak of P wave represents?
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max diff right and left sides. Move from endo to epi. Endo first to depol
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peak of R wave?
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have activated one half of wall.
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first cell to depolarize is the ___cell to repolarize
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last
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endo or epi have longest AP?
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endo bc first to depol and last to repol.
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AV valves. Define.
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tricuspid, 3 leaflets, right side and mitral, 2 leaflets, left side
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if mitrovalve doesn’t close completely
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will push blood out into aortic valve into aorta (good) but when contracts, will push back into left atrium (bad).
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valves ensure
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flow in system always forward
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semilunar valves
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aortic valve and pulmonic valve. At opening of aortic or pulminary arteries
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when left ventricle contracts, mitral valve _____
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closes
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approximation
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leaflets come together and close two compartments. Seal valve opening. Aka coaptation.
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if pressure in aorta is greater than pressure in ventricle, valve is open or closed?
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closed.
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pressure in left ventricle less than in left atrium
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mitral valve opens, bld comes into ventricle
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as put blood in aorta, pressure increases and semilunar valves close. Then what?
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see recoil of aorta against volume of blood. Pushes it into systemic circulation. Pressure declines.
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when left ventricle relaxed, pressure is?
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near zero
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at end of diastoe and beginning of systole, pressure?
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pressure in left ventricle greater then pressure in left atrium and mitral valve closes. Has low freq sound - low bc just a small pressure diff. this is lub of lub dub. AKA S1
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isovolumic contraction
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beginning of systole. Pressure rises rapidly within ventricles and exceeds pressure in atria. The AV valves close at beginning of this period and remain closed. SL valves closed too bc aortic and pulminary pressures greater than ventricular pressres also. no change in ventricular volume. at the end of this period, the SL valves open when pressure in ventricles greater than aorta/pulminary artery
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arotic valve closes when?
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when left ventricle relaxes and blood in aorta wants to flow back into left ventricle, slam valve shut. Pressure higher so high pitch. This is dub in lub dub. Aka S2.
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start with how much blood?
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150 mL
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as inject blood into aorta from left ventricle, ventricular volume decreases. What happens to pressure gradient?
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Diminished pressure gradient btwn aorta and left ventricle. Peak of the twich so less ability of ventricle to generate pressure.
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end systolic volume
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volume in ventricle after ejection of blood into aorta or pulminary artery
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filling of left ventricle is during what period?
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opening of mitral vavle through to the beginning of systole
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most filling of left ventricle when?
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rapid filling at beginning, opening of mitral valve.
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do the mitral valve and tricuspid valve act at same time?
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virtually yes. Bc activation passes down left and right bundle branches at same time so good synchrony of L and R systole.
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atrial contraction, systole counts for how much blood in end volume
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a couple millimeters, not very Impt for filling bld and end diastolic volume is Impt for activation.
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how do we know first heart sound is mitral valve closing and not tricuspid?
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depending on where you listen, you hear either one first. Localization of head of stethescope.
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when are atria impt?
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when exercise, diastolic interval shortens and it’s the atrial kick that enables you to reach an appropriate end diastolic volume.
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pressure falling in left ventricle, still pushing blood into aorta. Why?
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Envision column of blood moving into aorta. Has mass and velocity and thus momentum. As blood ejected into aorta, aorta expands to accept blood. If pressure falling in aorta and blood still ejected out of ventricle, into aorta, means aorta recoiling. rate of pumping of blood into aorta less than rate of exiting of blood out of other end of aorta. blood leaving faster than we can pump it in.
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momentum
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forward flow of blood at end of ventricular systole. Blood flows despite falling pressure.
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what happens when aortic valve closes and see a rebound of bp? no longer pumping blood into aorta but aorta is expanding. Why?
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volume of aorta increasing otherwise wouldn’t see expansion. Momentum of blood flowing out into systemic circulation, recoils some blood back into aorta after valve closes. Recoil is due to the systemic circulation which is expanded due to an ejection of a volume of blood into it. when upstream pressure source is eleminated due to closer of aortic valve, get recoil.
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when mitral valve is closed, see increase in atrial pressure. What is this?
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return of venous blood to right atrium. From lungs via pulminary vein to left atrium. Atrial filling.
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during ventricular filling what happens?
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pressures in right and left atrium are more than pressures in ventricle and filling begins.AV valves open.
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mitral valve opens when and what happens?
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when pressure from left atrium is greater than left venricle. blood flows into left ventricle from left atrium
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y descent
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a sudden fall in atrial pressure beginning with mitral valve opening at the end of isovolumic relaxation due to the rapid flow of blood from the atrium into the ventricle and secondarily as a consequence of suction due to ventricular relaxation
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a wave
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atria are contracting. Can be large when exercising majorly. Inc in pressure caused by atriole systole.
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when ejecting blood is aortic pressure less than ventricular pressue? Why?
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yes bc when ejecting blood aortic pressure has to be less than ventricular pressure.
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atrial kick
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final phase of ventricular filling. Impt in exercise, some diseases. Atrial kick is what propells the remainder of ventricular filling. Contributes little volume to person at rest.
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end diastolic volume
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after ventricules are filled, this is the volume they have. Volume determines the length of muscle fibers and thus force muscle fibers will have in subsequent contractions.
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what generates aortic pressure increase?
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muscular contraction in left ventricle generates pressure
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what are some determinants of ventricular filling?
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blood accumulated in atria during ventricular systole. Also relaxation of ventricle initially pulls blood into ventricle.
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increase heart rate what happens to filling?
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it decreases bc diastolic interval is shortening. The atrial kick helps you read your EDV. Above 180 bpm, filling is compromised.
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v wave
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inc pressure due to accumulation of blood within the atrium as it returns to the heart via the veins.
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c wave. Don’t need to know.
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small inc in pressure during isovolumic contraction caused by bulging of the av valves upward into the atrial cavity
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x descent. Don’t need to know.
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dec in atrial pressure during early ventricular ejection. During ejection the base of the ventricle moves downward toward the apex which pulls the av valve and atrium downward, thereby enlarging the atrium and causing atrial pressure to fall.
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PV loop, hidden, implied variable is what?
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time
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venous return is a volume of what if ESV is 75 mL and EDV is 150 mL?
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75 mL
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onset of systole, what happens?
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mitral valve closes, AV still closed. Isovolumic contraction. Building pressure within left ventricle. Pressure up to about 80mmHg. AV opens when reach 80 mmHg.
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arteriol presssure builds as ejecting blood into aorta. When exiting of blood in aorta exceeds exiting of left ventricular blood, where are you in PV loop?
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at top where you see pressure drop btwn where arotic valve opens and closes.
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end of systole is at what point?
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closure of aortic valve
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volume at end of systole is what volume?
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minimum volume needed for cardiac cycle
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how much blood ejected during cycle? End sytolic volume = what number?
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75 mL
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stroke volume =
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EDV - ESV
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how do you normalize stroke volume?
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take size of heart out of picture by normalizing SV to EDV
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ejection fraction =
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normalized stroke volume. = SV/EDV
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healthy individuals, ejection fraction is btwn?
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.6 and .7
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preload on heart
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load on heart before starts filling and contracting. Represented by EDV or EDP.
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as preload inc, what happens to SV?
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it increases
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greater filling in left ventricle, inc or dec pressure?
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inc
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when exercise, more venous return to heart. What happens to EDV and EDP?
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both inc
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preload normal is how much mmHg?
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a few to 14-15 mmHg
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heart failure, preload inc or dec?
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inc, can get up to 18-20 mmHg. Reflects congestion of venous blood in front of or upstream from left atrium. More blood comes into left atrium and ventricle and pressure inc.
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entry of capillary, what is pressure?
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30 mmHg
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need big or small pressure diffs for blood to move forward?
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minimal
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in diastole, always have pressure gradient?
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yes
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inc EDV, what happens to contraction?
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stretch cardiac cells so contraction becomes stronger
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frank-starling mechanism
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if we return more blood to heart, next beat will be stronger in a way that moves additional volume forward. If inc preload, heart beat stronger, SV inc to move extra preload forward. Intrinsic control mechanism.
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afterload
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load or pressure against which the heart must work.
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primary contributer to afterload?
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MABP
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if hypertensive, stroke volume is normal or no?
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normal.
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hypertensive has high MABP. What does this mean?
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left ventricle has to generate much more pressure to eject normal SV of blood. Works against higher afterload.
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hypertensive works against a greater load. Favorable? Why?
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unfavorable bc heart muscle hypertrophies to compensate for stress on heart muscle. Can have heart failure if not treated.
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wall stress
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stress per cross sectional area of muscle in a ventricular wall. Sigma = P in left ventricle X radius of left ventricle / (2X wall thickness).
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why is wall stress impt?
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if individual has calcium deposits on valve so stiff around periphery, and opening is narrow (stenotic), have NORMAL MABP, normal SV. BUT, if eject same amount of blood through a narrower opening, heart needs a TREMENDOUS systolic pressure. Not getting any idea of work that left ventricle is doing with MABP here. must measure left ventricle work using this method to get accurate afterload.
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if MABP high what does this tell us?
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person working against a higher afterload.
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Cardiac Work
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stroke work calculated as area of PV loop. Work to eject one stroke volume of blood. Pressure over a change in volume. CW = stroke work X heart rate.
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Cardiac Output normal is
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5 L/ min
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ejecting normal SV but inc afterload doing a lot more/less work to maintain normal CO?
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more
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sympathetic work inc?
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strength and speed of each contraction, in addition to inc. heart rate.
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heart failure, cant develop normal cardiac work with goal of maintaining normal what?
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mabp
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myocardial O2 consumption helps assess cardiac work. Determined by what three things?
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ventricular wall stress, heart rate, myocardial contractility
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ANS effectors?
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smooth and cardiac muscle, glands
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activation of effectos by what 2 things? In ANS
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reflexes, higher centers.
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primary functions of ANS?
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maintain constancy of internal environment, survival of organism, species.
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parasympathetic NS ?
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vegetative functions
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sympathetic NS?
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activated in response to stressors. Fight, flight, fright.
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origin of outflow tracts in PNS
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craniosacral tracts
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origin of SNS?
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thoracolumbar tracts
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efferent path has how many neurons in series?
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two
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sympathetic NS synapses in?
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paravertebral or collateral ganglia or chromaffin cells in adrenal medulla
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parasymp location of ganglia?
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in or near innervated organ
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location of ganglia in sympathetic
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paravertebral chain, collateral, no ganglian (Adrenal medulla)
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pregang axon in PNS
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long, myelinated, un branched
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pregang axon in SNS
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short, myelinated, branched
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postgang axon in PNS
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short, restricted distribution. Target organ discretely
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postgang axon in PNS
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long, widespread distribution
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responses in PNS
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localized
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responses in SNS
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generalized
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how do you distinguish btwn diff kinds of muscarinic receptros?
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depends on what activates and blocks them
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how many muscarinic receptors are there?
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5 but we need to know 2
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neuroeffector junction receptors are what?
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muscarinic
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parasymp neuro effector junction is always using what nuerotransmiter?
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Ach
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at rest, what is parasymp nervous system doing to heart rate?
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its slowing down the intrinsic heart rate. If block parasymp affects, heart rate will inc.
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is neuroeffector junction a nicotinic junction?
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no
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emotions and our conscious state effect autonomic outflow. T or f?
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true
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where are cell bodies in preganglionic axons of ANS?
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intermedial lateral gray area of SC
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neuroeffector junction in sympathetic nervous system is what? Is this inhibitory or stimulatory or both? What does this depend on?
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norepinephrine. If released in heart, inc heart rate etc. If released in gut, its inhibitory. Whether stimulating or inhib, has to do with adrenergic receptor in effector organ.
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salivary glands symp vs para
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symp small volume thick saliva, para large volume watery saliva
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pupils symp vs parasymp
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symp dilate para constrict
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lungs parasymp vs symp
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parasymp constrict and symp dilate
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digestive tract symp vs parasymp
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parasymp has inc in secretion and motility. Symp is opposite
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blood vessels. Sympathetic vs parasymp
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all innervation is symp (constricted or dilated). Amount of constriction etc. depends on sympathetic tone. Parasyp does not do anything to blood vessels. Usually symp will constrict BVs, but in skeletal muscle vascular beds you dilate BVs bc diverting blood there as part of fright or flight response.
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sympathetic, stimulus can be that MABP does what?
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simulus can be reduced MABP
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sweat glands are sym or parasymp?
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symp
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NE to one kind of receptor can be stimulus and to another no stim. T or f
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TRUE
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excitatory neurotransmitters? 2.
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aspartate and glutamate
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inhib neurotransmitters? 2.
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glycine and gaba
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modulators for regulating responses? 1.
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neuroactive peptides
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in autonomic ganglionic synapses, what is always the neurotransmitter released by the pregang axon?
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Ach
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receptor at autonomic ganglian are always what?
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nicotinic or cholinergic activated by Ach or nicotine
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if receptor is nicotinic, is post synaptic potential excitatory or inhib?
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excitatory when something binds to it. Inc in conductance to potassium and sodium. (neuromuscular junction is similar). Seek out potential somewhere between Na and K
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in nicotinic cholinergic receptor, what is the specific agonist?
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nicotine
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ingesting nictoine inc heart rate because?
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when ganglionic agonists are ingested, sympathetic effects dominate.
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inc a nicotine blocker inc resting heart rate. Effect suggests?
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the intrinsic heart rate is greater than the resting rate observed in healthy humans. Also parasymp activity dominates autonomic outflow at rest.
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resting heart rate is what?
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60-70 bmp
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at rest, parasymp flow to heart is __________automaticity?
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slowing
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muscarinic receptors are a type of what kind of receptor?
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cholinergic
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M2 vs M3 receptors. Excit or inhib and what do they act on?
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M2 activation of receptor is inhibitory (atria). M3 receptors are excitatory (gut smooth muscle).
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M2 receptors inhibit what?
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adenylate cyclase. Binding Ach to M2 blocks effects of symp on heart. (low protein PO4), high gk
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M3 receptors activate what?
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ach binding M3 activates PLC which gives high IP3, high DAG, high Ca release from inracellular stores, high PKC. If inc Ca in gut, see more contraction.
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in SYMP neuro effector jct, trammitters are typically what percept norepi and what percent epi?
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80% norepi and 20% epi. Exception is transmitter at neuroeffector junction to sweat glands in control of body temp, the sympathetic fiber is Ach here. Still symp bc outflow tract arises in thoracolumbar region. so anatomically its sympathetic.
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alpha receptors greatest affinity for what kind of neurotransmitters? Order.
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norepi >epi>isoproterenol
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beta receptors greatest affinity for what kind of neurotransmitters? Order.
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isoproterenol > Epi > Norepi
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sympathetic alpha one receptor agonists do what? What is their blocker?
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activates phospholipase C (which inc PKC and calcium). Inc Ca bc of IP3. in smooth muscle, activation is excitatory, see vasoconstriction. Alpha 1 receptor in GUT is inhibitory. Blocked by prasozin. Can identify alpha 1 receptors bc blocked by this.
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symp beta one receptor agonists activate what? Blockers are?
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adenylate cyclase which inc PKA. B blockers are propranolol and attenolol
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B1 receptors excitatory eg. Heart muscle. What happens?
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ion channel phosphorylation and contractile protein phosphorylation. 1. inc automaticity. Heart beat. 2. inc Ca delivery during EC coupling. 3. make conractile proteins more powerful and eager to contract by phosphorylating them.
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symp B2 receptors inhib to what?
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blocked by b blockers, propanolol and attenolol. If epi or norepi bind, activate PKA in effector tissue. When activate, B2 are inhib to gut smooth muscle, some vascular smooth muscle.
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what vascular smooth muscle might B2 receptors inhibit?
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get vasodilation with B2 receptors in SM within skeletal muscle (aka when exercise). coronary vasculature dilates and constricts based on oxygen level. Lots of O2 constrict. Not so much O2 dilate.
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symp B2 receptors do what biologically (specific)?
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PKA activation of Ca release from restricted sub sarcolemmal pool. THEN, Ca activation of K channels.
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sweating, thermal:
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control of body temperature. Sympathetic cholinergic nerves with generalized discharge. If body temp goes above normal temp, you activate sweating. Generalized all over body.
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emotional sweating
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sympathetic adrenergic discharge. Discrete patterns. Richard Nixon sweating on upper lip.
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fight or flight sweating
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sympathetic adrenergic. Generalized but can be localized: axillary is prominent
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gustatory sweating
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symathetic adrenergic. Face, neck, scalp. Overeaters have patterns of sweating through neck and on chest.
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alpha 1 and beta 1 excit or inhib?
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both can be both
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