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113 Cards in this Set

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Positive chronotopic effects
Things that *increase* heart rate. Ex: sympathetic n.s., where Norepi stimulates Beta-1 receptors in SA Node and activate AC through G-protein. This increases I[funny], which in turn icreases rate of Phase 4 depolarization.
Positive chronotopic effects
Things that decrease heart rate. Ex: parasympathetic n.s. releases ACh to activate muscarinic (M2) receptors in the SA node. Activates G-protein, G[k] that inhibits AC and decreases I[funny]. G[k] also increases potassium channels K+-ACh and increases outward K+. Hyperpolarizes.
Dromotropic effect
changes the conduction velocity of heart. Positive effect increases it, Negative effect decreases it. Ex: sympa increases conduction velocity through AV Node and I[calcium], parasympa decreases it through decreased I[calcium] and increased I[K-ACh].
Conduction velocity factors
depends on the size of the inward current. The larger this current, the more rapidly the current spreads. This also correlates with dv/dt (the rate of rise of upstroke of Acction potential), since dv/dt correlates with size of inward current.
EKG: P wave
The depolarization of atria. The P duration correlates with conduction time through atria. Ex: If conduction velocity decreases, P wave spreads out.
EKG: PR interval
The time from initial depolarization of atria to initial depolarization of ventricles. This flat part of curve is the “PR segment” and corresponds with “AV Node Conduction.” Normally 160ms. If increase conduction velocity, decreases the PR interval length.
EKG: QRS complex
The depolarization of ventricles. This time length is similar to P-wave because conduction velocity in His-Purkinje system is much faster than atrial conducting system.
EKG: T wave
The repolarization of ventricles.
EKG: QT interval
Represents 1st ventricular depolarization to last ventricular repolarization.
Heart Rate
On EKG: count the QRS complexes (or also R waves). …..Heart rate = 1/cycle length , where cycle length is one R to the next R. units is beats/sec. If heart rate changes, so does the duration of action potential, and thus the refractory periods and excitability.
If Heart Rate increases, results in:
Decreases the duration of action potential and its refractory period. But increase in number of action potentials per given time. This may cause arrhythmias.
Inotropic effect
Positive inotropic effect—increases contractility. Positive results in high peak tension, increased rate of tension development, and faster relaxation, so contraction twitch is shorter. Ex: Sympa n.s. works on Beta-1 receptors that activate AC, then cAMP, etc.
Protein that regulates Calcium ATPase in sarcoplasmic reticulum. When phosphorylated, it stimulates Calcium ATPase, results in uptake and storage of calcium, so faster relaxation.
Mean arterial pressure (P[a]) equals?
P[a] = (cardiac output) x (Total peripheral resistance)
where CO is units mL/min and TPR units is mm Hg/mL/min
*Be aware: the units are not independent. If you change TPR, it also changes CO, etc.
Found in carotid artery, which detects both increase and decrease in P[a], the mean arterial pressure and sends info to brain center via Carotid Sinus Nerve (of CN 9), to NTS Nucleus Tractus Solitarius, which either sends out positive info to parasym system or has an inhibitory pathway to sympa system. Also found in aortic arch, which detects only increase in P[a] and sends info via Vagus CN 10.
Brainstem CV centers
In reticular formation of medulla and the lower third of pons.
1) Vasoconstriction center, 2) Cardiac accelerator center, 3) cardiac decelerator center
Set-point normal pressue is about 100 mmHg.
It has tonically active control over sympa and parasympa. Parasympa sends info via Vagus nerve to SA Node.
Sympa has 4 effects: (1) to SA Node, (2) on cardiac muscle to increase contractility and stroke volume, (3)acts on arterioles for vasoconstriction to increase TPR, (4) and acts on veins for venoconstriction to decrease unstressed volume.
What is baroreceptor reflex’s response to increased arterial pressure?
The NTS receives info. Wants to reduce P[a] to normal, so NTS directs increase in parasympa activity, and to decrease sympa activity to the heart. Heart rate decreases (slows). This slow heart rate also decreases contractility. These lead to decreased cardiac output, which tends to reduce P[a] back to normal (since P[a] = cardiac output x Total Peripheral Resistance).
Also, sympa’s effects: less constriction of arterioles, so decrease TPR and thus P[a]. Also decrease constriction of vessel, so increases the Unstressed volume.
What is baroreceptor reflex’s response to hemorrhage?
Hemorrhage -> low P[a] and decreased stressed volume.
The reflex response is exactly opposite to that of an increased arterial pressure. Baroreceptors sense less stretch on their mechanoreceptors.
Sympa activity is increased in response. Heart rate and contractility increase. Results in increased cardiac output and constriction of arterioles (which increases TPR) and veins (which decreases unstressed volume but increases venous return and works via Frank-Starling.)
What is the Renin-angiotensin II-Aldosterone system’s response to hemorrhage?
Valsalva Maneuver
This tests the baroreceptor reflex.
Expire against a closed glottis (during coughin, defecation or heavy lifting). When doing this, increased intrathoracic pressure decreases venous return to heart. Low return leads to decreased CO and consequent decrease in P[a].
If baroreceptor reflex works, heart rate shows an increase, and when patient stops, heart rate decreases.
What is the Renin-angiotensin II-Aldosterone system? What’s its mxn?
It controls blood volume, and is a slower response than baroreceptor reflex.
Activated when P[a] decreases. So attempts to raise it to normal. Steps: 1) Decreased P[a] leads to low renal perfusion, sensed by mechanoreceptors in afferent arterioles in kidney. Renin thus made by JG cells.
Renin level influenced by?
1)      P[a] sensed by mechanoreceptors in afferent arterioles in kidney 2) Increased by sympa and by Beta-1 agonists like isoproterenol. 3) Decreased by Beta-1 antagonists like propanolol.
Action of Angiotensin II
An octopeptide. Acts on adrenal cortex, vascular smooth muscle, kidneys and brain: 1) zona glomerulosa of adrenal cortex: to increase synthesis & secretion of aldosterone (which acts on distal tubule and collecting duct to increase Sodium reabsorption to increase ECF volume and blood volume) 2) Arterioles: vasoconstricted, thus increase TPR and P[a].
Acts on distal tubule and collecting duct to increase Sodium reabsorption to increase ECF volume and blood volume.
Production is Stimulated by Angiotensis II.