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377 Cards in this Set
- Front
- Back
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Circulating plasma volume in a 70kg person
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3L
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Interstitial volume in a 70kg person
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12L
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Intracellular volume in a 70kg person
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30L
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Total blood volume in a 70kg person =
Plasma = Cellular components = |
5L
3L 2L |
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Homeostasis depends on three things:
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1. fresh circulating plasma
2. adequate blood flow 3. very small diffusion distance (10 micrometers) |
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Normal cardiac output for a resting person
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5 to 6 L/min
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Examples of organs that recondition the blood
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Lungs, kidneys, skin, most large abdominal organs
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Organs that use blood solely to supply metabolic needs
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Brain, heart muscle, skeletal muscle.
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Blood flow equation
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Flow = pressure difference / resistance
Q = change in P / R |
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Poiseuille equation for flow through a cylindrical vessel
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Q = change in P [ (pi x r^4) / (8Ln) ]
radius has a very large influence on the blood flow |
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cardiac output equation
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CO = SV x HR
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Five requirements for effective ventricular pumping
1. contractions synchronized 2. valves open fully 3. valves not leaky 4. contractions forceful 5. ventricles fill during diastole |
1. not arrhythmic
2. not stenotic 3. not insufficient or regurgitant 4. not failing |
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Sympathetic nerves release ___ which interacts with ___ receptors on cardiac muscle cells to ___ cardiac pumping.
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norepinephrine
B1 adrenergic increase |
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Sympathetic nerves increase heart pumping by ___, ___, and ___.
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heart rate
AP conduction velocity force of contraction |
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Parasympathetic nerves travel via ___ and innervate ___, ___, and ___.
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vagus nerve
SA node AV node atrial muscle |
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Parasympathetic nerves release ___ which interacts with ___ receptors to ___ heart pumping.
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acetylcholine
muscarinic decrease |
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Parasympathetic nerves decrease heart pumping by ___ on the SA node and __ on the AV node.
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decreasing heart rate
decreasing AP conduction velocity |
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Arteries are __ vessels.
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conduit (they have relatively low and unchanging resistance to flow)
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Arterioles are __ vessels.
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resistance (high and changeable resistance regulates peripheral blood flow)
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Capillaries are __ vessels.
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exchange (have no smooth muscle, can't change diameter actively)
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Peripheral veins and venules are __ vessels.
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capacitance (they normally contain more than 50% of total blood volume)
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Sympathetic nerves innervating arterioles release __ and interact with __ receptors to cause __.
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norepinephrine
alpha-adrenergic arteriolar constriction |
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Venules and veins are richly innervated by __ and constrict when activated, decreasing venous volume. This leads to __ cardiac filling and therefore ___ via __ law.
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sympathetic nerves
increased increased cardiac output Starling's |
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Hematocrit definition
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cell volume / total blood volume
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Inorganic electrolytes
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ions such as sodium, potassium, chloride, bicarbonate
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Plasma's normal osmolarity
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300 mOsm/L
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Concentration of sodium chloride in plasma (isotonic)
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150 mM solution
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Plasma proteins play an important osmotic role in transcapillary fluid movement, especially __ which is the most abundant.
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albumin
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Why does HR change when you stand up?
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Blood went to legs instead of heart when you stood up, stroke volume went down, aterial pressure went down, arterio baroreceptors detect, medullary respiratory center changes, sympathetic system increases HR.
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Three ways cardiac muscle cell APs are different from skeletal muscle cell APs
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1. can be self-generating
2. conduct directly from cell to cell 3. have long durations |
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K+ equilibrium potential
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roughly -90 mV
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Na+ equilibrium potential
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roughly +70 mV
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Electrolyte that is responsible for the fast depolarization in the fast response AP
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Na+ via i(Na) channel
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Electrolyte responsible for slow depolarization in the slow response AP
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Ca++ via the i(Ca) channel (slow inward L channels)
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Three mechanisms that contribute to slow depolarization in pacemaker cells
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1. progressive decr in permability to K+
2. perm of Na+ increases slightly 3. incr in perm of Ca++ |
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i(Na) current
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travels through Na+ channel (fast), voltage gated, accounts for phase 0 of AP, inactivation may contribute to phase 1 of AP
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i(K1) current
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K+ channel (inward rectifier), voltage gated, maintains high K+ permeability during phase 4, decay contributes to diastolic depolarization, suppression during phases 0-2 contribute to plateau
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i(To) current
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K+ channel (transient outward), voltage gated, contributes to phase 1 of AP (slightly repolarizes from high depol)
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i(Ca) current
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Ca++ channel (slow inward, L channels), voltage gated, phase 2 of AP, enhanced by sympathetic stimulation and B-adrenergic agents
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i(K) current
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K+ channel (delayed rectifier), voltage gated, phase 3 of AP, enhanced by incr extracellular Ca++
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i(KATP) current
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K+ channel (ATP-sensitive), ligand gated, increases K+ perm when ATP conc is low
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i(KACh) current
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K+ channel (ACh-activated), ligand gated, responsible for effects of vagus nerve, shortens phase 2 of AP
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i(f) "funny" current
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Na+ channel (pacemaker current), ligand and voltage gated, enhanced by sympathetic and B-adrenergic agents, suppressed by vagal stimulation, contributes to diastolic depolarization
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Intercalated disks btw myocytes contain firm mechanical attachments by proteins called __ in structures called __.
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adherins
desmosomes |
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Intercalated disks btw myocytes contain low resistance electrical connections btw adjacent cells by protein called __ in structures called __.
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connexin
gap junctions |
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Conduction over small-diameter cells in the AV node is __ than over large-diameter cells in the Purkinje system.
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slower
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Ventricular cells which are the last to depolarize have __ duration APs and are the __ to repolarize.
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shorter
first |
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P wave in ECG
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atrial depolarization
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QRS complex in ECG
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ventricular depolarization
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T wave in ECG
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ventricular repolarization
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Automaticity
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spontaneous electrical pacemaker activity like that of cells in the SA node
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Acetylcholine (interacting with __ receptors) increases the perm of resting membrane to __ and decreases the diastolic perm to __.
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muscarinic
K+ Na+ |
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Norepi (interacting with __ receptors) increases the inward currents carried by __ and by __ during diastolic interval
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B-adrenergic
Na+ (i(f)) Ca++ |
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Dromotropic
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conduction velocity (DRiving)
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Chronotropic
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HR change
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Sarcoplasmic reticulum sequesters calcium during diastolic interval with the help of the calcium-storage protein __.
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calsequestrin.
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Calcium-induced calcium release in the cardiac cell is a result of opening __ channels on the __.
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calcium sensitive release (L-type)
SR |
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When intracellular Ca++ is __, cross bridges form btw myosin and actin.
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high (>1.0 microMolar)
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In cardiac muscle contraction, Ca++ interacts with __ to cause __.
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troponin C
configuration change that removes inhibition of actin sites |
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80% of myocyte Ca++ is actively taken back up into the SR by the action of __ pumps which is regulated by the protein __ when it gets phosphorylated (for example, by __).
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Ca++-ATPase
phospholamban norepi |
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The cardiac glycoside, digitalis, slows the __ pump which results in an increase in __.
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Na+/K+
intracellular Ca++ |
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Inotropic
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contractility (increases the peak isometric tension that a muscle can develop at a FIXED LENGTH), causes myocytes to contract more rapidly and forcefully
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The most important inotropic modulator is __.
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Norepi (which also has a chronotropic effect)
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Norepi increases contractility via __ receptors, through the __ signaling pathway which phosphorylates the __ channel increasing inward __ current during the plateau phase.
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B1-adrenergic
Gs protein-cAMP-protein kinase A Ca++ Ca++ |
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Inotropic changes from norepi are due to increases in free __ during activation which allows more cross bridges to form.
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Ca++
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A secondary effect of norepi in myocyte contraction is phosphorylation of __ which increases __ and therefore __.
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phospholamban
Ca++ retrapping increased rate of relaxation |
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Lusitropic
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rate of relaxation
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Treppe
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staircase phenomenon when HR increases, more Ca++ enters the cell, then the more Ca++ causes a progressive increase in contractile force to a higher plateau
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Law of Laplace
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tension on the muscle of the ventricular wall (T) depends on intraventricular pressure (P) and intraventricular radius (r) as T = P x r
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Why do old people get edema?
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They lose their teeth, can't eat enough protein, and have edematous tissue because the proteins don't keep the fluid in the proper space.
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Why does permeability to Na+ remain low in the slow AP depolarization?
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The Na+ channels are inactivated
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What phase of depolarization do anti-arrhythmic drugs work on?
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Phase 2 - they are Ca++ channel blockers, which decrease the sustained refractory period (plateau)
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At rest in a myocyte, what is the channel configuration?
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K+ channels are open.
Na+ channels (fast) are closed ("m" gate for activation is closed, "h" gate for inactivation is open) Ca++ channels (slow) are closed ("d" gate for activation is closed, "f" gate for inactivation is open) |
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How does an irritable area in the myocardium generate an ectopic beat?
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K+ builds up outside the cell and can't be washed away. This starts a slow depolarization, like in the SA node, which inactivates Na+ channels and causes slow depolarization, leading to an ectopic beat.
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What does a prolongation of the PR interval on an ECG mean?
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Conduction delay, because this is the time from atrial depolarization to ventricular depolarization. This could be heart block or another conduction problem.
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At a normal heart rate, is atrial contraction necessary for ventricular filling?
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No. In fact, the ventricle has nearly reached its max diastolic volume before atrial contraction begins.
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Incisura or dicrotic notch
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An upward notch that appears in the aortic pressure trace because a small volume of aortic blood must flow backward to fill the aortic valve leaflets as they close
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Stroke Volume
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end diastolic volume - end systolic volume
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Pulmonary artery systolic and diastolic pressures
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24/8 mmHg
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Pressure pulsations from the right atrium can be seen where in the body?
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in the neck over the jugular veins in a person who is laying down
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The first heart sound S1 occurs at the beginning of __ because of the closure of the __.
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systole
AV valves |
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The heart sound S1 occurs at which point of the ECG?
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immediately after the QRS complex
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The second heart sound S2 arises from the closure of the __ at the beginning of __.
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aortic and pulmonic valves
the period of isovolumetric relaxation |
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The heart sound S2 is heard at which point of the ECG?
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about the time of the T wave
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S3 occurs __ and produces a __ gallop rhythm.
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shortly after S2
ventricular |
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S3 is associated with what cardiac condition?
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can sometimes be detected in normal children, but more commonly in patients with left ventricular failure
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S4 is heard __ and produces a __ gallop rhythm.
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shortly before S1
atrial |
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S4 is associated with what cardiac condition?
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increased ventricular diastolic stiffness associated with several cardiac disease states
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End-diastolic ventricular pressure is referred to as __ and systemic arterial pressure is often referred to as __.
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ventricular preload
ventricular afterload |
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How much does the cardiac output of an average person increase when going from rest to strenuous exercise?
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from 5.5 to maybe 15 L/min
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Increased afterload, at constant preload, has a __ effect on cardiac muscle shortening.
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negative
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What are the three distinct influences on stroke volume?
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contractility, preload, and afterload
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What are the two reasons cardiac output increases at constant filling pressure with an increase in cardiac sympathetic activity?
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sympathetic tone increases heart rate and increases stroke volume by increasing contractility
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What are some of the ATP energy substrates of the heart?
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glucose and pyruvate (esp after a high carb meal)
free fatty acids, TGs, and ketones (fasting) glycogen (during increased sympathetic stimulation) lactate (especially newborns) acetyl CoA |
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The basal metabolism of the heart accounts for __% of myocardial ATP use.
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25%
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The energy expended during the isovolumetric contraction phase accounts for __% of total myocardial oxygen consumption, this making __ a major determinant of O2 consumption.
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50%
cardiac afterload |
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Cardiac wall tension is related to __ and __ through the law of Laplace, so reductions in __ will reduce the energy required for isometric contraction.
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ventricular pressure
ventricular radius cardiac preload |
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Simplest index of energy demands
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peak systolic arterial pressure times heart rate (pressure-rate product)
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Fick principle
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amount of substance consumed by tissues is equal to what goes in minus what goes out times the blood flow
Q = Xtc / (Xa - Xv) |
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Ejection Fraction =
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stroke volume / end diastolic volume
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Normal ejection fraction range under resting conditions
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55% to 80% (less than 55% indicates depressed myocardial contractility)
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What are the 5 sympathetic effects on the heart?
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1. positive chronotropic (HR)
2. decr in AP duration, to minimize neg effect of decreased filling time 3. positive dromotropic (AP conduction velocity) 4. positive inotropic (contractility) 5. positive lusitropic (increased relaxing helps diastolic filling along with #2) |
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Methods to reduce myocardial oxygen demand
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1. decr HR (sympathetic drive)
2. decr afterload (BP) 3. Decrease preload (law of Laplace – if heart is dilated, make it smaller) 4. Decrease contractility |
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Fick principle
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"... what goes in (to the vascular bed) minus what comes out (of the vascular bed) must have been consumed by the tissue"... what goes in = flow (Q) times [X]a and what comes out = Q[X]v ... then solve for Q
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Duration of the normal PR interval
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from 120 to 200 ms
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Normal QRS complex duration
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between 60 to 100 ms
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The QT interval occurs during the period of __ and at a normal HR of 60 bpm will be a duration of __.
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ventricular systole
less than 380 ms |
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Einthoven's electrocardiographic conventions
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Voltage scale: 10mm upward = +1mV
Paper speed: 25mm = 1s |
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A left electrical axis deviation could be caused by these three things
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physical displacement of heart to the left
left ventricular hypertrophy loss of electrical activity to the right ventricle |
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A right electrical axis deviation exists in these three situations
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physical displacement of the heart to the right (for example in tall skinny people)
right ventricular hypertrophy loss of electrical activity in the left ventricle |
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What is the orientation (degrees) of Lead II?
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+60 degrees
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What does Lead II connect?
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right arm and left leg
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What is a vectorcardiogram and what does each loop indicate?
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starts from an isoelectric diastolic point and traces three loops during each cardiac cycle
atrial depolarization, ventricular depolarization, ventricular repolarization |
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Augmented unipolar limb lead from the right arm is called __, from the left arm is called __, and from the left leg is __.
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aVR
aVL aVF |
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6 characteristics of a normal sinus rhythm on an ECG
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1. frequency of QRS complexes are ~1 per second
2. shape of QRS complex is normal and duration is less than 120 ms 3. each QRS is preceded by a P wave 4. PR interval is less than 200 ms 5. QT interval is less than half of the R-to-R interval 6. no extra P waves |
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Supraventricular tachycardia occurs when __.
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atria are abnormally excited and drive the ventricles at a very rapid rate.
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What symptoms accompany SVT?
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low blood pressure and dizziness (extremely high HR doesn't allow enough diastolic filling time)
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What two mechanisms may cause SVT?
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abnormal pacemaker region (ectopic focus)
re-entry phenomenon |
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Atrial flutter is a special form of __ which is caused by a __ and shows up as __ on the ECG.
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SVT
large re-entry pathway a sawtooth pattern |
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First degree heart block is caused by __, shows __ on ECG, and __ clinically.
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unusually slow conduction through AV node
abnormally long PR interval (>0.2s) inconsequential |
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Second degree heart block occurs when __, shows __ on ECG, and __ clinically.
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some but not all atrial impulses are transmitted through AV node
some but not all P waves have QRS and T waves may not represent a serious clinical problem |
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Third degree heart block occurs when __, shows __ on the ECG, and __ clinically.
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no impulses are transmitted through the AV node, so some area in the ventricles assumes the pacemaker role
P waves and QRS complexes are totally dissociated ventricular rate is probably slower than normal and could impair CO |
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Atrial fibrillation occurs when __, shows __ on the ECG, and __ clinically.
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cells in atria depolarize, repolarize, and are excited again randomly (could be due to circus pathways)
no P waves may be well tolerated by most pts as long as ventricular rate is enough to maintain cardiac output |
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Bundle branch blocks often occur as a result of __.
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MI
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Bundle branch blocks occur when __, show __ on ECG, and __ clinically.
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ventricular depolarization is less synchronous than normal in half the heart
widening of the QRS (>0.12s) usually inconsequential |
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Premature ventricular contraction (PVC) are caused by __, show __ on ECG, and __ clinically.
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caused by APs from an ectopic focus in the ventricle, often followed by a missed beat
large amplitude, long-duration deflections palpitations due to stroke volume of beat after the compensatory pause being larger than normal |
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Ventricular tachycardia occurs when __, show __ on ECG, and __ clinically.
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ventricles are driven at high rates often by ectopic ventricular focus
large downward deflections very serious condition because the heart is pumping less effectively than normal and also, it often precedes ventricular fibrillation |
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Prolonged QT intervals occur when __, show __ on ECG, and __ clinically.
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delayed ventricular repolarization (could be due to inappropriate opening of Na+ channels or prolonged closure of K+ channels)
QT interval of more than 50% of cycle length (normal is less than 40%) can go into torsades de pointes or deteriorate rapidly into ventricular fibrillation, which is rapidly fatal |
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Ventricular fibrillation occurs when __, shows __ on ECG, and __ clinically.
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various areas of the ventricles contract asynchronously, and circus pathways can be triggered easily
especially vulnerable at the end of the T wave when ventricular cells are "hyperexcitable", just looks like a squiggle situation is fatal unless quickly corrected by cardiac conversion |
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In aortic stenosis, ventricular pressure is __ and aortic pressure __.
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very high
rises more slowly to a subnormal level |
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In aortic stenosis, pulse pressure is usually __.
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low
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There is an invariable increase in left ventricular muscle mass in __.
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aortic stenosis
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Which two valvular abnormalities result in a systolic (ejection) murmur?
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aortic stenosis
mitral insufficiency |
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Which two valvular abnormalities result in a diastolic murmur?
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mitral stenosis
aortic insufficiency |
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Symptoms of mitral stenosis
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pulmonary congestion
shortness of breath diastolic murmur |
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Symptoms of aortic valve insufficiency (regurgitation)
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large pulse pressure
diastolic murmur |
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Symptoms of mitral valve regurgitation (insufficiency)
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systolic murmur
mitral valve prolapse |
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Which of these arrhythmias might result in a reduced stroke volume?
SVT, ventricular tachycardia, atrial fibrillation, ventricular fibrillation, 3rd degree heart block |
SVT - filling time reduced
v. tach - filling time reduced a. fib - if ventricular rate is rapid v. fib not heart block, because slower HR usually leads to increased filling |
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What is the pressure abnormality associated with aortic stenosis?
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pressure dif btw left ventricle and the aorta during systolic ejection
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What is the pressure abnormality associated with mitral stenosis?
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pressure dif btw left atrium and left ventricle during diastole
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Fick principle of cardiovascular transport
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tissue rate of utilization of a substance = flow (arterial concentration of substance - venous concentration of substance)
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Rate at which a substance is carried to an organ depends on these two factors
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blood flow rate x concentration of substance in the blood
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Four factors that determine the diffusion rate of a substance between blood and interstitial fluid
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1. concentration difference
2. surface area for exchange 3. diffusion distance 4. permeability of capillary wall |
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Diameter of the lumen of a capillary
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5 micrometers
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Wall thickness of a capillary
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1 micrometer
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Lipid-soluble substances (like oxygen and CO2) cross the capillary wall __.
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easily
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The capillary permeability to small polar particles (like Na+ and K+) is __ than that of oxygen.
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10,000-fold less
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Small water-soluble substances like __ transport through capillary walls through water-filled channels.
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Na+, K+, Cl-, H2O, glucose
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Proteins in the blood cross the capillary membrane via __.
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pinocytosis, but they don't really cross and are normally confined to the plasma space.
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Hydrostatic pressure inside capillaries is __ and thus makes fluid want to move __.
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about 25 mmHg
out of the capillary |
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Total osmotic pressure of a solution is proportional to the __.
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total number of solute particles in the solution (oncotic pressure is colloid osmotic pressure)
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Because of plasma proteins, the oncotic pressure of plasma is about __ and due to the absence of proteins, the interstitial space is about __ which makes fluid want to move __.
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25 mmHg
0mmHg into the capillary to dilute the proteins |
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Relationship among factors that influence transcapillary fluid movement, known as Starling hypothesis
|
net filtration rate = K [(Pc-Pi) - (oncotic of capillary - oncotic of interstitium)] where K is a constant expressing how easily fluid can move across capillaries
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Histamine is often released in damaged tissue which __ capillary permeability so that __ leak into interstitium and cause __.
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increase
proteins net filtration and edema |
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Flow of lymph from the tissues into the circulatory system is promoted by these two things
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1. increases in tissue interstitial pressure
2. contraction of lymphatic vessels valves in vessels also prevent backward flow |
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Total resistance when vessels with individual resistances are connected in series
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Rs = R1 + R2 + . . . + Rn
always greater than the individual resistances |
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Total resistance when vessels with individual resistances are connected in parallel
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1/Rp = 1/R1 + 1/R2 + . . . 1/Rn
always less than that of any of the individual resistances |
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The more parallel elements that occur in a network, the __ the overall resistance of the network.
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lower
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Blood flows most rapidly in parts of the peripheral vasculature with the __ total cross-sectional area (__) and most slowly in the region with the __ total cross-sectional area (__).
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smallest
aorta largest capillary beds |
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Because blood is viscous, it exerts a __ on the walls of the vessel.
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shear stress
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With laminar blood flow, the shear stress on the wall of a vessel is proportional to __.
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the rate of flow through the vessel
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Detection of sounds from peripheral arteries called __ is abnormal and usually means __.
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bruits
significant pathological reduction of a large vessel's cross-sectional area |
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An increase in the central venous volume __ cardiac filling, which then __ stroke volume, according to the __ law of the heart.
|
enhances
augments Frank-Starling |
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Central venous pressure
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0 mmHg
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Because mean arterial pressure is relatively stable, large changes in an organ's blood flow are achieved by changes in __.
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its overall vascular resistance to blood flow
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Which vessels have the largest vascular resistance?
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arterioles
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Blood flow through an organ is primarily regulated by adjustment in the __.
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internal diameter of arterioles
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Increased organ blood flow caused by arteriolar dilation is accompanied by __ arterial pressure and __ capillary pressure.
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decreased
increased |
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Arteriolar constriction tends to cause transcapillary fluid __ while arteriolar dilation tends to cause transcapillary fluid __.
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reabsorption
filtration |
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Definition of compliance
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how much vascular volume changes in response to a given change in distending pressure
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Because veins are so compliant, __ in peripheral venous pressure can cause __ amount of circulating blood volume to shift into or out of the peripheral venous pool.
|
even small changes
a significant |
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Mean arterial pressure definition
|
Diastolic pressure + 1/3 (systolic pressure - diastolic pressure)
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Mean arterial pressure determinants
|
CO x TPR
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All changes in the mean arterial pressure result from changes in either __ or __.
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cardiac output
total peripheral resistance |
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Arterial pulse pressure definition
|
systolic pressure - diastolic pressure
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Arterial pulse pressure determinants
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stroke volume divided by arterial compliance
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Pa =
|
CO x TPR (determinants)
Pd + 1/3(Ps-Pd) (definition) |
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Pp =
|
Ps - Pd (definition)
SV/Ca (determinants) |
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Pulse pressure tends to increase with age in adults because of a decrease in arterial __.
|
compliance
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Decrease in arterial compliance is sufficient to cause __ pulse pressure even though __ decreases with age.
|
increased
stroke volume (remember Pp = SV/Ca) |
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|
Mean arterial pressure tends to increase with age because of an age-dependent increase in __ which is controlled primarily by __, not __.
|
TPR
arterioles arteries |
|
|
Changes in TPR have __ effect on pulse pressure because __.
|
little or no effect
parallel changes in both systolic and diastolic pressure |
|
|
Functional characteristics that distinguish smooth muscle from skeletal or cardiac muscle
|
1. contract and relax more slowly
2. develop active tension over a greater range of muscle lengths 3. can change contractile activity as a result of APs or changes in resting memb potential 4. may change contractile activity is absence oof changes in memb potential 5. maintain tension for prolonged periods at low energy cost 6. can be activated by stretch |
|
|
The actin filaments in smooth muscle are __ than those in striated muscle.
|
much longer
|
|
|
In smooth muscle, actin filaments don't attach to Z-lines but rather anchor to __ that are tethered to the surface membrane by cable-like __.
|
dense bodies
intermediate filaments |
|
|
Perhaps because of __ and __, smooth muscle can develop tension over a greater range of length changes than skeletal or cardiac.
|
long actin filaments
lack of sarcomere arrangement |
|
|
Steps that lead increased Ca++ to contraction in smooth muscle
|
1. Ca++ forms complex with calmodulin
2. Ca++-calmodulin activates a phosphorlyating enzyme called myosin light chain kinase 3. this enzyme causes phosphorylation of the light chain protein (part of the cross-bridge head of myosin) by ATP 4. myosin light chain phosphorylation enables cross-bridge formation and cycling during which energy from ATP is used for tension devt and shortening |
|
|
Vascular smooth muscle contractile activity is regulated not only by changes in intracellular free Ca++ levels but also by __.
|
changes in the Ca++ sensitivity of the contractile machinery
|
|
|
Smooth muscle action potentials are initiated primarily by __ and are developed __ like the slow type cardiac action potentials. This current flows through a __ channel.
|
inward Ca++ current
slowly voltage-operated calcium channel (VOC) |
|
|
The repolarization in smooth muscles occurs primarily by an __ flux of __ ions through both __ channels and __ channels.
|
outward
K+ delayed K+ calcium-activated K+ |
|
|
With pharmacomechanical coupling, chemical agents (eg NTs) can induce smooth muscle contraction without the need for __.
|
a change in membrane potential
|
|
|
In smooth muscle pharmacomechanical coupling, these two events cause intracellular Ca++ to increase:
|
1. the activated receptor opens the surface receptor-operated channels (ROC) for Ca++ that allows it to influx from the extracellular fluid
2. activated receptor may induce formation of an intracellular "second messenger" IP3 that opens channels to release Ca++ from SR inside the cell |
|
|
In ROC of smooth muscle, what does the activated receptor first stimulate in order to increase Ca++ concentration from extracellular and intracellular (via IP3 acting on the SR) stores?
|
specific GTP-binding proteins (G-proteins)
|
|
|
As in cardiac cells, smooth muscle cells actively pump Ca++ __ and __. Ca++ is also countertransported out of the cell in exchange for __.
|
into the SR
outward across the sarcolemma Na+ |
|
|
In ROC of smooth muscle, what does the activated receptor first stimulate in order to increase Ca++ concentration from extracellular and intracellular (via IP3 acting on the SR) stores?
|
specific GTP-binding proteins (G-proteins)
|
|
|
As in cardiac cells, smooth muscle cells actively pump Ca++ __ and __. Ca++ is also countertransported out of the cell in exchange for __.
|
into the SR
outward across the sarcolemma Na+ |
|
|
Vascular B-receptors are designated __-receptors and are pharmacologically distinct from the __-receptors found on cardiac cells.
|
B2
B1 |
|
|
Three mechanisms for relaxation of smooth muscle cells and vessel dilation:
|
1. hyperpolarization of the cell membrane
2. epinephrine (or histamine or vasoactive intestinal peptide) -> B2 receptors -> G-protein -> adenylate cyclase -> ATP to cAMP -> activation of protein kinase A -> phosphorylation of proteins -> stimulation of Ca++ efflux and membrane hypolarization 3. nitric oxide that operates via cGMP pathway (NO is produced by endothelial cells and nitrates) |
|
|
Arterioles remain in a state of partial constriction even when all external influences are removed, called basal tone. There are three categories of influences that can cause them to dilate or constrict:
|
1. local influences
2. neural influences 3. hormonal influences |
|
|
In all vascular beds except the lungs, exposure to low oxygen causes __ while high oxygen levels cause __.
|
vasodilation
arteriolar vasoconstriction |
|
|
When the metabolic rate of skeletal muscle is increase by exercise, tissue levels of O2 decrease while CO2, H+, and K+ increase, and all of these chemical alterations cause __.
|
arteriolar dilation
|
|
|
Local metabolic control of arterioles:
With increased metabolic activity or oxygen deprivation, cells in many tissues release __, a potent vasodilator. |
adenosine
|
|
|
The most important mechanism of local flow control is __.
|
local metabolism
|
|
|
ACh causes __ of intact vessels and __ of vessels stripped of their endothelial lining.
|
vasodilation
vasoconstriction (because ACh stimulates production of NO from endothelial cells) |
|
|
increased intracellular Ca++ -> NO synthase activated -> NO made from __ -> cGMP -> __
|
L-arginine
vasodilation |
|
|
Agents that stimulate endothelial cell NO production because their receptors on endothelial cells are linked to receptor-operated Ca++ channels
|
ACh, bradykinin, vasoactive intestinal peptide, substance P
|
|
|
Shear stress on endothelial cells stimulates their NO production presumably because __.
|
stretch-sensitive channels for Ca++ are activated
|
|
|
When released, histamine produces arteriolar __ (via the cAMP pathway), which leads to __.
|
vasodilation
edema and local tissue swelling |
|
|
Bradykinin is a small polypeptide that acts to __. It is involved in the vascular responses associated with __ and __.
|
increase capillary permeability
tissue injury immune reactions |
|
|
A sudden increase in the internal pressure within an arteriole (transmural pressure) produces first __ and then __ (called the __ response).
|
initial slight passive mechanical distention
active constriction myogenic |
|
|
Active constriction in arterioles is called myogenic response because __.
|
it originates in the smooth muscle itself
|
|
|
What is active hyperemia?
|
when you are exercising, have increased metabolic rate, and must create a higher blood flow
|
|
|
What is reactive hyperemia?
|
a higher than normal blood flow that occurs after a period of lower than normal blood flow - it may be caused by both local metabolic and myogenic mechanisms
|
|
|
What is the tissue pressure hypothesis of blood flow autoregulation?
|
an abrupt increase in arterial pressure causes transcapillary fluid filtration and thus increase in interstitial fluid volume and pressure, which would a decrease in vessel diameter by simple compression
|
|
|
What is the most important means of reflex control of the vasculature?
|
sympathetic vasoconstrictors
|
|
|
Norepinephrine causes an increase in the tone of arterioles after combining with __ receptors on smooth muscle cells.
|
alpha 1 adrenergic
|
|
|
T/F
Blood vessels, as well as the brain and heart, are innervated by sympathetic and parasympathetic fibers. |
False. Blood vessels, as a general rule, don't receive innervation from parasympathetics.
Parasympathetics do release acetylcholine in the vessels of the brain and heart, however. They also vasodilate in the vessels of the salivary glands, pancreas, gastric mucosa, and external genitalia. |
|
|
During activation of the sympathetic nervous system, the adrenal glands release the catecholamines __ and __.
|
epinephrine
norepinephrine |
|
|
Both epinephrine and norepinephrine can activate __ to increase HR and contractility.
|
cardiac B1-adrenergic receptors
|
|
|
Cardiac cells have __ receptors.
|
B1 adrenergic
|
|
|
Arterioles have __ receptors which __ and __ receptors which dilate.
|
alpha-1
constrict B2 |
|
|
__ receptors are more sensitive to epinephrine than are __ receptors, so moderately elevated levels of epi cause __ while higher levels cause __.
|
B2
alpha-1 vasodilation vasoconstriction |
|
|
Vasopressin is also known as __.
|
antidiuretic hormone, ADH
|
|
|
ADH, aka __, is released from the __ in response to __ or __.
|
vasopressin
posterior pituitary low blood volume high extracellular fluid osmolarity |
|
|
Vasopressin acts on collecting ducts in the kidneys to __ renal excretion of water.
|
decrease
|
|
|
Angiotensin II regulates __ release from the adrenal cortex as part of the system for controlling body sodium balance.
|
aldosterone
|
|
|
T/F Angiotensin II is a very potent vasodilator agent.
|
False. Angiotensin II is a potent vasoconstrictor. It may be partially responsible for the abnormal vasoconstriction that accompanies many forms of HTN.
|
|
|
Compared with arterioles, veins normally have __ basal tone, which means that __ have __ effect on veins.
|
little
vasodilator metabolites little |
|
|
Where do myocardial infarcts occur most frequently?
|
in the endocardial layers of the left ventricle
|
|
|
Why does an increase in sympathetic tone increase myocardial oxygen consumption?
|
by increasing HR and contractility
|
|
|
Flow through the cerebrum is autoregulated very strongly and is little affected by changes in arterial pressure unless it falls below about __.
|
60 mmHg
|
|
|
When does cerebral blood flow decrease?
|
whenever arterial blood P(CO2) falls below normal, although it appears that the cerebral arteries respond not to the changes in P(CO2) but to changes in the extracellular H+ conc (i.e. the pH) caused by changes in CO2.
|
|
|
What happens when arterial blood P(O2), such as that caused by oxygen inhalation, is higher than normal?
|
it does little to decrease cerebral blood flow, however lower than normal P(O2) causes cerebral arterioles to vasodilate
|
|
|
Sweat glands in human cutaneous tissue are innervated by __ that release __.
|
cholinergic sympathetic fibers
ACh |
|
|
ACh released by sympathetics in human sweat glands cause __.
|
sweating and marked cutaneous vasodilation
|
|
|
What is hypoxic vasoconstriction in the pulmonary vasculature?
|
pulmonary arterioles vasoconstrict in the presence of low P(O2), which is essential to efficient lung gas exchange because it diverts blood flow away from the areas of the lung that are underventilated
|
|
|
What structures are in the central venous compartment?
|
vena cavae and right atrium
|
|
|
What are the IA Na+ channel blockers?
|
quinidine
procainamide disopyramide |
|
|
What are the IB Na+ channel blockers?
|
lidocaine
mexilitine |
|
|
What are the IC Na+ channel blockers?
|
flecainide
propafenone |
|
|
Type IA Na+ channel blockers slow both the __ and __ phases of the fast sodium gates.
|
rate of activation (phase 0)
reactivation (phase 3) |
|
|
Type IB Na+ channel blockers __ the rate of activation (phase 0) of sodium channels and __ the rate of reactivation (phase 3).
|
do not affect
enhance |
|
|
Type IC Na+ channel blockers __ the rate of activation of the fast sodium gates and __ the rate of reactivation.
|
slow
do not alter |
|
|
What is a unique drug characteristic of procainamide?
|
it is mostly eliminated in the kidney so can be used in patients with liver problems
|
|
|
How is quinidine elimated from the body?
|
80/20 from the liver
|
|
|
What happens to the QT interval with type IA Na+ channel blockers?
|
prolonged - so caution Torsades after prolonged QT interval (esp with Quinidine and Procainamide, not as much with Disopyramide)
|
|
|
What happens to the QRS complex with the type IA Na+ channel blockers?
|
it is widened (is dose-dependent in Quinidine, not in Procainamide or Disopyramide)
|
|
|
What happens to the QRS complex in type IB Na+ channel blockers?
|
nothing - it is the QT interval that slightly shortens
|
|
|
What is unique about lidocaine when used for life threatening VT?
|
it must be used IV but works extremely quickly
|
|
|
What are the direct effects of the type IB sodium channel blockers?
|
delay opening of fast sodium gates
no change in the rate of activation enhances reactivation of fast sodium gates |
|
|
What happens to the QT interval with type IB Na+ channel blockers?
|
a slight shortening
|
|
|
What are the K+ channel blockers?
|
Amiodarone, Ibutilide, Dofetilide
|
|
|
What happens to the QT interval with K+ channel blockers?
|
it is prolonged with Amiodarone and Dofetilide and has a dose-dependent increase with Ibutilide
|
|
|
What is unique about Amiodarone?
|
it is a K+ channel blocker that has a very long plasma half-life of 20-100 days - also, it eliminated 99% in the liver (hard to get rid of!)
|
|
|
What is a common side effect of Amiodarone?
|
cough/pulmonary fibrosis
also, it has many drug interactions |
|
|
What are the Ca++ channel blockers?
|
Verapamil and Diltiazem
|
|
|
What channels do Verapamil and Diltiazem inhibit?
|
the L-type Ca++ channels (slow inward)
|
|
|
What do Ca++ channel blockers do to the sinus rate?
|
slow it down
|
|
|
What do Ca++ blockers do to the PR interval?
|
prolong it
|
|
|
What do Ca++ blockers do to the QRS complex?
|
they don't change it - they slow sinus rate and prolong PR interval
|
|
|
What do Ca++ blockers do to the QT interval?
|
don't change it - they slow sinus rate and prolong PR interval
|
|
|
What do the Ca++ channel blockers do to the AV node?
|
they prolong the refractory period of the AV nodal region, which would interrupt a re-entry pathway and convert a SVT to a normal sinus rhythm
|
|
|
What are some common adverse affects of Ca++ channel blockers?
|
sinus bradycardia
AV conduction block (because the whole point is that they prolong refractory period of AV node to stop a re-entry pathway) |
|
|
What are the Beta-adrenergic blockers?
|
Propranolol
Satalol Esmolol Acebutolol |
|
|
What do B-blockers do?
|
inhibit the effects of norepinephrine on the heart
|
|
|
What types of channel blockers do B-blockers seem to mimic?
|
Ca++ channel blockers also appear as sympatholytic drugs
|
|
|
What are the cardiac effects of B-blockers?
|
slows pace maker rate and conduction velocity of SA and AV nodal cells (Ca++ dependent) more than in atrial and ventricular cells (Na+ dependent), so they look like Ca++ blockers
they also prolong refractory period of nodal cells but shorten refractory period of atrial and ventricular cells |
|
|
What happens to the sinus rate with B-blockers?
|
slows
|
|
|
What happens to the PR interval with B-blockers?
|
prolongs
|
|
|
What happens to the QRS complex with B-blockers?
|
not really a change - they more mimic Ca++ blockers to slow sinus rate and prolong PR interval
|
|
|
What happens to the QT interval with B-blockers?
|
not really a change - they more mimic Ca++ blockers to slow sinus rate and prolong PR interval
|
|
|
How would you treat an exercise-induced ventricular tachyarrhythmia?
|
good to use B-blockers to slow down sympathetics on the heart, however this has a possibility of reducing athlete performance as well
|
|
|
What is the direct effect of adenosine on the heart?
|
potent inhibition of cAMP-induced Ca++ influx
|
|
|
What is unique about the cardiac drug adenosine?
|
it has an immediate onset of action, and the patient will convert in seconds from a life-threatening paroxysmal SVT to normal sinus rhythm - also, works so fast that there are few side effects
|
|
|
What does adenosine do to the PR interval?
|
prolongs it
|
|
|
What does adenosine do to the QRS complex?
|
nothing - it prolongs PR interval
|
|
|
What does adenosine do to the QT interval?
|
nothing - it prolongs the PR interval
|
|
|
What does atropine do?
|
blocks paraympathetics at muscarinic receptors
|
|
|
What does digitalis do?
|
poisons Na+/K+ pump, enhances cholinergic stimulation of the heart (vagomimmetic) or in other words increase the parasympathetic system, which leads to a slowing of the AV node, slowing of sinus heart rate, and it looks like a Ca++ channel blocker
|
|
|
What does digitalis do to the sinus rate?
|
slows it
|
|
|
What does digitalis do to the PR interval?
|
prolongs it (looks like a Ca++ blocker)
|
|
|
What does digitalis do to the QRS complex?
|
nothing - it prolongs PR interval
|
|
|
What does digitalis do to the QT interval?
|
nothing - it prolongs PR interval
|
|
|
What are the drugs of choice for atrial fib or atrial flutter?
|
Verapamil, Diltiazem, or B-blocker to slow ventricular response
|
|
|
What is a characteristic side effect of procainamide?
|
SLE - lupus
red butterfly rash |
|
|
What are two reasons for a tachyarrhythmia?
|
1. accelerated automaticity (pace-maker activity) of ectopic pace-maker cells
2. conduction defects resulting in re-entry |
|
|
What are three therapeutic strategies to treating tachyarrhythmias?
|
1. hyperpolarize the membrane (increase the maximum diastolic potential) - incr K+ perm or decr Na+ and Ca++ perm
2. make threshold firing potential less negative - decr potential for activating Na+ gates 3. slow rate of diastolic depolarization - slow closing of K+ channels or improve Na+/K+-ATPase activity |
|
|
If someone has premature ventricular contraction, what is the best way to stop the ectopic foci?
|
use a Na+ channel blocker (IA, IB, IC), because they would make the threshold firing potential less negative
|
|
|
What are the two major variables that affect the mean circulatory filling pressure?
|
circulating blood volume
state of peripheral venous vessel tone |
|
|
The rate at which blood leaves the central venous compartment is equal to the __.
|
cardiac output
|
|
|
Venous return is the rate at which __.
|
blood returns to the thorax from peripheral vascular beds and thus the rate at which blood enters the central venous compartment
|
|
|
The mean circulatory filling pressure is __.
|
the actual pressure that would exist throughout the system in the absence of flow, and it is about 7 mmHg (for an extra 1000mL of blood)
|
|
|
The amount of blood the vascular system could hold and the amount it does hold (with inflation and pressure)
|
3.5L
4.5L |
|
|
The venous function curve shows how venous return increases as __.
|
central venous pressure drops
|
|
|
Lowering central venous pressure below __ produces no additional increase in venous return.
|
0 mmHg
|
|
|
"Peripheral venous pressure" can be viewed as essentially equivalent to __.
|
"mean circulatory filling pressure"
|
|
|
Central venous pressure (i.e. cardiac filling pressure) has a __ influence on CO, and it has a __ effect on venous return.
|
positive
negative |
|
|
A/an __ in peripheral venous pressure can be as effective as a/an __ in central venous pressure in increasing venous return.
|
increase
drop |
|
|
Three things that increase peripheral venous pressure
|
increase circulating blood volume
increase sympathetic activity to veins increase any force compressing veins from the outside |
|
|
Increasing peripheral venous pressure shifts the whole venous function curve __.
|
upward and to the right
|
|
|
T/F Cardiac sympathetic nerves do not affect the venous function curve.
|
True. Venous return will be higher with activated sympathetics to the heart, but the venous function curve doesn't shift. Increased sympathetic activity to veins can shift the curve up and to the right.
|
|
|
What would you suspect if someone had an abnormally high central venous pressure?
|
congestive heart failure, because they have a combo of dysfunctional heart muscle (depressed cardiac function curve) and excessive fluid volume (right-shifted venous function curve)
|
|
|
What would you suspect if someone had an abnormally low central venous pressure?
|
low blood volume or lack of venous tone
|
|
|
What is normal central venous pressure and how would you check for it?
|
2 mmHg
put them in a semirecumbent position and see if their jugular vein distends more when the jugular vein is 7cm above the right atrium |
|
|
In sympathetic pathways, the cell bodies of the preganglionic fibers are located __.
|
within the spinal cord
|
|
|
In the parasympathetic system, the cell bodies of the preganglionic fibers are located __.
|
within the brainstem
|
|
|
Increased stretch of baroreceptors causes __ AP generation rate.
|
increased
|
|
|
Since baroreceptors sense absolute stretch and rate of change of stretch, __ and __ affect baroreceptor firing.
|
mean arterial pressure
arterial pulse pressure |
|
|
At low concentrations, epinephrine stimulates __ receptors and at high concentrations, epi stimulates __ receptors.
|
only beta2 adrenergic
beta2 and alpha adrenergic |
|
|
Alpha adrenergic receptors __ tone and vaso__ while beta2 receptors __ tone and vaso__.
|
increase
constrict decrease dilate |
|
|
At low concentrations, epinephrine acts on __ receptors and vaso__.
|
beta2
dilates |
|
|
At high concentrations, epinephrine acts first on __ and __ but then on mostly __ receptors and vaso__.
|
alpha
constrict beta2 dilate |
|
|
Aortic arch baroreceptors afferent travel in __ and carotid baroreceptors travel in __.
|
vagus nerves (X)
glossopharyngeal nerves (IX) |
|
|
Increased stretch causes __ APs by the arterial baroreceptors.
|
increased
|
|
|
APs generated by the carotid sinus baroreceptors join with the __ nerve.
|
glossopharyngeal (IX)
|
|
|
Afferent fibers from the aortic baroreceptors run with the __ nerve.
|
vagus (X)
|
|
|
Where does the integration of signals about regulation of arterial pressure occur?
|
medullary cardiovascular centers, in the medulla oblongata
|
|
|
Are the arterial baroreceptors active at normal arterial pressures?
|
Yes - they supply a tonic input to the central integration centers. This is why they can sense low blood pressure.
|
|
|
What three things occur when the arterial baroreceptors fire APs?
|
1. inhibit activity of sympathetic excitatory tracts
2. stimulate activity of spinal inhibitory tracts 3. stimulate activity of parasympathetic preganglionics |
|
|
What is the Bezold-Jarisch reflex?
|
marked bradycardia and hypotension from application of strong stimuli to coronary vessel chemoreceptors in the posterior wall of the left ventricle (people with MIs to this area will sometimes present with bradycardia)
|
|
|
Low P(O2) and/or high P(CO2) levels in the blood causes reflex increases in respiratory rate and mean arterial pressure. What two reflex receptors cause this?
|
arterial CHEMOreceptors (located in the carotids)
central chemoreceptors (located somewhere in the CNS) |
|
|
What is the cerebral ischemic response?
|
triggered by inadequate brain blood flow, produces a more intense sympathetic vasoconstriction and cardiac stimulation than any other influence on the CV control centers
|
|
|
What is the Cushing reflex?
|
When there is increased ICP (like by a tumor or a bleed), there is a parallel rise in arterial pressure (can cause Pa to get above 200mmHg) to prevent the collapse of cranial vessels and preserve adequate brain blood flow
|
|
|
What is the dive reflex?
|
remarkable bradycardia and intense vasoconstriction in all systemic organs except brain and heart in aquatic animals - sometimes it is used clinically to activate cardiac parasympathetic nerves to interrupt a. tach
|
|
|
What is the alerting reaction and where are the centers that signal it to occur?
|
"fight or flight" reaction, in which there is pupillary dilation, increased skeletal muscle tenseness, increase in blood pressure
signal comes from posterior hypothalamus |
|
|
What is vasovagal syncope and where does the signal for it occur?
|
extreme stress causes fainting because the depressor centers in anterior hypothalamus cause sudden loss in sympathetic tone and large increase in parasympathetic tone, which causes a loss in arterial blood pressure, which decreases cerebral blood flow suddenly and causes fainting
|
|
|
Superficial pain causes a __ in BP and deep pain causes a __ in BP.
|
rise
decrease deep pain sometimes accompanies vasovagal syncope and creates a state of shock in joint displacement and/or crushing injuries |
|
|
Are the arterial baroreceptors considered to be inhibitory or excitatory?
|
inhibitory - increase in arterial baroreceptor firing rate results in a decrease in sympathetic output
|
|
|
What are the nonarterial baroreceptor influences on the medullary cardiovascular centers?
|
things that raise the set point and increase sympathetics (like exercise, sense of danger, Cushing reflex, cerebral ischemic response, decr in central venous pressure, cutaneous pain)
things that lower the set point (vasovagal syncope, deep pain, incr central venous pressure) |
|
|
Nonarterial baroreceptor influences causes sympathetic activity and arterial pressure to change in __ direction.
|
the same
|
|
|
Arterial baroreceptor reflexes causes sympathetic activity and arterial pressure to change in __ direction.
|
reciprocal (opposite)
|
|
|
Same direction changes in arterial pressure and sympathetic activity suggest what?
|
problem isn't in the periphery but rather in abnormal pressure-raising or -lowering input to the medullary cardiovascular center
|
|
|
The physician should think of what when he or she sees a patient with increased HR and arterial pressure?
|
influences that raise the set point: exercise, sense of danger, Cushing reflex, cerebral ischemic response, decr in central venous pressure, cutaneous pain
|
|
|
Can the baroreceptor reflex effectively regulate arterial pressure in the long term?
|
no, because it adapts to prolonged changes in arterial pressure
|
|
|
What is the fluid volume mechanism for regulating arterial pressure?
|
increases in arterial pressure cause an increase in urinary output and thus decrease in blood volume
|
|
|
Sympathetic nerve activity leads to what hormone being released?
|
renin, which causes high angiotensin2, which leads to high aldosterone, which leads to increased renal absorption of sodium, water, and thus a decreased urinary output rate
|
|
|
Vasopressin (ADH) leads to what?
|
decreased urinary output rate
|
|
|
Which class of drugs will slow the pacemaker rate of the SA node?
|
calcium
|
|
|
Which class of drugs will slow the pacemaker rate of the ventricles?
|
sodium
|
|
|
Which class of drug will delay repolarization of the AV node?
|
calcium
(potassium would be next, because of Ca++ induced K+ release) |
|
|
Which class of drugs will delay the repolarization of the ventricles?
|
potassium
|
|
|
Which class of drugs will speed the condution of the AP across the AV node?
|
calcium
|
|
|
Which class of drugs will slow the speed of conduction of the AP in the ventricles?
|
sodium
|
|
|
Which class of drugs will prolong the AP duration (effective refractory period) in the ventricles?
|
Potassium (Na+ IA would be a second choice)
|
|
|
Which class of drugs prolongs the AP duration in the AV node?
|
calcium
|
|
|
Which class of drugs decreases the number of P waves on the ECG?
|
Calcium if in the sinus node, sodium if in the atria
|
|
|
Which class of drugs will prolong the PR interval of ECG?
|
calcium
|
|
|
Which class of drugs will prolong the QT interval of the ECG?
|
potassium is the first choice
sodium is the second choice |
|
|
Which class of drugs will widen the QRS complex of the ECG?
|
sodium
|
|
|
Which class of drugs will slow an etopic pacemaker in the atrium?
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sodium
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Which class of drugs will slow an ectopic pacemaker in the AV node?
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calcium
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Which class of drugs will slow an ectopic pacemaker in the ventricle?
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sodium
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Which class of drugs will increase the refractory period of cells in the ventricles?
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potassium
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Which class of drugs will treat sinus tachycardia?
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calcium
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Which class of drugs will treat multifocal atrial tachycardia?
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sodium
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Which class of drugs will treat atrial flutter or fibrillation due to a re-entry circuit in the atrial muscle?
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potassium
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Which class of drugs will treat PSVT (re-entry in the AV node)?
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calcium
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Which class of drugs will treat ventricular tachycardia due to a re-entry in the ventricular muscle?
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potassium
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Which class of drugs will treat premature ventricular contractions?
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sodium
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Which drug will prolong the refractory period of the AV node?
amiodarone flecainamide lidocaine quinidine verapamil |
verapamil
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Which drug does not prolong the refractory period of the AV node?
adenosine amiodarone digoxin metoprolol verapamil |
amiodarone
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Which drug prolongs the refractory period of the ventricles?
adenosine amiodarone digoxin lidocaine verapamil |
amiodarone
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Which drug slows the pacemaker rate of the atrium?
adenosine quinidine verapamil |
quinidine
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The Na+ channel blockers slow pacemaker rate of atrial and ventricular cells by which mechanism?
hyperpolarize resting MP raise Tm change slope of phase 4 change slope of phase 0 |
raise the threshold membrane firing potential
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Which drug does not widen the QRS complex of the ECG?
quinidine lidocaine flecainide |
lidocaine
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Which drug prolongs the QT interval of the the ECG?
quinidine lidocaine flecainide |
quinidine
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Which drug shortens the QT interval of the ECG?
quinidine lidocaine flecainide amiodarone |
lidocaine
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Which drug is orally effective and shortens the QT interval of the ECG?
quinidine disopyramide procainamide lidocaine mexilitine |
mexilitine
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Which drug variably shortens the PR interval of the ECG?
quinidine lidocaine flecainamide amiodarone ibutilide verapamil adenosine digoxin propranolol |
quinidine (blocks the vagus)
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What is the most common side effect of quinidine?
bradycardia SLE GI confusion dry cough |
GI
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Which drug is eliminated primarily as the unchanged parent drug in the urine?
adenosine amiodarone digoxin flecainamide ibutilide propafenone procainamide verapamil |
procainamide
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Dry cough is associated with which drug?
adenosine amiodarone digoxin flecainamide ibutilide propafenone procainamide verapamil |
amiodarone
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SLE-like symptoms are associated with which drug?
adenosine amiodarone digoxin flecainamide ibutilide propafenone procainamide verapamil |
procainamide
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Digitalis induced AV conduction block is most effectively treated with which drug?
adenosine amiodarone atropine digoxin flecainamide ibutilide propafenone procainamide verapamil |
atropine
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What is a first line Rx for a.fib? (protect ventricles)
adenosine amiodarone lidocaine quinidine |
adenosine
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Which drug would convert a.fib to a normal sinus rhythm?
adenosine amiodarone lidocaine quinidine verapamil |
amiodarone - since it is a re-entry phenomenon
or quinidine if it is an ectopic pacemaker |
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Which drug would convert a PSVT to a normal sinus rhythm?
adenosine amiodarone lidocaine quinidine |
adenosine
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