Cardiology Flashcards
1
Q
Membrane potential is measured on which side of the cell membrane?
A
the stated value (e.g. -70 mV) is the intracellular space relative to the extracellular space
2
Q
The magnitude of an ion’s chemical force depends on wha t two things? What equation describes this relationship?
A
- it is dependent on the ratio of extracellular and intracellular ion concentrations as well as the valence of the ion
- this is described by the Nernst potential
- E = (60/z)log(extracellular/intracellular concentration)
3
Q
The magnitude of an ion’s current depends on what two things?
A
- forces driving ion movement (i.e. electrochemical gradient)
- and the conductance of that ion
4
Q
What is conductance? What factors contribute to it’s value?
A
- it is a measure of how easily the ion can move across the membrane in response to the electrochemical gradient driving it
- it is related to the number of open ion channels, the number of leak channels, and to the ion concentration
5
Q
How does the conductance of potassium relate to the concentration of potassium?
A
potassium conductance is proportional to the extracellular concentration of potassium
6
Q
What equation is used to describe the current of an ion?
A
I = g x (V - E)
7
Q
How is fractional conductance of potassium and sodium calculated?
A
- fractional sodium conductance = sodium conductance/(sodium conductance + potassium conductance)
- fractional sodium conductance + fraction potassium conductance = 1 if we assume the cell is only permeable to sodium and potassium
8
Q
How can we determine the membrane potential for a cell mathematically, based on the assumption it is permeable only to sodium and potassium?
A
V = (E x fractional potassium conductance) + (E x fractional sodium conductance)
9
Q
What is the typical membrane potential of a resting neuron?
A
-70 mV
10
Q
What cardiac tissue is least excitable? Why is this important for cardiac function?
A
since the AV node is the least excitable cardiac tissue, it delays ventricular contraction until atrial contraction has finished and complete filling of the ventricle has occurred
11
Q
Describe the path or sequence of excitation through the heart.
A
- SA node exhibits pacemaker function
- atrial muscle
- AV node
- common bundle
- bundle branches
- purkinje fibers
- ventricular muscle
12
Q
What cardiac event do the p wave, pq interval, qrs complex, st segment and t wave each represent?
A
- p wave: atrial contraction
- pq interval: AV node depolarization
- qrs complex: phase 0/1 of ventricular contraction
- st segment: phase 2 of ventricular contraction
- t wave: depolarization of the ventricle
13
Q
Which pieces of the cardiac conduction pathway utilize calcium-dependent action potentials in which calcium is responsible for the upstroke of the AP?
A
the SA and AV nodes
14
Q
Which ions provide the depolarizing current or upstroke of the AP in each of the various segments of the cardiac conduction pathway?
A
- most utilize a sodium current
- the SA and AV nodes rely on a calcium current
15
Q
The magnitude of the depolarizing current during the upstroke of an action potential will determine what four things about that action potential?
A
- the threshold potential
- amplitude of the AP
- the rate of rise of the AP
- the conduction velocity of the AP
16
Q
What determines the conduction velocity of an action potential?
A
the magnitude of the depolarizing current during the upstroke of the AP
17
Q
Describe the phases of the SA node action potential.
A
- in phase 4, the funny sodium current (pacemaker potential) is greater than the repolarizing potassium current
- the difference between these two currents determines the steepness of phase 4 (how quickly threshold is met)
- when threshold is met, phase 0 begins as voltage-gated calcium channels open and depolarization occurs
- depolarization opens voltage-gated potassium channels, which open and begin to repolarize the cell
- during phase 3, the potassium current predominates over the funny sodium current, and there is a net polarization
- slowly, the voltage-gated potassium channels close again, and the funny sodium current predominates (phase 4)
18
Q
What is the maximum diastolic potential?
A
the most negative potential achieved in the SA node (typically -50 mV), determined by the balance of the repolarizing potassium current and the depolarizing funny sodium current
19
Q
What determines heart rate within the SA node?
A
the balance between the funny sodium current and the repolarizing potassium current
20
Q
Describe the phases of atrial and ventricular action potentials.
A
- during phase 4, there is a stable resting potential
- during phase 0, depolarization occurs due to a sodium current
- during phase 1, there is a transient repolarization attributed to potassium current
- during phase 2, there is a plateau in which the repolarizing potassium current is balanced by the voltage-gated calcium current
- during phase 3: the repolarizing potassium current outweighs the voltage-gated calcium current as L-type calcium channels close and repolarization occurs
21
Q
What role does the voltage-gated calcium current play in the ventricular action potential? What segment of the ECG describes this potential?
A
- it is needed to induce myocyte contraction
- it is represented by the length of phase 2 of the action potential, and those the QT interval
22
Q
What is the effect of sympathetic, noradrenergic activity in the heart on each of the various currents.
A
- it increases funny sodium current (increasing heart rate)
- it increases the current through L-type calcium channels
- it increases the potassium current
23
Q
What effects do sympathetic activity have on the various currents mediating the cardiac cycle? Through what mechanism is this? How do these molecular changes manifest?
A
- sympathetic nerves release NE on B1 receptors in the SA and AV nodes
- this serves to increase the funny sodium, L-type calcium, and potassium currents
- the net result is an increase in heart rate and an increase in conduction velocity through the AV node, which is seen as a smaller PR interval
- sympathetic firing does not change the magnitude of the sodium current in the atria or ventricles, so there is no change in the amplitude or width of the QRS complex or P wave
- the increase in potassium current, however, increases the rate of repolarization, so you see a spiked T wave and shorter QT interval
- the increase in L-type calcium current increases inotropic state and makes phase 2 potential more positive
24
Q
What effects do parasympathetic activity have on the various currents mediating the cardiac cycle? Through what mechanism does this occur? How do these molecular changes manifest?
A
- acetylcholine activates muscarinic receptors in the SA and AV nodes
- the result is to decrease the funny sodium and L-type calcium currents
- at low-to-moderate vagal activity, there is a decrease in potassium current; at high vagal activity, there is activation of the K(ACh) channel, which increases potassium current
- the net result is a decrease in heart rate and a decrease in conduction velocity through the AV node, which is seen as a prolonged PR interval
25
What effect does sympathetic activity have on MDR and phase 4 in the SA node?
- MDR is less negative
| - phase 4 is steeper
26
What effect does low-to-moderate parasympathetic activity have on MDR and phase 4 in the SA node?
- MDR is unchanged
| - phase 4 is less steep
27
Describe the changes in ECG following an increase in sympathetic activity to the heart.
- the heart rate increases with increased funny sodium current
- the inotropic state increases with increased L-type calcium current, and phase 2 of the AP is more positive (no change on ECG)
- the QT interval is shorter and the T wave is spiked due to the increased potassium current and faster repolarization
- because the sodium current is unaffected in the ventricles and atria, there is no change in the P wave or QRS complex
28
What receptors and second messengers mediate sympathetic and parasympathetic input to the heart?
- sympathetic: B1 receptors and Gs proteins
| - parasympathetic: M2 receptors and Gi proteins
29
What is the normal extracellular potassium concentration?
3.5-5 mEq/liter
30
How do hypokalemia and hyperkalemia affect the resting potential of cardiac myocytes? Why is this problematic?
- they both cause depolarization of the resting membrane potential
- the result is that both impair voltage-gated sodium current in the atria and ventricles
31
How do hyperkalemia and hypokalemia affect the ECG?
because they both impair voltage-gated sodium current in the atria ventricles, both conditions manifest with flattened and prolonged P waves and QRS complexes
32
Describe voltage-gated sodium channels.
they have two gates
- an activation gate, which is closed at normal resting potential but has fast kinetics and opens upon depolarization
- an inactivation gate, which is open at normal resting potential but closes at higher potentials with slow kinetics
33
Through what shared mechanism do hypokalemia and hyperkalemia impact sodium current?
- both cause depolarization of the resting membrane potential
- at higher resting potential, more resting sodium channels have inactivation gates that have already closed
- thus, a depolarizing current that opens the activation gate, doesn't actually result in a sodium current
- this serves to decrease the sodium current during the upstroke of the action potential
- as a result, the threshold potential is less negative (decreased excitability), the rate of rise of the AP is diminished, AP amplitude is decreased, and there is decreased conduction velocity
34
Through what mechanism do hypokalemia and hyperkalemia cause depolarization of the resting potential?
- in hypokalemia, there is a decrease in potassium conductance
- this increases the fractional conductance of sodium, which makes the resting potential more positive
- in hyperkalemia, the nernst potential for potassium becomes more positive, which makes resting potential more positive
35
How do the mechanisms of hypokalemia and hyperkalemia differ? How are they the same?
- they cause depolarization of the resting potential in different ways
- from there, however, they are the same as depolarization of the resulting potential serves to diminish the sodium current and make the threshold more positive
36
Compare and contrast the effects of hypokalemia and hyperkalemia on each of the following parameters:
- potassium nernst potential
- potassium conductance
- resting potential
- sodium channel inactivation
- conduction velocity
- QRS complex
- phase 3 repolarization
- AP duration
- T wave amplitude
- E is less negative in hyper and more negative in hypo
- g is increased in hyper and decreased in hypo
- resting potential is less negative in both
- Na channel inactivation is increased in both
- conduction velocity is decreased in both
- QRS complex is flat and wide in both
- phase 3 is faster in hyper and slower in hypo
- AP duration is decreased in hypo and increased in hyper
- T wave is spiked in hyper and depressed in hypo
37
What is a U wave on ECG characteristic of?
it is a characteristic feature of hypokalemia
38
How do hyper- and hypokalemia affect the SA node and heart rate?
- hypokalemia: MDP is less negative, phase 4 more steep, and so tachycardia occurs
- hyperkalemia: MDP is more negative, phase 4 is less steep, but there is no change in heart rate because the baroreflex is initiated by lower cardiac output
39
How is hypokalemia treated?
- an estimate of ECF is made
| - then potassium is slowly infused to avoid producing hyperkalemia
40
How is hyperkalemia treated initially?
- initially, increasing it is treated with calcium, which shifts the sodium-inactivation gate curve more positive
- this doesn't correct the problem but does restore excitability until you can correct potassium levels
41
List three options for correcting hyperkalemia and how each functions.
- sodium bicarb stimulates the Na/H exchanger, increasing sodium influx, thereby enhancing the Na/K pump
- insulin directly stimulates the Na/K pump
- diuretics enhance potassium excretion
42
What are the absolute, relative, and functional refractory periods?
- absolute: period during the AP at which depolarization is already occuring
- relative: period after the AP in which potassium current predominates and there is hyperpolarization
- functional: the combination of the two
43
What normally prevents re-entrant loops?
rapid depolarization and a smaller diameter of the ventricle ensures that the the conduction velocity is such that when the AP returns to a previously depolarized spot, it will still be in it's refractory period and won't be depolarized a second tie
44
Under what circumstances are re-entrant loops more likely?
- when conduction velocity is decreased
- when the duration of the AP is decreased
- when loop length is extended
45
What changes in currents are likely to produce re-entrant loops?
- those that decrease sodium current
- those that decrease potassium current
- those that increase potassium current
46
Describe early after depolarizations including the mechanism by which they arise and problems associated with them.
- they are slight depolarizations seen in late phase 2 or early phase 3
- they are associated with decreased potassium current (hypokalemia or cocaine use) and are a result of the "calcium window", a period when inactivation gates reopen during repolarization before activation gates have all closed
47
What is the calcium window? Why is it not usually a problem? When does it become a problem? What does it lead to?
- a current that arises due to opening of inactivation gates before activation gates have all closed
- usually, repolarization is faster than gate movement, so no calcium current arises
- when repolarization is slowed by a diminished potassium current (hypokalemia or cocaine use), the gates' kinetics allow for a calcium current to arise during phase 3
- additionally, sympathetic activity serves to shift the activation gate curve more negative, increasing the width/duration of the calcium window
48
How does sympathetic activity contribute to the formation of early after depolarizations?
- sympathetic activity increases the calcium current by shifting the activation gate curve more negative (so they open sooner during depolarization)
- however, this increases the size of the calcium window, increasing the potential for EADs
49
How do early after depolarizations trigger re-entrant loops?
if enough cells experience early after depolarizations, the calcium that moves intracellularly can spread through gap junctions and trigger action potentials in normal tissues
50
What are delayed after depolarizations? With what are they associated? Through what mechanism do they arise?
- they are small depolarizations that occur during phase 4 in ventricular myocytes
- associated with high heart rates, which cause the accumulation of calcium within myocytes since there is insufficent time to pump all the calcium out
- increased calcium levels activate the Na/Ca exchanger, which produces a net depolarizing current as 3 sodium enter for every one calcium out
- increased calcium also activates a non-specific cation channel, which allows extracellular cations to enter the cell
51
What is V fib? Why is it problematic? How is it treated?
- totally disorganized, chaotic ventricular rhythm due to multiple re-entrant loops with the ventricles causing depolarization
- there is no effective contraction and CO is markedly reduced to a life-threatening level
- defibrillation is the treatment of choice
52
Why is defibrillation used to treat V fib?
theoretically, the electrical shock depolarizes the entire heart at the same time, putting all myocytes into a refractory period until the SA node resumes supra ventricular rhythm
53
What is atrial fibrillation?
- the absence of discernible P waves, or a fluttering of P waves not matched to QRS complexes
- due to multiple re-entrant loops within the atria
- slightly reducing cardiac output
54
Why is atrial fibrillation not life threatening in the acute phase?
because atrial contraction only contributes to a small degree of ventricular filling, thus cardiac output is usually maintained
55
Why is atrial fibrillation a problem in the chronic phase?
because it results in stasis of the blood in the atria, increasing the risk of coagulation and thrombi
56
The arterial blood pressure depends on what?
the volume of blood within the arteries, determined by the rate of inflow and the rate of venous run off
57
How does TPR affect blood pressure?
it increases blood pressure by reducing the rate of runoff from arteries to veins
58
What is pulse pressure?
the difference between systolic and diastolic pressures
59
What three factors determine diastolic pressure? In what way does each do so?
arterial systolic pressure determines the starting point from which the rate and time of runoff control the drop in pressure by the amount of blood leaves the arterial system
60
Rate of runoff is determined by what cardiac factor?
the TPR
61
How does heart rate impact the diastolic pressure?
if the heart rate is faster, there is less runoff time, and diastolic pressure will be higher
62
What are the four primary determinants of arterial systolic pressure?
- arterial diastolic pressure determines the starting point
- stroke volume and ejection rate contribute
- as does arterial compliance
63
How is arterial compliance calculated and defined? How does it change with age and how does this affect systolic pressure?
- it is calculated as the change in volume/change in pressure
- aging reduces compliance and increases systolic pressure
64
How does arterial compliance affect systolic pressure?
- when compliance is high, the stroke volume is better accommodated without raising pressure in the vessel
- as such, the systolic pressure is lower
65
How does ejection rate affect systolic blood pressure?
when the rate of ejection is faster, systolic BP will reach a greater peak
66
How is MAP calculated?
MAP = diastolic pressure + (⅓)systolic pressure = CO x TPR
67
The baroreflex serves to maintain what cardiac measure/variable?
the MAP
68
What three factors determine stroke volume?
- preload
- afterload
- inotropic state
69
How is preload defined?
- as the stretch on myocardial fibers before contraction
- since myocardial stretch is difficult to measure, we use related variables related to ventricular filling as estimates instead (EDV, venous return, EDP)
70
How do heart rate and venous return affect preload?
- as heart rate increases, filling time is reduced as is preload
- as venous return increases, preload also increases
71
What is Starling's Law?
stroke volume increases when preload is increased
72
Why does the force of contraction increase with preload?
because greater preload results in a greater degree of stretch and thus a more favorable overlap of thick and thin filaments, contributing to the formation of more cross bridges
73
How is afterload calculated?
afterload = wall stress = (pressure x ventricular radius)/(2 x wall thickness)
74
What is inotropic state? What is it dependent on?
it is the contractility or force of contraction achieved by the heart dependent on the cytosolic calcium level within contracting myocytes
75
Why is cardiac muscle able to increase the force of contraction in response to higher intracellular calcium levels while skeletal muscle is not?
- when skeletal muscle contracts, calcium levels are supramaximal
- however, cardiac muscle contracts at sub maximal calcium levels, so there is additional reserve available and when calcium levels rise, more cross bridges form than under normal conditions
76
The greatest resistance to flow in the systemic circulation is in what vessels?
the arterioles
77
TPR is mainly determined by the resistance of which vessels?
arterioles
78
Describe how a starling curve is affected by changes in inotropy, heart rate, preload, and afterload.
- when inotropy increases, the curve shifts up
- when heart rate increases, there is movement down the normal curve
- when preload increases, there is movement up the normal curve
- when afterload increases, the curve shifts down
79
What are the three types of shock?
- hypovolemic
- distributive
- cardiogenic
80
Compare and contrast hypovolemic, distributive, and cardiogenic shock.
- hypovolemic is defined by decreased blood volume; central venous pressure will be low and the patient will be cool to touch
- cardiogenic is defined by inadequate cardiac output; central venous pressure will be high and the patient will be cool to touch
- distributive is defined by generalized systemic vasodilation; the patient will be warm to touch
81
List five causes of hypovolemic shock.
- dehydration
- burns
- hemorrhage
- impaired fluid reabsorption by kidney
- cholera
82
Blood flow to any particular systemic organ is determined by what equation?
flow = (MAP - RAP) / (resistance of organ)
83
Blood flow to the various organs varies because of what difference between organs?
vascular resistance
84
How do systemic arterioles respond to a decrease in MAP? How do those in the heart and brain respond?
- when MAP drops, systemic arterioles constrict in an effort to maintain MAP
- at the same time, arterioles of the heart and brain dilate to maintain adequate perfusion and nutrient delivery
85
List five factors that would increase the myocardial need for oxygen?
- increased inotropic state (B1 activation)
- increased afterload
- increased heart rate
- increased preload
- ventricular hypertrophy
86
Why might the heart experience myocardial ischemia during a period of hemorrhagic shock despite auto-regulation of arteriole diameter?
because although arteriole diameter expands to increase perfusion, the systemic drop in MAP increases sympathetic activity, which will increase the inotropic state of the heart, increasing oxygen demand
87
Describe how the baroreflex increases MAP in response to a decrease?
- increases heart rate
- increases inotropic state of the heart
- causes arteriole and venous constricition, increasing TPR and venous return (preload)
88
Which alters intracellular fluid volume, hemorrhage or dehydration?
dehydration creates a solute imbalance that moves water
89
What is an example of a hypertonic contraction?
dehydration
90
What sort of IV should be started for someone that is dehydrated? Why?
- 5% dextrose
- can't use saline because that will increase ECF but doesn't establish a gradient that will move water into cells, which have also lost fluid
- dextrose will be taken up by the cells and water will follow
91
How is the ventricular cycle curve affected by distributive shock?
- Po is the same because the heart's inotropic state hasn't changed and the filling curve is also unchanged
- afterload is decreased, however, so the curve is shorter than normal because the aortic valve increases earlier
- the heart empties more as well so the curve widens to the left (lower ventricular volume at the end of ejection
92
What mediates the drop in MAP that defines septic shock?
- inflammatory mediators cause endothelial cells to express iNOS, and EDNF is produced at extremely high levels, causing marked vasodilation
- inflammatory mediators also increase vascular permeability in the post-capillary venule, and blood volume is lost to edema
93
How do Epipens inhibit anaphylactic shock?
they activate a1 receptors to cause vasoconstriction, maintaining TPR and MAP while simultaneously activating B2 receptors to relax airways and improve oxygen delivery
94
List three causes of neurogenic shock and the mechanism through which they induce a decrease in MAP.
- deep anesthesia, pain reflex from deep trauma, or vasovagal syncope evoked by strong emotions
- all result in a decrease in sympathetic activity, which causes a generalized arteriolar vasodilation
95
What category of shock is neurogenic shock?
it is a distributive shock
96
How is neurogenic shock treated?
they will respond well to an alpha1 agonist
97
How does distributive shock affect the normal distribution of blood flow to the various organs?
- systemic organs receive higher than normal blood flow at the expense of blood flow to the brain and heart
- essentially, the ability to regulate blood flow to organs is lost in a person with distributive shock
98
What leads to acute heart failure in those with distributive shock?
- the oxygen demand of the heart is increased as it attempts to compensate for the decline in MAP by increasing CO
- however, the body has lost the ability to regulate blood flow to the organs and thus the heart doesn't receive adequate blood flow
99
How does cardiac tamponade affect the ventricular cycle curve?
it doesn't affect Po but it raises the passive filling curve
100
What is paradoxical pulse during cardiac tamponade? How does it originate?
- a greater than normal decline in systolic arterial pressure during inspiration
- the increase in venous return to the right ventricle during inspiration causes an exaggerated reduction in left ventricular volume because increased filling causes the septum to bulge into the left ventricle
101
What is physiologic S2 splitting?
- an effect of inspiration
- it increases intrathoracic volume and decreases pressure
- this lowers right atrial pressure and increases venous return
- EDV of the right ventricle increases as does stroke volume and thus ejection time
- the result is a delayed closure of the pulmonic valve
102
How does breathing affect heart rate?
- upon inspiration, intrathoracic volume increases and pressure decreases
- this causes distension of pulmonary veins and pooling in pulmonary veins
- the result is a decrease in flow to the left atrium, reducing preload and stroke volume
- there is a slight drop in MAP, which the baroreflex compensates for, in part, by increasing HR
103
How does cardiac tamponade affect an ECG?
- there are low amplitude ECG recordings since the pericardial sac diminishes the magnitude of electrical events recorded on the ECG
- heart sounds are diminished for the same reason
104
How does the baroreflex respond to shock?
- shock implies a decrease in MAP which equals CO x TPR
| - the baroreflex compensates by increasing CO or TPR, whichever the problem didn't originate with
105
What is irreversible shock?
a final take of shock in which death will ensue regardless of treatment
106
Why does shock become irreversible when prolonged?
- shock contributes to impaired organ blood flow and thus ischemia
- ischemia contributes to cell injury, which subsequent results in the release of toxic factors (e.g. myocardial depressant factor) which reduce contractility of the heart and reduce CO
- ischemia also triggers to the local accumulation of vasodilator metabolites and a thus a drop in TPR
- finally, ischemia initiates a switch to anaerobic glycolysis, lactate acid builds, inducing an acidosis, which further impairs cell functioning
- all these together contribute to irreversible shock as even a transfusion can't rescue these processes
- summary: myocardial depressant factor (low CO), local vasodilators (low TPR), acidosis
