Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cardiac > M&M Cardiac Physiology > Flashcards

M&M Cardiac Physiology Flashcards

Learn!!!

1
Q

The two vascular systems that the heart propels are arranged in a: ____

A

Series

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

At rest, myocardial cell membrane is nominally permeable to ___, but impermeable to ____.

A

Permeable to K+, impermeable to Na+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Explain the Na+/K+ pump in the heart

A

its an ATP pump that concentrates K+ INTRAcellularly, in exchange for extrusion of Na+ out of the cell.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Action potentials in skeletal muscle vs cardiac:

A

Skeletal: due to opening of voltage gated sodium channels. In cardiac: it is initiated by voltage gated sodium channels, and maintained by voltage gated calcium channels.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

SA node is located where:

A

junction of RA and SVC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

AV node is located:

A

Septal wall of right atrium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Why is it that the SA node controls the heart rate?

A

Because its faster.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Order of propogation:

A

SA node, AV node, Bundle of His, Purkinje system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What do inhaled anesthetics do to SA node automaticity?

A

They depress SA node automaticity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

At high concentrations, how do local anesthetics depress conduction?

A

By binding to sodium channels, and at extremely high concentrations, they can depress the SA node.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Types of Ca2+ channel blockers:

A

Dihydropyridine: amlodipine and nifedipine (plug channel),

Non-dihydropyridine: verapamil, diltiazem: block channel in its depolarized inactivated state

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How does sympathetic stimulation increase the force of contraction?

A

It raises intracellular Ca2+ concentration via B1 adrenergic receptor mediated increase in cAMP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How does digoxin work?

A

It increases intracellular Ca2+ concentration through inhibition of membrane bound Na/K+ ATPase; the small increase in intracellular Na+ allows for greater influx of Ca2+ via sodium calcium exchange mechanism.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Glucagon enhances contractility. How Sway?

A

By increasing the intracellular cAMP levles via activation of a specific nonadrenergic receptor.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

So, cAMP is good or bad for contractility?

A

Good

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Why does acidosis affect the heart?

A

Because it blocks slow calcium channels and therefore also depresses cardiac contractility by unfavorably altering intracellular calcium kinetics.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

T/F nitrous oxide also produces concentration dependent decreases in contractility by reducing the availability of intracellular Ca2+ during contraction

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Parasympathetic fibers primarily innervate what: _____. ACh acts on ____ to produce negative _____

A

Atria and conducting tissues. ACh acts on specific cardiac muscarinic receptors (M2) to produce negative chronotropic, dromotropic, and inotropic effects.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Sympathetic fibers are more widely distributed throught the heart compared to PS fibers (Tf)

A

True.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Cardiac sympathetic fibers originate where, and travel to the heart how.

A

Originate in T1-T4, and travel to the heart initially thrugh cervical (stellate) ganglia and from the ganglia as cardiac nerves.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

A wave:

A

Atrial systole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

C wave: ___ and is caused by:

A

ventricular contraction and is said to be caused by bulging of AV valve into atrium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

v wave:

A

pressure buildup from venous return before the AV valve opens again

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

X descent:

A

decline in pressure between c and v waves and is due to pulling down of atrium by ventricular contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Aortic notch:

A

brief pressure change from transient backflow of blood into LV just before aortic valve closure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the formula for cardiac index?

A

Cardac output/BSA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is normal Cardiac index:

A

2.5-4.2 L/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Why is Caridac index (CI) an insensitive measurement of ventricular performance?

A

becasue it has a wide range, and so abnormalities usually reflect gross ventricular impairment.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Why is measurement of mixed venous oxygen tension (or saturation) an excellent estimate of the adequacy of cardiac output? and in which conditions?

A

So only in the ABSENCE of hypoxia or severe anemia, . becasue a decrease in mixed venous Ox saturation in response to increased demand means inadequate tissue perfusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What three major factors determine Stroke volume:

A

preload, afterload, contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

T/F: Contractility is independent of both preload and afterload.

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Ventricular preload is aka:

A

End diastolic volume (AKT question)

33
Q

The most important determinant of RV preload is:

A

Venous return

34
Q

IN the absence of Pulmonary or RV dysxn, venous return is also the major deteminant of :

A

LV preload

35
Q

LVEDP can be used as a measure of preload ONLY when:

A

relationship between ventricular volume and pressure (ventricular compliance) is constant.

36
Q

which ventricle of heart is more compliant and why?

A

RV: because it is thinner.

37
Q

SVR equation (one with 80)

A

SVR=80 x (MAP-CVP)/CO

38
Q

Normal SVR:

A

900-1500 dyn.

39
Q

What is the formula for RV afterload? PVR

A

80x (PAP-LAP (aka PCWP))/CO

40
Q

Why is the right ventricle more sensitive to changes in afterload than the left?

A

Because it has a thinner wall

41
Q

How does NE enhance contractility?

A

Primarily via B1 receptor activation

42
Q

Name 3 things that can depress myocardial contractility:

A

hypoxia, acidosis, depletion of catecholamine stores within the heart.

43
Q

Hypokinesis:

A

decreased contraction,

44
Q

akinesis:

A

failure to contract

45
Q

dyskinesis:

A

paradoxic bulging

46
Q

Stenosis of an AV valve and semilunar valve both decrease stroke volume. How is it different for each one?

A

AV: decreases preload
Semilunar: increases ventricular afterload

47
Q

T/F valvular regurgitation can reduce stroke volume without changes in preload, afterload, contractility, and w/o wall motion abnormalities.

A

TRUE

48
Q

When is LVEF not a good measure of contractility?

A

Left ventricular EF is not an accurate measure of ventricular contractility in the presence of mitral insufficiency

49
Q

How can LV diastolic dysfunction be measured on TTE?

A

Left ventricular diastolic function can be assessed clinically by Doppler echocardiography on a transthoracic or transesophageal examination. Flow velocities are measured across the mitral valve during diastole.

50
Q

What do veins do when there is significant blood or fluid loss?

A

Following significant blood or fluid losses, a sympathetically mediated increase in venous tone reduces the caliber of these vessels and shifts blood into other parts of the vascular system.

51
Q

With reduced perfusion, arterioles:

A

Dilate

52
Q

Which autonomic nervous system controls the vasculature?

A

Although the parasympathetic system can exert important influences on the circulation, autonomic control of the vasculature is primarily sympathetic.

53
Q

Sympathetic outflow comes out of the spinal Sympathetic outflow to the circulation passes out of the spinal cord at all thoracic segments and the first two lumbar segments. cord where?

A

Sympathetic outflow to the circulation passes out of the spinal cord at all thoracic segments and the first two lumbar segments.

54
Q

Do sympathetic fibers innervate capillaries?

A

No

55
Q

Vasovagal syncope: How? When can it occur?

A

Vasodepressor (vasovagal) syncope, which can occur following intense emotional strain associated with high sympathetic tone, results from reflex activation of both vagal and sympathetic vasodilator fibers.

56
Q

How does pressure change once it leaves big vessels and goes into veins and arterioles?

A

The mean pressure falls to less than 20 mm Hg in the large systemic veins that return blood to the heart. The largest pressure drop, nearly 50%, is across the arterioles, and the arterioles account for the majority of SVR.

57
Q

Explain the baroreceptor reflex:

A

Elevations in blood pressure increase baroreceptor discharge, inhibiting systemic vasoconstriction and enhancing vagal tone

58
Q

Where are the peripheral baroreceptors located?

A

Peripheral baroreceptors are located at the bifurcation of the common carotid arteries and the aortic arch.

59
Q

How do the peripheral baroreceptors individually make changes?

A

Carotid baroreceptors send afferent signals to circulatory brainstem centers via Hering’s nerve (a branch of the glossopharyngeal nerve), whereas aortic baroreceptor afferent signals travel along the vagus nerve.

60
Q

Which baroreceptor is more important? Why?

A

Of the two peripheral sensors, the carotid baroreceptor is physiologically more important and is primarily responsible for minimizing changes in blood pressure that are caused by acute events, such as a change in posture. Carotid baroreceptors sense MAP most effectively between pressures of 80 and 160 mm Hg. Adaptation to acute changes in blood pressure occurs over the course of 1-2 days, rendering this reflex ineffective for longer term blood pressure control.

61
Q

What do volatile anesthetics due to the baroreceptor response?

A

All volatile anesthetics depress the normal baroreceptor response, but isoflurane and desflurane seem to have less effect. Cardiopulmonary stretch receptors located in the atria, left ventricle, and pulmonary circulation can cause a similar effect.

62
Q

Both angiotensin II and AVP are potent arteriolar vasoconstrictors.T/F:

A

True

63
Q

Diff in receptors for AT1 and AVP?

A

Angiotensin constricts arterioles via AT1 receptors. AVP mediates vasoconstriction via V1 receptors and exerts its antidiuretic effect via V2 receptors.

64
Q

In 85% of people, the RCA supplies:

A

In 85% of persons, the RCA gives rise to the posterior descending artery (PDA), which supplies the superior-posterior interventricular septum and inferior walL

65
Q

Formula for coronary perfusion pressure:

A

CPP: AoDP-LVEDP

66
Q

Why is the endocardium more susceptible o ischemia?

A

In 85% of persons, the RCA gives rise to the posterior descending artery (PDA), which supplies the superior-posterior interventricular septum and inferior wal

67
Q

What is the most important determinant of myocardial blow?

A

Myocardial oxygen demand is usually the most important determinant of myocardial blood flow. HR is most important part of demand.

68
Q

Why can the myocardium not compensate for reductions in blood flow by extracting more oxygen?

A

The myocardium usually extracts 65% of the oxygen in arterial blood, compared with 25% in most other tissues. Coronary sinus oxygen saturation is usually 30%. Therefore, the myocardium (unlike other tissues) cannot compensate for reductions in blood flow by extracting more oxygen from hemoglobin.

69
Q

Diastolic dysfunction. Tell me about, early, middle/psedonomalization, and late:

A

In the early stages of diastolic dysfunction, the primary abnormality is impaired relaxation. When left ventricular relaxation is delayed, the initial pressure gradient between the left atrium and the left ventricle is reduced, resulting in a decline in early filling, and, consequently, a reduced peak E wave velocity. The A wave velocity is increased relative to the E wave, and the E/A ratio is reduced. As diastolic dysfunction advances, the left atrial pressure increases, restoring the gradient between the left atrium and left ventricle with an apparent restoration of the normal E/A ratio. This pattern is characterized as “pseudonormalized.” Using the E/A ratio alone cannot distinguish between a normal and pseudonormalized pattern of diastolic inflow. As diastolic dysfunction worsens further, a restrictive pattern is obtained. In this scenario, the left ventricle is so stiff that pressure builds in the left atrium, resulting in a dramatic peak of early filling and a prominent, tall, narrow E wave. Because the ventricle is so poorly compliant, the atrial contraction contributes little to filling, resulting in a diminished A wave and an E/A ratio greater than 2:1.

70
Q

E wave and diastolic dysfunction:

A

An e’ wave less than 8 cm/sec is consistent with diastolic dysfunction.

71
Q

When is heart failure associated with an elevated CO?

A

Heart failure is less commonly associated with an elevated cardiac output. This form of heart failure is most often seen with sepsis, thyrotoxicosis, and other hypermetabolic states, which are typically associated with a low SVR

72
Q

Why is anesthesia in ppl with heart failure so scary?

A

Nonetheless, the failing heart becomes increasingly dependent on circulating catecholamines. Abrupt withdrawal in sympathetic outflow or decreases in circulating catecholamine levels, such as can occur following induction of anesthesia, may lead to acute cardiac decompensation.

73
Q

Tell me about BNP:

A

Brain natriuretic peptide (BNP) is produced in the heart in response to myocyte distention. Elevated BNP concentration (>500 pg/mL) usually indicates heart failure, and measurement of BNP concentration can be used to distinguish between heart failure and lung disease as a cause of dyspnea.

74
Q

Problem in Volume vs pressure overloaded ventricle/wall stress:

A

In the volume-overloaded ventricle, the problem is an increase in diastolic wall stress. The increase in ventricular muscle mass is sufficient only to compensate for the increase in diameter: The ratio of the ventricular radius to wall thickness is unchanged. Sarcomeres replicate mainly in series, resulting in eccentric hypertrophy. Although ventricular EF remains depressed, the increase in end-diastolic volume can maintain normal at-rest stroke volume (and cardiac output).

The problem in a pressure-overloaded ventricle is an increase in systolic wall stress. In this case, sarcomeres mainly replicate in parallel, resulting in concentric hypertrophy: The hypertrophy is such that the ratio of myocardial wall thickness to ventricular radius increases. As can be seen from Laplace’s law, systolic wall stress can then be normalized. Ventricular hypertrophy, particularly that caused by pressure overload, usually results in progressive diastolic dysfunction. The most common reasons for isolated left ventricular hypertrophy are hypertension and aortic stenosis.

75
Q

Normal PR interval:

A

0.12-0.2 seconds

76
Q

Shortened PR interval: what’s usually the cause? What can you see, and how can you differentiate the two?

A

Abnormally short P-R intervals can be seen with either low atrial (or upper AV junctional) rhythms or preexcitation phenomena. The two can usually be differentiated by P-wave morphology: With a low atrial rhythm, atrial depolarization is retrograde, resulting in an inverted P wave in leads II, III, and aVF; with preexcitation, the P wave is normal during sinus rhythm. If the pacemaker rhythm originates from a lower AV junctional focus, the P wave may be lost in the QRS complex or may follow the QRS.

77
Q

What is preexcitation?

A

Preexcitation usually refers to early depolarization of the ventricles by an abnormal conduction pathway from the atria.

78
Q

How does pre-excitation shorten the PR interval?

A

In patients with preexcitation, the normal cardiac impulse originating from the SA node is conducted simultaneously through the normal (AV nodal) and anomalous (bypass tract) pathways. Because conduction is more rapid in the anomalous pathway than in the AV nodal pathway, the cardiac impulse rapidly reaches and depolarizes the area of the ventricles where the bypass tract ends. This early depolarization of the ventricle is reflected by a short P-R interval and a slurred initial deflection (δ wave) in the QRS complex. The spread of the anomalous impulse to the rest of the ventricle is delayed because it must be conducted by ordinary ventricular muscle, not by the much faster Purkinje system. The remainder of the ventricle is then depolarized by the normal impulse from the AV node as it catches up with the preexcitation front. Although the P-R interval is shortened, the resulting QRS is slightly prolonged and represents a fusion complex of normal and abnormal ventricular depolarizations.

Cardiac (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions