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Cardiovascular and Pulmonary > Cardiovascular Systems Physiology and Pathophysiology IV > Flashcards

Cardiovascular Systems Physiology and Pathophysiology IV Flashcards

1
Q

Can target the SNS (i.e. beta blockers); or can impede the activation of Ca2+, Na+, or K+ channels. In so doing, these compounds modulate depolarization and/or repolarization of cardiac tissues

A

Antiarrythmics

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2
Q

In addition, certain of the above listed cardiac arrhythmias can be studied and treated by an

A

Electrophysiologist

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3
Q

In general, an electrophysiologist can do what 3 things?

A
  1. ) Assess cardiac conductance system
  2. ) Characterize recurrent arrythmias
  3. ) Map and potentially destroy arrythmogenic foci
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4
Q

An area of necrosis which develops due to a sudden loss of blood supply

A

Infarct

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5
Q

Results from a severe impediment of blood supply (ischemia) to a region of the myocardium

A

Myocardial Infarction

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6
Q

The most common location for the development of an MI is the

A

Left ventricle

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7
Q

Represent ischemia and are not diagnostic for the MI

A

T waves

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8
Q

Becomes elevated following an MI and returns to normal several hours later. This elevation signals an MI

A

ST segment

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9
Q

The pathogenesis of ST elevation is complex and involves localized increases in

A

Extracellular K+

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10
Q

Resting membrane potential (RMP) of the damaged myocardium becomes less negative and the observed ST elevation is basically the difference between

A

Healthy RMP and ichemic RMP

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11
Q

Indicates irreversible myocardial death

-represent the misdirection of current away from the dead area

A

New Q waves

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12
Q

Appear within a few hours of the infarct, but may take a few days to develop

-Do not resolve

A

Q waves

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13
Q

The inferior and posterior regions of the heart are supplied by the

A

Right coronary artery

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14
Q

If the inferior myocardium is affected, electrical activity within which leads would reflect MI changes in the ECG

A

Inferior leads: II, III, and aVF

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15
Q

The posterior heart does not have a dedicated lead so we rely on

A

V1

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16
Q

A posterior infarct would show as reciprocal changes, such as a prominant R wave that is not present in a healthy ECG, in

A

V1

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17
Q

Which leads show electrical activity in the region that is supplied by the left circumflex artery?

A

Left lateral leads: I, aVL, V5, and V6

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18
Q

The anterior myocardium is supplied by the

A

Left anterior descending artery

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19
Q

Damage to the portion of the heart supplied by the left anterior descending artery would show in the

A

Precordial leads (V1-V6)

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20
Q

What are the 4 heart sounds that occur and can be coordinated with an ECG?

A
  1. ) S1
  2. ) S2
  3. ) S3
  4. ) S4
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21
Q

The first heart sound

-represents the onset of ventricular systole

A

S1

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22
Q

The first heart sound (S1) is caused following closure of the

A

AV valves (lub)

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23
Q

Heard following closure of the semilunar valves due to
vibrations of the ventricular and large vessel walls due to recoil of arterial and ventricular blood against the valve leaflets

A

S2 (2nd heart sound, dub)

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24
Q

S2 is split into which 2 components?

A
  1. ) Aortic valve component (A2)

2. ) Pulmonic valve comonent (P2)

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25
Q

A2 and P2 are most easily elucidated upon

A

Inspiration

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26
Q

Under normal conditions, A2-P2 is fused on expiration, but splits into a distinct A2-P2 pattern on inspiration; this is known as

A

Psychologic splitting

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27
Q

Occurs due to the decreased intrathoracic pressure that is generated during inspiration

A

Psychologic splitting

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28
Q

Decreased intrathoracic pressure allows for increased venous return to the right heart which allows for lengthened

A

Systolic ejection

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29
Q

Also, low intrathoracic pressure increases capacitance of pulmonary arteries and veins; this reduces

A

Intravascular pressures

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30
Q

During inspiration, diastolic back pressure against the pulmonic valve is reduced so that

A

Later closure occurs

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31
Q

The decrease in intrathoracic pressure lowers pulmonary vein pressure and reduces left heart diastolic filling. With less volume, the time for systole is reduced and the

A

Aortic valve closes earlier

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32
Q

An increase in the delay between A2 and P2 that is often caused by right bundle branch block, which prolongs the cardiac cycle in the right heart

A

Widened splitting

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33
Q

P2 can also be delayed by the less common

A

Pulmonic valve stenosis

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34
Q

When P2 occurs before A2 and the splitting occurs on expiration

A

Paradoxal splitting

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35
Q

Paradoxal splitting is caused by a delay in aortic valve closure. This can be the result of

A

Left bundle branch block or aortic stenosis

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36
Q

If detectable, occurs during the beginning of the middle third of ventricular filling

A

S3

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37
Q

A low pitched sound that resembles S1 and S2 and has the cadence of the word Kentucky

A

S3

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38
Q

In adults, S3 can often be heard in the setting of elevated left heart filling pressures in adult patients with

A

Dilated cardiomyopathies

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39
Q

Can be ascultated in patients with left ventricular hypertrophy (a stiff ventricle)

A

S4

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40
Q

S4 sounds like S 1 and S2 and occurs in

A

Late diastole

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41
Q

The cadence of S1 + S2 + S4 is similar to the word Tennessee, where the first syllable is

A

S4

42
Q

Heart murmur when the aortic valve resists blood flow and there is a dramatic increase in LVP

A

Aortic valve stenosis

43
Q

Over time, aortic valve stenosis can result in

A

LV hypertrophy

44
Q

Heart murmur when the pulmonic valve resists blood flow and RVP is much greater than pulmonary arterial pressure

-Results in RV hypertrophy over time

A

Pulmonic valve stenosis

45
Q

The intensity of a pulmonic valve stenosis increases

A

During inspiration (loudest over 2nd intercostal space)

46
Q

Murmur resulting from the left atrium having to work harder to eject blood through the resistant valve, resulting in left atrial hypertrophy

-rare

A

Mitral stenosis

47
Q

Mitral stenosis is observed on an ECG as an increased amplitude and duration of the left atrial component of the P wave observed in leads

A

II and V1

48
Q

Murmur resulting from blood leaking back into the left atrium, which causes the left atrium to have to work harder against elevated pressures

A

Mitral regurgitation

49
Q

The increase in left atrial size accompanying a mitral regurgitation results in a

A

Notched P wave in the ECG

50
Q

A murmur cause by the reflux of blood during RV systole that causes an abnormal increase in jugular venous pressure

A

Tricuspid regurgitation

51
Q

Can cause pathologic systolic waveforms within the venous circulation

A

Tricuspid regurgitation

52
Q

Because of reflux through the inferior vena cava, tricuspid regurgitation can result in a

A

Pulsative liver

-liver pulsations can be palpated

53
Q

Patients with a murmur that intensifies during inspiration and present with a distended jugular vein likely have a

A

Tricuspid regurgitation

54
Q

A murmur that causes the over taxed LV to perform more work to pump blood through a leaky valve and against the high pressure within the aorta

A

Aortic valve regurgitation

55
Q

In an aortic regurgitation, LVV and LVP are increased and the result is

A

LV dilation and hypertrophy

56
Q

The cornerstone of diagnosing and quantifying murmurs, and certainly directs medical and surgical interventions

A

Electrocardiography

57
Q

In the event of low plasma volume (hypovolemia), the SNS triggers changes in cardiac, vascular, renal, and neuroendocrine function which raise

A

Intravascular volume, CO, and total peripheral resistance (TPR) (increase BP)

58
Q

With elevated plasma volume (hypervolemia) inducing a

concomitant rise in BP, alterations in renal function, CO, and vascular smooth muscle tone serve to

A

Lower BP

59
Q

Populations of high pressure sensory receptors (baroreceptors) are loated in the

A

Aortic arch and carotid sinus

60
Q

Low pressure baroreceptors (type A and B) are found in the

A

Right atrium/vena cava and left atrium/pulmonary vein regions

61
Q

Sensitive to stretch and therefore change firing rate with atrial systole and diastole

A

Low pressure baroreceptors

62
Q

Relatively inactive at blood pressures below 50-60 mm Hg, but progressively increase the rate of firing between pressures of approximately 60-180 mm Hg

A

High pressure baroreceptors

63
Q

Signals the medulla to increase SNS input to the heart if BP plummets below 60 mmHg

A

Low pressure baroreceptors

64
Q

Signal the ANS to attenuate SNS activity concomitant with an increase in PSNS ton in order to slow HR if BP soars

A

High pressure baroreceptors

65
Q

Located in the carotid sinus and aortic body where they sense decreases in blood partial pressure of O2 (PO2)

A

Chemoreceptors

66
Q

Elevated PCO2 and decreased blood pH increase the sensitivity of chemoreceptors to

A

Hypoxia

67
Q

Chemoceptors are exquisitely sensitive to tiny changes in PCO2; but are less sensitive to changes in

A

PO2

68
Q

Occurs when BP falls below approximately 60 mmHg because deoxygenated blood is not being removed quickly enough

A

Stagnant hypoxia (increase in PCO2:PO2 ratio and H+ concentration)

69
Q

In this scenario, chemoceptors are activated and signal a sequence of events resulting in augmented SNS cardiovascular activity, in conjunction with a block in

A

Cardiac PSNS tone

70
Q

Baroreceptors and chemoreceptors are designed to correct only

A

Acute changes in BP

-not chronic

71
Q

Episodes of hypertension increase high pressure baroceptor activity. High pressure baroceptors
activate fibers within the

A

Afferent vagal and glossopharyngeal tracts

72
Q

Within the medulla, the coordinated actions of stimulatory and inhibitory interneurons impair the activity of SNS preganglionic fibers that supply SNS tracts to the

A

Heart and vascular smooth muscle

73
Q

In addition, there is also an activation of interneurons connecting to medullary

A

PSNS fibers

74
Q

In response to hypertension, baroreceptors signals the medulla to downregulate SNS innervation while upregulating PSNS activity of the heart. The result is

A

Reduced TPR and slowed HR

75
Q

In addition, signals to the kidneys lead to increased

A

Urine excretion

76
Q

In an acute drop in BP, low pressure baroreceptors and chemoreceptors induce an upregulation in SNS activity. As a result, the following are increased

A
  1. ) Venous return to the heart
  2. ) HR
  3. ) Vascular resistance in skeletal muscle and splanchnic and renal tissues
77
Q

Chronic low BP activates elaborate and integrated renal and endocrine compensatory mechanisms involving the hormones

A

Angiotensin II, aldosterone, and arginine vasopressin

78
Q

What are the two types of hypertension (HTN)

A

Primary and secondary

79
Q

The form of HTN which develops somewhat gradually commonly within the age range of approximately 20-50 years-old

A

Primary HTN

80
Q

Around 95% of patients with HTN have which form?

A

Primary HTN

81
Q

Renal malfunctions resulting in increased Na+ and H2O retention, and/or hyperactive RAAS activity can be a cause of

A

Primary HTN

82
Q

Primary HTN can also be caused by the desensitization of baroreceptors to increased volume and pressure which results in the loss of

A

Normal feedback control

83
Q

In part defined as uncontrolled BP despite the use of optimal doses of 3 BP medications, one of which is a diuretic

A

Resistant (or secondary) HTN

84
Q

Secondary HTN usually manifests

A

Prior to age 20 or after age 50

85
Q

Kidney disease such as renal artery stenosis and renal parenchymal disease and adrenocortical hormone excess can cause

A

Secondary HTN

86
Q

Hypo- and hyperthyroidism and coarction of the aorta can cause

A

Secondary HTN

87
Q

A protein hormone that is synthesized within the renin-angiotensin system

-A potent vasoconstrictor

A

Angiotensin II (An-II)

88
Q

Angiotensin II bioactivity is regulated by which receptors?

A

AT1 and AT2

89
Q

Known to mediate angiotensin II activity in vascular smooth muscle and cardiac muscle

A

AT1

90
Q

Based upon what is known, AT1 is the predominant AnII receptor that mediates AnII-orchestrated

A

vasoconstriction

91
Q

Angiotensin II is a potent vasoconstrictor and this action is mediated by

A

An-II binding to AT1

92
Q

Has extra-vascular effects that can exacerbate renovascular hypertension

A

An-II

93
Q

Can block high pressure baroreceptor input; therefore, the counter-response to elevated BP is neutralized, and SNS has free-reign to maintain increased TPR

A

An-II

94
Q

An-II stimulates the adrenal cortex to secrete the steroid hormone

A

Aldosterone

95
Q

Augments kidney-mediated Na+ reabsorption from the forming urine

A

Aldosterone

96
Q

Increased Na+ resorption results in

A

H2O retention

97
Q

A vasoconstrictor that can modulate Na+ and K+

currents that regulate ventricular myocyte function in the heart

A

Aldosterone

98
Q

Directly linked with promoting ventricular hypertrophy, the induction of proinflammatory cascades, and profibrotic remodeling

A

Aldosterone

99
Q

Can directly stimulate the release of norepi from post-ganglionic SNS fibers

A

An-II

100
Q

Collectively then, An-II-induced vasoconstriction, An-II-dependent block in high pressure baroreceptor activity, increased aldosterone levels, and An-II-directed secretion of norepi, all factor into increased TPR and thus

A

Elevated BP

101
Q

Counteract transient increases in AII and aldosterone, as well as high BP

A

Renal and other mechanisms

102
Q

In the normotensive patient, urinary output is directly correlated with

A

Mean arterial Pressure (BP)

Cardiovascular and Pulmonary (25 decks)

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