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Health Challenges > Week 3: Cardiovascular > Flashcards

Week 3: Cardiovascular Flashcards

1
Q

3 layers of heart

A

endocardium, myocardium, epicardium

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2
Q

mitral valve separates

A

left atrium and ventricle

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3
Q

aortic valve seperates

A

left ventricle and aorta

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4
Q

tricuspid valve separates

A

right atrium and right ventricle

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5
Q

pulmonic valve separates

A

right ventricle and pulmonary artery

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6
Q

systole

A

contraction of the myocardium, results in ejection of blood from the cardiac
chamber.

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7
Q

diastole

A

relaxation of the myocardium, allows for filling of the chamber

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8
Q

cardiac output

A

amount of blood pumped by each ventricle in 1 minute.
It is calculated by multiplying the amount of blood ejected from the ventricle with
each heartbeat, the stroke volume (SV), by the heart rate (HR) per minute:

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9
Q

cardiac index

A

CO divided by the body mass index (BMI). A measure of the
CO of a patient per square metre of body surface area, the cardiac index adjusts the
CO to the body size. The normal cardiac index is 2.8 to 4.2 L/minute/m2

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10
Q

cardiac reserve

A 
refers to the heart’s ability to alter the CO in response to an increase
in demand (e.g., exercise, stress, hypovolemia).
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11
Q

baroreceptors

A

Baroreceptors, located in the aortic arch and carotid sinus, respond to stretch or
pressure within the arterial system.

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12
Q

chemoreceptors

A

located in the aortic arch and carotid body, can initiate changes in
HR and arterial pressure in response to decreased arterial O2 pressure, increased
arterial CO2 pressure, and decreased plasma pH.

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13
Q

two main factors influencing bp

A

cardiac output, systemic vascular resistance

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14
Q

electrocardiography

A

Deviations from the normal sinus rhythm can indicate abnormalities in heart
function.

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15
Q

exercise or stress testing

A

to evaluate the cardiovascular response to physical stress.

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16
Q

echocardiography

A

Provides information about (1) valvular structure and motion, (2) cardiac chamber
size and contents, (3) ventricular muscle and septal motion and thickness, (4)
pericardial sac, (5) ascending aorta, and (6) ejection fraction (EF) (percentage of
end-diastolic blood volume that is ejected during systole).

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17
Q

nuclear cardiography

A

includes MUGA, SPECT, PET, CMRI, MRA

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18
Q

Cardiac computed tomography

A 
Heart-imaging test in which CT technology, with or without intravenous contrast
medium (dye), is used to see the heart anatomy, coronary circulation, and great
blood vessels (e.g., aorta, pulmonary veins, artery).
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19
Q

coronary angiography

A 
Contrast media (introduced via a catheter inserted in a large peripheral artery) and
fluoroscopy are used to obtain information about the coronary arteries, heart
chambers and valves, ventricular function, intracardiac pressures, O2 levels in
various parts of the heart, CO, and EF.
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20
Q

electrophysiology study

A

Studies and manipulates the electrical activity of the heart using electrodes placed
inside the cardiac chambers. It provides information on SA node function, AV
node conduction, ventricular conduction, and source of dysrhythmias.

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21
Q

intracoronary ultrasound or intravascular ultrasound

A

Performed during coronary angiography. It obtains 2D or 3D ultrasound images to
provide a cross-sectional view of the arterial walls of the coronary arteries.

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22
Q

colour flow duplex imaging

A

Uses contrast media, injected into arteries or veins (arteriography and
venography) to diagnose occlusive disease in the peripheral blood vessels and
thrombophlebitis.

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23
Q

fractional flow reserve

A

Performed during a cardiac catheterization; a special wire is inserted into the
coronary arteries to gather these measurements, and the information is used to
determine need for angioplasty or stent placement on nonsignificant blockages.

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24
Q

hemodynamic monitering

A

Uses intra-arterial and pulmonary artery catheters to monitor arterial BP,
intracardiac pressures, CO, and central venous pressure (CVP).

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25
Q

nitric oxide helps

A

maintain
low arterial tone at rest, inhibits growth of the smooth muscle layer, and
inhibits platelet aggregation.

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26
Q

endothelin function

A

produced by the endothelial cells, is an extremely potent

vasoconstrictor.

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27
Q

how do kidneys contribute to BP reg

A

Sodium retention results in water retention, which causes an increased ECF
volume. This increases the venous return to the heart, increasing the stroke
volume, which elevates the BP through an increase in CO.

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28
Q

adrenal medulla function in bp

A

releases epinephrine in response to SNS stimulation.
Epinephrine activates 2-adrenergic receptors, causing vasodilation. In
peripheral arterioles with only 1-adrenergic receptors (skin and kidneys),
epinephrine causes vasoconstriction.

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29
Q

pituitary function in bp

A

ADH is released from the posterior pituitary gland in response to an increased
blood sodium and osmolarity level. ADH increases the ECF volume by
promoting the reabsorption of water in the distal and collecting tubules of the
kidneys, resulting in an increase in blood volume and BP.

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30
Q

isolated systolic hypertension

A

average SBP greater than or equal to 140 mm
Hg coupled with an average DBP less than 90 mm Hg. ISH is more common in older
adults. Control of ISH decreases the incidence of stroke, heart failure, cardiovascular
mortality, and total mortality.

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31
Q

primary hypertension

A

Elevated BP without an identified cause; this

accounts for 90% to 95% of all cases of HTN.

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32
Q

secondary hypertension

A

Elevated BP with a specific cause that often can be
identified and corrected; this accounts for 5% to 10% of HTN in adults, and more
than 80% of HTN in children.

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33
Q

hemodynamic hallmark of hypertension

A

increased SVR

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34
Q

genetic factors account for

A

30-60% variability in BP

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35
Q

hypertension is a amjor risk factor for

A

coronary artery disease, cerebral atherosclerosis, and stroke

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36
Q

hypertension is one of the leading causes of

A

end stage renal disease

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37
Q

pt and caregiver teaching for hypertension

A

(1) nutritional therapy, (2)
drug therapy, (3) lifestyle modification, and (4) home monitoring of BP (if
appropriate).

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38
Q

orthostatic hypotension

A

defined as a decrease of 20 mm Hg or more in SBP, a

decrease of 10 mm Hg or more in DBP.

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39
Q

hypertensive crisis

A

severe and abrupt elevation in BP, arbitrarily defined as a

DBP above 120 to 130 mm Hg.

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40
Q

hypertensive emergency

A

develops over hours to days, and is defined as BP that is

severely elevated with evidence of acute target-organ damage.

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41
Q

hypertensive urgency

A

develops over days to weeks, and is defined as a BP that is

severely elevated but with no clinical evidence of target organ damage.

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42
Q

artherosclerosis

A

a focal deposit of cholesterol and lipids within
the intimal wall of the artery. Inflammation and endothelial injury play a central role
in the development of atherosclerosis. It is the major cause of CAD.

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43
Q

fatty streaks

A

the earliest lesions of atherosclerosis, are characterized by lipid-
filled smooth muscle cells. As streaks of fat develop within the smooth muscle
cells, a yellow tinge appears.

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44
Q

fibrous plaque stage

A

beginning of progressive changes in the
endothelium of the arterial wall. These changes can appear in the coronary
arteries by age 30 and increase with age. LDLs and growth factors from platelets stimulate smooth muscle proliferation and thickening of the arterial wall.

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45
Q

complicated lesion

A

the final and most dangerous stage. As the fibrous plaque
grows, continued inflammation can result in plaque instability, ulceration, and rupture. Once the integrity of the artery’s inner wall is compromised, platelets
accumulate in large numbers, leading to a thrombus.

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46
Q

the growth and extent of collateral circulation are attributed to two factors

A

(1) the inherited predisposition to develop new blood vessels (angiogenesis), and (2) the presence of chronic ischemia.

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47
Q

modifiable risk factors of CAD

A

elevated serum lipids, hypertension, tobacco use,
physical inactivity, obesity, diabetes, metabolic syndrome, psychological states (e.g., depression, acute and chronic stress, anxiety, hostility and anger),
homocysteine level, and substance use.

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48
Q

statin drugs

A

inhibiting the synthesis of cholesterol in the liver. Liver

enzymes must be regularly monitored.

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49
Q

niacin

A

highly effective in lowering LDL and
triglyceride levels by interfering with their synthesis. Niacin also increases HDL
levels better than many other lipid-lowering drugs.

50
Q

fibric acid derivatives

A

accelerating the elimination of very-low-density

lipoproteins (VLDLs) and increasing the production of apoproteins A-I and A-II.

51
Q

bile acid sequestrants

A

sequestrants increase conversion of cholesterol to bile acids and
decrease hepatic cholesterol content. The primary effect is a decrease in total
cholesterol and LDLs.

52
Q

angina

A

clinical manifestation of reversible myocardial ischemia. It is an unpleasant feeling, often described as a “constrictive,” “squeezing,” “heavy,” “choking,” or “suffocating” sensation. It is rarely sharp or stabbing, and it usually does not change with position or breathing.

53
Q

chronic stable angina

A

refers to chest pain that occurs intermittently over a long period with the same pattern of onset, duration, and intensity of symptoms.

54
Q

prinzmetals angina

A

a rare form of angina that often occurs at rest, usually in
response to spasm of a major coronary artery. When spasms occur, the patient
experiences angina and transient ST segment elevation.

55
Q

1st line med tx of angina

A

short acting nitrates

56
Q

common diagnostics for a pt with CAD

A

chest
radiograph, a 12-lead ECG, laboratory tests (e.g., lipid profile); nuclear imaging;
exercise stress testing, and coronary angiography.

57
Q

acute coronary syndrome

A

develops when ischemia is prolonged and not immediately reversible. ACS encompasses the spectrum of unstable angina, non–ST-
segment–elevation myocardial infarction (NSTEMI), and ST-segment–elevation myocardial infarction (STEMI).

58
Q

ACS patho

A

associated with deterioration of a once-stable atherosclerotic plaque. This
unstable lesion may be partially occluded by a thrombus (manifesting as UA or NSTEMI) or totally occluded by a thrombus (manifesting as STEMI).

59
Q

unstable angina

A

chest pain that is new in onset, occurs at rest, or has a worsening pattern. UA is unpredictable and represents an emergency.

60
Q

myocardial infarction

A

(MI) occurs as a result of sustained ischemia, causing
irreversible myocardial cell death. Between 80 to 90% of all MIs are due to the
development of a thrombus that halts perfusion to the myocardium distal to the
occlusion.

61
Q

most common complication after MI

A

dysrhythmias, and

dysrhythmias are the most common cause of death in patients in the prehospitalization period.

62
Q

complications after MI

A

HF, cardiogenic shock, papillary muscle dysfunction, papillary muscle rupture, ventricular aneurysm, pericarditis

63
Q

primary diagnostic studies used to determine whether someone has UA or MI

A

ECG, serum cardiac markers, and coronary angiography. Other measures include exercise stress testing and echocardiography

64
Q

cardiac catheterization is used to

A

locate and assess blockage and implement treatment modalities if needed.

65
Q

fribrinolytic therapy aims to

A

stop infarction process by dissolving the thrombus in the coronary artery to reperfuse the myocardium.

66
Q

coronary revascularization

A

(an intervention to restore blood flow to the affected
myocardium) with coronary artery bypass graft (CABG) or PCI surgery is
recommended for patients who (1) do not achieve satisfactory improvement with
medical management, (2) have left main coronary artery or three-vessel disease, (3)
are not candidates for PCI (e.g., lesions are long or difficult to access), (4) have failed
PCI with ongoing chest pain, (5) have diabetes mellitus, or (6) are expected to have
longer-term benefits with CABG than with PCI.

67
Q

nursing mgt of angina

A

(1) administration of supplemental oxygen, (2) measurement of vital signs,
(3) 12-lead ECG, (4) prompt pain relief, first with a nitrate and followed by an opioid
analgesic if needed, (5) auscultation of heart sounds, and (6) comfortable positioning of the patient.

68
Q

cardiac rehab restores a pt to an optimal state of function in 6 areas:

A

physiological, psychological, mental, spiritual, economic, and vocational.

69
Q

sudden cardiac death

A

involves an abrupt disruption in cardiac function, producing an abrupt loss of cardiac output and cerebral blood flow. Death usually occurs within 1 hour of the onset of acute symptoms (e.g., angina, palpitations).

70
Q

risk factors for SCD

A

male gender (especially Black men), family history of
premature atherosclerosis, tobacco use, diabetes mellitus, hypercholesterolemia,
hypertension, and cardiomyopathy.

71
Q

heart failure

A

is an abnormal clinical
syndrome involving impaired cardiac pumping and/or filling. Not all patients with HF
will have pulmonary congestion or volume overload.

72
Q

HF chracteristics

A

ventricular dysfunction, reduced exercise tolerance,

diminished quality of life, and shortened life expectancy.

73
Q

Heart failure with reduced ejection fraction (HF-REF),

A

the most common
form of HF, results from an inability of the heart to pump blood effectively. It is
caused by impaired contractile function (e.g., myocardial ischemia), increased
afterload (e.g., hypertension), cardiomyopathy, and mechanical abnormalities
(e.g., valvular heart disease).

74
Q

Heart failure with preserved ejection fraction (HF-PEF)

A

often referred to as
diastolic HF—is the inability of the ventricles to relax and fill during diastole.
Decreased filling of the ventricles results in decreased stroke volume and cardiac
output (CO).

75
Q

most common form of initial HF

A

left sided failure

76
Q

primary cause of right sided failure

A

left sided failure

77
Q

acute decompensated hf manifests as

A

pulmonary
edema, an acute, life-threatening situation in which the lung alveoli become filled
with serous or serosanguineous fluid.

78
Q

clinical s&s of hf

A

fatigue, dyspnea (including paroxysmal nocturnal
dyspnea, which occurs when the patient is asleep and is caused by the reabsorption of
fluid from dependent body areas when the patient is lying flat), tachycardia, edema,
nocturia, skin changes, behaviour changes, chest pain, and weight changes.

79
Q

complications of hf

A

Pleural effusion, dysrhythmias, left ventricular thrombus formation, hepatomegaly,
and renal failure

80
Q

goal of therapy for acute decompensated hf and pulmonary edema

A 
improve ventricular
function by decreasing intravascular volume, decreasing venous return (preload),
decreasing afterload, improving gas exchange and oxygenation, and increasing CO.
81
Q

cardiac resynchronation therapy

A

involves pacing
both the right and left ventricles to achieve coordination of right and left ventricle
contractility.

82
Q

Intra-aortic balloon pump

A

used for short-term support for HF
patients with acute decompensation; however, the limitations of bed rest,
infection, and vascular complications preclude long-term use.

83
Q

Ventricular assist devices (VADs)

A

effective long-term support for up to 2 years

and have become standard care for acutely decompensated transplant candidates.

84
Q

drug management of hf

A

include: (1)
identification of the type of HF and underlying causes, (2) correction of sodium and
water retention and volume overload, (3) reduction of cardiac workload, (4)
improvement of myocardial contractility, and (5) control of precipitating and
complicating factors.

85
Q

goals of vasodilators in hf

A

(1) increasing venous capacity,
(2) improving EF through improved ventricular contraction, (3) slowing the
process of ventricular dysfunction, (4) decreasing heart size, and (5) avoiding
stimulation of the neuro-hormonal responses initiated by the compensatory
mechanisms of HF.

86
Q

overall goals of hf pt

A

(1) a decrease in peripheral edema,
(2) a decrease in shortness of breath, (3) an increase in exercise tolerance, (4)
adherence to the drug regimen, and (5) no complications related to HF.

87
Q

max acceptable time from harvesting the donor heart to transplantation

A

4-6 hours

88
Q

a normal cardiac impulse begins in the

A

SA node in the upper right atrium

89
Q

components of the ans that effect the hr are

A

right and left vagus nerve fibres of the psns and fibres of the sns

90
Q

The electrocardiogram

A

graphic tracing of the electrical impulses

produced in the heart.

91
Q

ECG waveforms are produced by

A

movement of charged ions across the

membranes of myocardial cells, representing repolarization and depolarization.

92
Q

p wave

A

depolarization of the atria (passage of an electrical

impulse through the atria), causing atrial contraction.

93
Q

pr interval

A

time period for the impulse to spread through the

atria, AV node, bundle of His, and Purkinje fibres.

94
Q

qrs complex

A

depolarization of the ventricles (ventricular

contraction), and the QRS interval represents the time it takes for depolarization.

95
Q

st segment

A

time between ventricular depolarization and
repolarization. This segment should be flat, or isoelectric, and represents the
absence of any electrical activity between these two events.

96
Q

t wave

A

repolarization of the ventricles.

97
Q

qt interval

A

the total time for depolarization and repolarization of

the ventricles.

98
Q

automaticity

A

property of specialized cells of the heart found in the (SA) node,
parts of the atria, the atrioventricular (AV) node, and the His–Purkinje system that are
able to discharge spontaneously.

99
Q

electrophysiological study (EPS)

A

identifies different mechanisms of

tachydysrhythmias, heart blocks, bradydysrhythmias, and causes of syncope.

100
Q

holter moniter

A

records the ECG while the patient is ambulatory and performing
daily activities.

101
Q

event monitors

A

recorders that are activated by the patient and can be used only
at the time the patient experiences symptoms.

102
Q

signal averaged ecg

A

a high-resolution ECG used to identify the patient at risk

for developing complex ventricular dysrhythmias.

103
Q

sinus bradycardia

A

the conduction pathway is the same as that in sinus rhythm, but
the SA node fires at a rate less than 60 beats/minute. This is referred to as absolute
bradycardia.

104
Q

sinus tachycardia

A

normal sinus rhythm, but the SA node fires at a rate greater

than 100 beats/minute as a result of vagal inhibition or sympathetic stimulation.

105
Q

premature atrial contraction

A

contraction originating from an ectopic

focus in the atrium in a location other than the sinus node.

106
Q

paroxysmal supraventricular tachycardia

A

a dysrhythmia originating in an ectopic focus anywhere above the bifurcation of the bundle of His.

107
Q

atrial flutter

A 
atrial tachydysrhythmia identified by recurring, regular, sawtooth-
shaped flutter (F) waves that originate from a single ectopic focus in the right atrium.
108
Q

atrial fibrillation

A

characterized by a total disorganization of atrial electrical
activity due to multiple ectopic foci resulting in loss of effective atrial contraction.

109
Q

junctional dysrhythmias

A

dysrhythmias that originate in the area of the AV
node, primarily because the SA node has failed to fire or the signal has been blocked.
In this situation, the AV node becomes the pacemaker of the heart.

110
Q

1st degree av block

A

type of AV block in which every impulse is

conducted to the ventricles but the duration of AV conduction is prolonged.

111
Q

2nd degree av block type 1

A

is a gradual lengthening of the PR interval. It occurs because of a prolonged AV
conduction time until an atrial impulse is nonconducted and a QRS complex is blocked (missing).

112
Q

2nd degree av block type 2

A

involves a P wave that is nonconducted without progressive antecedent PR lengthening. This almost always occurs when a block in one of the bundle branches is present.

113
Q

3rd degree av block

A

constitutes one form
of AV dissociation in which no impulses from the atria are conducted to the
ventricles.

114
Q

premature ventricular contraction

A

contraction originating in an ectopic
focus in the ventricles. It is the premature occurrence of a QRS complex, which is
wide and distorted in shape compared with a QRS complex initiated from the normal
conduction pathway.

115
Q

ventricular tachycardia

A

run of three or more PVCs. It occurs when an

ectopic focus or foci fire repetitively and the ventricle takes control as the pacemaker.

116
Q

ventricular fibrillation

A

severe derangement of the heart rhythm
characterized on ECG by irregular undulations of varying shapes and amplitude.
Mechanically the ventricle is simply “quivering,” and no effective contraction, and
consequently no CO, occurs.

117
Q

asystole

A

total absence of ventricular electrical activity. No ventricular
contraction occurs because depolarization does not occur.

118
Q

Synchronized cardioversion

A

therapy of choice for the patient with hemodynamically unstable ventricular or supraventricular tachydysrhythmias.
o A synchronized circuit in the defibrillator is used to deliver a countershock that is programmed to occur on the R wave of the QRS complex of the ECG.
o The synchronizer switch must be turned on when cardioversion is planned.

119
Q

Radiofrequency ablation therapy

A

An electrode-tipped ablation catheter is used to “burn” or ablate accessory pathways
or ectopic sites in the atria, AV node, and ventricles.

120
Q

Typical ECG changes seen in myocardial ischemia

A

ST-segment depression

and/or T wave inversion.

121
Q

typical ECG change seen during myocardial injury

A

ST-segment elevation.

Health Challenges (8 decks)

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