Week 3: Cardiovascular Flashcards
1
Q
3 layers of heart
A
endocardium, myocardium, epicardium
2
Q
mitral valve separates
A
left atrium and ventricle
3
Q
aortic valve seperates
A
left ventricle and aorta
4
Q
tricuspid valve separates
A
right atrium and right ventricle
5
Q
pulmonic valve separates
A
right ventricle and pulmonary artery
6
Q
systole
A
contraction of the myocardium, results in ejection of blood from the cardiac
chamber.
7
Q
diastole
A
relaxation of the myocardium, allows for filling of the chamber
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:
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
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).
11
Q
baroreceptors
A
Baroreceptors, located in the aortic arch and carotid sinus, respond to stretch or
pressure within the arterial system.
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.
13
Q
two main factors influencing bp
A
cardiac output, systemic vascular resistance
14
Q
electrocardiography
A
Deviations from the normal sinus rhythm can indicate abnormalities in heart
function.
15
Q
exercise or stress testing
A
to evaluate the cardiovascular response to physical stress.
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).
17
Q
nuclear cardiography
A
includes MUGA, SPECT, PET, CMRI, MRA
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).
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.
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.
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.
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.
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.
24
Q
hemodynamic monitering
A
Uses intra-arterial and pulmonary artery catheters to monitor arterial BP,
intracardiac pressures, CO, and central venous pressure (CVP).
25
nitric oxide helps
maintain
low arterial tone at rest, inhibits growth of the smooth muscle layer, and
inhibits platelet aggregation.
26
endothelin function
produced by the endothelial cells, is an extremely potent
| vasoconstrictor.
27
how do kidneys contribute to BP reg
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.
28
adrenal medulla function in bp
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.
29
pituitary function in bp
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.
30
isolated systolic hypertension
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.
31
primary hypertension
Elevated BP without an identified cause; this
| accounts for 90% to 95% of all cases of HTN.
32
secondary hypertension
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.
33
hemodynamic hallmark of hypertension
increased SVR
34
genetic factors account for
30-60% variability in BP
35
hypertension is a amjor risk factor for
coronary artery disease, cerebral atherosclerosis, and stroke
36
hypertension is one of the leading causes of
end stage renal disease
37
pt and caregiver teaching for hypertension
(1) nutritional therapy, (2)
drug therapy, (3) lifestyle modification, and (4) home monitoring of BP (if
appropriate).
38
orthostatic hypotension
defined as a decrease of 20 mm Hg or more in SBP, a
| decrease of 10 mm Hg or more in DBP.
39
hypertensive crisis
severe and abrupt elevation in BP, arbitrarily defined as a
| DBP above 120 to 130 mm Hg.
40
hypertensive emergency
develops over hours to days, and is defined as BP that is
| severely elevated with evidence of acute target-organ damage.
41
hypertensive urgency
develops over days to weeks, and is defined as a BP that is
| severely elevated but with no clinical evidence of target organ damage.
42
artherosclerosis
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.
43
fatty streaks
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.
44
fibrous plaque stage
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.
45
complicated lesion
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.
46
the growth and extent of collateral circulation are attributed to two factors
(1) the inherited predisposition to develop new blood vessels (angiogenesis), and (2) the presence of chronic ischemia.
47
modifiable risk factors of CAD
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.
48
statin drugs
inhibiting the synthesis of cholesterol in the liver. Liver
| enzymes must be regularly monitored.
49
niacin
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
fibric acid derivatives
accelerating the elimination of very-low-density
| lipoproteins (VLDLs) and increasing the production of apoproteins A-I and A-II.
51
bile acid sequestrants
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
angina
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
chronic stable angina
refers to chest pain that occurs intermittently over a long period with the same pattern of onset, duration, and intensity of symptoms.
54
prinzmetals angina
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
1st line med tx of angina
short acting nitrates
56
common diagnostics for a pt with CAD
chest
radiograph, a 12-lead ECG, laboratory tests (e.g., lipid profile); nuclear imaging;
exercise stress testing, and coronary angiography.
57
acute coronary syndrome
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
ACS patho
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
unstable angina
chest pain that is new in onset, occurs at rest, or has a worsening pattern. UA is unpredictable and represents an emergency.
60
myocardial infarction
(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
most common complication after MI
dysrhythmias, and
| dysrhythmias are the most common cause of death in patients in the prehospitalization period.
62
complications after MI
HF, cardiogenic shock, papillary muscle dysfunction, papillary muscle rupture, ventricular aneurysm, pericarditis
63
primary diagnostic studies used to determine whether someone has UA or MI
ECG, serum cardiac markers, and coronary angiography. Other measures include exercise stress testing and echocardiography
64
cardiac catheterization is used to
locate and assess blockage and implement treatment modalities if needed.
65
fribrinolytic therapy aims to
stop infarction process by dissolving the thrombus in the coronary artery to reperfuse the myocardium.
66
coronary revascularization
(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
nursing mgt of angina
(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
cardiac rehab restores a pt to an optimal state of function in 6 areas:
physiological, psychological, mental, spiritual, economic, and vocational.
69
sudden cardiac death
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
risk factors for SCD
male gender (especially Black men), family history of
premature atherosclerosis, tobacco use, diabetes mellitus, hypercholesterolemia,
hypertension, and cardiomyopathy.
71
heart failure
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
HF chracteristics
ventricular dysfunction, reduced exercise tolerance,
| diminished quality of life, and shortened life expectancy.
73
Heart failure with reduced ejection fraction (HF-REF),
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
Heart failure with preserved ejection fraction (HF-PEF)
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
most common form of initial HF
left sided failure
76
primary cause of right sided failure
left sided failure
77
acute decompensated hf manifests as
pulmonary
edema, an acute, life-threatening situation in which the lung alveoli become filled
with serous or serosanguineous fluid.
78
clinical s&s of hf
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
complications of hf
Pleural effusion, dysrhythmias, left ventricular thrombus formation, hepatomegaly,
and renal failure
80
goal of therapy for acute decompensated hf and pulmonary edema
```
improve ventricular
function by decreasing intravascular volume, decreasing venous return (preload),
decreasing afterload, improving gas exchange and oxygenation, and increasing CO.
```
81
cardiac resynchronation therapy
involves pacing
both the right and left ventricles to achieve coordination of right and left ventricle
contractility.
82
Intra-aortic balloon pump
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
Ventricular assist devices (VADs)
effective long-term support for up to 2 years
| and have become standard care for acutely decompensated transplant candidates.
84
drug management of hf
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
goals of vasodilators in hf
(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
overall goals of hf pt
(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
max acceptable time from harvesting the donor heart to transplantation
4-6 hours
88
a normal cardiac impulse begins in the
SA node in the upper right atrium
89
components of the ans that effect the hr are
right and left vagus nerve fibres of the psns and fibres of the sns
90
The electrocardiogram
graphic tracing of the electrical impulses
| produced in the heart.
91
ECG waveforms are produced by
movement of charged ions across the
| membranes of myocardial cells, representing repolarization and depolarization.
92
p wave
depolarization of the atria (passage of an electrical
| impulse through the atria), causing atrial contraction.
93
pr interval
time period for the impulse to spread through the
| atria, AV node, bundle of His, and Purkinje fibres.
94
qrs complex
depolarization of the ventricles (ventricular
| contraction), and the QRS interval represents the time it takes for depolarization.
95
st segment
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
t wave
repolarization of the ventricles.
97
qt interval
the total time for depolarization and repolarization of
| the ventricles.
98
automaticity
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
electrophysiological study (EPS)
identifies different mechanisms of
| tachydysrhythmias, heart blocks, bradydysrhythmias, and causes of syncope.
100
holter moniter
records the ECG while the patient is ambulatory and performing
daily activities.
101
event monitors
recorders that are activated by the patient and can be used only
at the time the patient experiences symptoms.
102
signal averaged ecg
a high-resolution ECG used to identify the patient at risk
| for developing complex ventricular dysrhythmias.
103
sinus bradycardia
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
sinus tachycardia
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
premature atrial contraction
contraction originating from an ectopic
| focus in the atrium in a location other than the sinus node.
106
paroxysmal supraventricular tachycardia
a dysrhythmia originating in an ectopic focus anywhere above the bifurcation of the bundle of His.
107
atrial flutter
```
atrial tachydysrhythmia identified by recurring, regular, sawtooth-
shaped flutter (F) waves that originate from a single ectopic focus in the right atrium.
```
108
atrial fibrillation
characterized by a total disorganization of atrial electrical
activity due to multiple ectopic foci resulting in loss of effective atrial contraction.
109
junctional dysrhythmias
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
1st degree av block
type of AV block in which every impulse is
| conducted to the ventricles but the duration of AV conduction is prolonged.
111
2nd degree av block type 1
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
2nd degree av block type 2
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
3rd degree av block
constitutes one form
of AV dissociation in which no impulses from the atria are conducted to the
ventricles.
114
premature ventricular contraction
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
ventricular tachycardia
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
ventricular fibrillation
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
asystole
total absence of ventricular electrical activity. No ventricular
contraction occurs because depolarization does not occur.
118
Synchronized cardioversion
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
Radiofrequency ablation therapy
An electrode-tipped ablation catheter is used to “burn” or ablate accessory pathways
or ectopic sites in the atria, AV node, and ventricles.
120
Typical ECG changes seen in myocardial ischemia
ST-segment depression
| and/or T wave inversion.
121
typical ECG change seen during myocardial injury
ST-segment elevation.
