Block 5 Flashcards
(578 cards)
1
Q
Comprise the most prevalent serious disorders in industrialized nations
A
CARDIOVASCULAR DISEASES
2
Q
Age-adjusted death rates for coronary heart disease have declined by _____ in the last four decades in US
A
2/3
3
Q
Remain the most common cause of death: → 35% of all death → Almost 1 million death each year
A
CARDIOVASCULAR DISEASES
4
Q
→ ¼ of cardiac deaths are?
A
sudden (sudden cardiac death)
5
Q
Cardiovascular diseases was considered to be more common in?
A
men than in women
6
Q
Percentage of all deaths due to CVD is higher among?
A
women (43%) than men (37%)
7
Q
o Chest discomfort
A
Myocardial ischemia
8
Q
Common symptoms of Heart Failure:
A
▪ Fatigue ▪ Peripheral Edema ▪ Dyspnea
9
Q
→ Obstruction to blood flow
A
o Valvular Stenosis → heart failure
10
Q
→ Abnormal cardiac rhythm or rate
A
o Palpitations o Dyspnea o Hypotension o Syncope
11
Q
Dyspnea
A
→ Pulmonary disease, marked obesity and anxiety
12
Q
Chest discomfort
A
→ Result from variety of non-cardiac and cardiac causes other than myocardial ischemia
13
Q
Edema
A
→ Primary renal disease and hepatic cirrhosis
14
Q
Syncope
A
→ Neurologic disorder
15
Q
CHARACTERISTIC FINDINGS OF CARDIAC PATIENTS
A
- Dyspnea/Chest Discomfort 2. Heart murmurs 3. Elevated arterial pressure 4. Abnormal ECG, CXR, and other imaging 5. Risk factors for CAD
16
Q
positive a wave on ECG
A
MI
17
Q
Biomarker for cardiac disease
A
C-reactive protein
18
Q
→ No limitation of physical activity → No symptoms with ordinary exertion → Mild form
A
Class I
19
Q
→ Slight limitation of physical activity → Ordinary activity causes symptoms o Patient is walking on a flat surface and experience difficulty of breathing
A
Class II
20
Q
→ Marked limitation of physical activity → Less than ordinary activity causes symptoms → Asymptomatic at rest
A
Class III
21
Q
→ Inability to carry out any physical activity without discomfort → Symptoms at rest → Worst classification for the patient to have
A
Class IV
22
Q
• Congenital Heart Disease • Ventricular Septal Defect • Perimembranous type • Qp:Qs Ratio = 1:2 (Measures pulmonary circulation and flow of blood in the circulation)
A
Functional Class II-B
23
Q
• Ischemic Heart Disease • S/P anterior wall myocardial infarction • Congestive Heart Failure
A
Functional Class III-C
24
Q
• Rheumatic Heart Disease • Mitral Stenosis(irreg cardiac rhythm) • Atrial Fibrillation • Pulmonary Hypertension (physiological dx)
A
Functional Class IV-E “worse final classification”
25
Mendellian transmission of single-gene defects
→ Hypertrophic cardiomyopathy, Marfan syndrome, long QT syndrome.
26
Failure by the noncardiologist to recognize important cardiac manifestations of systemic illnesses • Example: The presence of _______ in stroke.
mitral stenosis
27
Failure by the cardiologist to recognize underlying systemic disorders in patients with heart disease. • Example: ________ should be tested for in an elderly patient with atrial fibrillation and unexplained heart failure
Hyperthyroidism → Heart failure is just one of the clinical manifestations of hyperthyroidism.
28
Provide precise diagnostic information that is critical to clinical evaluation, which may be crucial in developing a therapeutic plan in patients with known or suspected CAD.
Cardiac catheterization and coronary arteriography
29
If the stress test is positive, request for?
Invasive coronary angiogram
30
Should not be carried out in lieu of a careful history in patients with chest pain suspected of having ischemic heart disease.
coronary arteriogram
31
Why should coronary arteriogram not be carried out in lieu of a careful history in patients with chest pain suspected of having ischemic heart disease?
Although coronary arteriography may establish whether the coronary arteries are obstructed, and if so the severity of the obstruction, the results of the procedure by themselves often do not provide a definite answer to the question of whether a patient’s complaint of chest discomfort is attributable to coronary arteriosclerosis and whether or not revascularization is indicated.
32
Asymptomatic or mildly symptomatic patients with valvular heart disease that is anatomically severe should be evaluated periodically, every \_\_\_\_\_\_\_\_\_, by clinical and noninvasive examinations.
6 to 12 months
33
Medical management for CAD
o Anti – anginal drugs o Antiplatelet or antithrombotic drugs o Statins
34
Percutaneous coronary intervention for CAD
Coronary angioplasty
35
Surgical revascularization
Coronary bypass surgery
36
Consist of an endothelial tube in contact with a discontinuous population of pericytes
Capillaries
37
Typically have thin medias and thicker adventitias
Veins
38
Consists of a prominent tunica media
Small muscular artery
39
Have a prominent media with smooth-muscle cells embedded in a complex extracellular matrix
Larger muscular arteries
40
Have circular layers of elastic tissue alternating with concentric rings of smooth-muscle cells
Larger elastic arteries
41
Smallest blood vessels
Capillaries
42
Consist of a monolayer of endothelial cells in close juxtaposition of occasional smooth muscle-like cells known as Pericytes
Capillaries
43
do not invest in the entire micro vessel to form a continuous sheath
Pericytes
44
the media can contain just a few layers of smooth-muscle cells
Veins
45
Have a Trilaminar structure
Arteries
46
→ Monolayer of endothelial cell → Continuous with those of the capillary trees
Tunica Intima
47
→ Middle layer → Layers of smooth-muscle cells
Tunica Media
48
In \_\_\_\_\_, the media can contain just a few layers of smooth muscle cells
veins
49
→ Consists of looser extracellular matrix → Occasional fibroblast, mast cells and nerve terminals
Tunica Adventitia
50
• have relatively thicker media relative to their adventitia
Smaller Arteries
51
• contain a prominent tunica media • Atherosclerosis commonly affects this type of muscular artery
Medium-size Arteries
52
• have a much more structural tunica media consisting of concentric bands of smooth-muscle cells interspersed with strata of elastin-rich extracellular matrix sandwiched between layers of smooth-muscle cells
Larger (elastic) Arteries
53
Veins: Tunica Media
contain a few layers of smooth muscle cells
54
Veins: Tunica Adventitia
(Some Veins) have thicker adventitia than intima
55
Arteries: Tunica Media
made-up of several layers of smooth muscle cells
56
Arteries: Tunica Adventitia
(Large Arteries) have their own vasculatures, the vasa vasorum, which nourishes the outer aspects of the tunica media
57
Often contains occasional resident smooth-muscle (SM) cells beneath the monolayer of vascular endothelial cells.
Intima
58
The embryonic origin of SM cells in arteries of the upper body is derived from?
neural crest
59
The embryonic origin of SM cells in arteries of the lower body is derived from?
mesodermal structures (somites)
60
\_\_\_\_\_\_\_ may also give rise to both vascular endothelial cells and SM cells.
Bone marrow
61
The cells of vascular intima
Endothelial cells (EC)
62
Forms the interface between tissues and blood compartment.
Endothelium
63
Regulates the entry of molecules and cells into the tissue in a selective manner.
Endothelium
64
Has the ability to serve as a permselective barrier.
Endothelium
65
Participates in the local regulation of the blood flow and diameter size of the blood vessel.
Endothelium
66
Vasodilators produced by the endothelium under physiologic conditions:
o Prostacyclin o Endothelium-derived hyperpolarizing factor (EDHF) o Nitric oxide (NO)
67
o Potent Vasoconstrictor o Occurs when there is Endothelial Dysfunction
Endothelin
68
Oxidative stress occurs when there is excessive production of reactive oxygen species, such as superoxide anion, by endothelial and SM cells under pathologic conditions such as excessive exposure to \_\_\_\_\_\_\_\_.
Angiotensin II
69
Oxidative stress may lead also to inactivation of?
NO
70
The endothelium produces more _________ if there is more endothelial dysfunction already.
The endothelium produces more vasoconstriction rather than vasodilation if there is more endothelial dysfunction already.
71
Contributes critically to inflammatory processes involved in normal host defenses and pathologic states.
Endothelial monolayer
72
The endothelial monolayer expresses _______ during infection and inflammatory process.
leukocytes adhesion molecules
73
Regulate thrombosis and hemostasis.
Endothelial monolayer
74
Both _____ and _____ limit and antagonize platelet activation and aggregation.
Both NO and prostacyclin limit and antagonize platelet activation and aggregation.
75
Through local generation of \_\_\_\_\_, the normal endothelial monolayer can promote the lysis of nascent thrombi.
plasmin
76
The endothelial cell surface contains ________ that furnish an endogenous antithrombin coating to the vasculature.
heparan sulfate glycosaminoglycans
77
It also participates actively in fibrinolysis and its regulation.
Endothelial cell surface
78
They express receptors for plasminogen activators and produce tissue-type plasminogen activator.
Endothelial cell surface
79
Homeostatic Phenotype of Endothelial Functions
o Vasodilation o Antithrombotic and Profibrinolytic o Anti-inflammatory o Anti-oxidant
80
Dysfunctional Phenotype of Endothelial Functions
o Impaired dilatation, vasoconstriction o Prothrombotic and Antifibrinolytic o Pro-inflammatory o Proproliferative o Prooxidant
81
Forearm circulation is assessed by performing occlusion of the ______ artery flow with BP cuff, after which the cuff is deflated.
brachial artery Assess the change in brachial artery diameter and blood flow using ultrasound (Doppler)
82
Use of agonists that stimulate release of endothelial NO
→ Acetylcholine → Methacholine
83
• The increase in vessel diameter size of at least 10%. • Increase in blood flow. • Reactive Hyperemia
Normal
84
• Endothelial dysfunction • Smaller increase in diameter (less than 10%) • In extreme cases - paradoxical vasoconstriction
Abnormal Results
85
Major cell type of the media layer of the blood vessels
VASCULAR SMOOTH MUSCLE CELL
86
→ Controls the Blood pressure → Regional blood flow → Left Ventricular afterload
Smooth Muscle Cell Contraction and Relaxation
87
→ Venous capacitance → Influence the venous return of both ventricles
Venous Smooth Muscle Cells
88
Proliferation and Migration of Arterial Smooth Muscle Cells contribute to development of?
Arterial Stenosis
89
Cerebral vascular disease
ischemic stroke
90
Coronary artery disease
Stable angina and Acute Coronary Syndrome
91
Angioplasty and stent deployment
Post-PCI restenosis (percutaneous coronary intervention)
92
The principal function of the vascular SM cells is to?
maintain vessel tone
93
Vascular SM cells contract when stimulated by a rise in?
intracellular calcium concentration after calcium influx through the plasma membrane and release from intracellular stores.
94
open during membrane depolarization
Voltage-dependent L-type calcium channels
95
Voltage-dependent L-type calcium channels are regulated by:
o Na+ , K+ -ATPase pump o Ca 2+ sensitive K+ ion channel
96
Vascular SM cell contraction is principally controlled by?
the phosphorylation of myosin light chain
97
The steady state is maintained by the balance between the actions of?
myosin light chain kinase & myosin light chain phosphatase
98
Myosin light chain kinase is activated by calcium through the formation of?
calcium-calmodulin complex
99
SM contraction is sustained due to increased myosin ATPase activity brought about by?
myosin light chain phosphorylation
100
\_\_\_\_\_\_\_\_\_, in contrary would reduce SM cells contractile force
Myosin light chain dephosphorylation
101
Both cAMP and cGMP _____ vascular SM cells
relax
102
Baroreceptors and chemoreceptors are found in?
within the aortic arch and carotid bodies
103
Thermoreceptors are found in?
the skin
104
Effect of NO
potent vasodilator
105
Process of growing new blood vessels that can occur in response to chronic hypoxia and tissue ischemia.
Angiogenesis
106
a signaling cascade is activated that stimulates endothelial proliferation and tube formation
Vascular Endothelial Growth Factor
107
About ¾ of the ventricle is composed of?
Individual striated muscle cells (myocytes/ cardiomyocytes) → Length: 60-140 um → Diameter: 17-25 um
108
• Multiple, rodlike crossbanded strands found in each cell that run the length of the cell and are, in turn, composed of serially repeating structures, the sarcomeres • Numerous mitochondria
Myofibrils
109
The sliding filament model for muscle contraction rests on: → The fundamental observation that?
both the thick and thin filaments are constant in overall length during both contraction and relaxation
110
During activation: → The actin filaments are propelled further into the \_\_\_\_\_\_
A band
111
In the process: → Describe the length of the A band, I band and Z line
The A band remains constant in length, whereas the I band shortens and the Z line move toward one another
112
It is the volume that decreases by about 70 milliliters as the ventricles empty during systole
Stroke Volume (SV)
113
amount of blood ejected by your left ventricle into the aorta during contraction in a single cardiac cycle
Stroke Volume (SV)
114
Stroke Volume (SV) =
Stroke Volume (SV) = (end diastolic volume) - (end systolic volume)
115
the volume of each ventricle that increases to about 110 to 120 milliliters during diastole
End-diastolic Volume
116
the remaining volume in each ventricle, about 40 to 50 milliliters,
End-systolic Volume
117
Cardiac Output (CO) =
Cardiac Output (CO) = (SV) x (Heart rate (HR)
118
Blood Pressure (BP) =
Blood Pressure (BP) = (CO) x PVR (peripheral vascular resistance)
119
3 DETERMINANTS OF VENTRICULAR STROKE VOLUME:
1. Length of the muscle at the onset of contraction (preload) 2. Tension that the muscle is called upon to develop during contraction (afterload) 3. Contractility of the muscle (extent and velocity of shortening at any given preload and afterload)
120
Determines the: → length of the sarcomere at the onset of the contraction → The relation between the initial length of the muscle fibers → and the developed force has prime importance for the function of the heart muscle
Preload
121
“Starling’s Law” of the heart
the force of ventricular contraction depends on the end-diastolic length of the cardiac muscle
122
is sometimes used as a surrogate for the end-diastolic volume
Ventricular end-diastolic or filling pressure
123
The load that opposes the shortening of the muscles
VENTRICULAR AFTERLOAD
124
May be defined as the tension developed in the ventricular wall during ejection
VENTRICULAR AFTERLOAD
125
The extent/velocity of shortening of the ventricular muscle fibers at any level of preload and of myocardial contractility is ________ related to the afterload
inversely
126
Determinants of ventricular afterload:
→ Aortic pressure → Ventricular volume → Ventricular wall thickness
127
→ Indicates that the tension of the myocardial fiber is a function of the product of intracavitary ventricular pressure and the ventricular radius divided by the wall thickness
Law of Laplace
128
Determinants of Aortic Pressure
→ Peripheral vascular resistance → Physical characteristics of the arterial tree o The degree of stiffness of the arteries → The volume of blood it contains at the onset of ejection
129
EXERCISE • Interactions among 3 determinants of stroke volume
→ Increase (↑) in preload o Hyperventilation, pumping action of exercising muscle and vasoconstriction -increase in venous return and ventricular filling → Decrease (↓) in afterload o Arterial vasodilation in exercising muscles → Increase (↑) in contraction o Inc. in circulating catecholamines
130
Ventricular Preload: Lying Position
(↑) ventricular preload
131
Ventricular Preload: (↑) Intrathoracic pressure
can reduce (↓) preload
132
Ventricular Preload: Intrapericardial pressure
can also reduce (↓) preload
133
Ventricular Preload: (↑) venous tone= (↑) venous return
(↑) preload
134
Ventricular Preload: (↑) Pumping action
(↑) preload
135
Ventricular Afterload: Systemic vascular resistance = Arteriolar Constriction = (↑) arterial tone
(↑) afterload
136
Ventricular Afterload: Reduced elasticity of arterial tree (In case of atherosclerosis)
(↑) afterload
137
Ventricular Afterload: (↑)Elasticity
(↓) afterload
138
Ventricular Afterload: Arterial blood volume
(↑) afterload
139
Ventricular Afterload: Ventricular wall tension “law of laplace” (↑) of ventricular radius (dilated ventricle) ↓ (↑) ventricular tension
(↑) afterload
140
Qp:Qs Ratio- measures?
pulmonary circulation and flow of blood in the circulation
141
More sensitive index of cardiac function
EJECTION FUNCTION (EF)
142
Ratio of SV to end-diastolic volume
EJECTION FUNCTION (EF)
143
Normal value of ejection function
67 ± 8%
144
Systolic function
EJECTION FUNCTION (EF)
145
ELEVATED VENTRICULAR END-DIASTOLIC VOLUME • Normal value = ?
75 ± 20ml/m2
146
ELEVATED VENTRICULAR END-SYSTOLIC VOLUME • Normal value = ?
25 ± 7ml/m2
147
NON-INVASIVE TECHNIQUES OF MEASURING EJECTION FRACTION
• Echocardiography • Radionuclide scintigraphy (nuclear medicine) • Cardiac MRI
148
• Useful index of ventricular performance • Results are not dependent on the degree of preload and afterload
END-SYSTOLIC LEFT VENTRICULAR PRESSURE VOLUME RELATIONSHIP
149
Assessment of ventricular filling
DIASTOLIC FUNCTION
150
Increase in ventricular stiffness
→ Ventricular hypertrophy → Amyloid infiltration of the ventricle
151
Continuously Measuring The Velocity of Blood Flow Across The Mitral Valve Using Doppler Ultrasound
DIASTOLIC FUNCTION
152
4 causes of increase pressure in the right atrium and the jugular venous pressure:
1. Heart failure 2. Fluid overload 3. Constrictive pericarditis 4. Cardiac tamponade
153
Jugular venous pressure is assessed by looking at what vein?
Right internal jugular vein visualized between the medial clavicle and the earlobe. It runs underneath the sternocleidomastoid muscle.
154
Is the external jugular vein medial or lateral to the internal jugular vein?
Lateral
155
Indirectly measures pressure in the right atrium and the venous system.
JVP
156
Increase right atrium (RA) pressure = ?
increase JVP
157
Why do we use the right internal jugular vein?
We use Right IJV because it is located most directly above the right atrium. It can give the best indication of what is happening in the right atrium.
158
How to visualize the JVP?
→ Have the patient sit on their back at angle 45 degrees and turn head slightly to the left. → Useful to shine light diagonally across patient’s neck so that you can see the change in shadows as you get the JVP pulsation. → Pulsation is like a wave in the neck with 2 pulses per heartbeat. More of a flutter underneath the SCM muscle. → Distinguished from carotid pulse in 2 ways: o 2 pulses per heartbeat o No palpable pulsation
159
Hepatojugular reflex
Press over the liver or right upper quadrant (RUQ) of the abdomen, cause temporary rise of JVP
160
How to measure the height of JVP?
→ On the sternal angle, measure vertically from this point and assess where JVP is. → On the vertical height from sternal angle to the level of JVP is the height of the JVP.
161
Normal JVP Height
Less than 3 cm
162
5 parts of JVP waveform
1. A wave 2. X descent o 1st part of X descent o 2nd part of X descent 3. C wave 4. V wave 5. Y descent
163
Happening during ATRIAL CONTRACTION
A WAVE
164
What causes A wave?
→ Right atrium is contracting against blood that’s inside it then pushes blood into tricuspid valve to the right ventricle. Increase pressure of right atrium not only pushes blood downwards but also upwards. → Level of the blood in the IJV rises. This rise is the A WAVE.
165
Is caused by RELAXATION OF THE ATRIA, and the blood flows into the relax atria from the IJV and causes a drop of JVP.
1st X DESCENT
166
What causes the 1st X descent?
→ Is caused by RELAXATION OF THE ATRIA, and the blood flows into the relax atria from the IJV and causes a drop of JVP. → At the start of, X descent, there is also a blood that flows from the atria into the ventricles to complete the ventricular filling, leading to fall of JVP.
167
→ At the start of systolic contraction, the right ventricle contracts and squeezes blood out into the pulmonary artery. → This pressure pushes up against the close tricuspid valve and cause to bulge slightly into tha atria. → This pressure into the atria from that bulging tricuspid valve extend in SVC (superior vena cava) into IJV (Internal Jugular Vein) and creates rise in JVP called?
C wave
168
Is caused by the final parts of the Right VENTRICULAR CONTRACTION where it squeeze so small that creates space in the pericardium or the sack that fills the heart for the right ventricle to fill.
2nd X DESCENT
169
→ Ventricles become very small and create more space inside that sack so that atrium has space to fill out. → This sack is like a vacuum and ventricle shrinks and creates space inside the pericardium for atria to fill. So they expand and suck in blood and causing JVP to fall.
2nd X DESCENT
170
→ Happens when ATRIA RELAXES and right atrium starts to fill with blood. At this point tricuspid valve is still closed at the end of the systolic contraction of the ventricles. → So as the atria fills completely, this filling starts to occur higher up into the SVC, IJV and as a result JVP rises. It is called the?
V wave
171
→ Occurs when the tricuspid valve opens and all the blood flows from the right atrium into the right ventricle. This emptying of the right atria causes JVP to fall. → At this point, whole cycle restarts and the atria contracts and cause an a wave and so on.
Y DESCENT
172
It is cause by atrial contraction, causing atrial pressure to rise forcing blood flow both downward and upward into the JVP.
A WAVE
173
Starts with the relaxation of the atria and the blood flows back into the atrium.
1st X DESCENT
174
Caused by Right ventricular contraction causing the tricuspid to bulge into the right atria.
C WAVE
175
Caused by right ventricular contraction causing the right ventricles to take up less room and the atria to expand and fill the space left by the right ventricle and drain blood from IJV.
2nd X DESCENT
176
Caused by Right atrium filling up with blood and in turn the SVC and IJV filling with blood.
V WAVE
177
Caused by opening of tricuspid valve and emptying of the right atrium.
Y Descent
178
Absent A waves Example:
→ Atrial fibrillation. o The right atrium is not contracting in a coordinated way. The coordinated atrial contraction is what causes A waves
179
Large A waves Examples:
→ Right ventricular hypertrophy → Pulmonary hypertension → Pulmonary stenosis → Tricuspid stenosis o Cause by anything that makes flow from RA to RV more difficult because atria will be contracting against resistance and this will cause more blood to flow upwards because it can’t flow downwards.
180
Large V waves Example:
→ Tricuspid regurgitation - Right ventricular contraction will lead to blood flowing back thru the tricuspid valve and up into the right atrium, SVC and IJV - Will also cause loss of X descent because the ventricular contraction increases the pressure into the right atria rather than relieving it because the blood is trying to go back into the tricuspid valve to the RA.
181
Rarely palpable compared to carotid pulse. It has soft, bi-phasic, angulating quality with 2 elevation and inward deflection.
IJV
182
More vigorous thrust with single outward component.
carotid
183
Eliminated by light pressure in the vein just above the sternal and the clavicle
IJV
184
Not eliminated by pressure in vein at sternal end of clavicle
carotid pulsation
185
Height of pulsation of IJV changes with pulsation normally dropping as the patient _________ but in carotid it is unchanged.
becomes more upright
186
The height of pulsation usually _____ with inspiration in IJV while in carotid is not affected.
falls
187
Waves part of diastole
A and C wave is part of diastole
188
Waves part of systole
X and V wave is part of systole
189
Atrial contraction
A wave
190
Bulging of tricuspid valve
C wave
191
Atrial relaxation
X descent
192
Atrial filling
V wave
193
Followed by a drop in the pressure
Y descent
194
Best way to palpate carotid
→ Just below the caudal portion of the neck (rather than in the higher portion because it’s covered by the SCM muscle)
195
best heard carotid bruit
In the middle portion of the neck
196
Pressure within the thoracic vena cava just before the RA. The SVC and the connecting jugular veins act as a column of blood as which the CVP can be approximated by determining the JVP. This is done by measuring the elevation of the neck veins above the sternal angle and correlating it to the height of the blood column in cm of water.
Central Venous Pressure (CVP)
197
Best in examining jugular venous pressure because it is directly connected to the RA.
right side IJV
198
Can the external jugular vein be used in examining the central venous pressure?
The exam can also be performed in the EJV but they often branch at right angles which can interfere with the test results.
199
How to examine central venous pressure?
At the beginning of the test; → Patient should be recumbent with the head turned slightly to the left. The jugular veins are now at the same level as the RA and should be significantly distended under physiological conditions. → The jugular veins present with the regular pulse featuring a twin peak. The IJV pulsations are not readily observable because it lies deeper within the neck. Its pulsation, the weak, can be observed ventro-medial to the EJV. → The CVP or the height of the column above the RA can now be estimated by slowly raising patient’s upper body by 30 to 45 degrees. → As soon as the distention of the jugular vein starts to decrease halt the movement of the patient upper body and locate the most cranial point at which jugular vein is still distended. → The vein now functions a as nanometer that represent CVP. → Draw and imagine horizontal line toward the sternum starting at the most cranial point to at which the vein is still distended. → Since the sternal angle lies about 5 cm above the level of the RA, add those 5 cm to the measured distance. The sum roughly measures the CVP measured in cm of H2O
200
Normal CVP
4 to 10 cm of H2O
201
Is a CVP of 10 considered high?
If sum is greater that 10 cm the CVP is considered too high as seen in heart failure, hypovolemia or pulmonary embolism.
202
Lub
S1
203
Caused by the closing of the atrioventricular valves (the tricuspid and mitral valves) at the start of the systolic contraction of the ventricles.
S1
204
As the ventricles try to push blood out of the heart, the valves between the atria and the ventricles need to close to prevent blood from flowing back to the atria.
S1
205
Dub
S2
206
Caused by the closing or the semilunar valves (the pulmonary and aortic valves) once the systolic contraction is complete. This is to prevent blood from flowing back to the pulmonary arteries or the aorta into the ventricles.
S2
207
Lub de dub
S3
208
A third heart sound (S3) is heard roughly ___ second after the second heart sound.
0.1 second
209
Think of it as rapid ventricular filling causing the chordae tendineae to pull to their full length and twang like a guitar string.
S3
210
S3 is seen normally in?
This can be normal in young (15-40 years) healthy people because the heart functions so well that the ventricles easily allow rapid filling.
211
What does S3 indicate on older patients?
In older patients it can indicate heart failure, as the ventricles and chordae are stiff and weak so they reach their limit much faster than normal. Picture this like tight hamstrings in an old de-conditioned patient sharply tightening as they start to bend over.
212
Le lub dub
S4
213
A fourth heart sound (S4) is heard directly before \_\_\_.
S1
214
This is always abnormal and relatively rare to hear.
S4
215
It indicates a stiff or hypertrophic ventricle and is caused by turbulent flow from an atria contracting against a non-compliant ventricle. The ventricles are really stiff and the atria are trying to force blood in that causes a turbulent flow.
S4
216
“It’s also common to patients with hypertension, ischemic heart disease and coronary artery disease. ”
S4
You can hear S4 brought about by elevated left ventricular pressure
217
Significance of a loud S2 Is presence of?
pulmonary hypertension
218
How to use the stethoscope when listening to heart murmurs?
Auscultate with the bell of your stethoscope to better hear low pitched sounds and the diaphragm to listen to high pitched sounds. To remember this think of a child’s high-pitched screaming from their diaphragm versus a church bell giving a deep “bong”.
219
Aortic
2nd ICS Right Sternal border
220
Pulmonic
2nd ICS Left Sternal border
221
Tricuspid
5th ICS Left Sternal border
222
Mitral
5th ICS Mid-clavicular line (Apex area)
223
If you have a mitral regurgitation, you expect your ________ to dilate because of the regurgitated blood coming from the left ventricle coming back and forth to your left atrium. Because of that you have a dilated left ventricle. Likely the point of the maximum impulse is not on the 5th ICS (mitral area) but it would be on the?
left atrium 6th ICS left anterior axillary line
224
If you have aortic regurgitation, you have a dilated \_\_\_\_\_\_\_\_. But in this case of aortic regurgitation, it can be heard to your mitral going to your aortic valve. This refers to the _________ of the mitral valve going to your aortic area.
left ventricle “aortic sash area”
225
Remember when you’re dealing with aortic stenosis, you could also hear a systolic murmur. It starts in the mitral valve going towards the aortic area with radiation to your \_\_\_\_\_\_\_.
carotids
226
A murmur involving your atrial septum is usually located in the?
2nd or 3rd ICS left sternal boarder
227
A ventricular septal murmur (systolic), can be heard in the?
3rd or 4th ICS left sternal boarder
228
This is in the third intercostal space on the left sternal boarder and is the best area for listening to heart sounds (S1, S2, S3 and S4)
Erb’s Point
229
Special maneuvers can be used to emphasize certain murmurs: o mitral stenosis
Patient on their left hand side
230
Special maneuvers can be used to emphasize certain murmurs: o aortic regurgitation
Patient sat up, leaning forward and holding exhalation
231
Assessing a Murmur (SCRIPT): S
Site: Where your murmur is loudest?
232
Assessing a Murmur (SCRIPT): C
Character: soft/ blowing/ crescendo (getting louder)/ decrescendo (louder then quieter)
233
Assessing a Murmur (SCRIPT): R
Radiation: can you hear the murmur over the carotids (AS) or left axilla (MR)?
234
Assessing a Murmur (SCRIPT): I
Intensity: what grade is the murmur?
235
Assessing a Murmur (SCRIPT): P
Pitch: Is it high pitched or low and grumbling? Pitch indicates velocity
236
Assessing a Murmur (SCRIPT): T
Timing: Is it Systolic or Diastolic?
237
Grade of Murmurs: 1
Difficult to hear
238
Grade of Murmurs: 2
Quiet
239
Grade of Murmurs: 3
Easy to hear
240
Grade of Murmurs: 4
Easy to hear with palpable thrill
241
Grade of Murmurs: 5
Can hear with stethoscope barely touching the chest
242
Grade of Murmurs: 6
Can hear with stethoscope off the chest
243
This patient has a harsh / soft / blowing, Grade …, systolic / diastolic murmur, heard loudest in the aortic / mitral tricuspid / pulmonary area, that does not / radiates to the carotids / left axilla. It is high / low pitched and has a crescendo / decrescendo / crescendo-decrescendo shape. This is suggestive of a diagnosis of ?
mitral stenosis / aortic stenosis
244
Mitral stenosis causes?
left atrial hypertrophy
245
Aortic stenosis causes?
left ventricular hypertrophy
246
Mitral regurgitation causes?
left atrial dilatation
247
Aortic regurgitation causes?
left ventricular dilatation
248
Is when an incompetent mitral valve allows blood to lead back through during systolic contraction of the left ventricle.
Mitral regurgitation
249
Mitral regurgitation results in ________ because the leaking valve causes a reduced ejection fraction and a backlog of blood that is waiting to be pumped through the left side of the heart.
congestive cardiac failure
250
It causes a pan-systolic, high pitched “whistling” murmur due to high velocity blood flow through the leaky valve. The murmur radiates to left axilla.
Mitral regurgitation
251
The radiation of your mitral regurgitation is usually at the __________ especially if it involves the anterior mitral valve leaflet.
back or at the axilla The non-quotation of the mitral valve causes the direction of the flow towards the back or the axilla.
252
If you have a flailing posterior mitral valve leaflet, the direction of the flow is \_\_\_\_\_\_\_.
anteriorly Which means the pan-systolic murmur is best heard in the anterior portion or in the area of your tricuspid valve (4th ICS left parasternal boarder)
253
You may hear a third heart sound in?
MITRAL REGURGITATION
254
Causes of mitral regurgitation:
→ Idiopathic weakening of the valve with age → Ischaemic heart disease → Infective Endocarditis → Rheumatic Heart Disease → Connective tissue disorders such as Ehlers Danlos syndrome or Marfan syndrome
255
“Burr”
mitral regurgitation
256
The most common valve disease you will encounter.
Aortic stenosis
257
Narrow Aortic Valve
Aortic stenosis
258
It causes an ejection-systolic, high pitched murmur (high velocity of systole).
Aortic stenosis
259
The high pitch murmur which is common in the erderly is sometimes called a “cooing murmur”
Aortic stenosis
260
Diamond shaped murmur
Aortic stenosis
261
This has a crescendo-decrescendo character due to the speed of blood flow across the value during the different periods of systole.
Aortic stenosis
262
The differential diagnosis for aortic stenosis is?
hypertrophic cardiomyopathy
263
The presentation looks like an aortic stenosis EXCEPT THAT IT DOES NOT RADIATE TO THE CAROTIDS because the obstruction is in the left ventricular outflow tract. IT DOESN’T INVOLVE YOUR AORTIC VALVE.
hypertrophic cardiomyopathy
264
Flow during _____ is slowest at the very start and end and fastest in the middle.
systole
265
Other signs of aortic stenosis?
→ The murmur radiates to the carotids as the turbulence continues up into the neck → Slow rising pulse → Narrow pulse pressure → Patients may complain of exertional syncope (light headedness and fainting when exercising) due to difficulty maintaining good flow of blood to the brain
266
Causes of aortic stenosis?
→ Idiopathic age related calcification → Rheumatic Heart Disease
267
“Burr Dub”
Aortic stenosis
268
Aortic Valve Incompetent
AORTIC REGURGITATION
269
Typically causes an early diastolic, soft murmur
AORTIC REGURGITATION
270
Aortic regurgitation is also associated with a _________ pulse.
Corrigan’s pulse
271
A Corrigan’s pulse is also called a?
collapsing pulse
272
Is a rapidly appearing and disappearing pulse at carotid as the blood is pumped out by the ventricles and then immediately flows back through the aortic valve back into the ventricles.
Corrigan’s pulse
273
Aortic regurgitation results in ______ due to a back pressure of blood waiting to get through the left side of the heart.
heart failure
274
It can also cause an “Austin-Flint” murmur.
Aortic regurgitation
275
This is heard at the apex and is an early diastolic “rumbling” murmur.
“Austin-Flint” murmur
276
This is caused by blood flowing back through the aortic valve and over the mitral valve causing it to vibrate.
“Austin-Flint” murmur
277
Causes of aortic regurgitation?
→ Idiopathic age related weakness → Connective tissue disorders such as Ehlers Danlos syndrome or Marfan syndrome
278
“Lub Tarrr”
aortic regurgitation
279
A wave that is produced by cardiac systole traversing peripheral direction in the arterial tree at a rate faster than the column of blood
ARTERIAL PULSE
280
A wave being produce in the arteries which is transmitted in the arteries
Ventricular Systole
281
A peripheral transferring wave is felt as the arterial pulse with three fingers:
→ Index → Middle → Ring
282
Pulses that you can palpate:
→ Radial → – best suited for contour, volume and Brachial consistency → Carotid → Popliteal → Femoral → Posterior Tibial → Dorsalis Pedis
283
Normal pulse rate?
Ranges between 60-100 bpm (beats per minute)
284
Variations of pulse rate with age?
→ One week of age (Infant) – 140 bpm → One year of age – 120 bpm → Puberty – 70-80 bpm
285
\> 100 bpm
Tachycardia
286
Sinus rhythm → QRS in ECG is preceded by the P wave → Impulse originate in Sinus Node travels to the AV Node reaches Left Ventricle through the His and Purkinje Fibers
Tachycardia
287
\<60 bpm
Bradycardia
288
Sinus rhythm → QRS in ECG is also preceded by the P wave
Bradycardia
289
Tachycardia sinus rhythm physiologic causes:
o Infancy o Early Childhood o Exercise o Excitement o Anxiety o Emotional Stress
290
Bradycardia Sinus Rhythm physiologic causes:
o Athletes who undergo training o During sleep
291
Tachycardia Sinus Rhythm pathologic causes:
o Cardiovascular causes Congested Heart Failure Acute Myocardial Infarction Pulmonary Thromboembolism or MyocarditisShock o Non-Cardiac causes Fever Anemia Pregnancy Thyrotoxicosis Paget’s Disease Beri-Beri (Vitamin B1 deficiency ) Hemorrhage Hypotension
292
Bradycardia Sinus Rhythm pathologic causes:
o Cardiovascular causes Inferior Wall Myocardial Infarction Sinus-Atrial Block Post Cardiac Transplantation o Non-Cardiac causes Myxedema Chagas Disease Hypothermia Mental Depression
293
Tachycardia Sinus Rhythm pharmacologic causes:
o Epinephrine o Isoproterenol o Ephedrine o Alcohol o Nicotine o Caffeine
294
Bradycardia Sinus rhythm pharmacologic causes:
o Beta Blockers o Amiodarone o Propafenone o Lithium
295
Regularly Irregular Pulse
→ Sinus Arrhythmia Pulsus Bigeminus → Pulsus Alternans Heart Block
296
Irregularly Irregular Pulse
→ Atrial Fibrillation → Multifocal Atrial Tachycardia → Frequent Premature Ventricular Complexes
297
→ Used in ancient times → A piece of glass with water inside, the rest of the air has been evacuated out to create a vacuum. → When pointed to a particular direction, the water would rush from one side to the other, hitting the bulb and makinga sound.
Water Hammer Pulse (Collapsing Pulse)
298
Water Hammer Pulse (Collapsing Pulse) Aortic Run-Off → Aortic Regurgitation
o Patent Ductus Arteriosus
299
Water Hammer Pulse (Collapsing Pulse) Aortic Run-Off → Aorto-Pulmonary Window
o Rupture of Sinus of Valsalva
300
Water Hammer Pulse (Collapsing Pulse) Cyanotic Congenital Heart Disease
→ Truncus Arteriosus → Pulmonary Atresia with Broncho-Pulmonary Collaterals → Tetralogy of Fallot with Blalock-Taussig Shunt
301
Twice Beating Pulse A. Anacrotic Pulse
→ Aortic Stenosis
302
Twice Beating Pulse B. Bisferiens Pulse
→ Aortic Regurgitation → Hypertrophic obstructive cardiomayopathy (HOCM) → Aortic Regurgitation and Aortic Stenosis → Hyperkinetic circulatory states → Patent ductus arteriosus
303
Twice Beating Pulse C. Dicrotic Pulse
→ Enteric fever → Cardiomyopathy → Hypovolemic Shock → Intra-arterial balloon pulsation
304
Dicrotic pulse
305
Bisferiens pulse
2 peaks before the dicrotic notch
306
Bisferiens of HOCM
1 peak is taller, 2nd peak coincides with the dicrotic notch
307
→ Variations in Left Ventricular Output Volume
→ Large wave from a large volume injected from the heart
→ Small wave with less volume injected from the heart
→ Result of left ventricular failure
Pulsus Alternans
308
The pulse wave from the alternated (large and small) given the name?
“Pulsus Alternans”
309
Pulsus alternans
310
Normal inspiration in normal individuals blood pressure falls down but in \_\_\_\_\_\_\_\_\_\_, on inspiration blood pressure falls down exaggerated (more than 10 mmhg)
Pulsus Paradoxus
311
Defined as Exaggeration of systolic fall of blood pressure by more than 10 mmhg.
PULSUS PARADOXUS
312
On deep inspiration in a patient with tamponade:
o There is an increased flow in the right side of the heart
o There is also a pressure from the outside resulting in increased ventricular transmural pressure
o Shift of the septum from the right to the left to accommodate the increased blood volume
o The left ventricle becomes small because the inter-ventricular septum is pushed towards the left ventricle results to a exaggerated fall of systolic blood pressure.
PULSUS PARADOXUS
313
CAUSES OF PULSUS PARADOXUS
Cardiovascular
o Cardiac tamponade
o Effusive constrictive pericarditis
o Restrictive cardiomyopathy
o Massive pulmonary embolism
o Severe hypovolemic shock
Pulmonary
o Chronic Obstructive Pulmonary Disease (COPD)
Absence of Pulsus Paradoxus when there is presence of tamponade
o Atrial Septal defect (ASD)
314
Type of pulsus paradoxus:
Due to Severe cardiac tamponade
Total Paradox
315
Type of pulsus paradoxus:
o Due to positive pressure breathing with ventilators, Isorhythmic Atrioventricular Dissociation and Hypertrophic Obstructive Cardiomyopathy
o Means there is increased blood pressure during deep sleep inspiration
Reversed pulsus paradoxus
316
VOLUME OF THE PULSE
(delayed systolic peaking in a slow rising pulse)
o Caused by Aortic Stenosis
Pulsus Parvus et Tardus
317
VOLUME OF THE PULSE:
o Caused by Aortic Regurgitation
Pulsus Magnus
318
Hyperdynamic States (causes a high volume pulse)
o Pregnancy
o Thyrotoxicosis
o Beri-Beri
o Fever
o Paget’s Disease
319
Radial pulse synchronicity can be abnormal in?
Takayasu’s Arteritis
Thoracic Outlet Syndrom
Subclavian Steal Syndrome
Chronic Atherosclerosis
Coarctation of Aorta
Dissection of Aorta
320
CHARACTERISTIC PULSE IN VALVULAR HEART DISEASE:
AORTIC STENOSIS
Pulvus Parvus et Tardus (slow rising pulse with delayed systolic peaking)
Anacrotic Pulse
Pulsus Alterans (left ventricular failure)
Pulsus Bisferiens (severe aortic stenosis)
321
CHARACTERISTIC PULSE IN VALVULAR HEART DISEASE:
AORTIC REGURGITATION
Water Hammer Pulse
Pulsus Bisferiens
Pulsus Magnus
322
Blood pressure in Aortic Regurgitation
Wide pulse pressure \>70 mmHg
323
Hill’s sign is seen in?
Aortic Regurgitation
324
o Greater velocity of blood flow below lower limbs
o Greater gradient between posterior tibial and radial arteries
Hill’s sign
325
Severity of Aortic Regurgitation:
60 mmHg
Severe
326
Severity of Aortic Regurgitation:
40-60 mmHg
Moderate
327
Severity of Aortic Regurgitation:
20-40 mmHg
Mild
328
Other signs seen in aortic regurgitation:
1. Landolfi’s Sign
2. Becker’s Sign
3. De Musset’s Sign
329
Alternative dilation and constriction of the pupil
Landolfi’s Sign
330
prominent retinal artery pulsation
Becker’s Sign
331
Named after Alfred de Musset, a French philosopher who had a habit of synchronous nodding of head with his heartbeat
De Musset’s Sign
332
Signs of Aortic Regurgitation in Head and Neck
Corrigan’s sign
Muller’s sign
Minervini’s sign
Logue sign
333
dancing carotid pulsations
Corrigan’s sign
334
pulsation of uvula
Muller’s sign
335
pulsations of the tongue
Minervini’s sign
336
pulsation of sterno-clavicular joint
Logue sign
337
Signs of Aortic Regurgitation in Upper Extremity
Locomotor brachialis
Quincke’s pulse
Palfrey’s sign
338
dancing brachial pulsations
Locomotor brachialis
339
pulsation of nail bed
Quincke’s pulse
340
pistol shot over radial artery
Palfrey’s sign
341
Signs of Aortic Regurgitation in Lower Extremity
Hill’s sign
Traube’s Sign
Duroziez’s murmur
342
pistol shot sounds over femoral artery
Traube’s Sign
343
Three D's of Duroziez’s murmur
→ Duroziez
→ Distal
→ Diastolic
344
On placing the stethoscope in an inclined fashion, with the inclined towards the foot end, that is displaced distally, the patient will have a diastolic murmur. A systolic murmur will be normal because we are obstructing the artery with the stethoscope. However, if this murmur is also present in the diastolic phase, then this is called the __________ which is pathologic.
Duroziez murmur
345
Signs of Aortic Regurgitation in Abdomen
Rosenbach’s sign
Gerhardt sign
Dennision’s sign
346
pulsation of liver
Rosenbach’s sign
347
pulsation of spleen
Gerhardt sign
348
pulsation of the cervix
Dennision’s sign
349
Case: A 78 year old male presents complaining of dyspnea on exertion and exertional angina for the past 3 months. On exam, you note a 2/6 systolic murmur when your stethoscope is placed in the apical area. Which of the following is the correct murmur?
Step 1: Know if it is diastolic or systolic:
Systolic
350
Case: A 78 year old male presents complaining of dyspnea on exertion and exertional angina for the past 3 months. On exam, you note a 2/6 systolic murmur when your stethoscope is placed in the apical area. Which of the following is the correct murmur?
Step 2: Know the location of the murmur:
Apical
351
Step 1: Know if it is diastolic or systolic: Systolic
Step 2: Know the location of the murmur: Apical
Basing on the picture above and the given data, it is now obvious that the murmur is of the _____ area.
mitral area
352
the only time you hear this is when blood flows across the mitral valve when the left atrium is trying to throw blood into the ventricles as it fills that ventricle during diastole
Mitral stenosis
353
blood ejects out of the left ventricle and has the potential of going back across the mitral valve if it will regurgitate back to the left atrium which is called a?
mitral regurgitation
354
Systolic Murmurs
Mitral Regurgitation
Tricuspid Regurgitation
Aortic Stenosis
Pulmonic Stenosis
355
Diastolic murmurs
Mitral Stenosis
Tricuspid Stenosis
Aortic Regurgitation
Pulmonic Regurgitation
356
Mnemonics: MRS. ASS
→ Mitral Regurgitation – Systolic
→ Aortic Stenosis – Systolic
357
Murmurs are louder during:
→ Right sided murmurs in Inspiration
o RINspiration
→ Left sided murmurs in Expiration
o LEXpiration
358
o heart becomes hypertrophied and the septum bulges and blocks the outflow tract
o normally more blood flow across the valve or into the heart makes the murmur louder but in \_\_\_\_\_\_\_\_\_\_, more blood or pressure in the heart actually pushes the septum back to its normal physiologic condition and re-opens the outflow tract obstruction
Hypertrophic Obstructive Cardiomyopathy (HOCM)
359
o prolapsing and blocking normal blood flow
o more blood going to the heart and returning the mitral valve leaflets back into their normal position
o you don’t hear the midsystolic click that goes along with the mitral valve prolapse
Mitral Valve Prolapse (MVP)
360
→ Done every time you increase preload to get a louder murmur during auscultation
→ more blood is going to flow through the heart and more blood flows over a valve whether it is stenotic or regurgitant
Maneuvers: Squatting / Leg raising
361
HOCM – less blood flow, less blood is there to push the septum back to its normal position so the sounds are louder or worse
Decreased preload
362
MVP – less blood to return the mitral valves back to their normal position
Decreased preload
363
→ Used to decrease decrease preload
→ Tell the patient bear down and pretend like having a bowel movement
→ this prevents blood from returning to the heart aka decreases preload
Maneuver: Valsava
364
means more pressure is being exerted upon the left ventricle as it tries to eject the blood out of the heart
Increased afterload
365
→ used to increase afterload
→ tell the patient to squeeze their left hand
Maneuver: Hand grip
366
regurgitant murmur becomes louder
Increased afterload
367
HOCM and MVP on the other hand has softer murmurs
→ in increased afterload, HOCM and MVP have more pressure propping the septum and those valve leaflets back into its normal position respectively
→ softer HOCM and MVP means that murmur is getting better; you don’t hear it as much because there’s less mechanical issue since there is more pressure returning to the heart to its physiologic position
368
achieved by using a drug called amyl nitrate
Decreased afterload
369
In HOCM, because less pressure is forcing that septum back into its normal position, the outflow tract gets obstructed and murmur gets worse or louder
Decreased afterload
370
In MVP, because less pressure is being forced upon those mitral valve leaflets, the mitral valve is going to prolapse more and get worse or louder
Decreased afterload
371
Cresendo-Decresendo
AORTIC STENOSIS
372
Present in Old patients (70 years old or older)
AORTIC STENOSIS
373
SAD- Syncope, angina, dyspnea
AORTIC STENOSIS
374
Calcified valve- deposits of calcium crystal present around the aortic valve resulting to decrease in space
AORTIC STENOSIS
375
Radiates to the carotids
AORTIC STENOSIS
376
Holosystolic- same volume throughout; continuous murmur
MITRAL REGURGITATION
377
History of Rheumatic fever
MITRAL REGURGITATION
“Rheu-mitral”
378
Radiates to the axilla
MITRAL REGURGITATION
379
Holosytolic- murmur between S1 and S2
TRICUSPID REGURGITATION
380
History of Intravenous Drug Abuse-
TRICUSPID REGURGITATION
“Want to TRI some drugs?”
381
damage is primarily on the tricuspid valve due to presence of pathogens in the blood due to intravenous drug abuse
TRICUSPID REGURGITATION
382
in the Philippines, common cause of Tricuspid regurgitation is?
severe pulmonary hypertension and rheumatic heart disease (due to infective endocarditis)
383
Opening snap- hard to hear
MITRAL STENOSIS
“Operating System is MicroSoft” (the OS is MS)
384
Family History of sudden cardiac death
HYPERTROPHIC OBSTRUCTIVE MYOPATHY
385
Similar to other murmurs- maneuvers give it away
HYPERTROPHIC OBSTRUCTIVE MYOPATHY
386
HYPERTROPHIC OBSTRUCTIVE MYOPATHY with decreased preload:
→ Louder (worse) with decreased pre-load-
o less blood going to the heart, septum can push over more and obstruct more which means the murmur is louder
387
HYPERTROPHIC OBSTRUCTIVE MYOPATHY with decreased afterload:
→ Louder (worse) with decreased afterload-
o less pressure forcing the septum over which means the septum is going to block the outlet so the murmur gets louder
388
HYPERTROPHIC OBSTRUCTIVE MYOPATHY with increased preload:
→ Softer (better) with increased pre-load-
o Have the patient do some leg raising or squatting so more blood goes back to the heart. More blood will force the septum push into the side and make the murmur better or softer
389
HYPERTROPHIC OBSTRUCTIVE MYOPATHY with increased afterload:
→ Softer (better) with increased afterload-
o have the patient do some handgrip of squeeze their left hand making the heart pump against a greater pressure which means more pressure is going to force the septum back to its normal position which makes it sound softer or better
390
Midsystolic click
o Young woman with psychiatric history- young women who are anxious and depressed
o Myxomatous valve disease
MITRAL VALVE PROLAPSE
“to win MVP, your team has to click”
391
\<60- junctional rhythm
Tachycardia and or Ventricular Tachycardia
392
below 60 but not less than 40 bpm
Sinus bradycardia-
393
o Below 40 bpm
2nd degree AV block or complete heart block
394
For patients experiencing syncopal attacks/ near syncope, dizziness, and HR is below 60/min, request for a ________ to find out if you are dealing with a pathologic type of bradyrrythmia
holter monitor
395
Atrial fibrillation- can be seen in patients with ?
Mitral Stenosis, Dilated Cardiomyopathy, Hyperthyroidism
396
can be seen in young normal individuals; no treatment needed
Sinus arrhythmia
397
A midsystolic nonejection sound (C) occurs in \_\_\_\_\_\_and is followed by a late systolic murmur that crescendos to the second heart sound (S2).
mitral valve prolapse
398
\_\_\_\_\_\_\_\_\_ decreases venous return; the heart becomes smaller; C moves closer to the first heart sound (S1), and the mitral regurgitant murmur has an earlier onset.
Standing
399
With prompt \_\_\_\_\_\_\_\_, venous return and afterload increase; the heart becomes larger; C moves toward S2; and the duration of the murmur shortens. The systolic murmur of hypertrophic obstructive cardiomyopathy behaves similarly.
squatting
400
Peripheral cyanosis:
Congenital Heart Disease/Heart Failure
401
Splinter Hemorrhages:
Infective endocarditis
402
Xanthomata:
Hypercholesterolemia
403
Tar Staining:
Smoking
404
Finger Clubbing:
Infective endocarditis and Congenital heart disease
405
Schamroth’s window test:
lost with finger clubbing
406
Capillary refill time:
less than 2 seconds is normal
407
Assess for radio-radial delay:
aortic coarctation
408
Assess for a collapsing pulse:
aortic regurgitation
409
Auscultate the carotid arteries to detect bruits
o Patient should hold their breath upon auscultation
o Palpate the carotid pulse if no bruits identified
410
Xanthelasma and Corneal Arcus:
Hyperlipidemia
411
Conjuctival Pallor:
Anemia
412
Radiation of an ejection systolic murmur is often heard in ?
aortic stenosis
413
Aortic murmurs- (patient sits up)
o will get louder with \_\_\_\_\_\_
expiration
414
Mitral murmurs- (rolls on left side)
o Will get louder with \_\_\_\_\_\_
o Auscultate the _____ listening for radiation of a mitral murmur
expiration
axilla
415
Assess for sacral edema-
o Right ventricular failure
416
Assess for pedal edema
o Right ventricular failure
417
CORONARY ARTERY DISEASE:
Cerebrovascular
* Ischemic stroke
* Transient ischemic attack
418
CORONARY ARTERY DISEASE:
Coronary artery
* Myocardial infarction
* Angina
419
CORONARY ARTERY DISEASE:
Peripheral
* Intermittent claudication
* Rest pain
* Gangrene
* Necrosis
420
supplies the anterior portion, the
atrioventricular septum and the apex
left anterior descending artery
421
supplies the lateral portion of the heart
Left main coronary artery
422
→ supplies the inferior posterior portion of the
heart
→ supplies right portions of the heart as well as
the inferolateral portions
Right coronary artery
423
Generally refers to atherosclerosis of the
coronary arteries that may result in significant
obstruction to coronary blood supply leading to
myocardial ischemia.
Coronary artery disease
424
Refers to a condition in which there is an
imbalance between the oxygen supply and
oxygen demand of the myocardium usually due to
severe fixed or dynamic obstruction of the
myocardial blood supply, or an increase in
myocardial oxygen requirements or both.
Myocardial ischemia
425
most common cause of life threatening illness
ISCHEMIC HEART DISEASE
426
Major determinants of myocardial oxygen demand
• heart rate
• myocardial contractility
• myocardial wall tension (stress)
In managing patients with ischemia, reducing the
determinants will improve blood supply.
427
Oxygen carrying capacity of the blood
* Inspired oxygen
* pulmonary function
* hemoglobin concentration
428
3 sets of coronary arteries regarding coronary
resistance flow
• large epicardial arteries (R1)
• prearteriolar vessels (R2)
• arteriolar and intramyocardial capillary vessel
(R3)
429
Occurs when too much cholesterol, triglyceride or
lipid substances are deposited in the arterial wall.
ATHEROSCLEROSIS
430
Obstruction is significant if more than
\_\_\_% involving the left vein, also Left circumflex
and right coronary artery obstruction is significant
if more than \_\_\_\_%.
Obstruction is significant if more than
50% involving the left vein, also Left circumflex
and right coronary artery obstruction is significant
if more than 70%.
431
But a \_\_\_\_\_% luminal obstruction
is enough to have ischemia, at rest is okay but if
you increase workload that can result to
myocardial ischemia.
50%
432
major site of
atherosclerotic disease
Epicardial coronary arteries
433
sub intimal collections of
fat, smooth muscle cells, fibroblasts and
Intracellular matrix
atherosclerotic plaque
434
CASCADE OF MECHANISMS AND
MANIFESTATIONS OF ISCHEMIA
* endothelial and microvascular dysfunction
* decreased sub endocardial perfusion
* altered metabolism/abnormal ST segment
* micro-infarction/myocardial fibrosis
* diastolic dysfunction
* decreased segmental perfusion
* regional wall motion
* systolic dysfunction
435
o Clenched fist
o squeezing
o Central substernal chest discomfort
Levine’s sign:
436
Normal ABI (ankle-brachial index)
\< 0.8
437
HOW TO
OBTAIN ABI:
get systolic pressure of
dorsalis pedis and systolic pressure or
brachial artery.
Usually, LE would have higher systolic
blood pressure compared to UE. For
example: systolic pressure sa imo upper
arm is 100, the systolic pressure in your
dorsalis pedis would be above 100 ---
normal
In opposite, dorsalis pedis systole is 90 and
brachial index is above 100 or 110, that’s
significant. You have presence of arterial
occlusive disorder.
438
Cause of Increase demand for Oxygen by the heart
muscle
→ increase in heart rate
→ increase in contraction
→ increase in blood pressure
439
Cause of inadequate supply of Oxygen to the heart
Either due to:
1) Atherosclerosis
2) Spasm of the coronary artery
- Which is the Prinzmetal angina
440
Emergency medications for angina pectoris
• Nitroglycerin gr 1/150 tablet
• Isordil 5 mg
→ one tablet sublingual
→ Iban na ginahatag spray. You give that every 5
minutes. Mas dasig ang spray. Diri sa
Philippines, indi available ang spray.
→ Butang mo under the tongue. After 5 minutes,
stop it. After 5 minutes, repeat it if may chest
pain pa. After 5 minutes, liwat. After 3 tries and
the px is still having chest discomfort, tell the px
“go to the hospital and probably you’re dealing
already with acute coronary syndrome.
441
Warning to patients who take Emergency Nitrates
Headache
Hypotension
442
Anti-Anginal Agents
Nitrates
Beta blocker
Calcium channel blocking agent
443
Administration of \*trace amount of molecule, \*labeled with radionuclide, to provide diagnostic information and assess therapeutic response long before changes can be seen at anatomical level
Nuclear Medicine
444
Simply an unstable nuclide or nuclear species that undergoes radioactive decay.
Radionuclide
445
Radionuclide signal is for \_\_\_\_\_detection
external
446
the biological distributor
Pharmaceutical
447
= Radiopharmaceutical
Suitable Radionuclide + Specific Pharmaceutical
448
detects or captures what is happening with the organ of interest because it traces the radiation being emitted by the unstable radionuclide; This produces the images
Gamma camera
449
Unstable nuclides → Stable
Radioactive Decay
450
→ A device which narrows a beam of particles or waves
→ To narrow can mean either to cause the direction of motion to become more aligned in specific direction or to cause the spatial cross section of the beam to become smaller
→ It also removes the energy that is not needed and not in the path
→ It only absorb the specific energy to produce the specific structure or images
“Collimator”
451
Gamma emissions must be of suitable energy between __________ (ideal of gamma camera)
50-200 KeV
452
Desirable Characteristics of Radionuclide
1. Gamma emissions must be of suitable energy between 50-200 KeV (ideal of gamma camera)
2. Effective half-life and bio distribution is long enough and suitable for its intended use
3. Do not emit particulate particle
453
Nuclear Medicine Imaging
Two broad classes:
→ Single Photon Emission Tomography (SPECT)
→ Positron Emission Tomography (PET)
454
It is similar to a conventional nuclear medicine planar imaging using a gamma camera (scintigraphy) but is able to provide true 3D information. This information is typically presented as cross-sectional slices through the patient but can be freely reformatted or manipulated as required.
SPECT Imaging
Single Photon Emission Computer Tomography
455
Radionuclides use that decay by positron emission.
Positron Emission Tomography
456
one particular angle
Planar
457
collected from many angles around the patient
Tomographic
458
depth information
Cross-sectional images
459
positive electron released from the nucleus wherein it interacts with the electrons of the tissue. They undergo annihilation and produce energy wherein the gamma camera captures.
Positron
460
Advantages of Functional Imaging (Scintigraphy)
Early diagnosis
Increased test sensitivity
Directly demonstrates effects of therapy
Complements anatomical imaging
461
Indications of MPI (MYOCARDIAL PERFUSION IMAGING)
1. Suspected with Coronary artery disease (CAD)
2. Symptomatic patients with pretest probability of CAD 15%-85% with LVEF of \>50%; or in patients unable to exercise adequately with ECG characteristic such as Left bundle branch block.
3. Pretest probability 66-85% for CAD or LVEF \<50% without typical of angina.
4. Patients with known CAD diagnosed by an anatomical imaging modality in whom the functional significance of the stenosis should be determined.
5. To exclude ischemia as a trigger for rhythm disorders.
6. Patients with persistent symptoms after revascularization procedures.
7. Patients with \>3 risk factors who will undergo high risk surgery.
8. To assess viability of dysfunctional myocardium; sometimes followed by viability testing with FDG.
9. Patients with Agatston calcium score of \>400 and any risk.
462
Contraindications of MPI
Pregnancy
Unstable angina pectoris and recent Myocardial Infarction (MI) less than 4 days are contraindicated to stress MPI.
463
O2 supply below the metabolic requirements because of inadequate blood circulation cause by coronary stenosis.
Myocardial Ischemia
464
Necrosis of myocardial tissue as a result of coronary occlusion.
Myocardial Infarction
465
Necrosis involves all layers from endo to epicardium.
Transmural Infarction
466
Necrosis involves only muscles adjacent to endocardium.
Subendocardial Infarction
467
late result of infarction.
Myocadial scar
468
Chronic ischemia with decreased blood flow and down regulation of contractility. Reversible with restoration of blood flow. No perfusion on rest imaging poor ventricular contraction. Improved perfusion given a long recovery between rest-rest imaging or delayed reinjection T1 201.
Hibernating Myocardium
469
myocardium with persistent contractile dysfunction despite restoration of perfusion after a period of ischemia; usually improves with time. Normal perfusion imaging. Poor ventricular contraction. Uptake by FDG metabolic imaging.
Stunned Myocardium
470
2 clinical reasons for selecting MPI:
→ The desirability of highly sensitive test for detecting ischemia over time bec of the presence of coronary angioplasty or restenosis.
→ Extent & severity of ischemia of potential residual ischemia may help govern the indication for repeat intervention.
471
MPI Basic Concepts
A tracer must be delivered to the myocardium
A viable, metabolically active myocardial cells must be present to localize the tracer
→ HEALTHY = (+) UPTAKE
→ INFARCTED = (-) UPTAKE
472
Myocardial Perfusion agents
→ Thallium
→ Technetium (Tc99m) + Sestamibi
→ Technetium (Tc99m) + Tetrosfosmin
473
Infarct Myocardium Scintigaphy agents
Technetium (Tc99m) Pyrophosphate
474
Radionuclide Ventriculography
Technetium (Tc99m) + RBC
475
Biokinetic properties similar but not identical to potassium.
Thallium (TL)
476
Images immediately after injury- flow dependent initial distribution- regional myocardial blood flow.
Thallium (TL)
477
Delayed images (2-24 hours)- distribution of K+ pool- myocardial viability
Thallium
478
Principle is that it is not static over time
Thallium
479
Redistribution
→ Filling in of the myocardial perfusion defect occurring shortly (between 3-5 hours) after injection is related to 2 factors.
Thallium
480
Negative charge cross the membrane and affinity with mitochondria.
Distribution remained relatively fixed over time, reflecting the distribution of myocardial blood flow at the time of injection and is frozen over time- can be imaged for several hours.
2 separate injections are required (during rest and exercises)
Tc-99m SESTAMIBI
481
Manifestations of Myocardial Ischemia:
EKG
→ Ion flux across cell membrane is impaired, therefore produces ST segment depression.
482
Manifestations of Myocardial Ischemia:
Perfusion Scintigraphy
→ Decrease in regional flow produces cold defect area on scintigraphy
483
Manifestations of Myocardial Ischemia:
Radionuclide Ventriculography
→ Regional wall motion abnormality or fall in left ventricular ejection fraction
More on functional imaging; Way better than 2d-echo; Invasive and very expensive.
484
Pharmacologic Stress Study
Indications:
→ Inability to exercise (can’t walk, obese, pain in the body)
→ Inadequate exercise heart rate or workload
→ Left bundle branch block or ventricular pacemakers
485
→ An indirect vasodilator
→ Blocks cellular absorption of Adenosine increase concentration of Adenosine (vasodilation)
Dipyridamole or persantine
486
Dipyridamole Infusion Protocol
o 0.142 mg/kg/min is infused for 4 mins.
o Maximal vasodilation after the 4th min
o Tracer is injected after the 4th min
487
Side Effects of Dipyridamole or persantine
o HA, flushing, nausea, angina
o Reversed quickly by IV Aminophylline which blocks Adenosine receptors
488
Ischemia may be induced by __________ (inc. bld flow in NL CA steals bld away from vasc. bed supplied by stenotic CA
CORONARY STEAL
489
an endogenous vasodilator
Adenosine
490
Adenosine Infusion Protocol
o 40 ug/kg/min is infused via infusion pump for 6 minutes
o Radiotracer is injected on the 5th minute
o Has more potent and consistent vasodilatory effect than Dipyridamole
491
Side effects of adenosine:
- more common (75%)
o HA, nausea, flushing, chest pain, AV blocks
o Reversed instantaneously by terminating the infusion
492
→ Sympathomimetic agent increase myocardial oxygen demand by increasing HR and BP even flat in bed
→ Used for patients with contraindication to Dipyridamole or Adenosine (BA, COPD, patients taking Xanthine derivatives and those who have consumed caffeine)
Dobutamine
493
The computer acquires imaging data synchronous with the ECG R wave
Arrythmic beats are filtered out of the data collection cycle
The R-R interval is usually divided into 8 – 16 frames
Enable to display sequential gated images in a cinematic display to assess tracer distribution, regional wall motion, Ejection Fracton, wall thickening.
It permits 3D display of the myocardium
Gated SPECT Imaging Acquisition
494
IMAGE RECONSTRUCTION
Filtered back projection
Filtering – to correct for reconstruction artifacts, suppress noise and enhance image quality
Tomo SPECT Imaging
495
short axis view
Apex to base
496
horizontal/ long axis view- from inferior going upward
Coronal view
497
from septum to lateral- vertical long axis view
Sagittal cut
498
Gold standard in viability study-
PET
499
Polar Map Circumferential Profiles
→ Advantage
o provides graphic display of the relative distribution of the tracer uptake in the myocardium and the degree of perfusion abnormality in comparison to a normal reference data base
500
Polar Map Circumferential Profiles disadvantage:
o unable to distinguish between true perfusion defects and artifacts
501
Glucose analog transported into the cell by glucose transporter (GLUT) express on the cell membrane, phosphorylated by the enzyme hexokinase and trapped. (Half-life 1 hour and 10 mins)
Fluorodeoxyglucose (FDG)
502
GOLD STANDARD study to detect viable myocardium considered for revascularization in order to predict outcome benefit and for correct stratification and guide further treatment.
Positron Emission Tomography (PET)
503
Assess regional and global wall motion
predictor of long term outcome of MI
Cardiac chamber volumes and morphology
distinguish systolic from diastolic CHF
Ventricular systolic and diastolic function indices including LV and RV EF-prognosis value.
evaluation of patient undergoing chemotherapy in monitoring cardiotoxicity induced by chemo agents.
Equilibrium Radionuclide Angiocardiography
504
To calculate LV and RV EF. (More on RV EF)
Assess wall motion abnormality
Quantify left to right cardiac shunt.
Measure cardiac output and absolute ventricular chamber volume.
Evaluate diastolic volume.
First Pass Radionuclide Ventriculography
505
All of the ff are important in xray
A. Projection
B. Inspiration
C. Rotation
D. artifact
B. Inspiration
506
A good inspiraroty film should be:
A. Below the 9th rib
B. Above the 10th rib
C. At the level of 12th rib
D. Equidistant clavicles
B. Above the 10th rib
507
pulmonary artery supply deoxygenated blood in this chamber?
A. R atrium
B. R ventricle
C. L atrium
D. L ventricle
B. R ventricle
508
Pulmonary veins drain blood into what chamber?
A. RA
B. LA
C. RV
D. LV
B. LA
509
Which chamber does the blood to the aorta come from?
A. RA
B. LA
C. RV
D. LV
D. LV
510
Projections of chest heart radiograph?(ang major ata na ginagamit)
A. PA
B. PA lateral
C. AP
D. AP lateral
A. PA
511
What projection will show retrocardiac fullness
A. PA
B. AP
C. Lateral
D. Oblique
C. Lateral
512
most posteriorly and superiorly located in chest PA xray
a. RA
b. LA
c. RV
d. LV
b. LA
513
What cardiac chamber forms the right cardiac border in PA view?
A. Right atrium
B. Left atrium
C. Right ventricle
D. Left ventricle
A. Right atrium
514
It forms the left border of the heart in chest PA
A. Left ventricle
B. Left atrium
C. Right Ventricle
D. Right atrium
A. Left ventricle
515
Normal cardiothoracic ratio on PA--
0.5
516
signs of cardiomyopathy-
water bottle sign
517
Most common cardiomyopathy
A. Restricted cardiomyopathy
B. Constricted cardiomyopathy
C. Hypertrophic cardiomyopathy
D. Dilated cardiomyopathy
D. Dilated cardiomyopathy
518
Which is not a mogul of the heart at the left mediastinal outline?
A. Aortic knob
B. Pulmonary artery
C. Left atrial appendage
D. Left hemidiaphragm
D. Left hemidiaphragm
519
Heart mogul commonly unseen but when seen denotes prominence/enlargement.
Ans. Left atrial appendage
520
Not true in ABI
A. most powerful indicator of LVH
B. Ankle\>Branchial
C. Diagnosis fir peripheral art. Disease
D. Normal 0.70
D. Normal 0.70
521
Which is not true about A Wave - ang answer ko lang ang A wave ha - para atrial contraction that pushes blood from RA to RV -may choice to nga wave after P wave( confirm lng kung amo ni ang answer)
| (INCOMPLETE CHOICES)
522
Which is true about V wave?
Ans. Ventricular filling
523
Not have LV heave
A. Mitral stenosis
B. Aortic stenosis
C. Mitral regurgitation
D. Aortic regurgitation
A. Mitral stenosis
524
RV heave -
atrial septal defect
525
Pulsus parvus et tardus
- Aortic stenosis
526
Pulsus paradoxus
-
Cardiac Tamponade
527
Water hammer pulse
-
Aortic Regurgitation
528
Pulsus alternans
-
LV Systolic dysfunction
529
Soft S1 sound
Coronary Artery Disease
530
Loud Second Heart Sound
Hypertension
531
Mid systolic clicks
Mitral Valve Prolapse
532
hypertrophic cardiomyopathy
increased murmur when standing
533
Aortic stenosis
-
crescendo decrescendo midsystolic murmur radiating to neck
534
Atrial septal defect
-
holosystolic murmur at 2nd ICS
535
Aortic regurgitation
-
diastolic blowing murmur, located at 2nd and 3rd ICS
536
PDA
continuous murmur at pulmonic area
537
Ventricular septal defect
Holosystolic murmur heard best at 3rd-4th midclavicular ics
538
18 yo female, chest discomfort. LV heave @ 6th ICS LAAL, holosystolic murmur @ 4th & 5th ICS MCL. Diagnosis
A. Mitral regurgitation
B. VSD
C. ASD
D. Hypertrophic cardiomyopathy
B. VSD
539
Mitral Regurgitation -
radiates to the axilla
540
40 yo male (+) dyspnea, bipedal edema, RV heave, apex at 5th ICS LMCL, grade3/6 systolic murmur @ 3rd and 4th ICS left parasternal, diastolic rumbling murmur at apex. Give the diagnosis:
A. Mitral regurgitation and tricuspid regurgitation
B. Mitral Valve Prolapse and Aortic Regurgitation
C. Tricuspid Stenosis and Mitral Regurgitation
D. Aortic Regurgitation and Mitral Regurgitation
C. Tricuspid Stenosis and Mitral Regurgitation
541
ECG basically used to detect ischemic diseases and cardiac arrhythmia.
-
True
542
HOLTER recorder basically used to detect ischemic diseases and cardiac arrhythmia.
| (True or False)
True
543
Radiology does not include the shadow of the heart.
-False
544
Doppler Flow shows color flow directions of blood flow and shunts
(True or False)
True
545
Color coding is used in the direction of the blood flow.
(True or False)
True
546
Red color indicate blood flow away from the tracer. -
(True or False)
False
547
Holter is used to detect asymptomatic cardiac arrthymia-
(True or False)
True
548
Holter can be used to identify/detect asymptomatic ST segment elevation -
(True or False)
True
549
Made up of smooth muscle cells.
A. Media
B. Intima
C. Adventitia
D. Pericytes
A. Media
550
Consists of loose extracellular matrix -
Adventitia
551
Monolayer of Endothelial cells
A. Media
B. Intima
C. Adventitia
D. Pericytes
B. Intima
552
Forms an interface between tissue and blood component.
A. Extracellular matrix
B. Intima
C. Endothelium
D. Capillary
C. Endothelium
553
Type of vessel that has few layers of media:
Vein
554
Type of blood vessel that is commonly affected by atherosclerosis.
A. Capillaries
B. Veins
C. Medium-sized arteries
D. Elastic arteries
C. Medium-sized arteries
555
Type of vessel that has prominent tunica media
a. Veins
b. Capillary
c. Medium size artery
d. Elastic artery
c. Medium size artery
556
Embryonic origin of smooth muscle of the upper body parts. -
neural crest
557
Embryonic origin of smooth muscle of lower body parts. -
Somites
558
Reactive oxygen species produced by endothelium:
A. Phosphorylation of myosin light chain
B. Oxidative stress
C. Responsive oxygenation
D. Sympathetic activation
B. Oxidative stress
559
It is used to assess noninvasively endothelial dysfunction.
A. Methacholine
B. Doppler study
C.
D.endothelin
B. Doppler study
560
It is an agonist used to assess endothelial function invasively.
A. Methacholine\*
561
Normal endothelium function after clinical assessment
A. Decrease blood flow
B. Paradoxical vasoconstriction
C. less than 10%
D. Reactive hyperemia
B. Paradoxical vasoconstriction
562
NO is associated with what type of ANS
a. sympathetic
b. parasympathetic
c. nonadrenergic
nonadrenergic
563
A potent vasoconstrictor that endothelium produce
A. NO
B. Prostacyclin
C. Endothelin
C. Endothelin
564
What is the principal function of vascular smooth muscle cells
A.
B. To maintain vessel tone
C.
D. Improve blood flow
B. To maintain vessel tone
565
Not a determinant of aortic pressure
A. Peripheral Vascular Resistance
B. Degree of stiffness of arteries
C. Hyperventilation
D. Volume of blood on onset of ejection
C. Hyperventilation
566
Length of muscle before the onset of contraction?
A. Afterload
B. Contractility
C. Wall stress
D. Preload
D. Preload
567
Nuclear Medicine
A. Used unsealed radionuclide for ... theranostic
B. Uses sealed radionuclide for... Theranostic
C. pure therapeutic
D. Uses safe radionuclide? (lipat ko kay kalaba)
A. Used unsealed radionuclide for ... theranostic
568
The advantages of functional imaging (scintigraphy):
A. Early diagnosis, increased test sensitivity and complements anatomical imaging
B. Indirectly demostrates effects of therapy
C.
D. AOTA
A. Early diagnosis, increased test sensitivity and complements anatomical imaging
569
Basic principle of nuclear medicine
A. Radiotracer must be delivered to the myocardium with the viable myocardium extracting the tracer
B. Radiotracer must be delivered to the myocardium with the non-viable myocardium extracting the tracer (Only 2 choices were given)
A. Radiotracer must be delivered to the myocardium with the viable myocardium extracting the tracer
570
Clinical Application of Myocardial Perfusion test?
A. Diagnosis of Myocardial Ischemia
B. To know location, duration and severity of Myocardial Ischemia
C. Planning for PTCA by identifying lesions.
D. AOTA
D. AOTA
571
Indication of exercise stress imaging?
A. Inability to exercise
B. Inadequate exercise heart rate or workload
C. Left bundle branch block
D. Aota
D. Aota
572
Contraindications in taking Adenosine and Dypiridamole
A. Asthma
B: 2nd or 3rd deg AV block
C. Systolic BP of 90 or less
D. AOTA
D. AOTA
573
Contraindications in using Dobutamine.
A. Recent acute coronary syndrome
B. Severe Aortic stenosis
C. Left ventricular outflow tract obstruction
D. All of the above
D. All of the above
574
Adenosine is a potent vasodilator that increases cgmp and camp-
(True or False)
True
575
Perfusion scintigraphy: decrease regional blood flow produces cold defect in areas of scintigraphy. -
TRUE or FALSE
TRUE
576
True or false Mechanism of ischemia Radionuclide ventriculography: regional wall motion abnormality or fall in left ventricular ejection fraction.
(TRUE or FASLE)
TRUE
577
True or false: perfusion-like scintigraphy detect abnormal motion cold defect TRUE
85. True or false Adenosine is a potent vasodilator that forms adenyl cyclase and camp
(TRUE or FALSE)
TRUE
578
True or False Dipyridine block the cellular uptake of adenosine
TRUE or FALSE
TRUE
