Review Q's Week 4 Flashcards
1. biochem artherosclerosis (1-32) 2. pharma anti angina (33-46) 3. physio hemodynamics (47-71) 4. patho atherosclerosis (72-88) 5. patho IHD (89-108) 6. nuclear cardiology (109-124) 7. physio seminar ECG leads (125-171) 8. clinical med acute coronary syndromes (172-197)
1
Q
What are four things plaques are made up of?
A
cholesterol
lipids
inflammatory cells
Ca deposits
2
Q
What occurs if the femoral artery gets occluded due to atherosclerosis?
A
intermittent claudication (condition in which cramping pain in the leg is induced by exercise)
3
Q
What occurs if the internal carotid artery gets occluded due to atherosclerosis?
A
ischemia and cerebral infarction
4
Q
What is the predominant cell in early atherosclerotic lesions?
A
macrophages
5
Q
Where dos lipid accumulate in the arteries?
A
tunica intima
6
Q
What are foam cells? Where can they be found?
A
Foam cells are a type of macrophage that localize to fatty deposits on blood vessel walls, where they ingest low-density lipoproteins and become laden with lipids, giving them a foamy appearance.
7
Q
Where are smooth muscle cells located in the blood vessels?
A
in the tunica media
8
Q
What occurs to the smooth muscle cells (SMC) of blood vessels during atherosclerosis?
A
foam cells release cytokines and growth factors that induce the SMCs to move to the tunica intima (they’re also changed to a repair phenotype instead of a contractile phenotype)
9
Q
early atherosclerotic lesions are also called
A
fatty streaks/fatty dots (the first grossly visible lesion in the development of atherosclerosis)
10
Q
Which lipoprotein reduces risk of atherosclerosis? Why?
LDL or HDL
A
HDL; it moves the lipids from the body back to the liver, this is why its called the good cholesterol.
LDL moves lipids to the body
11
Q
What are the two ways cholesterol inflex is regulated?
A
too much free cholesterol inhibits the main cholesterol synthesis enzyme (HMG-CoA reductase) and it can also inhibit the DNA transcription of LDL receptors
12
Q
What occurs to the cell if ACAT enzyme is defective?
A
the cell would get damaged. The ACAT enzyme acts to esterify and store free cholesterol, without it the free cholesterol would build up and cause damage to the cell (its toxic)
13
Q
What are the receptors that uptake cholesterol via regulated versus unregulated pathway?
A
regulated= LDL receptors (they uptake native LDL)
unregulated= SR-A, CD36, oxLDL receptor (they uptake modified LDL’s!!)
14
Q
What are the three uses for free cholesterol in the cell?
A
make steroids
make cell membrane
esterify and store it
15
Q
Which of the following is a full transporter?
a. ABCA1: ATP-Binding Cassest Transporter A1
b. ABCG1: ATP-Binding Cassest Transporter G1
A
a. ABCA1: ATP-Binding Cassest Transporter A1
(ABCA1 gives both phospholipids and cholesterol esters to form the small HDL; ABCG1 only gives cholesterol esters to make the HDL bigger)
16
Q
Where/Which receptor do the full HDL lipoproteins bind to?
A
the SR-B1 receptor in the liver
(it takes the lipids from the fat HDL and returns it to the circulation as a skinny legend)
17
Q
How do modified LDL’s lead to inflammation?
A
by binding to toll like receptors (those activate inflammation)
(these modified/oxidized LDL’s get consumed by the macrophages by the unregulated scavenger receptors, but they also bind to the toll-like receptors on these macrophages and activate inflammation)
18
Q
How does adaptive immunity play a role in atherosclerosis? explain.
A
dendritic cells (antigen-presenting) uptake the oxidized LDL, go to lymph, and present them to naive T cells. The naive T cells differentiate and go to the plaque to kill the oxidized LDL- this causes inflammation
19
Q
What can be used biomarkers in coronary vascular disease?
A
inflammatory mediators
(use to diagnose)
20
Q
What are the two hypotheses that explain how atherosclerosis develops?
A
1- response to injury (injury to endothelium caused the lipoproteins to go into the vessel wall and oxidize)
2- lipid retention (hyperlipidemia causes a the lipoproteins to go into the vessel wall and bind to matrix protein, aggregating and oxidizing) (…but why does it go into the vessel wall? because it’s going from the high lipid concentration in the blood to low lipid concentration on the vessel wall)
21
Q
T/F: once the atherosclerotic plaque ruptures, occlusion is imminent
A
false, it doesn’t have to cause an occlusion, it can heal and cause stenosis instead
22
Q
What can reduce the size of plaques?
A
efferocytosis (when dying cells are removed by phagocytic cells) or when cells migrate out of the plaque
23
Q
Explain how plaques initiate
A
LDL accumulates in tunica intima and they get oxidized
oxidized LDL makes endothelial cells make adhesion receptors (ICAM, VCAM)
adhesion receptors attract monocytes and transform them into macrophages
macrophages express the scavenger receptors to uptake the oxidized LDL and transform to foam cells
24
Q
What are four harmful effects of oxidized LDL?
A
- proliferation and migration of smooth muscle cells
- inducing endothelial cells to make adhesion molecules
- inducing MCP-1 (macrophage chemotactic factor protein-1) so monocytes get attracted to the site
- increase MCSF (macrophage colony-stimulating factor) so monocytes can differentiate into macrophages
25
Which cells mainly aid in producing the fibrous cap? how?
vascular smooth muscle cells; they are the ones that migrate into the tunica intima and produce extracellular matrix, collagen, elastin, etc. This forms the fibrous cap while the inner portion is filled with foam cells/macrophages.
26
Which plaque enzyme acts to degrade the fibrous cap?
metalloprotease
27
How does the necrotic/lipid core of the plaque form?
the macrophages that have lots of free cholesterol die first (they die because the free cholesterol is toxic), and release the free cholesterol into the plaque killing cells and forming the core (lipids and debris)
28
T/F: thrombosis symptoms appear as soon as the lipid core is formed
false; the lipid core doesn't cause any symptoms when its under the fibrous cap, but when the plaque ruptures and the core interacts with the circulation, symptoms appear
29
T/F: apoptosis of macrophages is good for the atherosclerotic plaque development
false; apoptosis of macrophages can be **both good and bad** for the atherosclerotic plaque development. In the early lesion the apoptotic debris gets cleared, so it hinders plaque development. But later on when the plaque is bigger, the debris doesn't get cleared, thus making the plaque bigger.
30
What plays a physical role in disrupting the continuity of the fibrous cap?
the free cholesterol makes sharp crystals that can mechanically/physically pierce the fibrous cap open
31
After a plaque ruptures and a thrombus is formed, what process can result in stenosis?
constrictive remodeling
32
What's the difference between M1 and M2 macrophages?
M1= proinflammatory, initiate the plaque formation
M2= antiinflammatory, reduce plaque size and help tissue remodeling (matrix synthesis)
33
Patient feels severe chest pain when playing soccer, what kind of angina is this?
stable/classic/typical angina
34
What is Prinzmetal’s Angina?
Caused by coronary artery spasm (vasospastic angina) which reduces coronary blood flow leading to reduction of blood flow to the myocardium
35
Which administration method allows Nitroglycerin to reach a therapeutic dose faster?
a. Oral route
b. Transdermal route
c. Sublingual
c. Sublingual
36
What location does Nitroglycerin have the biggest effect on?
large veins (affected at lower doses)
37
Mechanism of action of Nitroglycerin. How does it reduce angina?
dilate veins, which decreases preload and venous return causing the oxygen consumption of myocardial muscle to be reduced
dilate arteries, which decreases resistance and afterload causing the oxygen consumption of myocardial muscle to be reduced
38
Explain how organic nitrates increase the blood supply to the heart.
Organic nitrates increase NO, which increase cGMP synthesis, which then relaxes vascular smooth muscle. This dialates coronary muscles and allows the blood supply to the heart to increase.
39
What drugs are contraindicated when organic nitrates are taken? why?
PDE5 inhibitors EX/sildenafil
it enhances the action of nitric oxide (NO) and cGMP and severely lowering blood pressure
40
How do beta 1-receptor Antagonists work to treat angina?
Reduce heart rate and force of contraction, thus reducing work done and oxygen demand.
41
When are beta 1-receptor Antagonists contraindicated?
in variant (vasospastic/Prinzmetal’s) angina (they man worsen symptoms)
42
Which Ca channel blockers is cardioselective?
a. Nifedipine
b. Verapamil
c. Amlodipine
d. Diltiazem
b. Verapamil
| (a nondihydropyridine)
43
Side effect of Calcium Channel Blockers?
constipation
44
What kind of anti-anginal drug is Ranolazine? Where is it metabolized?
Sodium Channel Blocker; Extensively metabolized in the liver by CYP enzymes
45
Patient comes in with unstable angina, what can you prescribe?
aspirin
heparin
clopidogrel
46
What's the long term effect of aspirin? explain.
reduced platelet aggregation; aspirin selectively inhibits thromboxane synthesis by inhibiting COX-1 (COX is the precursor to thromboxane)
thromboxane= hypertensive agent that facilitates platelet aggregation
platelets do not possess a cell nucleus and are therefore unable to resynthesize COX
47
Describe the relationship between blood flow and resistance versus blood flow and pressure gradient
↑Resistance= ↓ blood flow
↑pressure gradient= ↑ blood flow
48
What is the normal value of Pulse pressure?
40mmHg
Pulse pressure is the difference between systolic and diastolic; so the difference between them 120/80 mmHg
49
An increase in which of the following increases resistance?
a. viscosity of blood
b. radius of vessel
c. length of vessel
d. A+B
e. A+C
e. A+C
50
In a healthy patient, in which location can the blood flow become turbulent during exercise?
ascending aorta
51
What are four things that facilitate turbulent flow?
large blood vessels diameters
high velocities
low blood viscosity
stenotic cardiac valves
52
T/F: the total cross sectional area of capillaries are higher than the aorta
true
53
What's the major mechanism of regulating blood flow and blood pressure?
**Vascular tone** (the degree of contraction of vascular smooth muscle cells)
(for the record, both vascular tone and CO regulate BP)
54
Describe the role of the arterioles in regulating the blood pressure and the blood flow
They use vascular/arterial tone to regulate each of the following; its a war between increasing the pressure and allowing the blood flow, they're opposite forces
55
What occurs if the arterioles were fully dilated?
anaphylactic shock; we don't have enough blood to fill all the arteries, that's partly why they're always constricting
56
How do extrinsic factors affect arteriole contraction?
extrinsic factors mostly constrict the arterioles
(they're selfish and want a higher blood supply, so they constrict to get more.)
57
How do the intrinsic factors affect arteriole contraction? Where do these factors come from?
They usually dilate the arteries, they're selfish and only care about the blood they're getting, not about any other organ's blood supply.
These factors come from the endothelial cells of the arterioles and from the surrounding tissue **autocrine/paracrine.**
58
In theory, when blood pressure increases the blood flow would also increase, this doesn't happen in the body, why?
because the vessels contract to compensate
When the pressure increases, the diameter of the vessels increases with it- this causes a blood flow increase. However, right after, the vascular smooth muscles **constrict** to reduce the diameter and bring blood flow back to normal.
59
How do the vascular smooth muscle cells know when to contract?
(they contact when the blood pressure increases abruptly)
There are pressure/tension receptors that sense these changes and start the cation influx which leads into contraction.
TRPC6 receptors (Transient receptor potential cation channel)
60
After running for 5 minutes, the blood flow to skeletal muscle increased drastically. What do you call this? Explain the mechanism.
active hyperemia
This occurs due to tissue hypoxia and the generation of vasoactive metabolites
61
What is passive/reactive hyperemia?
higher blood flow after a period of ischemia
62
How will endothelial damage affect vessels? Would it cause vasoconstriction or vasodilation? Why?
**vasoconstriction**, because endothelial damage causes decreased secretions of Nitric oxide and Prostacyclin (which are both vasodilators) so the substances that cause constriction go unchallenged.
63
What are four endothelium produced substances that cause vasodilation?
Nitric oxide
Prostacyclin
Endothelium derived hyperpolarization factor
Acetylcholine (when endothelium is intact, it causes dilation. if not, then constriction)
64
How do **bradykinin** and **histamine** affect both arterioles and veins? What can this lead to?
they dilate arterioles and constrict veins
this causes the blood to easily leave the heart (low afterload) and get stuck in the dilated veins- leading to edema
65
Describe the vessel constriction/dilation from point A to point B. How is the relationship between the pressure and blood flow in this interval?
vessels maximally dilated, so the resistance is as low as possible.
pressure and blood flow are linearly proportional
66
Describe the vessel constriction/dilation from point B to point C. How is the relationship between the pressure and blood flow in this interval?
During this stage, the vessels are constricting to neutralize the pressure changes, so when you increase the pressure you don't see as much change in the blood flow. The resistance is increasing
67
Describe the vessel constriction/dilation from point C to point D. How is the relationship between the pressure and blood flow in this interval?
The vessels in this area are maximally constricted and the resistance is as high as it can be. So the vessels did what they could do, but the relationship between pressure and blood flow is linearly proportional.
68
Explain the long term pressure increase. In what ways to the vessels adapt to the higher pressure?
the pressure changes have very low effect on the blood flow (because it occurs slower and the body has time to adapt)
Adaption occurs by the proliferation of vascular smooth muscle cells of the vessels, so they become thicker and the diameter decreases. This allows them to withstand higher pressure.
69
Explain how an acute increase in pressure (and thus blood flow) is counteracted by **metabolic response**s.
As the pressure increases, it initially dilates the vessels and increases flow (occurs before the muscles contract in response) This flow of blood dilutes the dilatory substances, causing the vessels to constrict.
70
What organs have the highest autoregulation? lowest?
highest= brain, kidney, heart
lowest= skin
71
What are the autoregulation range? (the pressures that the body can successfully regulate) Explain why these limitations exist.
around 50-120mmHg or 60-180mmHg
we can't regulate below 50mmHg because at that pressure the vessels are fully dilated
We can't regulate above 180/200mmHg because the vessels are fully contracted (what else do you want them to do? they're trying their best!)
72
arteriosclerosis vs arteriolosclerosis
differentiate between them
arteri**o**sclerosis= in arteries (large and medium sized)
arteri**olo**sclerosis= in arterioles (small sized)
73
Which of the following does atherosclerosis mostly affect?
a. tunica intima
b. tunica media
c. tunica adventitia
a. tunica intima
(tunica media indirect affect)
74
Which hormone has a protective effect from atherosclerosis?
estrogen
75
What are a few things that can result in endothelial dysfunction?
high BP, fungi, toxins, nicotine, oxidized LDL, homocysteine
76
What attracts smooth muscle cells from the tunica media to intima?
monokines made by macrophages
77
What induces smooth muscle cell proliferation?
platelet-derived growth factors and other cytokines
78
T/F: thrombosis is the initial step of atherogenesis
false, its a complication of atherogenesis
79
What is a mural thrombus?
a thrombus that adheres to **the wall** of a blood vessel. They occur in **large vessels** such as the heart and aorta, and can restrict blood flow but usually **do NOT block it entirely.**
80
Explain what happened to this vessel.
layering of many mural thrombi, which then resulted in stenosis over time
81
Where are raised plaques most likely found?
medium-sized vessels
(they won't cause any significant stenosis in large sized vessels like the aorta)
82
What is the blue circle highlighting?
calcification
83
Describe the fibro/fatty proportions of this plaque.
it's a fibrous plaque
84
What process does this picture show? (wall very thick and to the side)
**remodeling of lesion**
the lesion invaded the tunica adventitia and grew into it instead of growing into the lumen of the vessel
**Eccentric coronary stenosis**
85
Which lesion if more susceptible to rupture? one with a thick or thin cap?
thin cap (duh!)
86
What is an intramural thrombus?
thrombus found inside the wall of the vessel, it pushes the wall from the inside and may rupture thus causing luminal narrowing
87
Which vessels does atherosclerosis affect more?
the large and medium blood vessels
it does **not** affect small blood vessels
88
What's the major cause of ischemic organ damage?
atherosclerosis
89
What kind of thrombus is "M"?
intramural thrombus
90
What kind of thrombus is this?
occlusive/luminal thrombosis
91
T/F: hemorrhage in vessel walls only occurs when a rupture of the vasa vasorum occurs
false, it may occur with or without a rupture
92
What causes sudden coronary spasms?
hemorrhage (in the blood vessel)
a rupture (in the blood vessel)
a rupture that causes hemorrhage
(vascular spasm causes pain)
93
What can you seen near the lumen of the vessel? What does this indicate?
you can see **cholesterol crystals** (white and pointy) so that means that there was a **rupture** nearby and that's how they ended up in the lumen. Its an **atheromatous embolus,** which is due to the fragmentation of cholesterol crystals or atheromatous debris from atherosclerotic vessels.
94
What's the difference between a thrombus and an embolus?
**thrombus=** or blood clot, _develops in a blood vessel_ and reduces the flow of blood through the vessel
**embolus=** **piece** of a blood clot that broke loose, **foreign object, or other bodily substance** becomes stuck in a blood vessel and largely obstructs the flow of blood
(both can cause coronary occlusion)
95
When does unstable angina happen and why?
Happens when patient at rest because of an **unstable legion** (thin fibrous capsule!) so it's susceptible to rupture and will cause a **nonocclusive thrombosis**
96
What are the two types of acute MI?
transmural (due to a complete occlusion)
subendocardial (due to partial thrombus that causes low perfusion, leading the endocardium of the heart to die)
97
When does a circumferential subendothelial MI occur?
When there's more than 75% stenosis in all three vessels, so severe hypoperfusion occurs and the subendothelial becomes ischemic
98
What can you see in this myocardial tissue?
contraction band necrosis (happens because myocytes die while contracting)
there's also fewer nuclei present
\*early myocardial necrotic changes
99
Describe the process of healing after an MI.
MI occurs and **necrosis** develops. Then **neutrophils** come to **digest** the necrotic tissue with enzymes (neutrophilic infiltrate). Now that the tissue is digested, **macrophages** come via new **capillaries** and eat the necrosis. The new blood supply/capillaries also bring **fibroblasts** to replace the dead tissue.
100
Describe the state of the myocardial tissue.
advanced necrosis and neutrophilic infiltration
101
identify cells
blue arrow= macrophages
yellow arrow= fibroblasts
\*this is granulation tissue
102
describe the state of the myocardial tissue
fibrous tissue formation
103
What's are complications of MI? What do these complications result in?
mainly **ventricular fibrillation** (a type of arrhythmias)
**cardiogenic shock** is also a complication that occurs due to acute left ventricular failure (aka pump failure)
\* these complications result in sudden death
104
What is Myocardial rupture? When does it occur?
Its when an area of the **muscular wall** of the heart weakens and ruptures (it ruptures because of the high pressure in the heart, like a baloon with no contracitlity). If this happens, then blood from witlhin the heart can leak into the pericardium.
This usually **because of a heart attack**; after the MI inflammation occurs and polymorphonuclear cells are trying to digest the dead tissue causing the area to be less rigid and more liquefactive, leading to rupture.
105
myocardial rupture→hemopericardium→cardiac tamponade
Explain.
When a myocardial rupture occurs, the heart wall explodes and blood goes to the pericardium and is stuck there, this is Hemopericardium (blood in the pericardial sac of the heart).
When a lot of blood is present in the pericardium, that leads to cardiac tamponade- which is the accumulation of fluid in the pericardial space, resulting in **reduced ventricular filling** and subsequent hemodynamic compromise (and diastole oopsie).
106
What occurs in the infract of the heart affects papillary muscles?
mitral valve prolapse
107
This is a heart of a hypertensive patient with a previous MI. explain what happened.
the previous MI may have **weakened** his heart (and **dilated** it) causing the ejection fraction to decrease. This would cause a build-up of blood in the ventricle that would coagulate and form a mural thrombus (it can also be pumped and become a systemic embolism)
108
What is a Ventricular aneurysm? What causes it?
aneurysm= a bulge in a wall
It occurs after an MI, the heart wall is **fibrotic and weak** so the high pressure in the heart would bulge the wall outwards. This is not dangerous by itself, but it makes **thrombus formation** more likely due to turbulence changes.
109
How does Myocardial perfusion imaging (MPI) work? What two radiotracers are used for its uptake?
you give the radiotracers and they get taken up by the areas with high perfusion (more blood flow= more uptake of radiotracers) this causes high extraction in the myocardium.
**99mTc Sestamibi/Tetrofosmin (Myoview)** and **201Thallium chloride** are used
110
When using Myocardial Perfusion Imaging, what's the best way to identify coronary artery stenosis?
the easiest way to identify is to compare the patient during rest and during stress (reduces uptake in stress!)
111
What's the difference between the two radiotracers?
1- 99mTc Sestamibi/Tetrofosmin (Myoview)
2- 201Thallium chloride
1= Lipid soluble chelates, 50% extracted by heart, no redistribution- so you have to take two studies (one in rest and one during stress)
2= Potassium analog so its taken up by the cells as K, 75% extracted by heart, go to areas with reduced perfusion, not used as much cuz of bad image quality
112
During the stress test, when should the radiotracer be injected?
one minute before exhaustion
113
How can we perform a stress test if the patient is unable to perform exercise? What 3 things do we use?
Adenosine
Dobutamine
Dipyridamole (persantine)
114
Which of the following is used in the stress test if a patient is asthmatic?
a. Adenosine
b. Dobutamine
c. Dipyridamole (persantine)
b. Dobutamine
| (Adenosine makes it worse)
115
Diagnose.
The short axis (one on top) is different during rest and exercise, the inferolateral wall of the ventricle doesn't have enough circulation during exercise. This reversible quality means that it's **ischemia** (change during stress, not permanent)
116
Diagnose.
Block appears in rest and during stress so it's infarct/blocked artery. Scarring is what caused this result.
117
How do you diagnose coronary artery disease? describe the findings.
You do a stress ECG and find ST depressions.
if the patient cannot exercise, use Myocardial perfusion imaging or Angiography (angiography is diagnostic and therapeutic)
118
When is the exercise tolerance test (ETT) not accurate?
the elderly
people with disabilities
women (less accurate)
people with conduction abnormalities
119
diagnose the scintigraphy image.
dilated left ventricle (bad prognosis)
120
diagnose
MI (regions of necrosis, which have a bad supply at rest and in stress)
121
T/F: MUGA analysis is based on qualitative data
false, it's based on quality (ex/ size of cardiac chambers) and quantity (ex/stroke volume)
122
The MUGA scan is mainly indicated for which patients?
(mainly) Patients receiving anthracycline chemotherapy
(Adriamycin) to monitor cardiac toxicity
+ Presurgical evaluation of patients
(as well as patients who have coronary artery disease, but these patients have many options for tests)
123
Describe the viability of the tissue. explain.
The tissue is not viable (scar tissue) because the blood flow and the metabolism are absent, meaning that the tissue is fully dead- irreversible damage.
124
Describe the viability of the tissue. explain.
The tissue is hybernating and viable. The blood flow is not reaching some regions, but they still have active metabolic processes. So if you reperfuse the tissue it will still function.
125
Which of the following does an ECG detect?
a. conduction
b. contraction
a. conduction
126
What are the three bipolar limb leads?
leads I, II, II
| (eithoven leads)
127
What are the three unipolar limb leads?
leads aVR, aVL, aVF
128
Which two of the following leads have the **negative** electrode on the right arm?
a. lead 1
b. lead 2
c. lead 3
d. aVF
e. aVR
f. aVL
a. lead 1
+
b. lead 2
129
Which of the following leads have the **positive** electrode on the left foot?
a. lead 1
b. lead 2
c. lead 3
d. aVF
e. aVR
f. aVL
b. lead 2
+
c. lead 3
+
d. aVF
130
Which of the following leads have the positive electrode on the left arm?
a. lead 1
b. lead 2
c. lead 3
d. aVF
e. aVR
f. aVL
a. lead 1
+
f. aVL
(lead 3= negative electrode on left arm)
131
Which leads provide a horizontal view of the heart?
the 6 chest leads
132
Which of the following are the inferior leads?
a. lead 1
b. lead 2
c. lead 3
d. aVF
e. aVR
f. aVL
b. lead 2
+
c. lead 3
+
d. aVF
133
Which of the following are the left lateral leads?
a. lead 1
b. lead 2
c. lead 3
d. aVF
e. aVR
f. aVL
a. lead 1
+
f. aVL
134
Which of the following leads have the highest reaction to this vector?
a. lead 1
b. lead 2
c. lead 3
c. lead 3
135
T/F: the 6 chest leads are unipolar
true
(they use the positive electrodes applied to the chest wall and a virtual/null electrode)
136
T/F: unipolar chest leads have one pole
false, they have the positive pole and a null/near-zero pole (created by averaging out three electrodes- this average acts like it's in the center of the heart)
137
What causes the P wave to become too **tall**? how about too **broad**? **inverted** P wave?
tall= right atrial hypertrophy
broad= left atrial hypertrophy
inverted= ectopic atrial rhythm
138
What are the leads with a positive (normal) P wave?
a. lead 1
b. lead 2
c. lead 3
d. aVF
e. aVR
f. aVL
b. lead 2
+
d. aVF
139
Which of the following chest leads appears biphasic during atrial depolarization?
V1
140
Which of the following chest leads are left lateral leads?
V5&6
141
Which of the following chest leads are anteroseptal leads?
V1, 2, 3, 4
(picture= V1+2 detect septal changes while V3+4 detect anterior changes.)
142
How to classify **chest** leads:
based on their location
VS
based on electrical changes they see
**(you can ignore this if you want, I got this info from Dr.Najeeb)**
**based on their location:**
V1+2= over the right side of heart (right leads)
V3+4= over the septum of heart (septal leads)
V5+6= over the left side of heart (left leads)
**based on electrical changes:**
V1+2= see septal changes (septal leads)
V3+4= see anterior changes ( anterior leads)
V5+6= see left changes (left leads)
143
name
qRs
144
name
Qr
145
name
qR
146
name
rS
147
name
QS
148
name
rsR'
If the initial deflection is positive = an R wave
A negative deflection following an R wave = an S wave
A second positive deflection (Another R) = an R’ wave
149
name
Rs
150
Which of the chest leads have a higher R wave amplitude?
V6
(amplitude gets higher as you the leads become more lateral)
151
Which of the chest leads have a deeper S wave?
V1
(S wave becomes less deep as you move laterally)
152
What bundle branch has to be defective in order for the M shaped ECG to appear in lead V6?
left bundle branch
153
During left bundle branch, what can you seen in the V1 chest lead? how about V6?
V1= W pattern
V6= M pattern
154
Which of the following causes ST elevation?
a. myocardial infarction
b. myocardial injury
c. myocardial ischemia
b. myocardial injury
+ a. myocardial infarction
155
Which of the following causes ST depression?
a. myocardial infarction
b. myocardial injury
c. myocardial ischemia
c. myocardial ischemia
156
Which of the following may cause R wave elevation?
a. myocardial infarction
b. myocardial injury
c. myocardial ischemia
b. myocardial injury
157
Which of the following causes deep Q waves?
a. myocardial infarction
b. myocardial injury
c. myocardial ischemia
a. myocardial infarction
158
Which of the following may cause T wave inversion?
a. myocardial infarction
b. myocardial injury
c. myocardial ischemia
c. myocardial ischemia
159
Which produces a tall P wave?
a. Right ventricular hypertrophy
b. Left ventricular hypertrophy
a. Right ventricular hypertrophy
160
**Right** ventricular hypertrophy: Which waves are affected? inverted?
**Tall P wave** (why? because right ventricular hypertrophy causes right arterial hypertrophy)
(^ because ventricular hypertrophy leads to atrial hypertrophy)
**T wave inversion in V1, V2, (V3, V4)**
161
**Left** ventricular hypertrophy: Which waves are affected? inverted?
**T wave inversion in I, aVL, V5, V6**
**ST depression in V5, V6**
(Changes are particularly in V5, V6)
(the **P wave** would also get **broad** because left ventricular hypertrophy also causes left atrial hypertrophy)
162
T/F: deeper Q waves remain present even after the patient healed
true, they're permanent. So if an old MI occurred, the Q waves never go back to normal.
163
Which leads are used to see infarctions in each of the following heart walls?
Anterior wall=
Anterolateral wall=
Inferior wall=
Posterior wall=
Anterior wall= V2-V4 (V5) (Q wave)
Anterolateral wall= V3-V6, I, aVL (Q wave)
Inferior wall= II, III, aVF (Q wave)
Posterior wall= V1 (R wave)
164
What two things cause ST elevation?
acute infarction, pericarditis
165
What causes ST depression?
ischemia, exercise, or subendocardial MI
166
how does K concentration affect T wave?
hypokalemia= low T wave
hyperkalemia= high T wave
167
In which leads is T wave normally inverted?
aVR
168
Which kind of MI causes ST segment elevation/deep Q waves?
a. Transmural MI
b. Subendocardial MI
a. Transmural MI
169
T wave inversion is associated with
myocardial ischemia (increased cardiac death)
(we also said that some leads go through T wave inversion during ventricular hypertrophy)
170
What is the J point?
The point between the end of the QRS complex and the ST segment
171
Which of the following shows J point depression only? (not ST-segment depression)
**E**
(Up-sloping depression of less than 1 mm at 80 ms beyond the J point (E) is simply J point depression)
172
After a coronary occlusion, how long does it take for the myocardial tissue to start dying?
30 minutes
173
What causes a STEMI?
ST segment elevation myocardial infarction most commonly occurs when thrombus formation results in **complete occlusion** of a major epicardial coronary vessel.
174
What's the cardinal symptom of acute coronary syndrome?
chest pain (severe pressure)
175
What are some radiation sites of ischemic chest pain?
retrosternal
Ulnar aspect of left arm
Neck
Jaw
Epigastrium
Back (interscapular)
176
T/F: radiation sites of ischemic chest pain can be the only/primary sight of pain
true (ex/ of someone who only has jaw pain)
177
T/F: men and women have a likely chance of presenting with unusual ischemic pain
false, women have a higher chance of having unusual symptoms
178
How do you differentiate between unstable angina pain and MI pain?
unstable angina= less than 30 minutes
MI= more than 30 min, severe, high troponin
179
Women comes in due to chest pain that has been present for 5 months, but it has been getting worse recently that she has pain while resting. diagnose
unstable angina
(crescendo angina- escalating angina- and the fact that she has pain while resting indicates this)
180
Patient comes in with chest pain. He points with one finger towards the left side of his chest to indicate the location of the pain. He says it hurts most when inhaling rapidly. Diagnose.
chest wall pain/ MSK pain/ costochondritis
181
Patient comes on sudden chest pain. He described it as tearing pain that caused shortness of breath, faintness, and loss of vision. After checking his pulse, the right arm has a weaker pusle than the left. diagnose.
aortic dissection
182
Whats the most common cause of chest pain?
chest wall pain
| (MSK)
183
Patient comes in with sharp pain on his sides that gets worse when he sneezes. He also has a fever and a productive cough. diagnose.
pneumonia
184
Patient comes in with sharp chest pain that radiates to the shoulder (trapezius muscle). Pain improves when he leans forward.
acute pericarditis
185
T/F: all unstable angina patients can be diagnosed with ECG
false, 1/3 have a normal ECG
(even MI patients may initially present with normal ECG- we treat them and keep checking ECG till we see abnormality)
186
T/F: MI patient with ST deviation have a worse prognosis
true
187
How long after MI does it take for troponin levels to elevate? How long will they stay high?
Modern assays can detect troponins as early as 3-4 hours after onset of myocardial damage. **(the note says 4-6 hours)**
**stays elevated for 2 weeks**
(this is why we use it to _confirm_ the diagnosis)
188
How do you diagnose MI?
elevated troponin levels + _one_ of the following things
motion abnormality, myocardial viability, ischemia signs, ST-segment or Q wave abnormalities, thrombus
189
What are some noncardiac reasons for increased troponin?
Renal failure, pulmonary causes, burns, **s**evere illness, **s**troke, **s**ubarachnoid hemorrhage, **s**epsis
190
You have a patient with a STEMI, whats the first thing you must do?
Dual Antiplatelet Therapy (Aspirin + P2Y12inhibitors Clopidogrel)
this is to prepare the artery for reperfusion
191
Whats the best treatment for a STEMI?
Percutaneous coronary intervention (**PCI** or angioplasty with stent)
if that's not possible then fibrinolysis therapy/ thrombolytic therapy
192
Patient comes in with STEMI, you apply dual antiplatelet therapy and see that the closest hospital that has a facility for PCI is 150 minutes away. What's the next course of action?
use the Fibrinolytic therapy (aka thrombolytic therapy)
Why? the PCI is the best treatment but it must be done within 2 hours- if thats not possible fibrinolytic therapy is the way to go.
193
Patient comes in with a STEMI and hemophilia A. The closest PCI facility is five hours away. What is the next course of action?
travel the five hours for a PCI facility. fibrinolytic therapy is absolutely contraindicated.
194
When is fibrinolytic therapy is absolutely contraindicated?
stroke or intracranial hemorrhage of unknown cause
ischemic stroke less than 6 months ago
recent head trauma (1 month)
recent GI bleeds
noncompressible punctures
aortic dissection
bleeding disorders
195
How to treat an NSTEMI?
Dual Antiplatelet therapy + Parenteral anticoagulation
196
When does fibrinolytic therapy stop being useful in treating a STEMI?
if the STEMI went on for 12 hours, the fibrinolytic therapy won't do anything. PCI is the only option.
197
After an MI the ejection fraction of the patient is below 40%. How do you treat this?
ACE inhibitor= to treat
aldosterone antagonist= secondary prevention drug
(if we keep the ejection fraction this low, remodeling will occur to compensate.)
198
What is a Q wave MI?
myocardial infarctions that in a Q wave forming on the 12-lead ECG once the infarction is completed. Many **Q-wave infarctions are often non-transmural**, and conversely, transmurality may occur in the absence of Q-waves.
199
A patient is suspected of having an MI. Lab tests also show elevated creatinine and glucose levels. What does this indicate?
elevated creatinine= renal impairment (maybe due to renal failure, which will increase the risk of MI)
elevated glucose= indicates necrosis (higher MI risk)
