Quiz 1 Flashcards
1
Q
What two factors principally determine the cardiac output?
A
Heart Rate
Stroke Volume
2
Q
What are LVEDV and LVESV?
A
LVEDV- Left ventricular end diastolic volume
LVESV- Left ventricular end systolic volume
3
Q
What is the formula for stroke volume?
A
SV = LVEDV - LVESV
4
Q
What is the formula for Ejection fraction (EF)?
A
EF = SV / LVEDV
5
Q
What is the range for a normal ejection fraction?
A
55-70%
6
Q
What is the general definition of preload?
A
7
Q
What is the definition of preload as it pertains to the heart? What factor primarily determines preload?
A
8
Q
What is the definition of afterload as it pertains to the heart? What is it often approximated by?
A
9
Q
What is contractility in the heart? What nervous system regulates contractility? What effect does it have on ESV (LVSEV)?
A
10
Q
What is venous return?
A
11
Q
What are the three main factors that affect venous return?
A
1) Right atrial pressure
- decreased RAP increases VR
2) Mean systemic filling pressure
- Increased MSFP increases venous return
3) Total peripheral resistance
-Decreased TPR increases venous return
12
Q
What is right atrial pressure? What is the normal range? What can cause it to decrease/increase?
A
13
Q
What is MSFP? What causes it to increase/decrease?
A
14
Q
What proportion of resistance to venous return is determined by arteriolar/small artery resistance? What proportion by venous resistance?
A
15
Q
What is the resting membrane potential for a contractile cardiac mucle cell?
A
-80 mV
16
Q
What occurs during phase 4 of a ventricular myocyte action potential?
A
17
Q
What occurs during phase 0 of a ventricular myocyte action potential?
A
18
Q
What occurs during phase 1 of a ventricular myocyte action potential?
A
19
Q
What occurs during phase 2 of a ventricular myocyte action potential?
A
20
Q
What occurs during phase 3 of a ventricular myocyte action potential?
A
21
Q
What occuring during phase 4 of a ventricular myocyte action potential?
A
22
Q
What event during a cardiac myocyte action potential induces muscle contraction?
A
23
Q
In a healthy heart, the only viable pathway for electrical signaling between the atria and the ventricles is what structure?
A
The bundle of His
24
Q
Myocytes specializing in conduction have notably smaller levels of what two contractile proteins?
A
Myosin and Actin
25
What occurs during phase 4 of a cardiac pacemaker cell action potential?
26
What occurs during phase 0 of a cardiac pacemaker cell action potential?
27
What occurs during phase 3 of a cardiac pacemaker cell action potential?
28
What is the sarcolemma as found in cardiac myocytes?
29
What are T-tubules as found in cardiac myocytes (also present in other muscle types)?
30
What are L-type Ca2+ channels as found in cardiac myocytes?
31
What is the Ryanodine receptor? What is its function?
32
What elements does a couplon consist of?
33
What is the role of the sarcoplasmic reticulum?
34
What is the first step of excitation contraction coupling?
35
What is the second step of excitation contraction coupling?
36
What is the third step of excitation contraction coupling?
37
What is the fourth step of excitation contraction coupling?
38
What is the role of SERCA in step 5 of excitation contraction coupling?
39
What is the role of NaCaX in step 5 of excitation contraction coupling?
40
What is the role of the Ca2+ pump in step 5 of excitation contraction coupling?
41
Descrie which leads should be observed in the "quick and dirty" axis determination method:
42
What are three potential causes of a left axis deviation?
43
What are three potential causes of a right axis deviation?
44
STEMI localized to the LCX or diagonal branch of LAD arteries will involve which EKG leads?
45
STEMI localized to the RCA or LCX arteries will involve which EKG leads?
46
STEMI localized to the LAD will involve which EKG leads?
47
What is true about the relationship between ST elevations and ST depressions?
48
What is a hallmark on an EKG denoting a prior MI?
49
What is Ohm's law?
I = V/R
V= IR
50
How can Ohm's law (picture attached) be related to blood flow?
51
What is the formula for MAP derived from Ohm's law?
52
What are two formulas for MAP using SBP and DBP?
53
What is the formula for calculating resistance to blood flow in a vessel?
54
What is the signifance of Poiseuille's law in terms of blood flow?
55
Why is Poiseulle's law referred to as a fourth power law?
The relationship between radius and flow (or resistance in medical applications) is massive due to r being raised to the 4th power
56
What is the most important factor determing blood flow in the CV system?
Vessel radius
57
How is resistance totaled when the resistors are arranged in a series?
58
How is resistance totaled when the resistors are arranged in parallel?
59
What is the formula for compliance? How is compliance different from elastance? Of arteries and veins, which are more compliant? Which are more elastance?
60
What are three notable causes of blood viscosity? What is a notable cause of low viscosity?
61
How is pulse pressure calculated? What is its relation to stroke volume and to arterial compliance?
62
What is the law of Laplace in context of ventricular myocardium?
*where h is the thickness of the ventricular myocardium
63
At what structure does an AP orginating from the SA node slow before entering the ventricles?
The AV node
64
Which two catecholamines are the most responsible for binding adrenergic receptors?
Epinephrine and Norepinephrine
65
What G protein is preferred by a-1 adrenergic receptors?
66
What G protein is preferred by a-2 adrenergic receptors?
67
What G protein is preferred by b-1 adrenergic receptors?
68
What G protein is preferred by b-2 adrenergic receptors?
69
Which alpha adrenergic receptor acts pre-synaptically, inhibiting the release of NE?
alpha-2 receptors
70
Which alpha receptor acts post-synaptically, stimulating phospholipase C to cause vasoconstriction and pupil dilation?
alpha-1 receptors
71
What effect does alpha-1 receptor activation have on associated muscle?
72
What three tissues are associated with alpha-1 receptors? What are the associated responses at each tissue?
73
Where are alpha-2 receptors found? What response is associated with receptor activation?
74
What two tissues are beta-1 receptors associated with?
The heart and kidneys
75
Which parts of the heart and kidney are beta-1 receptors associated with? What responses are associated with receptor activation?
76
In which five tissues are beta-2 receptors principally found? What responses are associated with activation of these receptors?
77
Which catecholamine has a preference for alpha receptors over beta receptors?
NE
78
Does EPI have a preference for alpha or beta receptors?
Neither; EPI stimulates alpha and beta receptors equally
79
If a tissue has only beta receptors, will EPI or NE be the effective stimulant?
EPI
80
T/F: NE has an 100 fold greater affinity for the beta-2 receptor than EPI
False; EPI has an 100 fold greater affinity for the B2 receptor relative to NE
81
What signaling molecule binds to cholinergic receptors?
Acetylcholine (ACh)
82
What are the two types of cholinergic receptors?
Nicotinic
Muscarinic
83
What are the two synapse types where muscarinic receptors are found?
84
What tissues are M1 receptors found in? What response is associated with receptor activation?
85
Which four parts of the heart are M2 receptors associated with? What are the responses to receptor activation?
The fourth is to decrease contractility in the ventricles
86
What six tissues/organ systems are M3 receptors associated with?
87
What occurs in response to M3 receptor activation in secretory glands and in sweat glands?
88
What three divisions of the respiratory system are associated with M3 receptors? What response is associated with receptor activation?
89
What 5 elements of the GI tract are associated with M3 receptors? What responses occur as a result of receptor activation?
90
What two elements of the urinary bladder are associated with M3 receptors? What responses are associated with receptor activation?
91
What three elements of the eye are associated with M3 receptors? What responses are associated with receptor activation?
92
What is the cell membrane permeable to?
Water ghosts on steroids
-H20
-Gasses (O2, CO2)
- Lipid based molecules like steroid hormones
93
Which of the Starling forces has the greatest effect on fluid movement?
Capillary hydrostatic pressure (Pc)
94
If lymphatic capillaries are blind-ended tubes, how does excess interstial fluid enter them?
95
Using this diagram, explain how right-sided HF can lead to edema
Good job!
96
A patient with hypoalbuminemia and edema is given an infusion of albumin with normal saline. What happens to the following:
-Plasma volume
-Interstitial volume
-Intracellular volume
-Plasma osmolality
-Cellular osmolality
97
What would be the most likely cause of sustained dyspnea with a finding of pulmonary edema?
Left-sided heart failure
98
Which organ produces angiotensinogen?
99
Which is the direct action of Renin?
100
How is angiotensin I converted to angiotensin II? In what type of capillary does the majority of this conversion take place in the body?
101
What are the direct effects of angiotensin II in the body (besides stimulating aldosterone secretion)?
102
What are the direct effects of aldosterone secretion? In which part of the kidneys do they exert their effect?
103
Lymph nodes in which parts of the body drain into the thoracic duct? In which parts of the body do they drain into the right lymphatic duct?
104
Into what structure(s) does the thoracic lymphatic duct drain?
Into the internal jugular vein, the subclavian vein, or the joint between the two (L. brachiocephalic vein)
105
The major vein draining a tissue is partially occluded. What would be the expected effects on the following:
-Capillary hydrostatic pressure
-Interstitual fluid hydrostatic pressure
-Lymph flow rate
106
Why does concentration of EPI matter in regards to vasoconstriction/vasodilation?
107
What is the perfusion pressure of the coronary arteries approximated by?
108
What three types of factors do the coronary arteries use to control their own blood flow?
Metabolic factors
Endothelial factors
Neural factors
109
What is the main metabolic factor that coronary arteries use to control blood flow during hypoxemia? What are other metabolites that act as vasodilators?
110
What endothelial factors can be used by coronary arteries to control their blood flow? Which factor is a vasoconstrictor?
111
What is nitric oxide a metabolite of? How does it cause SM relaxation and vasodilation?
112
What is NO a metabolite of? How does it cause SM relaxation and vasodilation?
113
What are the two ANS (neural) factors that coronary arteries use to control blood flow? Which is the main contributor?
114
How is the change in pressure calculated using Ohm's law in context of blood flow?
115
In Poiseuille's law, blood flow has what relationship to vessel radius and resistance?
116
What are the three major determinants of myocardial oxygen demand?
117
In Laplace's law, what relationship does wall stress have to pressure, radius and thickness?
118
What is atherosclerosis? In what type of arteries does it occur? How common is it?
119
What are the two types of arteriolosclerosis? In what type of arteries does it occur? How common is it?
120
What is Monckeberg medial arteriosclerosis? How common is it? In what types of arteries does it occur?
121
What are the top 4 locations (in descending order) that are most commonly involved in atherosclerosis?
122
Which landmark study identified common risk factors for CVD?
123
What are 4 nonmodifiable RF for atherosclerosis? What are 4 modifiable RF?
124
What is the first step in the "Response to Injury" hypothesis for atherosclerosis?
Explain the pathogenesis using the diagram
125
What is the second step in the "Response to Injury" hypothesis for atherosclerosis?
Explain the pathogenesis using the diagram
126
What is the third step in the "Response to Injury" hypothesis for atherosclerosis?
Explain the pathogenesis using the diagram
127
What is the fourth step in the "Response to Injury" hypothesis for atherosclerosis?
Explain the pathogenesis using the diagram
128
What is the fifth step in the "Response to Injury" hypothesis for atherosclerosis?
Explain the pathogenesis using the diagram
129
What pathology of early atherosclerosis can be seen here?
A fatty streak
130
What are the color and pattern of formation of atherosclerotic plaques (gross findings)? Where are they particularly common?
131
What are the three main differences between a vulnerable plaque and a stable plaque?
132
What are the three stages of progression of atherosclerosis in the pre-clinical phase?
133
What are the three major complications of atherosclerosis in the clinical phase?
134
What is an abdominal aortic aneurysm often associated with?
135
What sizes of an aortic mural thrombus are high risk for rupture?
136
What atherosclerotic pathology finding is seen here?
Lines of Zahn
137
What are lines of Zahn?
138
Atherosclerosis complications include peripheral vascular disease (PVD) What is the progression of symptoms in PVD?
139
T/F: Atherosclerosis is not a realistic cause of stroke
False
140
What type of arteriosclerosis is displayed here? What is it commonly seen in?
141
What type of arterosclerosis is displayed here? What is it seen in?
142
What are the etiologies of hyaline arteriosclerosis and hyperplastic arteriosclerosis?
Hyaline art- proteins leak into damaged vessel wall (pink "glassy" material)
Hyperplastic art- proliferation of SM and BM ("onion skinning" layers of SM and BM)
143
What type of arteriosclerosis is seen here? In what patient population is it often found?
Monckeberg’s arteriosclerosis
144
What are the syndromes that compose ischmeic heart disease?
145
How many deaths in the US are due to ischemic heart disease? After what age does risk increase?
146
How long after 90+% of coronary flow is lost does myocyte death begin? Is it reversible?
20-30 minutes
It is irreversible
147
What microscopic changes are seen less than four hours after an infarction?
148
What microscopic changes are seen between 4-24 hours after an infarction?
149
What microscopic changes are seen between 1-3 days after an infarction?
150
What microscopic changes are seen between 4-7 days after an infarction?
151
What microscopic changes are seen between 1-3 weeks after an infarction?
152
What microscopic changes are seen months after an infarction?
153
How long after an infarction is a ruptured septum, ventricular free wall, or papillary muscle seen?
154
How long after an infarction is an aneurysm, mural thrombus, or Dressler syndrome seen?
155
What complications are possible within the first 24 hours of an infarction?
156
Based on the histology slide, how recently has this patient had an MI?
Less than four hours (normal findings)
157
Based on the histology slide, how recently has this patient had an MI? What findings can be seen?
Between 4 and 24 hours
Necrosis (loss of nuclei)
Hemorrhage
158
What is the etiology of the wavy fibers seen in this biopsy? How long after an MI can this be seen?
159
Based on the histology slide, how recently has this patient had an MI? What findings can be seen?
Between 1-3 days
Inflammation of predominantly neutrophils
160
Based on the histology slide, how recently has this patient had an MI? What findings can be seen?
Between 4-7 days
Inflammation of predominantly macrophages
161
Based on the histology slide, how recently has this patient had an MI? What findings can be seen?
Between 1-3 weeks
162
Based on the histology slide, how recently has this patient had an MI? What findings can be seen?
4+ weeks
163
What MI complication is seen here?
Ventricular free-wall rupture
164
What MI complication is seen here?
Septal rupture
165
What MI complication is seen here?
Papillary muscle rupture
166
What MI complication is seen here?
Fibrinous pericarditis
167
What MI complication is seen here?
Mural thrombus
168
What MI complication?
Aneurysm
169
What is Dressler's syndrome? How is it differentiated from fibrinous pericarditis?
170
What are the physical symptoms associated with the following effects of myocardial ischemia?
171
According to the Canadian cardiovascular society (CCS) What constitutes classes I- IV of chest pain?
172
How is unstable angina defined according to the CCS?
173
What are the three acute coronary syndromes (ACS)?
STEMI
NSTEMI
Unstable angina
174
What five factors play a major role in diagnosis of CAD?
175
What are the two types of stress testing? Which is always accompanied by imaging (PET, ECG, MRI)?
Exercise
Pharmacologic
Pharmacologic stress testing is accompanied by imaging
176
What two medication regimens are used for pharmacologic stress testing?
Dobutamine -> increase HR and contractility
Adenosine/Dipyridamole- vasodilation
177
What three questions should be asked in determing a cardiac stress test? In what situations should imaging be done?
178
What are the three main goals of tx of angina?
179
What does PCI stand for? What are examples of PCI?
Percutaneous coronary intervention
Ballon, stent, rotoblation
180
What treatment for angina (CAD) can be employed if PCI is insufficient?
Coronary artery bypass grafting (CABG)
181
What is the pathophysiology of 90% of ACS cases?
182
After a patient history of chest pain denotes probable ACS, how is a UA/NSTEMI differentiated from a STEMI?
183
What two areas of an ECG can help differentiate between UA/NSTEMI and a STEMI?
184
How can a UA be differentiated from an NSTEMI?
185
Why is troponin measured? When does it begin to be elevated? When does it peak?
186
What is the door to balloon time for a STEMI? What is the door to lytic time? When are thrombolytics indicated?
DTB < 90 minutes
DTL < 30 minutes
Thrombolytics are only used for STEMI AND DTB time estimated at over 90 minutes
187
When are thrombolytics used in treatment of ACS? What are two types of thrombolytics used?
188
What two classes of drugs are used to increase blood supply apart from thrombolytics?
189
What are three types of anticoagulants used to increase blood supply during ACS? What are 2 types of antiplatelets besides aspirin?
190
What are three examples of P2Y12 inhibitors used to treat ACS?
191
What are the six primary treatments used in cases of UA/NSTEMI? What secondary treatment is preferred?
192
What specific reasons might there be for an urgent/invasive stratery in treatment of a UA/NSTEMI?
193
A patient between what ages presenting with aortic stenosis would be most lie to have a rheumatic etiology? (95% mitral disease)
Ages 40-60
*also some congenital bicuspid presentations
194
A patient between what ages presenting with aortic stenosis would be most likely to have a degenerative etiology?
70+
195
A patient between what ages presenting with aortic stenosis would be most likely to have a congenital (unicuspid/bicuspid) etiology?
Under 30
196
How common is a bicuspid aortic valve? What is the inheritance pattern? With what changes/pathologies is it associated?
197
What are the three main symptoms of aortic stenosis?
198
What type of murmur is expected with aortic stenosis? Which heart sound maybe absent?
199
What is the treatment for aortic stenosis?
200
What is a TAVR?
201
What is the most common etiology of mitral stenosis? Is it more common in men or women?
202
What is the hallmark of rheumatic valve disease?
203
What are common symptoms of mitral stenosis? Why are pulmonary and right sided heart symptoms common?
204
Between what sounds can mitral stenosis be auscultated?
205
What treatments are available for mitral stenosis?
206
At what point is heart disease class III or class IV according to the NYHA?
207
What three surgical procedures are available for a mitral stenosis?
208
How common is tricuspid stenosis? What are 2 common symptoms? How is it treated?
209
Though rare, what are two significant causes of pulmonic stenosis? What type of heart sound abnormalities can be auscultated? What is the first line treatment?
210
What are the four most likely causes of acute mitral regurgitation?
211
What are the symptoms of acute mitral regurgitation?
212
What treatments are administered for acute mitral regurgitation?
213
What are the most likely etiologies for chronic mitral regurgitation? In what ways are etiologies different from acute MR?
Involvement or mitral annulus, left ventricle, and additional leaflet etiologies.
Unlikely to have rupture or involvement or papillary muscles or chordae tendinae
214
How much of the population is affected by mitral valve prolapse (Barlow's syndrome, myxomatous mitral valve)? What is the inheritance pattern? What other diseases is it associated with?
215
What symptoms typically present with chronic mitral regurgitation? Why are symptoms associated with low CO and pulmonary congestion?
216
Between what heart sounds can chronic mitral regurgitation be auscultated? How is it differentiated from acute mitral regurgitation?
217
What kind of imaging can be done to diagnose chronic mitral regurgitation?
218
What are the clinical symptoms of acute aortic regurgitation?
219
Between what heart sounds is an acute aortic regurgitation able to be auscultated?
220
How serious is acute aortic regurgitation? What treatments are usually given? What treatments are CI?
221
What symptoms are common with chronic aortic regurgitation? Walk through how these symptoms relate to the pathophysiology of the disease.
222
Between what heart sounds can chronic aortic regurgitation be auscultated?
223
What kind of imaging is used to diagnose chronic aortic regurgitation?
224
What three criteria are used to determine if Aortic valve replacement is necessary?
225
Do mechanical or bioprothetic valves last longer? Which requires anticoagulative therapy?
226
Do mitral valve or aortic valve replacements result in thrombosis more often? How is thrombosis of an artificial valve treated?
227
How serious is prothetic valve endocarditis?
228
