Exam 2 Flashcards
1
Q
Size of a current in an ECG is proportional to?
A
Mass of tissue (# of cells)
2
Q
What medium does an ECG use to detect electrical activity?
A
Extracellular fluid
3
Q
Which way does the ECG dipole always point?
A
From center of negative electrical field to center of positive electrical field
4
Q
What does the P wave signify?
A
Atrial depolarization
5
Q
What does the QRS wave signify?
A
Ventricular depolarization
6
Q
What does the T wave signify?
A
Ventricular repolarization
7
Q
What is the PR interval?
A
The beginning of the P wave to the beginning of the QRS wave
8
Q
How long should a PR interval be?
A
<0.2 sec
9
Q
What happens if a PR interval is longer than 0.2 sec or shorter than 0.02 sec?
A
Conduction problems from atria to ventricle
10
Q
How long should the QRS complex be?
A
<0.1 sec
11
Q
What does it mean if the QRS complex is longer than 0.1sec?
A
-Block in bundle branches
or
-Rhythm originating in ventricular myocytes
12
Q
What should the ST segment always be?
A
Isoelectric
13
Q
What happens if the ST segment is not isoelectric?
A
Injury currents which lead to ischemia
14
Q
What does it mean if the T wave is inverted?
A
Chronic ischemia
15
Q
Where are the three standard electrode leads?
A
Left and right arms, and left leg
16
Q
What do the 3 standard electrode leads make up?
A
Einthoven’s triangle
17
Q
What are the normal axis values for a 12 lead ECG?
A
-30 to 110
18
Q
What happens with a left axis deviation (<-30)?
A
- Left ventricular hypertrophy
- Hypertension or cardiomyopathy
19
Q
What happens with a right axis deviation (>110)?
A
- Right ventricular hypertrophy
- Pulmonary hypertension disease
20
Q
What is the sequence of depol in the heart?
A
1) Left septum
2) Septum and endocardium
3) Epicardium
4) Base of heart (Back of left ventricle)
21
Q
What is the sequence of repol in the heart?
A
1) Epicardium and base repol
2) Endocardium and septum
22
Q
What is bradycardia?
A
<60 bpm resting heart rate
23
Q
What is tachycardia?
A
> 100 bpm resting heart rate
24
Q
Who usually experiences a sinus arrythmia?
A
Young adults and children
25
What happens to heart rate with sinus arrythmia?
- Faster during inspiration
| - Slower during expiration due to parasympathetic activation
26
What is an arrythmia?
Irregular heart rythm
27
What is a circus rythm?
Smaller AP, longer refractory period, and slow conduction velocity due to ischemic area of heart becoming pacemaker
28
What do injury currents do in myocardial ischemia?
Alter the ST segment to elevate or depress it
29
What cardium is most susceptible to ischemia?
endocardium
30
Why is endocardium more susceptible to ischemia?
- Higher pressures (which squeeze blood vessels)
| - Farther from blood supply of coronary arteries
31
What are the common sites of conduction blocks?
- AV node
| - Bundle branches
32
What are the common causes of conduction blocks?
- Ischemia in the conduction system
| - Degenerative changes with age
33
Is 1st degree heart block life threatening?
no
34
What are the symptoms of 1st degree heart block?
none
35
What happens with 1st degree heart block?
Delay of conduction through AV node
| ->Increased PR interval >0.2 sec
36
What are the common causes of 1st degree heart block?
- Ischemia
- Hyperkalemia
- Drugs that block AV node conduction (Beta blockers, digitalis, Ca blockers)
37
Is type 1 2nd degree heart block life threatening?
No
38
What happens in type 1 2nd degree heart block?
Progressive increase in PR interval until a P wave is not conducted
39
Is type 2 2nd degree heart block life threatening?
Yes
40
What can treat a type 2 2nd degree heart block?
Pacemaker
41
What happens in a type 2 2nd degree heart block?
Series of non-conducted P waves, followed by one conducted P wave
42
What are symptoms of type 2 2nd degree heart block?
- Very slow HR
| - Very slow ventricular depol rate
43
Where is a 3rd degree heart block found?
Between AV node and bundle branches
44
Is 3rd degree heart block life threatening?
Yes
45
What happens in a 3rd degree heart block?
No communication between atria and ventricles which causes
- Atria: 88 bpm
- Ventricle: 47 bpm
46
What are symptoms of 3rd degree heart block?
-Fainting (Stokes-Adams attacks)
47
What can treat 3rd degree heart block?
Pacemaker
48
What type of QRS wave is observed in a Bundle branch block?
Wide QRS wave
49
What does a right bundle branch block do to ventricular depolarization?
Causes the last phase of it to extend
50
What does a Left bundle branch block do to ventricular depolarization?
Causes the early phase of it to extend
51
What can cause a Right bundle branch block?
- Pulmonary hypertension
- Pulmonary stenosis
- Elderly degeneration
52
Is a right bundle branch block life threatening?
no
53
What can cause a Left bundle branch block?
- Systemic hypertension
- Aortic stenosis
- Elderly degenration
- Cardiomyopathy
- Coronary artery disease
54
What does a left bundle branch block indicate?
Underlying disease
55
How can a Left bundle branch block be treated?
Pacemaker
56
What happens to the QRS wave and T wave in premature ventricular contraction?
- Wide, irregular QRS
| - Inverted T wave
57
What generates a Premature ventricular contraction?
Group of ventricular myocytes
58
What is a string of Premature ventricular contractions called?
Ventricular tachycardia
59
What are the symptoms of ventricular tachycardia?
- may be no pulse
- Unconscious in seconds
- Can be fatal within minutes
60
What 3 factors effect stroke volume?
1) Preload
2) Afterload
3) Contractility
61
What are the two main mechanisms to increase contractility?
1) Frank-Starling mechanism
| 2) Sympathetic stimulation
62
Stroke work is directly proportional to?
Stroke volume
63
What happens to the stroke work/ filling pressure chart with sympathetic stimulation?
Curve shifts upward and to the left, increases stroke volume with less pressure
64
What does exercise do to the heart with respect to stimulation?
- Increase SNS stim
- Venoconstriction
- Muscle pump
65
What does exercise do to the heart with respect to stroke volume?
- Increased contractility
- Increased filling pressure
- Increased ejection fraction
- Increased left ventricular end diastolic pressure
66
Is increase in contractility and/or heart rate enough to increase steady state cardiac output?
no
67
What is required to increase central venous pressure?
Coordinated cardiovascular response ( more blood returned to heart)
68
What is the formula for stroke work?
∆P x ∆V
69
What can exercise do to stroke volume?
About double it
70
What can only SNS stim do to stroke volume?
Increase stroke work, but only a little bit of volume
71
What is the formula for total work of the heart?
∆P x ∆V + 1/2mv^2
72
What is the kinetic work of the heart like at rest?
~1% of total work on left side
| ~5% of total work on right side
73
What is the kinetic work of the heart like during heavy exercise?
~14% of total work on left side
| ~50% of total work on right side
74
What is the formula for efficiency of the heart?
External work / energy expended
75
What causes energy expense to be so high in the heart?
- Tension generation
| - Ionic pumps
76
Is efficiency low or high in the heart?
Low
77
What is the formula for energy expense?
Time-tension index= Heart Rate x Systolic Blood Pressure
78
What is the efficiency of the heart at rest?
~5-10%
79
What is the efficiency of the hear during exercise?
~15%
80
About what percent of the hearts energy is used for ionic pumps?
~25%
81
O2 consumption is directly proportional to?
Coronary blood flow
82
What percent of O2 does the heart extract at rest?
65-75%
83
How does coronary blood flow match O2 needs?
- Increased metabolic activity causes cells to release metabolites
- Coronary vessels vasodilate in response
84
How does coronary blood flow move?
-Behind aortic valve-> Sinus of valsalva-> Opening for coronary arteries-> Coronary arteries-> Capillaries-> Veins-> Coronary sinus-> Right atrium
85
What are the three types of flow?
1) Laminar
2) turbulent
3) Single file
86
Which layer is the slowest in laminar flow?
The outermost layer
87
What is the formula for shear stress?
SS=(4 x Flow x Viscosity)/ π x r^3
88
What is shear stress?
Frictional force caused by sliding lamina of blood
89
What is an acute adjustment to increased flow and subsequently sheer stress?
Dilation to bring ss down to normal level
90
What is a chronic adjustment to increased flow and subsequently sheer stress?
remodeling of arteries to become larger
91
What happens if there is very low shear stress?
Endothelial cell dysfunction
92
What happens if there is very high sheer stress?
Dissecting aneurysm (Tearing of the wall)
93
What are cells subject to low shear stress susceptible to?
Atherosclerosis
94
How does the shape of endothelial cells change from high shear stress to low shear stress?
More taut with high ss, blocky with low ss
95
What is the formula for the turbulent flow equation (or reynolds #)?
Re=(Velocity x diameter x density)/Viscosity
96
At what reynolds number does turbulent flow begin to happen?
2000
97
How do the relationship between flow and pressure change once a reynolds number of 2000 is reached?
- Before 2000 is reached Q is directly proportion to P
| - After 2000 is reached Q is directly proportional to √P
98
Where is turbulent flow seen?
- Aortic root at peak flow
- Blood vessel with atherosclerotic plaques
- Artery branch points
99
Where does single file blood flow happen?
Capillaries
100
What is the diameter of a capillary compared to that of a red blood cell?
Capillary= 5-6µm
| RBC=8µm
101
What is the formula for viscosity of blood?
Shear stress/ Shear rate
102
What is the formula for shear rate?
∆Velocity/ diameter
103
What is blood serum?
Plasma without the clotting factors
104
What is hematocrit?
% of red blood cells
105
What is the relationship between hematocrit and viscosity?
Hematocrit is directly proportional to viscosity
106
What mainly causes the viscosity of blood?
Red blood cells
107
What type of fluid is blood?
Non Newtonian fluid
108
How does viscosity relate to the size of the tube in which the liquid is contained?
- The smaller the tube the less viscous the liquid
| - The bigger the tube the more viscous the liquid
109
How does viscosity relate to shear rate?
As shear rate goes up viscosity goes down
110
How does high shear rate lower viscosity?
It keeps RBCs spread out
111
How does low shear rate raise viscosity?
It allows RBCs to stick together
112
What happens to hematocrit in microvessels?
It decreases from aaroun 40% in central to 24% in arteriolar
113
What is the formula for Pousilles law?
Q=(∆P x π x r^4)/ (8 x Viscosity x L)
114
What is the formula for resistance in series?
Rtotal= R1+R2+R3.....
115
What is the formula for resistance in series?
1/Rtotal=1/R1+1/R2+1/R3....
116
What is the formula for tension?
Tension= Pressure x Radius
117
What is the formula for wall stress?
Wall stress= (Pressure x radius)/ wall thickness
118
What is the acute vessel reaction to hypertension?
Constriction
119
What is the long term vessel reaction to hypertension?
Increase in wall thickness
120
What is the formula for Mean Arterial Pressure at rest?
MAP= Diastolic BP + (Systolic BP - Diastolic BP)/3
121
What is the usual speed of blood flow?
~0.2 m/s
122
What happens to a pressure wave as arteries stiffen?
The pressure wave begins to move faster
123
What is the pressure wave difference between someone young and someone old?
```
Young= ~4-5 m/s
Old= ~10 m/s
```
124
What effect does a fast pressure wave have on the vascular system?
Increases Mean arterial pressure
125
How does venous shape change from low volume to high volume?
At very low volume it becomes dumbbell like, works its way up to circular
126
What happens to venous blood when someone goes from supine to standing?
Shifts ~500mL blood to the lower extremities
127
What causes hypotension of the veins?
Decreased central venous pressure and decreased stroke volume
128
What is the long term compensation to hypotension?
Venoconstriction
129
What two factors maintain flow with posture change?
- Increase in arterial pressure
| - Increase in Venous pressure
130
What two pumps assist venous flow?
- Respiratory
| - Muscle
131
What do muscle and respiratory pumps do to capillary pressure in the foot?
Decrease it
132
What happens during a inspiration respiratory pump?
- Decreased pressure in thoracic veins
- Increased abdominal pressure
- Increased filling in thoracic veins
133
What happens during a expiration respiratory pump?
- Increased Pressure in thoracic veins
- Decreased abdominal pressure
- Decreased filling in thoracic veins
134
What are the 4 regulated Hemodynamic factors?
1) MAP
2) Tissue flow
3) Shear Stress
4) Wall Stress
135
What is the formula for MAP?
MAP= Q x Total peripheral resistance
136
What regulates Tissue flow?
∆ing artery/arteriole diameter
137
What regulates shear stress?
Artery/arteriole diameter
138
What regulates wall stress?
- Artery/arteriole diameter acutely
| - Wall thickness chronically
139
Where does endothelial cell paracellular transportation happen?
Between junctions
140
Where does endothelial cell transcellular transportation happen?
Through the actual cell
141
Describe endothelial cells on the arterial side
- Elongated with prominent stress fibers
| - Low permeability (complex tight junctions)
142
Describe endothelial cells on the venous side
- Have receptors for inflammation
| - Very leaky when inflammation occurs
143
Name the type of capillaries by premeability from lowest to highest.
Lowest: Continuous
Mid: Fenestrated
Highest: Discontinuous
144
What are the main inflammatory factors?
- VEGF
- Histamine
- Substance P
145
What do the inflammatory factors do?
Increase permeability on the venous side
146
What does a rise in cAMP do?
Decrease permeability by increasing tight junction formation
147
What does a rise in cGMP do?
Increase permeability
148
What does an increase in shear stress do?
- Acutely increases permeability
| - Chronically decreases permeability
149
Where are vesicula-vacular organelles found?
In venules within tumors or areas of high inflammation
150
How does VVO permeability compare to caveolae permeability?
About 2 x as wide as caveolae and much more permeable
151
What inflammation factors are normally found where VVOs are?
- VEGF*
- Serotonin
- Histamine
152
How do endothelial cells control blood vessel diameter?
Release of vasoactive factors
153
What 3 vasoactive factors relax smooth muscle cells?
1) NO* (nitric oxide)
2) PGI2 (prostacyclin)
3) EDHF (Endothelial derived hyperpolarizing factor)
154
How does EDHF move from ECs to SMCs?
Through gap junction
155
What vasoactive factor constricts smooth muscle cells?
Endothelin
156
What two channels do endothelial cells have?
- ATP K/NA channel (Na-K ATPase)
| - Kir (inward rectifier potassium channel)
157
What is the range of a EC resting membrane potential?
-30 to -68 mV
158
Why do ECs not have action potentials?
No voltage gated Na or Ca channels so no upstroke
159
What is IP3?
Inositol triphosphate
| -A membrane phospholipid metabolite
160
What two things does an increase in EC Ca do?
1) Activates Nitric Oxide synthase-> release NO-> SMC relaxation
2) Increases permeability in venules
161
What does hyperpolarization of a EC do?
1) Increases the driving force for Ca entry
| 2) Travels from EC-> SMC to hyperpolarize it-> relaxation
162
How does PGI2 move from ECs to SMCs?
Uses a g protein receptor (7 crossing)
163
What is Prostacyclin (PGI2)?
A metabolite of arachidonic acid which is a membrane phospholipid derived molecule
164
What is COX?
Cyclo Oxygenase
165
What does aspirin (a NSAID) do?
Blocks COX from converting arachidonic acid to PGI2
166
How is PGI2 made?
PLA2->arachidonic acid -COX> PGI2
167
What are NO*s 4 anti-atherosclerotic effects?
1) Relaxes SMC
2) Inhibits platelet aggregation
3) Inhibits EC and SMC proliferation
4) Inhibits luekocyte adhesion
168
What is NO*s non anti-atherosclerotic effect?
-Involved in increased venular permeability with inflammation
169
What two things produce NO*?
- Shear Stress
| - Agonists
170
What is PI3K?
PI3 Kinase
171
What is eNOS?
Endothelial Nitric oxide synthase
172
How does increased intracellular Ca stimulate eNOS?
Increased Ca->Ca-Calmodulin->Binds to eNOS and activates
173
What is the other way (not Ca but still requires calmodulin) to stimulate eNOS?
Phosphorylation of eNOS
174
What is EDHF?
Probably a metabolite of arachidonic acid
175
What causes dilation in large arteries?
Mainly NO, very little EDHF
176
What causes dilation in small arteries and arterioles?
Primarily EDHF
177
What is required for EDHF to move?
Myoendothelial gap junctions (MEJs)
178
When do Myoendothelial gap junctions increase?
With a decrease in arteriole/artery size
179
How long does endothelin constriction last?
2-3 hours after washed away
180
What does Endothelin participate in?
Remodeling-> Stimulates vascular and cardiomyocyte proliferation-> Participates in hypertrophy
181
What is endothelin implicated in?
- Carcinogenesis
- Bronchoconstriction
- Fibrosis
- Heart failure
- ***Pulmonary hypertension (Vasoconstriction in lungs)
182
What is ECE?
Endothelium converting enzyme
183
What percentages of endothelin go where?
25% to Circulation
| 75% to SMC
184
What can decrease the production of ET-1 mRNA?
Increase in NO and PGF2
185
What regulates production of ET-1?
Increase or decres in Pre-Pro ET-1
186
What can raise Pre-Pro ET-1?
- Vasoconstrictors (Shear stress, Angiotensin, vasopresin, and catecholamines)
- LDL
187
What can lower Pre-Pro ET-1?
-Vasodilators (NO*, PGI2, atrial natriuretic peptide, estrogen)
188
What does ET-1 usually play a role in?
total amount of vasoconstriction in body
189
Where is ET-1 the highest?
In the lungs by about 5x
190
What can improve pulmonary hypertension caused by ET-1?
Endothelin receptor blockers
191
What is the rate limiting reagent in the RAAS system?
Renin
192
How is angiotensin made?
Angiotensinogen -renin> Angiotensin I-> Angiotensin II
193
What is ACE?
Angiotensin converting enzyme
194
What releases renin?
The kidneys
195
What releases angiotensinogen?
Liver
196
What releases ACE?
Lungs
197
What do ACE inhibitors do?
Treat hypertension
198
What does angiotensin II do?
- Increase SNS activity
- Potent vasoconstriction
- Increase H2O kidney reabsorption
- Increase thirst
- Increase Mean arterial pressure
199
What are the clotting effects after there is a tear or rupture of small blood vessels?
-Vascular constriction-> Platelet plug formation-> 3-6 minutes later blood coagulation
200
What is the process of clotting after vessel damage?
Vessel damage-> Activates clotting cascade-> activation of thrombin in blood which allows fibrinogen to create an insoluble fiber network
201
What is a thrombus?
-Clot attached to blood vessel wall
202
What is a embolus?
-Free floating clot
203
What are the 4 main causes for thromboembolisms?
1) Imbalance between clotting and anticlotting factors due to atherosclerosis or age
2) Slow moving blood
3) Large mass of traumatized tissue
4) Septicemic shock
204
How can a large mass of traumatized tissue cause a thromboembolism?
Widespread clotting
205
How can septicemic shock cause a thromboembolism?
Bacterial infection can intitate clotting cascade
206
What are the steps to allow infiltration of leukocytes in venules?
1) Acitvated EC
2) Slow rolling
3) Arrest leukocytes
4) Diapedis
