Cardio Physiology Flashcards
1
Q
Carries deoxygenated blood to the lungs
A
Pulmonary artery
2
Q
Carries oxygenated blood from the lungs
A
Pulmonary vein
3
Q
Pressure in the right atrium (Central Venous Pressure)
A
0 mmHg
4
Q
Mitral & Tricuspid valves
A
AV Valves
5
Q
Aortic & Pulmonic valves
A
Semilunar Valves
6
Q
64% of blood volume is found in:
A
Veins (Reservoir of blood)
7
Q
Found between myocardial cell membranes
A
Intercalated discs (with Gap junctions)
8
Q
Found in Intercalated discs
A
Gap Junctions
9
Q
Heart Rate (HR) x Stroke Volume (SV)
A
Cardiac Output (CO)
10
Q
Cardiac output of Left & Right Heart
A
Equal (Resting: 5L/min) (due to higher resistance in pulmonary vessels)
11
Q
Blood Flow Velocity: Highest
A
Aorta
12
Q
Blood Flow Velocity: Lowest
A
Capillaries
13
Q
“Stressed Volume”; Thick-walled, under high-pressure
A
Arteries
14
Q
“Control conduits for blood flow”; Mainly under sympathetic control
A
Arterioles
15
Q
Alpha 1: smooth muscle contraction ➡️ Vasoconstriction
A
Increases Total Peripheral Resistance (TPR) or Systemic Vascular Resistance (SVR)
16
Q
Beta 2: smooth muscle relaxation ➡️ Vasodilation
A
Decreases Total Peripheral Resistance (TPR) or Systemic Vascular Resistance (SVR)
17
Q
No Vasoconstriction or Vasodilation; Composed of single layer of endothelial cells; No smooth muscle layer; Closed Loop
A
Capillaries
18
Q
“Unstressed Volume”; Thin-walled, under low pressure; With one-way valves
A
Veins
19
Q
What happens when systemic arterioles vasoconstrict?
A
TPR/SVR: IncreasesBlood flow: Decreases
20
Q
What happens when systemic arterioles vasodilate?
A
TPR/SVR: DecreasesBlood flow: Increases
21
Q
What happens to blood pressure when TPR increases?
A
Blood Pressure: Increases (BP=COxTPR)
22
Q
What happens when veins vasoconstrict?
A
Venous Return: Increases (CO & BP: Increases too)
23
Q
Change in Pressure / Resistance
A
Ohm’s Law
24
Q
Viscosity x Length / Radius
A
Poiseuille’s Law
25
Density x Diameter x velocity / viscosity
Reynold's Number
26
Volume / Pressure
Compliance orCapacitance
27
Streamlined (straight line) flow; Velocity: highest at the center, lowest at the walls
Laminar Flow
28
Disorderly flow; Associated with High Reynold's Number; Seen in Anemia
Turbulent Flow
29
Reynold's Number: Laminar Flow
<2000
30
Reynold's Number: Turbulent Flow
>2000
31
"A strain in the structure of a substance produced by pressure, when its layers are laterally shifted in relation to each other"
Shear
32
Highest Shear
At the Walls of the vessels
33
Lowest Shear
At the Center of the vessel
34
Consequence of Shear
Decreases Blood Viscosity
35
Compliance of Veins vs Arteries
24x Higher Compliance
36
Compliance: Effect of Aging
Decreases Compliance
37
Highest arterial pressure
Systolic Pressure
38
Lowest arterial pressure
Diastolic Pressure
39
Difference: Systolic Pressure - Diastolic Pressure
Pulse Pressure
40
Stroke Volume (SV) / Arterial Compliance
Pulse Pressure
41
Synonym: Right Atrial Pressure
Central Venous Pressure
42
2/3 (Diastole) + 1/3 (Systole)
Mean Arterial Pressure
43
Used to estimate Left Atrial Pressure
Pulmonary Capillary Wedge Pressure
44
Blood Pressure: Large Arteries
120/80 mmHg
45
Blood Pressure: Systemic Capillaries
17 mmHg
46
Blood Pressure: Vena cava
0 mmHg
47
Blood Pressure: Pulmonary arteries
25/8 mmHg
48
Blood Pressure: Pulmonary Capillaries
7 mmHg
49
True or False: BP Systemic Circulation < BP Pulmonic Circulation
False (>)
50
True or False: CO Systemic Circulation > CO Pulmonic Circulation
False (=)
51
Increased Systole; Normal Diastole; Increased Pulse Pressure
Arteriosclerosis
52
Decreased Systole; Normal Diastole; Decreased Pulse Pressure
Aortic Stenosis
53
Increased Systole; Decreased Diastole; Increased Pulse Pressure
Patent Ductus Arteriosus (PDA)
54
Increased Systole; Decreased Diastole; Increased Pulse Pressure (End-diastolic Pressure increases)
Aortic Regurgitation
55
Atrial Depolarization
P wave
56
Corresponds to AV Node Conduction
PR Segment
57
Correlates with conduction time/velocity through AV Node
PR Interval
58
Ventricular Depolarization
QRS Complex
59
Ventricular Repolarization
T wave
60
Period of Depolarization + Repolarization of Ventricles
QT Interval
61
Correlates with plateau of Ventricular action potential
ST Segment
62
What happens when Sympathetic NS stimulates the AV Node?
Conduction Velocity: IncreasesPR Interval: Decreases
63
What happens when Parasympathetic NS stimulates the AV Node?
Conduction Velocity: DecreasesPR Interval: Increases
64
What is the effect of Potassium on the ECG?
Hyperkalemia: Tall T WavesHypokalemia: Flat T waves
65
What is the effect of Calcium on the ECG?
Hypercalcemia: Shortened QT IntervalHypocalcemia: Prolonged QT Interval
66
What is the effect of MI on the ECG?
STEMI: ST Elevation, Q WavesNSTEMI: ST Depression
67
Abnormally prolonged interval between the QRS Complex and T Wave that may cause Sudden Cardiac Death in the children?
Long QT Syndrome (In Adults: Brugada Syndrome; In Athletes: Hypertrophic Cardiomyopathy)
68
Master pacemaker; Has unstable RMP; No sustained plateau
SA Node
69
Slowest conduction velocity (0.01-0.05m/sec)
AV Node
70
Fastest conduction velocity (2-4m/sec)
Bundle of His, Purkinje Fibers, Ventricles
71
Intrinsic Firing Rate: SA Node
70-80 beats/min (overdrive suppression)
72
Intrinsic Firing Rate: AV Node
40-60 beats/min
73
Intrinsic Firing Rate: Bundle of His
40 beats/min
74
Intrinsic Firing Rate: Purkinje Fibers
15-20 beats/min
75
What is the basis for AV Nodal Delay (0.13sec)?
Decreased Gap Junctions in that area
76
Which Na+ channel accounts for SA Node Automaticity?
I-f Channels (slow "funny" Na+ channels)
77
Which is responsible for setting the heart rate?
Rate of Phase 4 Depolarization
78
Inhibition of "pacemaking" of latent pacemakers by the SA Node?
Overdrive Suppression
79
AV block that causes fainting in patients due to initially suppressed state of Purkinje Fibers?
Stokes-Adams Syndrome
80
Condition when latent pacemaker assume pacemaking activity?
Ectopic Pacemaker
81
Conduction Velocity is dependent on which phenomenon?
Size of inward current during upstroke of Action Potential; Not dependent on duration of Action Potential
82
All Na+ inactivation gates close; No new Action Potential can be generated
Absolute Refractory Period (ARP)
83
At the end, some Na+ inactivation channels start to open; Action Potential cannot be conducted
Effective Refractory Period (ERP=ARP+RRP)
84
Action Potential can be generated and conducted but higher-than-normal stimulus is required
Relative Refractory Period (RRP)
85
All Na+ inactivation gates are open & membrane potential is higher than RMP (nearer to threshold); Cell is more excitable than normal
Supranormal Period (SNP)
86
Basis for ventricular fibrillation; Occurs when, in the propagation of AP around the ventricles, the signal never reaches an area with ARP
Circus Movements
87
Causes of Circus Movements: Dilated Cardiomyopathy
Long Conduction Pathway
88
Causes of Circus Movements: Ischemic Heart, Hyperkalemia, Blocked Purkinje
Decreased Conduction Velocity
89
Causes of Circus Movements: Epinephrine, Electrical stimulation
Short Refractory Period
90
Produces changes in Contractility
Inotrophic Effect
91
Produces changes in Rate of Relaxation
Lusitrophic Effect
92
Produces changes in heart rate
Chronotrophic Effect
93
Produces changes in Conduction Velocity
Dromotrophic Effect
94
Inotropes affect:
Stroke Volume
95
Chronotropes affect:
SA Node
96
Dromotropes affect:
AV Node
97
Beta 1 stimulation of the heart would result in
Stronger (positive inotrope), Briefer (positive lusitrope), & more frequent (positive chronotrope) Contractions
98
Left Ventricular End-Diastolic Volume (LVEDV)
Pre-load of the Heart
99
Aortic Pressure
Afterload of the Heart
100
An increase in Pre-load will increase Stroke Volume (and consequently, Cardiac Output) within certain physiologic limits
Frank-Starling Mechanism
101
LVEDV is directly proportional to what?
Venous Return & Right Atrial Pressure
102
What happens when After-load increases?
Stroke Volume & Cardiac Output: Decreases Velocity of Sarcomere Shortening: Decreases
103
What happens when Pre-load increases?
Stroke Volume & Cardiac Output: Increases
104
Blood ejected of the ventricle per heart beat; Equal to EDV - ESV; Normal value: 70ml
Stroke Volume
105
Percentage of EDV that is actually ejected of the ventricle; Equal to SV/EDV; Normal value: 55%
Ejection Fraction
106
Total blood volume ejected per unit of time; Equal to HR x SV; Normal Value: 5L/min (resting)
Cardiac Output
107
Work the heart performs on each beat; Equal to SV x Aortic Pressure; Fatty Acids are the primary source of energy
Stroke Work
108
Work per unit of time; Equal to CO x Aortic Pressure; With 2 components: Volume Work (Cardiac Output) & Pressure Work (Aortic Pressure)
Cardiac Minute Work
109
Increased by increased Afterload, size of the heart, contractility, heart rate
Myocardial O2 Consumption
110
Ratio of work output to total chemical energy expenditure; Normal value: just 20-25% (Most of the energy used by the heart is just converted to heat)
Maximum Efficiency of Cardiac Contraction
111
Right Atrial Pressure at which venous return is zero; Pressure in the blood vessels when the heart is stopped experimentally
Mean Systemic Pressure (MSP)
112
Increase in blood volume; Decrease in Venous Compliance
Increases MSP
113
Increased TPR
Decreases VR & CO
114
Positive Inotrophic Agent
Increases CO
115
Cardiac events that occur in a single heartbeat
Cardiac Cycle
116
Occurs during the distal 3rd of Diastole; Preceded by P Wave in the ECG; Not essential for ventricular filling
Atrial Contraction
117
Preceded by QRS Complex in the ECG; C Wave of atrial pressure is seen; AV valves will close; Semilunar valves are still closed; 1st Heart Sound (S1) is heard; Key Findings: Ventricular Pressure Increases & Ventricular Volume Remains the same
Isovolumic Contraction
118
Atrial filling begins; Semilunar valves open; Key Findings: Ventricular Pressure rapidly Increase & Ventricular Volume Decreases
Rapid Ventricular Ejection
119
T-wave occurs in the ECG; Airtic pressure also decreases; Key Findings: Ventricular Pressure Decreases & Ventricular Volume Decreases
Reduced Ventricular Ejection
120
Incisura of aortic pressure is seen; V wave of atrial pressure is seen; Semilunar valves closes, AV valves still closed; 2nd heart sound is heard; Key Findings: Ventricular Pressure Decreases & Ventricular Volume Remains the same
Isovolumic Relaxation
121
Opening of the AV valves; 3rd heart sound is heard; Ventricular Volume rapidly increase; Occurs during 1/3 of diastole
Rapid Ventricular Filling
122
Longest cardiac cycle phase; Ventricular Volume reduced increase; Dependent on heart rate; Occurs during middle 3rd of diastole
Reduced Ventricular Filling (Diastasis)
123
Atrial Pressure
0-4 mmHg
124
Peaks of Atrial Pressure: Atrial Contraction
A Wave
125
Peaks of Atrial Pressure: Contraction of Ventricles
C Wave
126
Peaks of Atrial Pressure: Venous blood going to the atrium
V Wave
127
In general, increases during systole and decreases during diastole
Aortic Pressure
128
Slight increase in aortic pressure during isovolumic relaxation
Incisura
129
Heart Murmur: 2nd ICS R Parasternal border
Aortic
130
Heart Murmur: 2nd ICS L Parasternal border
Pulmonic
131
Heart Murmur: 4th ICS L Parasternal border
Tricuspid
132
Heart Murmur: 5th ICS L MCL
Mitral
133
Physiologic murmurs occur only during systole or diastole?
Systole (all diastolic murmurs are pathologic)
134
Centers responsible for regulation of HR & BP; Found in medulla
Vasomotor Area
135
Respond to increase/decrease in pressures from 50-180 mmHg
Carotid Baroreceptors
136
Respond to increase in pressures >80 mmHg
Aortic Baroreceptors
137
Transmits afferent signal from Carotid Sinus to the medulla
Herring's Nerve (Branch of CN IX)
138
Transmits afferent signals from Aortic sinus to the medulla; Transmits efferent signals from medulla to the heart
Vagus Nerve (CN X)
139
Response of Baroreceptor reflex to Increase in BP
Decrease in HR & SV; Vasodilation of arterioles & veins
140
Response of Baroreceptor reflex to Decrease in BP
Increase in HR & SV; Vasoconstriction of arterioles & veins
141
Forced expiration on closed glottis; Demonstrates Baroreceptor Reflex
Valsalva maneuver
142
Responds to low O2, high CO2 concentration whenever BP is <80 mmHg
Chemoreceptors
143
Detects "fullness" of vascular system (increased intravascular volume)
Low-pressure Receptors (Cardiopulmonary Baroreceptors)
144
In response to increased intravascular volume: Atrial Natriuretic Peptide (ANP)
Increases (counter regulatory of Aldosterone)
145
In response to increased intravascular volume: Anti-Diuretic Hormone (ADH)
Decreases
146
In response to increased intravascular volume: Renal
Vasodilation (increase GFR)
147
In response to increased intravascular volume: Heart Rate
Increases (Bainbridge Reflex)
148
The "last-ditch" stand; Very powerful systemic vasoconstriction; Vasomotor center itself responds directly to ischemia during low BP; Starts at <60 mmHg and optimal at a BP = 15-20 mmHg
CNS Ischemic Response
149
Occurs in response to increased intracranial pressure; Triad: HPN, Bradycardia, Irregular respirations
Cushing Reaction or Cushing Reflex
150
What are the only two organs spared from powerful vasoconstrictive effects of the CNS Ischemic Response?
Heart (Coronary Circulation) & Brain (Cerebral Circulation)
151
Activated when faster mechanisms fail to regulate BP; Also responsible for maintaining normal BP despite wide variation in salt Intake
Renin-Angiotensin-Aldosterone-System (RAAS)
152
Describes fluid movement into (absorption) or out of (filtration) the capillary
Starling Forces
153
Positive fluid movement; fluid moves out of capillary
Filtration
154
Negative fluid movement; fluid moves into the capillary
Absorption
155
Favors filtration; Determined by pressure & resistance in arteries & veins; Normal value: 25 mmHg
Capillary Hydrostatic Pressure
156
Opposes filtration, Favors absorption; Increased by increases in plasma protein concentration; Normal value: 28 mmHg
Capillary Oncotic Pressure
157
Opposes filtration, favors absorption; Slightly negative due to lymphatic pump; Normal value: -3 mmHg
Interstitial Hydrostatic Pressure
158
Favors filtration; Determined by Interstitial Protein Concentration; Normal value: 8 mmHg
Interstitial Oncotic Pressure
159
Normal Net Filtration
2 ml/min
160
Hydraulic Conductance of Capillary Wall
Filtration Coefficient
161
Lymph produced per day
2-3L
162
Has 1-way valves and unidirectional flow; Reabsorbs proteins and wxcess fluid back to the circulatory syatem; Absorbs fat (using Lacteals)
Lymphatic System
163
Excess fluid in the interstitial spaces beyond the capability of the lymphatic system to return in to the blood vessels
Edema
164
When vascular smooth muscle are stretched, there's a reflex contraction and vice versa; May explain autoregulation, but not active or reactive hyperemia
Myogenic Theory
165
Vasodilator metabolites are produced as a result of metabolic activity
Metabolic Theory
166
Substances increase blood flow during deoxygenation; Vasodilators: Adenosine, CO2, Adenosine phosphate compounds, K, H
Vasodilator Theory
167
O2 is needed for vascular muscle contraction; Lack of O2 would lead to Vasodilation
Oxygen Lack Theory orNutrient Lack Theory
168
Increase in blood flow in response to brief period of decreased blood flow
Reactive Hyperemia
169
Blood flow increases to meet increased metabolic demand
Active Hyperemia
170
Afferent arteriole constriction/dilation occurs to maintain appropriate renal blood flow & GFR; Macula densa in the distal tubile detects fluid levels
Tubuloglomerular Feedback orMacula Densa Feedback
171
Most Potent Vasoconstrictor
Vasopressin
172
Release as a result of blood vessel damage; Causes arteriolar vasoconstriction; Implicated in Migraine
Serotonin
173
Released by damaged endothelium
Endothelin
174
Counteracts TXA2
Prostacyclin
175
Vasodilates upstream blood vessels
Nitric Oxide
176
Causes arteriolar dilation & venous constriction leading to increased filtration (local edema)
Bradykinin & Histamine
