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physiology > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Carries deoxygenated blood to the lungs

A

Pulmonary artery

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2
Q

Carries oxygenated blood from the lungs

A

Pulmonary vein

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3
Q

Pressure in the right atrium (Central Venous Pressure)

A

0 mmHg

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4
Q

Mitral & Tricuspid valves

A

AV Valves

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5
Q

Aortic & Pulmonic valves

A

Semilunar Valves

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6
Q

64% of blood volume is found in:

A

Veins (Reservoir of blood)

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7
Q

Found between myocardial cell membranes

A

Intercalated discs (with Gap junctions)

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8
Q

Found in Intercalated discs

A

Gap Junctions

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9
Q

Heart Rate (HR) x Stroke Volume (SV)

A

Cardiac Output (CO)

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10
Q

Cardiac output of Left & Right Heart

A

Equal (Resting: 5L/min) (due to higher resistance in pulmonary vessels)

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11
Q

Blood Flow Velocity: Highest

A

Aorta

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12
Q

Blood Flow Velocity: Lowest

A

Capillaries

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13
Q

“Stressed Volume”; Thick-walled, under high-pressure

A

Arteries

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14
Q

“Control conduits for blood flow”; Mainly under sympathetic control

A

Arterioles

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15
Q

Alpha 1: smooth muscle contraction ➡️ Vasoconstriction

A

Increases Total Peripheral Resistance (TPR) or Systemic Vascular Resistance (SVR)

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16
Q

Beta 2: smooth muscle relaxation ➡️ Vasodilation

A

Decreases Total Peripheral Resistance (TPR) or Systemic Vascular Resistance (SVR)

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17
Q

No Vasoconstriction or Vasodilation; Composed of single layer of endothelial cells; No smooth muscle layer; Closed Loop

A

Capillaries

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18
Q

“Unstressed Volume”; Thin-walled, under low pressure; With one-way valves

A

Veins

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19
Q

What happens when systemic arterioles vasoconstrict?

A

TPR/SVR: IncreasesBlood flow: Decreases

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20
Q

What happens when systemic arterioles vasodilate?

A

TPR/SVR: DecreasesBlood flow: Increases

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21
Q

What happens to blood pressure when TPR increases?

A

Blood Pressure: Increases (BP=COxTPR)

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22
Q

What happens when veins vasoconstrict?

A

Venous Return: Increases (CO & BP: Increases too)

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23
Q

Change in Pressure / Resistance

A

Ohm’s Law

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24
Q

Viscosity x Length / Radius

A

Poiseuille’s Law

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25
Q

Density x Diameter x velocity / viscosity

A

Reynold’s Number

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26
Q

Volume / Pressure

A

Compliance orCapacitance

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27
Q

Streamlined (straight line) flow; Velocity: highest at the center, lowest at the walls

A

Laminar Flow

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28
Q

Disorderly flow; Associated with High Reynold’s Number; Seen in Anemia

A

Turbulent Flow

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29
Q

Reynold’s Number: Laminar Flow

A
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30
Q

Reynold’s Number: Turbulent Flow

A

> 2000

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31
Q

“A strain in the structure of a substance produced by pressure, when its layers are laterally shifted in relation to each other”

A

Shear

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32
Q

Highest Shear

A

At the Walls of the vessels

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33
Q

Lowest Shear

A

At the Center of the vessel

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34
Q

Consequence of Shear

A

Decreases Blood Viscosity

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35
Q

Compliance of Veins vs Arteries

A

24x Higher Compliance

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36
Q

Compliance: Effect of Aging

A

Decreases Compliance

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37
Q

Highest arterial pressure

A

Systolic Pressure

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38
Q

Lowest arterial pressure

A

Diastolic Pressure

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39
Q

Difference: Systolic Pressure - Diastolic Pressure

A

Pulse Pressure

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40
Q

Stroke Volume (SV) / Arterial Compliance

A

Pulse Pressure

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41
Q

Synonym: Right Atrial Pressure

A

Central Venous Pressure

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42
Q

2/3 (Diastole) + 1/3 (Systole)

A

Mean Arterial Pressure

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43
Q

Used to estimate Left Atrial Pressure

A

Pulmonary Capillary Wedge Pressure

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44
Q

Blood Pressure: Large Arteries

A

120/80 mmHg

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45
Q

Blood Pressure: Systemic Capillaries

A

17 mmHg

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46
Q

Blood Pressure: Vena cava

A

0 mmHg

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47
Q

Blood Pressure: Pulmonary arteries

A

25/8 mmHg

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48
Q

Blood Pressure: Pulmonary Capillaries

A

7 mmHg

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49
Q

True or False: BP Systemic Circulation

A

False (>)

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50
Q

True or False: CO Systemic Circulation > CO Pulmonic Circulation

A

False (=)

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51
Q

Increased Systole; Normal Diastole; Increased Pulse Pressure

A

Arteriosclerosis

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52
Q

Decreased Systole; Normal Diastole; Decreased Pulse Pressure

A

Aortic Stenosis

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53
Q

Increased Systole; Decreased Diastole; Increased Pulse Pressure

A

Patent Ductus Arteriosus (PDA)

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54
Q

Increased Systole; Decreased Diastole; Increased Pulse Pressure (End-diastolic Pressure increases)

A

Aortic Regurgitation

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55
Q

Atrial Depolarization

A

P wave

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56
Q

Corresponds to AV Node Conduction

A

PR Segment

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57
Q

Correlates with conduction time/velocity through AV Node

A

PR Interval

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58
Q

Ventricular Depolarization

A

QRS Complex

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59
Q

Ventricular Repolarization

A

T wave

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60
Q

Period of Depolarization + Repolarization of Ventricles

A

QT Interval

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61
Q

Correlates with plateau of Ventricular action potential

A

ST Segment

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62
Q

What happens when Sympathetic NS stimulates the AV Node?

A

Conduction Velocity: IncreasesPR Interval: Decreases

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63
Q

What happens when Parasympathetic NS stimulates the AV Node?

A

Conduction Velocity: DecreasesPR Interval: Increases

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64
Q

What is the effect of Potassium on the ECG?

A

Hyperkalemia: Tall T WavesHypokalemia: Flat T waves

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65
Q

What is the effect of Calcium on the ECG?

A

Hypercalcemia: Shortened QT IntervalHypocalcemia: Prolonged QT Interval

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66
Q

What is the effect of MI on the ECG?

A

STEMI: ST Elevation, Q WavesNSTEMI: ST Depression

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67
Q

Abnormally prolonged interval between the QRS Complex and T Wave that may cause Sudden Cardiac Death in the children?

A

Long QT Syndrome (In Adults: Brugada Syndrome; In Athletes: Hypertrophic Cardiomyopathy)

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68
Q

Master pacemaker; Has unstable RMP; No sustained plateau

A

SA Node

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69
Q

Slowest conduction velocity (0.01-0.05m/sec)

A

AV Node

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70
Q

Fastest conduction velocity (2-4m/sec)

A

Bundle of His, Purkinje Fibers, Ventricles

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71
Q

Intrinsic Firing Rate: SA Node

A

70-80 beats/min (overdrive suppression)

72
Q

Intrinsic Firing Rate: AV Node

A

40-60 beats/min

73
Q

Intrinsic Firing Rate: Bundle of His

A

40 beats/min

74
Q

Intrinsic Firing Rate: Purkinje Fibers

A

15-20 beats/min

75
Q

What is the basis for AV Nodal Delay (0.13sec)?

A

Decreased Gap Junctions in that area

76
Q

Which Na+ channel accounts for SA Node Automaticity?

A

I-f Channels (slow “funny” Na+ channels)

77
Q

Which is responsible for setting the heart rate?

A

Rate of Phase 4 Depolarization

78
Q

Inhibition of “pacemaking” of latent pacemakers by the SA Node?

A

Overdrive Suppression

79
Q

AV block that causes fainting in patients due to initially suppressed state of Purkinje Fibers?

A

Stokes-Adams Syndrome

80
Q

Condition when latent pacemaker assume pacemaking activity?

A

Ectopic Pacemaker

81
Q

Conduction Velocity is dependent on which phenomenon?

A

Size of inward current during upstroke of Action Potential; Not dependent on duration of Action Potential

82
Q

All Na+ inactivation gates close; No new Action Potential can be generated

A

Absolute Refractory Period (ARP)

83
Q

At the end, some Na+ inactivation channels start to open; Action Potential cannot be conducted

A

Effective Refractory Period (ERP=ARP+RRP)

84
Q

Action Potential can be generated and conducted but higher-than-normal stimulus is required

A

Relative Refractory Period (RRP)

85
Q

All Na+ inactivation gates are open & membrane potential is higher than RMP (nearer to threshold); Cell is more excitable than normal

A

Supranormal Period (SNP)

86
Q

Basis for ventricular fibrillation; Occurs when, in the propagation of AP around the ventricles, the signal never reaches an area with ARP

A

Circus Movements

87
Q

Causes of Circus Movements: Dilated Cardiomyopathy

A

Long Conduction Pathway

88
Q

Causes of Circus Movements: Ischemic Heart, Hyperkalemia, Blocked Purkinje

A

Decreased Conduction Velocity

89
Q

Causes of Circus Movements: Epinephrine, Electrical stimulation

A

Short Refractory Period

90
Q

Produces changes in Contractility

A

Inotrophic Effect

91
Q

Produces changes in Rate of Relaxation

A

Lusitrophic Effect

92
Q

Produces changes in heart rate

A

Chronotrophic Effect

93
Q

Produces changes in Conduction Velocity

A

Dromotrophic Effect

94
Q

Inotropes affect:

A

Stroke Volume

95
Q

Chronotropes affect:

A

SA Node

96
Q

Dromotropes affect:

A

AV Node

97
Q

Beta 1 stimulation of the heart would result in

A

Stronger (positive inotrope), Briefer (positive lusitrope), & more frequent (positive chronotrope) Contractions

98
Q

Left Ventricular End-Diastolic Volume (LVEDV)

A

Pre-load of the Heart

99
Q

Aortic Pressure

A

Afterload of the Heart

100
Q

An increase in Pre-load will increase Stroke Volume (and consequently, Cardiac Output) within certain physiologic limits

A

Frank-Starling Mechanism

101
Q

LVEDV is directly proportional to what?

A

Venous Return & Right Atrial Pressure

102
Q

What happens when After-load increases?

A

Stroke Volume & Cardiac Output: Decreases Velocity of Sarcomere Shortening: Decreases

103
Q

What happens when Pre-load increases?

A

Stroke Volume & Cardiac Output: Increases

104
Q

Blood ejected of the ventricle per heart beat; Equal to EDV - ESV; Normal value: 70ml

A

Stroke Volume

105
Q

Percentage of EDV that is actually ejected of the ventricle; Equal to SV/EDV; Normal value: 55%

A

Ejection Fraction

106
Q

Total blood volume ejected per unit of time; Equal to HR x SV; Normal Value: 5L/min (resting)

A

Cardiac Output

107
Q

Work the heart performs on each beat; Equal to SV x Aortic Pressure; Fatty Acids are the primary source of energy

A

Stroke Work

108
Q

Work per unit of time; Equal to CO x Aortic Pressure; With 2 components: Volume Work (Cardiac Output) & Pressure Work (Aortic Pressure)

A

Cardiac Minute Work

109
Q

Increased by increased Afterload, size of the heart, contractility, heart rate

A

Myocardial O2 Consumption

110
Q

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)

A

Maximum Efficiency of Cardiac Contraction

111
Q

Right Atrial Pressure at which venous return is zero; Pressure in the blood vessels when the heart is stopped experimentally

A

Mean Systemic Pressure (MSP)

112
Q

Increase in blood volume; Decrease in Venous Compliance

A

Increases MSP

113
Q

Increased TPR

A

Decreases VR & CO

114
Q

Positive Inotrophic Agent

A

Increases CO

115
Q

Cardiac events that occur in a single heartbeat

A

Cardiac Cycle

116
Q

Occurs during the distal 3rd of Diastole; Preceded by P Wave in the ECG; Not essential for ventricular filling

A

Atrial Contraction

117
Q

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

A

Isovolumic Contraction

118
Q

Atrial filling begins; Semilunar valves open; Key Findings: Ventricular Pressure rapidly Increase & Ventricular Volume Decreases

A

Rapid Ventricular Ejection

119
Q

T-wave occurs in the ECG; Airtic pressure also decreases; Key Findings: Ventricular Pressure Decreases & Ventricular Volume Decreases

A

Reduced Ventricular Ejection

120
Q

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

A

Isovolumic Relaxation

121
Q

Opening of the AV valves; 3rd heart sound is heard; Ventricular Volume rapidly increase; Occurs during 1/3 of diastole

A

Rapid Ventricular Filling

122
Q

Longest cardiac cycle phase; Ventricular Volume reduced increase; Dependent on heart rate; Occurs during middle 3rd of diastole

A

Reduced Ventricular Filling (Diastasis)

123
Q

Atrial Pressure

A

0-4 mmHg

124
Q

Peaks of Atrial Pressure: Atrial Contraction

A

A Wave

125
Q

Peaks of Atrial Pressure: Contraction of Ventricles

A

C Wave

126
Q

Peaks of Atrial Pressure: Venous blood going to the atrium

A

V Wave

127
Q

In general, increases during systole and decreases during diastole

A

Aortic Pressure

128
Q

Slight increase in aortic pressure during isovolumic relaxation

A

Incisura

129
Q

Heart Murmur: 2nd ICS R Parasternal border

A

Aortic

130
Q

Heart Murmur: 2nd ICS L Parasternal border

A

Pulmonic

131
Q

Heart Murmur: 4th ICS L Parasternal border

A

Tricuspid

132
Q

Heart Murmur: 5th ICS L MCL

A

Mitral

133
Q

Physiologic murmurs occur only during systole or diastole?

A

Systole (all diastolic murmurs are pathologic)

134
Q

Centers responsible for regulation of HR & BP; Found in medulla

A

Vasomotor Area

135
Q

Respond to increase/decrease in pressures from 50-180 mmHg

A

Carotid Baroreceptors

136
Q

Respond to increase in pressures >80 mmHg

A

Aortic Baroreceptors

137
Q

Transmits afferent signal from Carotid Sinus to the medulla

A

Herring’s Nerve (Branch of CN IX)

138
Q

Transmits afferent signals from Aortic sinus to the medulla; Transmits efferent signals from medulla to the heart

A

Vagus Nerve (CN X)

139
Q

Response of Baroreceptor reflex to Increase in BP

A

Decrease in HR & SV; Vasodilation of arterioles & veins

140
Q

Response of Baroreceptor reflex to Decrease in BP

A

Increase in HR & SV; Vasoconstriction of arterioles & veins

141
Q

Forced expiration on closed glottis; Demonstrates Baroreceptor Reflex

A

Valsalva maneuver

142
Q

Responds to low O2, high CO2 concentration whenever BP is

A

Chemoreceptors

143
Q

Detects “fullness” of vascular system (increased intravascular volume)

A

Low-pressure Receptors (Cardiopulmonary Baroreceptors)

144
Q

In response to increased intravascular volume: Atrial Natriuretic Peptide (ANP)

A

Increases (counter regulatory of Aldosterone)

145
Q

In response to increased intravascular volume: Anti-Diuretic Hormone (ADH)

A

Decreases

146
Q

In response to increased intravascular volume: Renal

A

Vasodilation (increase GFR)

147
Q

In response to increased intravascular volume: Heart Rate

A

Increases (Bainbridge Reflex)

148
Q

The “last-ditch” stand; Very powerful systemic vasoconstriction; Vasomotor center itself responds directly to ischemia during low BP; Starts at

A

CNS Ischemic Response

149
Q

Occurs in response to increased intracranial pressure; Triad: HPN, Bradycardia, Irregular respirations

A

Cushing Reaction or Cushing Reflex

150
Q

What are the only two organs spared from powerful vasoconstrictive effects of the CNS Ischemic Response?

A

Heart (Coronary Circulation) & Brain (Cerebral Circulation)

151
Q

Activated when faster mechanisms fail to regulate BP; Also responsible for maintaining normal BP despite wide variation in salt Intake

A

Renin-Angiotensin-Aldosterone-System (RAAS)

152
Q

Describes fluid movement into (absorption) or out of (filtration) the capillary

A

Starling Forces

153
Q

Positive fluid movement; fluid moves out of capillary

A

Filtration

154
Q

Negative fluid movement; fluid moves into the capillary

A

Absorption

155
Q

Favors filtration; Determined by pressure & resistance in arteries & veins; Normal value: 25 mmHg

A

Capillary Hydrostatic Pressure

156
Q

Opposes filtration, Favors absorption; Increased by increases in plasma protein concentration; Normal value: 28 mmHg

A

Capillary Oncotic Pressure

157
Q

Opposes filtration, favors absorption; Slightly negative due to lymphatic pump; Normal value: -3 mmHg

A

Interstitial Hydrostatic Pressure

158
Q

Favors filtration; Determined by Interstitial Protein Concentration; Normal value: 8 mmHg

A

Interstitial Oncotic Pressure

159
Q

Normal Net Filtration

A

2 ml/min

160
Q

Hydraulic Conductance of Capillary Wall

A

Filtration Coefficient

161
Q

Lymph produced per day

A

2-3L

162
Q

Has 1-way valves and unidirectional flow; Reabsorbs proteins and wxcess fluid back to the circulatory syatem; Absorbs fat (using Lacteals)

A

Lymphatic System

163
Q

Excess fluid in the interstitial spaces beyond the capability of the lymphatic system to return in to the blood vessels

A

Edema

164
Q

When vascular smooth muscle are stretched, there’s a reflex contraction and vice versa; May explain autoregulation, but not active or reactive hyperemia

A

Myogenic Theory

165
Q

Vasodilator metabolites are produced as a result of metabolic activity

A

Metabolic Theory

166
Q

Substances increase blood flow during deoxygenation; Vasodilators: Adenosine, CO2, Adenosine phosphate compounds, K, H

A

Vasodilator Theory

167
Q

O2 is needed for vascular muscle contraction; Lack of O2 would lead to Vasodilation

A

Oxygen Lack Theory orNutrient Lack Theory

168
Q

Increase in blood flow in response to brief period of decreased blood flow

A

Reactive Hyperemia

169
Q

Blood flow increases to meet increased metabolic demand

A

Active Hyperemia

170
Q

Afferent arteriole constriction/dilation occurs to maintain appropriate renal blood flow & GFR; Macula densa in the distal tubile detects fluid levels

A

Tubuloglomerular Feedback orMacula Densa Feedback

171
Q

Most Potent Vasoconstrictor

A

Vasopressin

172
Q

Release as a result of blood vessel damage; Causes arteriolar vasoconstriction; Implicated in Migraine

A

Serotonin

173
Q

Released by damaged endothelium

A

Endothelin

174
Q

Counteracts TXA2

A

Prostacyclin

175
Q

Vasodilates upstream blood vessels

A

Nitric Oxide

176
Q

Causes arteriolar dilation & venous constriction leading to increased filtration (local edema)

A

Bradykinin & Histamine

physiology (12 decks)

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