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Step 1 - Cardiovascular > Physiology > Flashcards

Physiology Flashcards

1
Q

Cardiac output

A

Stroke volume x Heart rate

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2
Q

Cardiac output according to Fick’s principle

A

Rate of oxigen consumption / (arterial O2 content - venous O2 content)

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3
Q

Mean arterial pressure

A

CO x total peripheral resistance (TPR)

2/3 Dyastolic pressure x 1/3 systolic pressure

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4
Q

Pulse pressure

A

Systolic pressure - diastolic pressure

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5
Q

Pulse pressure is proportional to _______ and inversely proportional to ________

A

Stroke volume

Arterial compliance

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6
Q

End diastolic volume - end systolic volume

A

Stroke volume

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7
Q

CO is mantained by ____ and _____ during EARLY stages of exercise

A

Heart rate

Stroke volume

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8
Q

During LATE stages of exercise CO is mantained by

A

Heart rate only

Stroke volume plateaus

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9
Q

Preferentially shortened by high heart rate

A

Diastole

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10
Q

Isolated systolic hypertension in elderly

A

Aortic stiffening

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11
Q

Stroke volume depends on

A
  1. Contractility: directly
  2. Preload: directly
  3. Afterload: inversly
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12
Q

Contractility increases with

A
  1. Cathecolamine stimulation via B1 Rc
  2. Higher intracellular Ca
  3. Lower extracellular Na
  4. Digitalis (Blocks Na/K pump: more ic Na: less Na/Ca exchanger: more intracellular Ca)
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13
Q

Cathecolamine stimulation via B1 receptor effects

A
  1. Ca channels phosphorilated: more Ca entry: more Ca induced ca release and Ca storage in sarcoplasmic reticulum
  2. Phospholamban phosphorylation: active Ca ATPase: Ca storage in sarcoplasmic reticulum
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14
Q

Contractility decreases with

A
  1. Beta 1 blockade: less cAMP
  2. Heart failure with systolic dysfunction
  3. Acidosis
  4. Hypoxia/hypercapnia
  5. Non dihydropyridine Ca channel blockers
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15
Q

Myocardial oxygen demand increases with

A
  1. Contractility
  2. Afterload
  3. Heart rate
  4. Diameter of ventricle: more wall tension
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16
Q

Wall tension

A

Follows Laplace’s law:

Pressure x radius

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17
Q

Wall stress

A

Pressure x radius (tension) / 2 x wall thickness

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18
Q

Decreases preload

A

Venous vasodilators: nitroglycerin

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19
Q

Decreases afterload

A

Arterial vasodilators: hydralazine

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20
Q

Decrese preload and afterload

A 
ACE inhibitors (IECA)
ARB (ARA-II)
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21
Q

Chronic hypertension (increased MAP) produces

A

Left ventricle hypertrophy to overcompensate for high afterload in order to decrease wall tension

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22
Q

Ejection fraction

A

Stroke volume / End diastolic volume

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23
Q

Index of ventricular contractility

A

Ejection fraction

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24
Q

loss of contractility

A
  1. Loss of myocardium: myocardial infarct
  2. Beta blockers
  3. Non dihydropypiridine Ca
  4. Channel Blockers
  5. Dilated cardiomyopathy
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25
Q

Digoxine is a

A

Positive inotrope

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26
Q

_____ account for most of TPR

A

Arterioles

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27
Q

Highest cross-sectional area

Lowest flow velocity

A

Capillaries

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28
Q

Volumetric flow rate (Q)

A

Flow velocity x cross sectional area

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29
Q

Viscosity depends mostly on

A

Hematocrit

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30
Q

Viscosity increases in (examples)

A

Hyperproteinic states: multiple myeloma

Polycitemia

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31
Q

Viscosity decreases in

A

Anemia

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32
Q

Inotropic + effect

A

Cathecolamines

Digoxin

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33
Q

Inotropic - effect

A

Uncompensated HF
Narcotic overdose
Sympathetic inhibition

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34
Q

Increases venous return

A

Fluid infusion

Sympathetic activity

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35
Q

Decreases venous return

A

Accute hemorrage

Spinal anesthesia

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36
Q

Decreases total peripheral resistance

A

Exercise

AV shunt

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37
Q

Increase total peripheral resistance

A

Vasopressors

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38
Q

Period of the highest ventricular O2 consumption

A

Isovolumetric contraction

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39
Q

Isovolumetric contraction

A

Between mitral valve closing and aortic valve opening

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40
Q

Isovolumetric relaxation

A

Between aortic valve closing and mitral valve opening

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41
Q

Rapid filling

A

Period just after mitral valve opening

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42
Q

Reduced filling

A

Period just before mitral valve closing

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43
Q

Phases of left ventricle

A
  1. Isovolumetric contraction
  2. Systolic ejection
  3. Isovolumetric relaxatio
  4. Rapid filling
  5. Reduced filling
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44
Q

S1

A

Mitral and tricuspid valve closure

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45
Q

S2

A

Aortic and pulmonary valve closure

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46
Q

S3: when, meaning, pathological/normal

A
  • Early diastole, during rapid ventricular filling
  • High filling pressures: mitral regurgitation, HF
  • Dilated ventricles, normal in children and young adults
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47
Q

S4: when, meaning, pathological/normal

A
  • Late diastole, atrial kick
  • High atrial pressure
  • Ventricular noncompliance: hypertrophy: left atrium must push against stiff LV wall
  • ABNORMAL, regardless of patient age
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48
Q

S4 is normal when

A

IT’s never normal, regardless of patient’s age

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49
Q

a wave (JVP)

A

atrial contraction

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50
Q

a wave is absent in

A

atrial fibrillation: a=atrial

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51
Q

c wave

A

RV contraction: c=contraction

Closed tricuspid valve bulging into atrium

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52
Q

x descent

A

Downard displacement of closed tricuspid valve during rapid ventricular ejection phase

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53
Q

v wave

A

high atrial pressure due to filling against closed tricuspid valve

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54
Q

y descent

A

RAtrium emptYing into RV

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55
Q

Prominent y descent

A

Constrictive pericarditis

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56
Q

Absent y descent

A

Cardiac tamponade

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57
Q

Normal splitting of S2 occours

A

During inspiration due to the higher venous return and higher RV filling because of the drop in intrathoracic pressure

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58
Q

Wide spitting of S2 occours in

A

Conditions that delay RV emptying:

  • Pulmonic stenosis
  • Right bundle branch block
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59
Q

Fixed splitting

A

Atrial septal defect: left to right shunt: higher Righ atrial and right ventricle volume

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60
Q

Paradoxical splitting

A

Delayed aortic valve closure:
-Aortic stenosis
-Left bundle branch block
On inspiration P2 moves closer to A2, thereby paradoxically eliminating the split

61
Q

Increases intensity of right heart sounds

A

Inspiration

62
Q

Increases intensity of hypertrophic cardiomyopathy murmur

A 
Valsalva (phase II)
Standing up (decreases preload)
63
Q

Decreases intensity of hypertrophic cardiomyopathy

A

Handgrip

Squating

64
Q

Hand grip…

A

Increases afterload:

  • Less intensity of HCM
  • More intensity of MR, AR, VSD murmurs
65
Q

Decreases intensity of most murmurs

A

Valsalva phase II

Standing up

66
Q

Earlier onset of MVP click/murmur

A

Valsalva

Standing up

67
Q

Aortic stenosis murmur

A

Crescendo-decrescendo systolic ejection murmur

Click may be present

68
Q

Aortic stenosis symptoms

A

SAD:
Syncope
Angina
Dyspnea

69
Q

Most common cause of aortic stenosis

A

Age related calcification in older patients: >60 years old

Early onset calcification of bicuspid aortic valve

70
Q

Mitral/tricuspid regurgitation: murmur characteristics

A

Holosystolic

High pitched: blowing murmur

71
Q

MR is often due to

A

Ischemic heart disease: post-MI
Mitral valve prolapse
Left Ventricle dilatation

72
Q

TR is often due to

A

Right ventricle dilatation

73
Q

Most frequent valvular lesion

A

Mitral valve prolapse

74
Q

Mitral valve prolapse: murmur characteristics

A

Late systolic crescendo murmur with midsystolic click

75
Q

Midsistolic click in mitral valve prolapse is due to

A

Chordae tendinae sudden tensing

76
Q

Mitral valve prolpase can be caused by

A

Myxomatous degeneration: Marfan, Ehler-Danlos
Rheumatic fever
Chordae tendinae rupture

77
Q

Ventricular septal defect murmur

A

Holosystolic
Harsh-sounding
Loudest at tricuspid

78
Q

Can predispose to infective endocarditis

A

Mitral valve prolapse

79
Q

Pulsus parvus et tardus

A

Aortic stenosis: pulses are weak with a delayed peak

80
Q

Aortic regurgitation murmur

A

High pitch
Early diastolic
Decrescendo

81
Q

Watson’s water hammer pulse or corrigan pulse or magnus and celer pulse

A

Aortic regurgitation

82
Q

Severe aortic regurgitation can produce _____ when severe and chronic

A

head bobbing

83
Q

Aortic regurgitation is due to

A

Aortic root dilation
Bicuspid aortic valve
Endocarditis
Rheumatic fever

84
Q

Interval between S2-OS and severity of mitral stenosis

A

Shorter interval=higher severity

85
Q

Mitral stenosis murmur

A

Opening snap: abrupt halt in leaflet motion in diastole, after rapid opening due to fusion at leaflet tips
Mid to late diastolic murmur

86
Q

Late and highly specific sequela of rheumatic fever

A

Mitral stenosis

87
Q

Chronic Mitral Stenosis can result in

A

LA dilatation

88
Q

Continuous murmur

A

Patent ductus arteriosus: continuous machine like murmur loudest at S2
Due to congenital rubella or prematurity

89
Q

Phases of myocardial action potential

A

0: rapid upstroke and depolarisation
1: initial repolarisation
2: plateau
3: rapid repolarization
4: resting potential

90
Q

Phase 0 of myocardial action potential

A

Rapid upstroke and depolarisation

Voltage gated Na channels open

91
Q

Phase 1 of myocardial action potential

A

Initial repolarisation: inactivation of voltage gated Na channels
Voltage gated K channels begin to open

92
Q

Phase 2 of myocardial action potential

A

Ca influx through voltage gated Ca channels balances K efflux
Ca influx from ECF triggers Ca release from sarcoplasmic reticulum and myocyte contraction

93
Q

Phase 3 of myocardial action potential

A

Massive K efflux due to opening of voltage gated slow K channels and closure of voltage gated Ca channels

94
Q

Phase 4 of myocardial action potential

A

Resting potential

High K permeability through K channels

95
Q

3 differences cardiac muscle vs skeletal muscle

A
  1. Cardiac muscle action potential has a plateau, due to Ca influx and K efflux
  2. Cardiac muscle contraction requires Ca influx from ECF to induce Ca release from sarcoplasmic reticulum
  3. Cardiac myocytes are electrically coupled to each other by gap junctions
96
Q

Refractory periods in cardiac cycle

A
  1. Absolute refractory period: no stimulus can cause depolarisation
  2. Effective refractory period: may allow for non propagated depolarization
  3. Relative refractory period: allows a normal than stronger stimuli to cause a full depolarization
  4. Supranormal period: hyperexcitable period, even a weak stimulus can trigger an action potential
97
Q

Pacemaker action potentials occour in

A

SA and AV nodes

98
Q

Phase 0 of pacemaker action potential

A

Upstroke: opening of voltage gated Ca channels

99
Q

Phase 1 of pacemaker action potential

A

Doesn’t exist

100
Q

Phase 2 of pacemaker action potential

A

Doesn’t exist

101
Q

Phase 3 of pacemaker action potential

A

Inactivation of Ca channels and activation of K channels: K efflux

102
Q

Determines HR

A

Slope of phase 4 in the Sa node

103
Q

Adenosine effect on phase 4 of pacemaker action potential

A

Like ACh decreases the rate of diastolic depolarization and decreases HR

104
Q

Phase 4 of pacemaker action potential

A

Slow spontaneous diastolic depolarisation due to If: funny current
If channels are responsible for a slow mixed Na/K inward current

105
Q

AV node blood supply

A

Right coronary artery

106
Q

pacemaker rates vs speed of conduction

A

SA>AV>Bundle of His>Purkinje/ventricles

Speed of conduction: Purkinje>atria>ventricles>AV node

107
Q

Bachmann bundle

A

Conducts from AV node to left atrium

108
Q

AV node location

A

Posterioinferior part of interatrial septum

109
Q

PR interval

A

Time from start of atrial depolarization to start of ventricular depolarization
Usually less than 200 msec= 0.2 seg= 5 squares

110
Q

QT interval

A

Ventricular depolarization
Mechanical contraction of the ventricles
Ventricular repolarisation

111
Q

T wave

A

Ventricular repolarization

T wave inversion may indicate ischemia or recent MI

112
Q

J point

A

Junction between end of QRS complex and start of ST segment

113
Q

ST segment

A

Isoelectric, ventricles depolarised

114
Q

U wave

A

Prominent in:

  • Hypokalemia
  • Bradycardia
115
Q

Torsades de pointes

A

Ventricular tachycardia

Can progress to ventricular fibrillation

116
Q

_________ predisposes to torsades de pointes

A

Long QT interval

117
Q

Drug induced long QT

A 
ABCDE
AntiArrhythmics: class IA, III
AntiBiotics: macrolides
Anticychotics: haloperidol
AntiDepressants: TCA
AntiEmetics: ondansetron
118
Q

Treatment of torsades de pointes includes

A

magnesium sulfate

119
Q

Congenital long QT syndrome

A

Inherited disorder of myocardical repolarisation typically due to ion channel defects
Increase risk of sudden cardiac death (SCD) due to Torsades de Pointes

120
Q

Congenital QT syndrome includes

A
  • Romano-Ward syndrome

- Jervell and Lange-Nielsen syndrome

121
Q

Romano Ward syndrom

A

Congenital QT syndrome

Pure cardiac phenotype (no deafness)

122
Q

Jervell and Lange Nielsen syndrome

A

Congenital QT syndrome
Autosomal recessive
Sensorineural deafness

123
Q

Brugada syndrome

A

Autosomal dominant
Asian males
ECG pattern of pseudo-right bundle branch block + ST elevations in V1-V3
Risk of ventricular tachyarrhytmias and SCD
Prevent with implantable Cardioverter defibrillator (ICD)

124
Q

Most common type of ventricular pre excitation syndome

A

Wolff-parkinson White

125
Q

Wolff parkinson white syndrome

A
  • Abnormal fast accessory conduction pathway from atria to ventricle (Bundle of Kent)
  • Bypasses the rate slowing AV node
  • Ventricles depolarize earlier: delta wave with widened QRS complex and shortened PR interval on ECG
  • May result in reentry circuit: SV tachycardia
126
Q

Atrial fibrillation

A

Chaotic and erratic baseline with no descrete P waves in between IRREGULARLY spaced QRS complexes

127
Q

Atrial fibrillation tratment

A
  • Anticoagulation
  • Rate control
  • Rhythm control
  • Cardioversion
128
Q

Atrial flutter

A

A rapid succession of IDENTICAL, back to back atrial depolarization wave: sawtooth pattern

129
Q

Definitive treatment of flutter

A

Catheter ablation

130
Q

No discernible rhythm

A

Ventricular fibrillation

131
Q

AV block: First degree

A

PR >200 mseg

Benign and asymptomatic, no treatment required

132
Q

Progressive lengthing of PR interval until a beat is dropped: P wave not followed by QRS

A

AV block: Second degree: Mobitz type I: Wenckebach

133
Q

Mobitz type II

A

Dropped beats are not preceded by a change in the length of the PR interval
May progress to 3rd degree block
Treat with pacemaker

134
Q

Third degree (complete block)

A

Atria and ventricles beat independently of each other.
P waves and QRS complexes not rhytmically associated
Atrial rate >Ventricular rate

135
Q

Can be caused by Lyme disease

A

Third degree (complete) block

136
Q

Third degree block treatment

A

pacemaker

137
Q

Mobitz type II treament

A

pacemaker

138
Q

Atrial natriuretic peptide is released from, when, effects

A
  • atrial myocites
  • increase in blood volume and atrial pressure
  • increase cGMP, vasodilation and less Na absorption at renal collecting tubule. Dilates afferent renal arterioles and constricts efferent arterioles, promoting diuresis
  • Contributes to aldosterone escape
139
Q

Brain natriuretic peptide is released from, when, effects

A
  • ventricular monocytes
  • response to high tension
  • Similar action to ANP, longer half life
  • Dx of HF: High NPV
  • Nesiritide for treating HF
140
Q

Cushing reflex

A

Triad:

  • hypertension
  • bradycardia
  • respiratory depression
141
Q

Central chemoreceptors respond to

A

pH and Pco2 of brain

Doesn’t respond to PO2

142
Q

Peripheral chemoreceptors respond to

A

Low PO2 (<60 mmHg)
High PCO2
Low pH blood

143
Q

Aortic arch chemo and baroreceptors transmit via

A

Vagus nerve to solitary nucleus of medulla

144
Q

Carotid sinus baroreceptor transmits via

A

Glossopharyngeal nerve to solitary nucleus

145
Q

Good aproximation of left atrial pressure

A

Pulmonary capillary wedge pressure

146
Q

PCWP in mitral stenosis

A

PCWP> LVED pressure

147
Q

PCWP is measured with

A

Pulmonary artery catheter: Swan Ganz catheter

148
Q

Causes vasodilation in brain

A

CO2: lower pH

149
Q

Determine fluid movement through capillary membranes

A

Starling forces:

  • capillary pressure
  • intersticial fluid presure
  • plasma oncotic presure
  • intersticial oncotic pressure

Step 1 - Cardiovascular (5 decks)

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