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First Aid Cardiovascular > Anatomy/Physiology > Flashcards

Anatomy/Physiology Flashcards

1
Q

Acute Marginal Artery

A

supplies right ventricle

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2
Q

Post. descending/interventircular artery

A

supplies posterior 1/3 of IV septum and posterior walls of ventricles

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3
Q

Left anterior descending artery

A

supplies anterior 2/3 of IV septum, anterior papillary muscles and anterior surface of left ventricle

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4
Q

Left Circumflex coronary artery

A

supplies lateral and posterior walls of left ventricle

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5
Q

Blood supply for SA and AV nodes

A

Right Coronary Artery - infarct can cause nodal dysfx

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6
Q

Right Dominant Circulation

A

85% population, posterior descending artery arises from RCA

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7
Q

Left Dominant Circulation

A

8% of population, posterior descending artery arises from LCA

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8
Q

Codominant circulation

A

7% of population, posterior descending artery arises from both Left Circumflex artery and RCA

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9
Q

Peak of coronary blood flow

A

Early Diastole

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10
Q

Most posterior part of heart

A

Left Atrium, enlargment can cause dysphagia or hoarseness (compresses Left reccurrent laryngeal)

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11
Q

Cardiac Output

A

SV * HR -or-

rate of O2 consumption)/(arterial O2 content-venous O2 content

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12
Q

Mean Arterial Pressure

A

MAP = CO * TPR

2/3DBP + 1/2SBP

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13
Q

Pulse Pressure

A

systolic - diastolic
proportional to SV
inversely proportional to arterial compliance

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14
Q

Stroke Volume

A

EDV-ESV

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15
Q

Cardiac Output during exercise

A

Early - CO is maintained by increase HR and SV

Late - CO is maintained by increased HR only (SV plateaus)

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16
Q

Causes for increased Pulse Pressure

A

Hyperthyroidism, Aortic regurgitation, arteriosclerosis, obstructive sleep apnea, transiently with exercise

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17
Q

Causes for decreased Pulse Pressure

A

aortic stenosis, cardiogenic shock, cardiac tamponade, and advanced heart failure

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18
Q

Causes for increased stroke volume

A

increased contractility, increased preload, or decreased afterload
anxiety, pregnancy, exercise

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19
Q

Increased intracellular Calcium

A

increases contractility

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20
Q

Decreased Extracellular Sodium

A

increases contractility because it decreases the Na/Ca exchanger

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21
Q

Catecholamines effect on Heart

A

Increases activity of calcium pump in sarcoplasmic reticulum

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22
Q

Digitalis on Contractility

A

blocks Na/K pump thus increase intracellular Na and decreasing Na/Ca exchanger therefore INCREASING intracellular Calcium

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23
Q

Ways to decrease contractility and stroke volume

A

beta-1 blockade, HF with systolic dysfunction, acidosis, hypoxia/hypercapnea, non-dihydropyridine CCB

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24
Q

Increase of myocardial O2 demand

A

increased afterload, increased contractility, increased heart rate, increased ventricular diameter

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25
Q

Preload

A

depends on venous tone and circulating blood volume

approximated by ventricular EDV

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26
Q

Venodilators

A

nitroglycerin, decreases preload

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27
Q

Afterload

A

approximated by MAP

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28
Q

Compensation for increased afterload

A

LV compensates by thickening (hypertrophy) to decrease wall tension

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29
Q

Drugs that decrease both preload and afterload

A

ACE-inhibitors and ARBs

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30
Q

Vasodilators

A

hydralazine, decrease afterload

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31
Q

Wall Tension

A

Associated with Afterload

Pressureradius) / (2wall thickness

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32
Q

Ejection Fraction

A

EF = (SV)/(EDV) or (EDV-ESV)/EDV

left ventricular EF is an index of ventricular contractility

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33
Q

Normal EF

A

> 55%

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34
Q

EF in systolic heart failure

A

<55%

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35
Q

EF in diastolic heart failure

A

normal, >55%

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36
Q

Pressure =

A

Pressure = flow * resistance

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37
Q

Resistance of vessels in series

A

TR = R1+R2+R3…

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38
Q

Resistance of vessels in parallel

A

1/TR = 1/R1 + 1/R2 + 1/R3….

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39
Q

Causes of increased viscosity of blood

A

polycythemia, hyperproteinemic states (multiple myeloma), spherocytosis

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40
Q

Causes of decreased velocity of blood

A

ANEMIA

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41
Q

Resistance equation

A

(8(viscosity)length) / (pi*r^4)

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42
Q

Type of vessel that accounts for majority of TPR

A

arterioles, they regulate capillary flow

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43
Q

Inotropy

A

Strength of contraction

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44
Q

(+) inotropy

A

catecholamines, digoxin

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45
Q

negative inotropy

A

uncompensated heart failure and narcotic overdose

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46
Q

Decreases venous return

A

acute hemorrhage, spinal anesthesia

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47
Q

Increases venous return

A

fluid infusion, sympathetic activity

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48
Q

Increases TPR

A

vasopressors

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49
Q

Decreases TPR

A

Exercise and AV shunt

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50
Q

S1

A

mitral and tricuspid valve closure. Loudest at mitral area

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51
Q

S2

A

aortic and pulmonary valve closure, loudest at left sternal border

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52
Q

S3

A

Early diastole during rapid ventricular filling phase
associated with mitral regurgitation and CHF
more common in dilated ventricles

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53
Q

Heart sound normal in children and pregnant women

A

S3

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54
Q

S4

A

atrial kick - in late diastole, High atrial pressure. associated with ventricular hypertrophy. Left atrium must push against stiff LV wall.

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55
Q

Jugular venous pulse - a wave

A

atrial contraction

56
Q

Jugular venous pulse - c wave

A

RV contraction (close tricuspid valve)

57
Q

Jugular venous pulse -x descent

A

atrial relaXation and downward displacement of close tricuspid valve during ventricular contraction
absent in tricuspid regurg

58
Q

Jugular venous pulse -v wave

A

increased right atrial pressure due to filling against closed tricuspid valve

59
Q

Jugular venous pulse - y descent

A

blood flow from Rt Atria to Rt Ventricle

60
Q

Normal Heart Split

A

delayed closure of pulmonic valve during inspiration

from decreased intrathoracic pressure so more blood returns

61
Q

Wide Splitting

A

Seen in conditinos that dela right ventricular emptying
pulmonic stenosis, RBBB
Exaggeration of normal splitting

62
Q

Fixed Splitting

A

Seen in ASD which causes left-to-right shunt

regardless of breath, pulmonic valve is greatly delayed due to increased blood flow

63
Q

Paradoxical Splitting

A

Conditions that delay LV emptying
aortic stenosis, LBBB
P2 closes before A2 and on inspiration, no split

64
Q

Auscultation over aortic area

A

Systolic murmurs like: aortic stenosis, flow murmur, aortic valve sclerosis

65
Q

Auscultation over Left Sternal Border

A

Diastolic murmurs: aortic regurgitation, pulmonic regurgitation
Systolic murmurs: hypertrophic cardiopathy

66
Q

Auscultation over Pulmonic Area

A

Systolic ejectino murmur: pulmonic stenosis and physiologic murmur

67
Q

Auscultation over tricuspid area

A

Pansystolic murmur: tricuspid regurgitation, VSD

Diastolic Murmur: tricuspid stenosis, ASD

68
Q

Auscultation over Mitral Valve Area

A

Systolic Murmur: mitral regurgitation

Diastolic Murmur: mitral stenosis

69
Q

Inspiration

A

increases intensity of right heart sounds

70
Q

Hand Grip

A

increases intensity of MR, AR, VSD murmurs

MVP: increases murmur intensity and later onset of click/murmur

71
Q

Valsalva, Standing

A

increases hypertrophic cardiomyopathy murmur

MVP: decreases murmur intensity, earlier onset of click/murmur

72
Q

Rapid Squating

A

increases intensity of aortic stenosis murmur

MVP: increases murmur intensity and later onset of click/murmur

73
Q

Systolic Heart Sounds

A

aortic/pulmonic stenosis, AV regurgitation, VSD

74
Q

Diastolic Heart Sounds

A

Aortic/Pulmonic Regurgitation, AV stenosis

75
Q

Holosystolic, high-pitched “blowing murmur” at apex and radiates toward axilla

A

Mitral Regurgitation

76
Q

Holosystolic, high-pitched “blowing murmur” loudest left sternum 5th intercostal space to right sternal border

A

Tricuspid regurgitation

77
Q

Crescendo-decrescendo systolic ejection murmur

loudest at heart base; radiates to carotids

A

Aortic Stenosis

78
Q

“pulsus parvus et tardus”

A

pulses are weak with a delayed peak, aortic stenosis

can lead to syncope, angina and dyspnea on exertion

79
Q

Holosystolic, harsh-sounding murmur. Loudest at tricuspid area, accentuated with hand grip

A

VSD

80
Q

Late systolic Crescendo with midsystolic click

A

MVP

81
Q

Cause of midsystolic click

A

due to sudden tensing of chordae tendinae

82
Q

High-pitched “blowing” early diastolic decrescendo murmur. Bounding pulses and head bobbing

A

Aortic Regurgitation (wide pulse pressure is chronic)

83
Q

Aortic Root dilation, bicuspid aortic valve, endocarditis, or rheumatic fever

A

Aortic Regurgitation

84
Q

Follows opening snap. delayed rumbling diastolic murmur

A

Mitral Stenosis

85
Q

Continuous machine-like murmur, loudest at S2, left infraclavicular area

A

PDA, often due to congenital rubella

86
Q

ACh/adenosine on Heart

A

decrease the rate of diastolic depolarization and HR (longer for depolarization to occur)

87
Q

P wave

A

atrial depolarization (repolarization of atria in QRS)

88
Q

PR interval

A

conduction delay through AV node (normally <200msec)

89
Q

QRS complex

A

ventricular depolarization

90
Q

QT interval

A

Mechanical contraction of ventricles

91
Q

T wave

A

Ventricular repolarization

92
Q

T wave inversion

A

recent MI

93
Q

ST segment

A

Isoelectric, ventricles depolarized

94
Q

U wave

A

caused by hypokalemia, bradycardie

95
Q

Speed of conduction

A

Purkinje > Atria > ventricles > AV node

96
Q

Pacemakers

A

SA > AV > bundle of His/Purkinje/Ventricles

97
Q

Tx of Torsades de Pointes

A

Magnesium Sulfate

98
Q

Drugs that prolong QT

A

Sotalol, Risperidone, Macrolides, Chloroquine, Protease inhibitor (-navir), quinidine, Class Ia and III antiarrhythmics, thiazides

99
Q

Romano-Ward Syndrome

A

autosomal dominant, pure cardiac phenotype (no deafness) congenital long QT syndrome

100
Q

Jervell and Lange-Nielsen Syndrome

A

Autosomal Recessive, Sensorineural deafnes, congenital long QT syndrome

101
Q

Delta wave

A

Wolff-Parkinson-White Syndrome; abnormal fast accessory conduction pathway from atria to ventricle (bundle of Kent) to bypass the rate-slowing AV node so ventricles depolarize earlier

102
Q

Prolonged PR interval (>200msec)

A

1st Degree AV block

103
Q

Progressive lengthening of PR interval until a beat is dropped

A

2nd degree Mobitz Type I (Wenckebach)

104
Q

Chaotic and erratic baseline (irregularly irregular) with nodiscrete P waves inbetween irregularly spaced QRS complex

A

Atrial fibrillation

105
Q

“saw tooth” appearance of flutter waves

A

Atrial flutter

106
Q

Tx for Atrial Flutter

A

Class IA, IC, or III antiarrhythmics
Rate Control use beta-blocker or CCB
Definitive tx: catheter ablation

107
Q

completely erratic rhythm with no identifiable waves

A

Ventricular arrhythmia (tx with CPR and defibrillation)

108
Q

Dropped QRS beats, no change in PR interval
(2 more P waves than QRS)
(3 more P waves than QRS)

A

2nd degree AV block; Mobitz type II

2: 1
3: 1

109
Q

2nd degree AV block; Mobitz type II

A

Pacemaker

110
Q

Atria and ventricle beat independently of each other

A

3rd Degree heart block or complete heart blood, tx with a pacemaker

111
Q

Lyme disease

A

can result in 3rd degree heart block

112
Q

“aldosterone escape” mechanism

A

ANP

113
Q

Release from atrial myocytes in response to increase blood volume and atrial pressure

A

ANP

114
Q

Cause vasodilation and decrease sodium reabsorption at renal collecting tubues. Constricts efferent arterioles and dilates afferent arterioles

A

ANP

115
Q

Released from ventricular myocytes in response to increased tension

A

B-type (brain) natriuretic peptide

116
Q

longer t1/2 than ANP, with similar mechanism

A

BNP

117
Q

Nesiritide

A

recombinant form of BNP for treatment of heart failure

118
Q

Aortic Arch Receptors

A

vagus nerve to solitary nucleus of medulla responds to increased BP only

119
Q

Carotid sinus receptors

A

glossopharyngeal nerve to solitary nucleus of medulla, responds to increase and decreased BP

120
Q

Baroreceptors

A

respond to hypotension, decrease of afferent firing increase efferent sympathetic firing and decrease parasympathetic leading to vasoconstriction. Important in hemorrhage

121
Q

Carotid Massage

A

increased pressure on carotid sinus will increase AV node refractory period and decrease HR

122
Q

Cushing Reaction

A

hypertension, bradycardia and respiratory depression

increased ICP contricts arterioles leading to cerebral ischemia and sympathetics thus HTN and reflex bradycardia

123
Q

Peripheral Chemoreceptors

A

carotid and aortic bodies stimulated by decreased oxygen when pO2 is <60mmHg

124
Q

Central Chemoreceptors

A

stiulated by changes in pH and pCO2 of brain interstitial fluid, which in turn are influenced by arterial CO2

125
Q

Organ with largest blood flow

A

Lung

126
Q

Largest share of systemic cardiac output

A

Liver

127
Q

Highest blood flow per gram of tissue

A

Kidney

128
Q

Largest AV O2 difference because O2 extraction is ~80%

A

Heart

129
Q

Increased oxygen demand for heart is met by

A

increase coronary artery flow

130
Q

PCWP in mitral stenosis

A

PCWP > LV diastolic pressure

normal <12

131
Q

Autoregulation blood flow in heart

A

Local metabolites (vasodilatory) - CO2, adenosine, NO

132
Q

Autoregulation blood flow in Brain

A

Local metabolites (vasodilatory) - CO2 (pH)

133
Q

Autoregulation blood flow in Kidneys

A

Myogenic and tubuloglomerular feedback

134
Q

Autoregulation blood flow in Lungs

A

Hypoxia causes vasoconstriction

135
Q

Autoregulation blood flow in Skeletal Muscle

A

Local Metabolites - lactate, adenosine, K, H, CO2

136
Q

Autoregulation blood flow in Skin

A

Sympathetic stimulation most important mechanism - temperature control

137
Q

Whose head is on a rat?

A

Molly’s!!! (weird punch bowl)

First Aid Cardiovascular (4 decks)

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