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First Aid Chapters > Cardiac > Flashcards

Cardiac Flashcards

1
Q

what does truncus arteriosus give rise to

A

ascending aorta and pulmonary trunk

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2
Q

what does bulbus cordis give rise to

A

smooth parts of the right and left ventricles

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3
Q

what does primitive atria give rise to

A

trabeculated part of right and left ventricles

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4
Q

what does primitive pulmonary vein give rise to

A

smooth part of the left atrium

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5
Q

what does left horn of sinus venosus give rise to

A

coronary sinus

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6
Q

what does right horn of the sinus venosus give rise o

A

smooth part of the right atrium

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7
Q

what do the common cardinal vein and right anterior cardinal vein give rise to

A

superior vena cava

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8
Q

cause of patent foramen ovale

A

failure of septum primum and septum secundum to fuse after bith.

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9
Q

where do VSDs most often occur

A

in the membranous septum. acyanotic at birth- left to right shunt

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10
Q

order of fetal erythropoiesis

A 
Yuli Likes Sweet Blueberries
Yolk sac
Liver
Spleen
Bone Marrow
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11
Q

fetal hemoglobin

A

alpha 2 gamma 2

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12
Q

adult hemoglobin

A

alpha 2 beta 2

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13
Q

why does HbF pick up more oxygen?

A

greater affinity for oxygen and less binding of 2,3 DPG. this allows the HbF to extract oxygen from the maternal hemoglobin across the placenta

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14
Q

umbilical vein turns into the

A

ligamentum teres hepatis

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15
Q

umbilical arteries turn into the

A

medial umbilical ligament

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16
Q

ductus arteriosus turns into the

A

ligamentum arteriosum

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17
Q

ductus venosus turns into the

A

ligamentum venosum

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18
Q

foramen ovale turns into the

A

fossa ovalis

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19
Q

allantois turns into the

A

Urachus, mediaN umbilical ligament

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20
Q

notochord turns into

A

nucleus pulposus of the intervertebral disc

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21
Q

where is ligamentum teres hepatis

A

contained in the falciform ligament

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22
Q

what supplies the SA and AV nodes

A

RCA

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23
Q

what artery supplies the anterior papillary muscle

A

LAD

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24
Q

in the majority of people where does the PDA arise from

A

RCA

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25
Q

most posterior part of the heart

A

Left atrium

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26
Q

what supplies the right ventricle

A

acute marginal artery

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27
Q

what supplies the posterior wall of the ventricles and posterior 1/3 of the septum

A

PDA

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28
Q

what supplies the lateral and posterior wall of the left ventricle

A

left circumflex

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29
Q

MAP or mean arterial pressure equation

A

MAP = CO x TPR

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30
Q

another equation for MAP

A

MAP = 2/3 diastolic + 1/3 systolic

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31
Q

pulse pressure

A

systolic- diastolic

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32
Q

how to maintain CO in the early phases of exercise

A

increase HR and increase SV

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33
Q

how to maintain CO in the later phases of exercise

A

increase HR (SV plateues)

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34
Q

increasing HR shortens…

A

filling time- shortens diastole and therefore less time to fill the heart and a smaller cardiac output.

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35
Q

what conditions increase pulse pressure

A

hyperthyroidism, AR, arteriosclerosis, obstructive sleep apnea (increased sympathetic tone), exercise

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36
Q

what conditions decrease pulse pressure

A

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

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37
Q

3 conditions that increase stroke volume

A

anxiety, pregnancy and exercise.

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38
Q

what increases myocardial demand

A

increased afterload, increased contractility, increased heart rate and increase ventricular diameter (increased wall tension)

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39
Q

wall tension equation

A

wall tension = pressure x radius / 2 x wall thickness

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40
Q

vasodilators

A

decrease afterload- example is hydralazine

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41
Q

function of ACE inhibitors and ARBs on preload and afterload

A

decrease both of them

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42
Q

ejection fraction

A

measure of contractility. normal in diastolic failure and decreased in systolic failure

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43
Q

what correlates with contractility

A

end diastolic length of cardiac muscle fibers- preload

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44
Q

resistance equation

A

Resistance = 8 viscosity x length / r^4

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45
Q

what conditions increase viscosity

A

polycythemia
hyperproteinemic states like mulitple myeloma
hereditary spherocytosis

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46
Q

on the cardiac graph, things that increase contractility

A

catecholamines and digoxin

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47
Q

on the cardiac graph, things that decrease contractility

A

uncompensated heart failure and narcotic overdose

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48
Q

on the cardiac graph, things that increase venous return or volume

A

fluid infusion or sympathetic activity

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49
Q

on the cardiac graph, things that decrease venous return or volume

A

acute hemorrage or spinal anesthesia

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50
Q

change in the slope of the cardiac curves

A

this is a change in the TPR= total peripheral resistance

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51
Q

less steep curve on the cardiac graph (below)

A

this is an increase in TPR and this is from vasopressors

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52
Q

more steep curve on the cardiac graph (above)

A

this is a decrease in TPR and it is from exercise or AV shunt

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53
Q

S1

A

mitral and tricuspid closing. loudest in mitral area

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54
Q

S2

A

aortic and pulmonary valves closing. loudest at left sternal border

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55
Q

S3

A

early diastole. seen with Mitral regurg and CHF and more common in dilated ventricles. normal in children and pregnant women

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56
Q

S4

A

atrical kick. late diastole. associated with ventricular hypertrophy. left atrium must push against a still LV wall.

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57
Q

a wave in JVP

A

this is atrial contraction

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58
Q

c wave in JVP

A

this is RV contraction against a closed valve (T valve)

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59
Q

v wave in JVP

A

this is right atrial filling against a closed T valve

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60
Q

X wave in JVP

A

this is descent. it is atrial relaxation and downward descent during VENTRICULAR contraction. absent in tricuspid regurgitation

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61
Q

Y wave in JVP

A

this is descent. it is from blood flowing from RA to RV.

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62
Q

what causes normal splitting of the heart sounds

A

this is from with inspiration, there is a drop in intra thoracic pressure and this leads to more blood on the right side of the heart. get A2 then P2.

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63
Q

wide splitting of the heart sounds

A

seen in conditions that delay the RV from emptying like pulmonic stenosis, right bundle branch block). exageration of normal splitting

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64
Q

fixed splitting

A

this is seen in ASD. increase in blood on the right side of the heart regardless of inspiration so it is fixed and doesn’t change with breathing.

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65
Q

paradoxical splitting

A

seen when the left ventricle is delayed for whatever reason. things like aortic stenosis and left bundle branch block. now P2 occurs before A2. this is the opposite

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66
Q

what does inspiration do to heart sounds

A

increases the murmurs on the RIGHT side of the heart

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67
Q

which murmurs are increased with hand grip

A

MR, AR, VSD, MVP

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68
Q

murmurs increased with valsalva or standing

A

hypertrophic cardiomyopathy

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69
Q

what does valsalva and standing do

A

decreases venous return

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70
Q

what does rapid squatting do to the heart sounds

A

increases venous return, increases preload, increases afterload

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71
Q

diastolic heart sounds

A

ARMS

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72
Q

description of TR/MR murmur

A

holosytolic high pitched blowing murmur

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73
Q

where is MR heard

A

loudest at the apex. radiates to the axilla

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74
Q

AS murmur description

A

crescendo decrescendo systolic ejection murmur. LV pressure is greater than the aortic pressure. loudest at the base of teh heart and radiates to the carotids. assocaited wit pulses parvus et tardus. often due to age related disease or congenital bicuspid valve.

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75
Q

VSD murmur description

A

holosystolic harsh sounding murmur. loudest at the tricuspid area.

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76
Q

MVP murmur description

A

late systolic crescendo with midsystolic click.

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77
Q

what causes the midsystolic click in MVP

A

sudden tensing of the chordae

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78
Q

where is MVP best hear

A

over the apex

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79
Q

what determines if MVP is less severe

A

it is less severe with earlier onset. this can be brought about with valsalva

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80
Q

AR murmur description

A

high pitched blowing early diastolic decrescendo murmur. wide pulse pressure. bounding pulses and head bobbing. vasodilators decrease the murmur.

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81
Q

MS murmur description

A

follows an opening snap. delayed rumbling late diastolic murmur.

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82
Q

what correlates with severeity of MS

A

decreased interval between S2 and the opening span means worse.

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83
Q

most common cause of MS

A

this is from chronic rheumatic heart disease

84
Q

PDA murmur

A

continuous machine like murmur. loudest at S2.

85
Q

most common cause of PDA

A

congenital rubella or prematurity. best heard at the left infraclavicular region.

86
Q

what is phase 4 in SA and AV nodes

A

this is the slow diastolic depolarization. membrane potential spontaneously depolarizes as Na+ conductance increases. this is the If or funny channels. gives automaticity of SA and AV noes.

87
Q

what decreases the slope of phase 4 and therefore the HR

A

adenosine and ach

88
Q

what increases the slope of phase 4 and therefore HR

A

sympathetic stimulation (increases chance of If channels being open), and catecholamines

89
Q

what is the p wave

A

atrial depolarization

90
Q

what is the PR interval

A

conduction delay through the ventricle

91
Q

what is the QRS complex

A

ventricular depolarization

92
Q

what is the QT internat

A

mechanical contraction of the ventricles

93
Q

what is the T wave

A

ventricular repolarization. T wave inversion means recent MI

94
Q

ST segment is

A

time when the ventricles are depolarized

95
Q

what is the U wave

A

hypokalemia and bradycardia

96
Q

order of speed of conduction

A 
Park AT Ventura Avenue
Perkinje fibers
Atria
Ventricles
AV node
97
Q

what is torsades de pointes

A

this is polymorphic ventricular tachycardia. can progress to V fib

98
Q

treatment of torsades de pointes

A

magnesium sulfate

99
Q

drugs that prolong QT and predispose to torsades de pointes

A 
Some Risky Meds Can Prolong QT
Solatol (class 3)
Risperidone (and other anti psychotics)
Macrolines
Chloroqine
Protease inhibitors (navir)
Quinidine (class 1a)
Thiazides
100
Q

congenital QT syndrome

A

Romano Ward Syndrome- just cardiac issues

Jervell and Lange Nielsen syndrome- cardiac and deafness

101
Q

Wolff Parkinson White

A

abnormally fast pathway from the atria to the ventricles known as the bundle of Kent. this bypasses the normal slowing of the AV node. this means the ventricles start to depolarize too soon. see a delta wave with a shortened PR interval. can result in supraventricular tachycardia

102
Q

chaotic baseline ECG with no discrete P waves

A

this is atrial fibrilation

103
Q

sawtooth appearance on the bottom of the ECG line

A

this is atrial flutter

104
Q

prolonged PR interval

A

this is 1st degree heart block

105
Q

progressive lengthening of the PR interval until a dropped QRS

A

this is 2nd degree heart block type 1

106
Q

dropped beats that are not preceeded by a change in the length of the PR interval

A

this is 2nd degree heart block type 2

107
Q

P waves and QRS that are not associated with each other

A

3rd degree heart block

108
Q

function of ANP

A

released from ATRIAL myocytes in response to increased blood volume and atrial pressures. causes vasodilation and decreased Na re-absorption at the renal collecting tubule. constricts efferent renal arterioles and dilates the afferent ones promoting diuresis and giving an aldosterone escape mechanism

109
Q

function of BNP

A

this is released from the VENTIRCULAR myocytes. done in response to increased tension. similar to ANP but a longer half life. used to diagnose heart failure.

110
Q

what does the aortic arch receptor respond to

A

only responds to high (increased) BP

111
Q

what does the carotid sinus receptor respond to

A

both increased and decreased BP

112
Q

how does the carotid sinus respond?

A

through CN 9 to the solitary nucleus of the medulla

113
Q

how does the aortic arch respond

A

through CN 10 or vagus nerve to the solitary nucleus of the medulla

114
Q

how do baroreceptors work

A

icnreased pressure, or massage of them, leading to increased stretch, increased firing, increased AV node refractory period and therefore–> decreased HR

115
Q

cushing reaction

A

hypertension, bradycardia and respiratory depression

116
Q

peripheral chemoreceptors

A

located in the aorta or in the carotid bodies. stimualted by decreased Po2 increased Pco2 or decreased pH of blood

117
Q

central chemoreceptors

A

located in the brain. stimulated by changes in pH and PCo2 of brain interstitial fluid. do not respond direclty to Po2

118
Q

which organ gets 100% or largest amount of blood flow

A

lung

119
Q

which organ gets largest share of systemic cadiac output

A

liver

120
Q

which organ gets highest blood flow per gram of tissue

A

kidney

121
Q

which organ can extract oxygen the best

A

heart.

122
Q

what does tricuspid atresia require to be viable

A

ASD and VSD

123
Q

what congenital heart problem gives the boot shape on x ray

A

tetrology of fallot

124
Q

total anomalous pulmonary venous return

A

pulmonary veins drain into the right heart.

125
Q

what cardiac anomaly is assocaited with notching of teh ribs

A

adult form of coarctation of the aorta. this leads to hypertension in the upper extremities and hypotension and claudication in the lower extremities. this is distal to the ligamentum arteriosum.

126
Q

what heart defect is maternal lithium associated with

A

Eisenmenger syndrome

127
Q

what maternal behavior can cause a VSD

A

alcohol

128
Q

what heart problems are assocaited with 22q11

A

Truncus arteriosus and tetrology of fallot

129
Q

what heart problems are assocaited with Downs syndrome

A

ASD, VSD, AV septal defect (endocardial cushion defect)

130
Q

what heart problems are assocaited with congenital rubella

A

septal defects and PDA as well as pulmonary artery stenosis. but the big one is PDA

131
Q

what heart defects assocaited with Turner syndrome

A

bicuspid aortic valve, pre ductal or infantile coarctation of the aorta

132
Q

what heart defects are assocaited with maternal diabetes

A

transposition of the great vessels.

133
Q

definition of hypertension

A

> 140 /90

134
Q

genetic cause of hypertension in young woman

A

fibromuscular dysplasia (narrowing of the renal artery)

135
Q

what is systolic blood pressure related to

A

stroke volume

136
Q

what is diastolic blood pressure related to

A

TPR

137
Q

what cells are present in xanthomas

A

histiocytes

138
Q

corneal arcus

A

lipid deposition in the cornea. appears early with hypercholesterolemia.

139
Q

monkenberg -medial calcific sclerosis

A

this is calcificaion o the media of the arteries like the radial and ulnar arteries. usually benign. can be picked up on an xray or mammo. INTIMA IS NOT INVOLVED

140
Q

cause of hyaline arteriosclerosis

A

proteins leak into vascular wall making it so pink. from benign hypertension or diabetes with non enzymatic gycosylation. likes the kidneys

141
Q

cause of hyperplastic arteriolosclerosis

A

thickening of the vessel wall by hyperplasia of smooth muscle. onion skin appearance. main cause is malignant hypertension. can cause end organ ischemia with fibrinoid necrosis. acute renal failure from this- flea bitten appearance.

142
Q

what two factors are involved in smooth muscle cell migration in atherosclerosis

A

PDGF and FGF.

143
Q

locations of atherosclerosis

A

abdominal aorta > coronary artery > popliteal artery > carotid artery

144
Q

what are abdominal aortic aneurysms associated with

A

atherosclerosis. more frequently in hypertensive male smokers greater than 50. likes to go below the renal artery but above the aortic bifurcation

145
Q

what are thoracic aortic aneurysms associated with

A

cystic medial degeneration due to hypertension in older patients, or Marfans in younger patients. also historically assocaited with tertiarry syphilis (bliterative endarteritis of the vasa vasorum).

146
Q

where is the tear in an aortic dissection

A

tear is in the intima. requires though pre-existing medial weakness from either hypertension or inherited defects like with marfans. hypertension does this because you get hyline arteriolosclerosis of the vaso vasorum in the proximal aorta and you can’t feed the thick muscle so it becomes weaker.

147
Q

ECG findings with stable Angina

A

as long as it is subendocardial damage and not throughout the entire wall, this shows ST depression.

148
Q

ECG findings in unstable angina

A

this is still just ST depression

149
Q

ECG findings in an MI

A

this is where there has been blockage for more than 20 minutes. if transmural, ECG will show ST elevation. if subendocardial still, the ECG will show ST depression. cardiac biomarkers are diagnostic.

150
Q

what is Prinzmetal angina

A

occurs at rest secondary to coronary artery spasm. transient ST elevation can be seen. known triggers include tobacco, cocaine, triptans etc. treat with calcium channel blockers, nitrates and smoking cessation.

151
Q

coronary steal syndrome

A

this is when you give a vasodilator and this makes all the normal vessels dilate and the area of the coronary artery that is stenosed then gets less blood and this means increased ischemia. vasodilating drugs associated with this include dipyridamole and regadenoson)

152
Q

sudden cardiac death

A

this is death from cardiac causes within 1 hour of onset of symptoms. most commonly due to a lethal arrythmia like v fib.

153
Q

changes seen in the heart post MI after 0-4 hours

A

none. death is from arrythmias in general. or cardiogenic shock

154
Q

changes seen in the heart post MI 4-12 hours

A

early coagulative necrosis. release of necrotic cell contents into the blood, edema, hemorrgahe, wavy fibers etc. grossly get dark discoloration.

155
Q

changes seen in the heart post MI seen after 24 hours

A

neutrophils start to come in. grossly the heart looks yellow from this. extensive coagulative necrosis and tissue surrounding the infarct shows lots of neutrophils. complications at this point are fibrinous pericarditis. only seen with transmural infarct- chest pain and friction rub.

156
Q

changes seen in the heart post MI days 4-7

A

this shows the presence of macrophages and they come in and eat the tissue. the tissue is still yellow. it gets maximally soft by 10 days. this is when there is a risk of free wall rupture which leads to tamponade. can also get papillary muscle rupture leading to mitral regurg.

157
Q

changes seen in the heart post MI weeks 1-3

A

this is the start of the granulation tissue. it has a red border.

158
Q

changes seen in the heart post MI weeks 2- several months

A

poor movement of the ventricle as it forms a scar. the scar will be white at this point. fibrosis. complications include dressler syndrome

159
Q

dressler syndrome

A

this is pericarditis from an autoimmune reaction and antibodies that formed against the pericardium. remember this is fibrinous pericarditis

160
Q

cardiac troponins..

A

cardiac troponin I rises after 4 hours and is increased for 7-10 days. most specific

161
Q

cardiac CkMB

A

this rises quickly but falls quickly- good for re-infacrtion. less specific- also in skeletal muscle

162
Q

Q waves in leads VI-V4

A

anterior wall (LAD)

163
Q

Q waves in leads V1-V2

A

anteroseptal (LAD)

164
Q

Q waves in leads V4-V6

A

anterolateral (LAD or LCX)

165
Q

Q waves in I and aVL

A

Lateral wall (LCX)

166
Q

Q waves in II, III and avF

A

inferior wall (RCA)

167
Q

histology of dilated cardiomyopathy

A

eccentric hypertrophy with sarcomeres added in series

168
Q

common causes of dilated cardiomyopathy

A

alcohol abuse, beri beri, coxsackie B virus, chronic cocain use, chagas disease, doxurubicin tocicity, hemochromatosis, and peripartum cardiomyopathy

169
Q

findings in dilated cardiomyopathy

A

heart failure, S3, dilated heart on echo, balloon appearance of the heart of CXR

170
Q

histology of hypertrophic cardiomyopathy

A

marked ventricular hypertrophy with often septal predominance and myofibrillary disarray and fibrosis.

171
Q

mutation commonly seen in hypertrophic cardiomyopathy

A

mutation in sarcomere proteins- beta myosin heavy chain

172
Q

disease hypertrophic cardiomyopathy is assocaited with

A

friedrich’s ataxia

173
Q

obstructive hypertrophic cardiomyopathy

A

hypertrophied septum such that it is too close to the anterior mitral leaflet, leading to outflow obstruction and subsequent dyspnea and syncope

174
Q

most common cause of sudden death in athletes

A

hypertrophic cardiomyopathy

175
Q

Loffler syndrome

A

restrictive cardiomyopathy. endomyocardial fibrosis with a prominent eosinophilic infiltrate

176
Q

hypertrophic cardiomyopathy leads to

A

diastolic dysfunction

177
Q

infiltrative cardiomyopathy leads to

A

diastolic dysfunction

178
Q

dilated cardiomyopathy leads to

A

systolic dysfunction

179
Q

what does left heart failure cause in CHF

A

pulmonary edema, orthopnea and paroxysmal nocturnal dyspnea

180
Q

what type of fluid is pushed out in CHF

A

transudate

181
Q

what does right heart failure cause

A

hepatomegaly (nutmeg liver)- usually painful, peripheral edema, and jugular venous distension. this gives pitting edema which again is a transudate.

182
Q

symptoms of bacterial endocarditis

A

fever, new murmur, roth spots (round white spots on the retina surrounded by hemorrage), osler nodes (tender), janeway lesions (non painful on palms and soles), anemia, splinter hemorrages,

183
Q

S aureus and endocarditis

A

infects previously normal valves and gives acute bacterial endocarditis

184
Q

Strep viridans and endocarditis

A

this is low virulence so it infects congenitally abnormal or disease valves. sequela of dental procedures. sub acute in nature. gradual onset. smaller vegitations

185
Q

culture negative endocarditis

A

most likely Coxiella burnetti or Bartonella. also think about HACEK organisms- hemophilis, acinobacilius, cardiobacterium, Ekinella, Kingella

186
Q

S bovis endocarditis

A

seen in colon cancer patients

187
Q

S epidermidis endocarditis

A

prosthetic valves

188
Q

vegitations on both sides of the valve

A

this is liebman sacks endocarditis and is secondary to lupus. sterile vegitations.

189
Q

non bacterial thrombotic endocarditis

A

sterile vegitations seen in a hyper coagulable state or with adeno carcinoma underlying.

190
Q

rheumatic fever

A

consequence of pharyngeal infection with group A beta hemolytic strep.

191
Q

early cause of death with rheumatic fever

A

myocarditis

192
Q

late issues with rheumatic fever

A

valve disease. loves the mitral then the aortic valve. early lesion is MR and then progresses to MS.

193
Q

what disease is assocaited with Aschoff bodies

A

rheumatic fever tese are granulomas with giant cells and Anitschkow cells with wavy catepillary like nuclei).

194
Q

what type of HS reaction is rheumatic fever

A

type 2

195
Q

what skin disease is assocaited with rheumatic fever

A

erythema marginatum

196
Q

pericarditis pain

A

classic. sharp pain, aggrevated by breathing in (inspiration) and relieved by sitting up and leaning forward. presents with a friction rub. can see ST elevation or PR depression.

197
Q

serous pericarditis

A

tends to be viral or non infectious diseases

198
Q

fibrinous pericarditis

A

tends to be from Dressler syndrome, uremia, radiation,

199
Q

Beck triad of cardiac tamponade

A

hypotension, muffled heart sounds, distended neck veins

200
Q

ECG findings in cardiac tamponade

A

low voltage QRS and electrical alternans due to swining movement of the hear in large effusion

201
Q

pulsus paradoxus

A

decrease in systolic blood pressure by 10 mm Hg during inspiration. seen in cardiac tamponade, asthma, obstructive sleep apnea, pericarditis and croup

202
Q

“tree bark aorta”

A

this is the description for tertiary syphilis. calcification of the aortic root and ascending aorta. can lead to an aortic aneurysm and it is thoracic

203
Q

what is a cardiac myxoma

A

most common heart tumor (primary). mostly in the LA. ball valve and can obstruct the flow of blood. gelatinous in appearance. mesenchymal tumor with abundant ground substance.

204
Q

rhabdomyomas

A

most common primary cardiac tumor in children. usually in ventricles

205
Q

Kussmal sign

A

this is an increase in JVP with inspiration even though it should decrease because inspiration pulls the blood into the right heart. this means there is impaired filling of the ventricle. seen in constrictive pericarditis, restrictive cardiomyopathies and right atrial or ventricular tumors

206
Q

common mets to the heart

A

brest and lung
melanoma
lymphoma

often go to the pericardim and give pericardial effusion

First Aid Chapters (8 decks)

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