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Step 1 > Cardio > Flashcards

Cardio Flashcards

1
Q

Cardiac looping

A

week 4

primary heart tube loops to estabilish left right polarity

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2
Q

Kartaneger syndrome

A

defect in left right dyenin can lead to dextrocardia via ciliary dyskinesia

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3
Q

Septation and chambers

A
  1. Septum primum grows toward endocardial cushions, narrowing foramen primum
  2. Foramen secundum forms in septum primum
  3. Septum, secundum develops on the right side of septum primum, as foramen secundum maintains right left shunt
  4. Septum secundum expands and covers most of the foramen secundum. Residual foramen is foramen ovale
  5. remaining portions of septum primum forms one way valve of the foramen ovale
  6. septum primum closes against septum secundum sealing the foramen ovale soon after birth
  7. Septum secundum and septum primum fuse during infancy forming atrial septum
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4
Q

PFO

A

caused by failure of the septum primum and septum secundum to fuse after birth
lead to paradoxical emboli

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5
Q

Ventricle morphogenesis

A
  1. Muscular interventricular septum forms.
  2. Aorticopulmonary septum rotates and fuses with muscular ventricular septum to form membranous interventricular septum, closing interventricular foramen
  3. growth of endocardial cushions separates atria from ventricles and contributes to both atrial septation and membranous portion of the interventricular septum
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6
Q

VSD

A 
membranous septum
Most common
Holosystolic harsh sounding murmur
tricuspid area
asymptomatic at birth
May lead to LV overload and HF
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7
Q

Outflow tract formation

A

Neural crest and endocardial cell migrations –> truncal and bulbar ridges that spiral and fuse to form articopulmonary trunk

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8
Q

Conotrunal abnormalities

A

associated with failure of NCC to migrate

transposition of the great vessels, tetralogy of Fallot, persistent truncus arteriosus

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9
Q

Valve Development

A

Aortic/pulmonary- derived from endocardial cushions of outflow tract
mitral and tricuspid- fused endocardial cushions of the AV canal

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10
Q

Truncus arteriosus

A

ascending aorta and pulmonary trunk

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11
Q

bulbus cordis

A

smooth parts of left and right entricles

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12
Q

Primitive ventricle

A

trabeculared part of left and right ventricles

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13
Q

Primitive atrium

A

trabeculated part of left and right atria

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14
Q

left horn of sinus venosus

A

coronary sinus

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15
Q

right horn of sinus venosus

A

smooth part of right atrium

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16
Q

endocardial cushion

A

atrial septum, membranous interventricular septum, AV and semilunar valves

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17
Q

right common cardinal V and right anterior cardinal V

A

SVC

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18
Q

Posterior, subcardinal and surpacardinal V

A

IVC

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19
Q

primitive pulmonary V

A

smooth part of L atrium

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20
Q

Fetal circulation

A
  1. Blood entering fetus through the umbilical V is conducted via ductus venosus into the IVC, bypass hepatic circulation
  2. most of the oxygenated blood reaching the heart via IVC is directed through foramen ovale into the L atrium
  3. Deoxygenated blood from SVC passes through the RA –> RV –> main pulmonary A –> Ductus arteriosus –> descending aorta
    At birth, infant takes deep breath –> decrease resistance in pulmonary vasculature –> increase LA pressure –> foramen ovale closes
    High O2 and low prostaglandins –> closure of ductus arteriosus
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21
Q

Indamethacin

A

close patent ductus arteriosus –> Ligamentum arteriosum

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22
Q

Prostaglandin E 1 and 2

A

Keep PDA open

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23
Q

Ductus arteriosus

A

Ligamentum arteriosum

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24
Q

Ductus venosus

A

Ligamentum venosum

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25
Q

Foramen ovale

A

Fossa ovalis

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26
Q

Allantois –> urachus

A

median umbilical L

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27
Q

Umbilical A

A

Medial umbilical L

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28
Q

Umbilical V

A

Ligamentum teres hepatis

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29
Q

Notochord

A

nucleus pulposus

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30
Q

Enlargement of the LA

A

compression of the esophagus and or the L recurrent laryngeal N –> hoarseness

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31
Q

Most commonly injured part of the heart

A

RV

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32
Q

Pericardium

A 
Fibrous pericardium
Parietal layer of serous pericardium
Visceral layer of serous pericardium
Pericardial cavity lies between parietal and visceral layers
innervated by phrenic N
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33
Q

Pericarditis

A

can cause referred pain to neck arms or shoulders

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34
Q

LAD

A

anterior 2/3 of interventricular septum, anterolateral papillary muscle and anterior surface of LV
Most common occlusion

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35
Q

PDA

A

supply AV node, posterior 1/3 of intraventricular septum, posterior 2/3 walls of ventricles and posteromedial papillary M

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36
Q

RCA

A

supplies SA node

infarct may cause nodal dysfunction

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37
Q

Right dominant

A

Posterior descending A arise from RCA

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38
Q

Left dominant

A

Posterior descending A arise from LCX

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39
Q

Stroke volume

A

increased by high contractility, low afterload and high preload
SV= EDV-ESV

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40
Q

Contractility

A

increase with catecholamine stimulation via B1 receptor, high intracellular Ca2+, low extracellular Na+, digitalis
decreased with B1 blocker, HF, acidosis, hypoxia, CCB
Ejection fraction = ventricular contractility

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41
Q

Preload

A

depend on venous tone and circulating blood volume

Vasodilators decrease preload

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42
Q

Afterload

A

increase wall tension –> increase pressure –> increase afterload
Arterial vasodilators decrease afterload
LV compensates fro increase afterload by thickening to decrease wall stress.

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43
Q

Myocardial O2 demand

A

increase with high contractility, high afterload, high HR, high diameter of ventricle

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44
Q

Cardiac Output

A

SV x HR

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45
Q

Pulse pressure

A

SBP-DBP
directly proportional to SV
increase in hyperthyroidism, aortic regurgitation, aortic stiffening, obstructive sleep apnea, anemia, exercise
decrease in aortic stenosis, cardiogenic shock, cardiac tamponade, advance HF

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46
Q

MAP

A

CO x TPR

2/3DBP + 1/3 SBP = DBP + 1/3 PP

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47
Q

Starling curve

A

Force of contraction is proportional to end diastolic length of cardiac muscle fiber (preload)
increase contractility with catecholamines and positive inotropes
decreased contractility with loss of functional myocardium, B blockers, CCB, dilated cardiomyopathy

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48
Q

Resistance, pressure, flow

A

capillaries have highest total cross sectional area and lowest flow velocity
Pressure gradient drives flow from high pressure to low pressure
Arterioles account for TPR and veins provide most blood storage capacity

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49
Q

PV loop

A
  1. isovolumetric contraction- period between mitral valve closing and aortic valve opening HIGHES O2 CONSUMPTION
  2. Systolic ejection- period between aortic valve opening and closing
  3. isovolumetric relaxation- period between aortic valve closing and mitral valve opening
  4. Rapid filling- period just after mitral valve opens
  5. reduced filling- period before mitral valve closes
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50
Q

S1

A

Mitral and tricuspid close

LOUDEST AT MITRAL AREA

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51
Q

S2

A

Aortic and pulmonary valve close

LOUDEST AT LEFT UPPER STERNAL BORDER

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52
Q

S3

A

early diastole, during rapid ventricular filling phase.
HEARD AT APEX with patient in L lateral decubitus position
Associated with increased filling pressures (MR, AR, HF)
normal in children, athletes, pregnant

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53
Q

S4

A

in late diastole
HEARD AT APEX with patient in left lateral decubitus position
high atrial pressure
associated with ventricular hypertrophy

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54
Q

a wave

A

atrial contraction

absent in a fib

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55
Q

c wave

A

RV contraction

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56
Q

x descent

A

downward displacement of closed tricuspid valve during rapid ventricular ejection phase. Reduced or absent in tricuspid regurgitation and right HF because pressure gradients are reduced

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57
Q

v wave

A

high RA pressure due to filling agasint closed tricuspid valve

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58
Q

y descent

A

RA emptying into RV

Prominent in constrictive pericarditis, absent in cardiac tamponade

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59
Q

Aortic stenosis

A 
High LV pressure
high ESV
no change in EDV
low SV
systolic murmur
crescendo - descendo systolic ejection murmur
soft S2
loudest at base and radiates to carotids
lead to syncope, angina, dyspnea
age related calcification
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60
Q

Mitral Regurgitation

A

no true isovolumetric phase
low ESV due to low resistance and high regurgitation into LA during systole
high EDV due to high LA volume from regurgitation –> ventricular filling
high SV
Holosystolic high pitched murmur
loudest at apex and radiates to axilla
ischemic heart disease, mitral valve prolapse or LV dilation
Rheumatic fever and infective endocarditis

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61
Q

Aortic regurgitation

A

No true isovolumetic phase
high EDV
high SV
high pitched blowing early diastolic decrescendo murmur
heard at base or left sternal border
Bicuspid aortic valve, endocarditis, aortic root dilation, rheumatic fever

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62
Q

Mitral stenosis

A 
high LA pressure
low EDV
low ESV
low SV
follow opening snap
delayed rumbling mid to late diastolic murmur
late rheumatic fever
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63
Q

Physiological splitting of S2

A

inspiration –> drop in intrathoracic pressure –> high venous return –> high RV filling –> high RV SV –> high RV ejection time –> delayed closure of pulmonic valve

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64
Q

Wide splitting of S2

A

conditions that delay RV emptying, pulmonic stenosis, RBBB

causes delayed pulmonic sound

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65
Q

Fixed splitting of S2

A

ASD

left to right shunt –> high RA and RV volume –> high flow through pulmonic valve –> delayed pulmonic valve closure

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66
Q

Paradoxical splitting of S2

A

conditions that delay aortic valve closure
Aortic stenosis, LBBB
Normal order of semilunar valve closure is reversed so that P2 sound occurs before delayed A2 sound
split heard in expiration

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67
Q

Aortic systolic murmur

A

aortic stenosis
flow murmur
aortiv valve stenosis

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68
Q

Left Sternal border murmurs

A

Diastolic- aortic regurgitation, pulmonic regurgitation

Systolic- hypertrophic cardiomyopathy

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69
Q

Pulmonic systolic ejection murmuur

A

pulmonic stenosis, ASD, flow murmur

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70
Q

Tricuspid murmus

A

holosystolic- VSD, tricuspid regurgitation

diastolic- tricuspid stenosis

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71
Q

Mitral murmur

A

holosystolic- mitral regurgitation
systolic- mitral valve prolapse
diastolic- mitral stenosis

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72
Q

Stadning Valsalva position

A

decrease preload
murmurs that increase- mitral valve prolapse and hypertrophic cardiomyopathy
murmurs that decrease- most murmurs

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73
Q

passive leg raise

A

increase preload
murmurs that increase- most murmurs
murmurs that decrease- mitral valve prolapse and hypertrophic cardiomyopathy

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74
Q

Squatting

A

increase preload, increase afterload
murmurs that increase- most murmurs
murmurs that decrease- mitral valve prolapse and hypertrophic cardiomyopathy

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75
Q

Hand grip

A

increase afterload
murmurs that increase- AR, MR, VSD
murmurs that decrease- AS, hypertrophic cardiomyopathy

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76
Q

Inspiration

A

increase venous return to right heart and decrease venous return to left heart
murmurs that increase- right sided murmurs
murmurs that decrease- left sided murmurs

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77
Q

Mitral valve prolapse

A

late systolic crescendo murmur with midsystolic click via chordae tendinae
hear over apex
loud just before S2
benign
caused by myxomatous degeneration, rheumatic fever, chordae rupture

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78
Q

Patent ductus arteriosus

A 
continuous machine like murmur
left infraclavicular area
loudest at S2
congenital rubella or prematurity
patency maintained by PGE and low O2
late cyanosis of lower extremities
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79
Q

Torsades de pointe

A

polymorphic ventricular tachy
shifting sinusoidal waveforms on ECG
can progress to V fib
caused by drugs that decrease K+, Mg2+, Ca2+

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80
Q

Congenital long QT syndrom

A

inherited disorder of myocardial repolarization due to ion channel defects
increase risk of cardiac death due to torsades de pointes
Romano- Ward syndrome- AD pure cardiac phenotype
Jervell and Lange Nielson syndrome- AR, sensorineural deafness

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81
Q

Brugada syndrome

A

AD Asian males
Pseudo RBBB and ST elevation in V1-3
increased risk of t-tach and SCD
prevent SCD with implantable cardioverter defibrillator

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82
Q

Wolf parkinson White syndrome

A

ventricular pre-excitation syndrome
abnormal fast accessory conduction pathway from atria to ventricle bypass the rate slowing AV node –> ventricles begin to partially depolarize earlier –> delta wave with wide QRS and short PR interval

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83
Q

A- fib

A

chaotic and erratic baseline with no discrete P wave between irregularly spaced QRS complex
irregularly irregular
HTN, CAD, post binge drinking

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84
Q

Atrial flutter

A

rapid succession of identical back to back atrial depolarization
Sawtooth

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85
Q

V-fib

A

erratic rhythm with no identifiable waves

Fatal without CPR and defibrillation

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86
Q

First Degree AV block

A

PR interval is prolonged

benign and asymptomatic

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87
Q

Mobitz Type 1

A

Second degree AV block
progressive lengthening of PR interval until a beat is dropped
asymptomatic
regularly irregular

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88
Q

Mobitz Type 2

A

Second degree AV block
dropped beats that are not preceded by a change in length of PR interval
may progress to third degree

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89
Q

Third degree AV block

A

atria and ventricles beat independently of each other
p waves and QRS complexes not rhythmically associated
caused by lymes

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90
Q

Atrial natriuretic peptide

A

released from atrial myocytes in response to increase blood volume and atrial pressure
via cGMP
vasodilation and decrease Na+ reabsorption at the renal collecting tubule
Dilate afferent and constrict efferent –> diuresis

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91
Q

B type natriuretic peptide

A

Released by ventricular myocytes in response to tension
longer half life to ANP
diagnose HF

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92
Q

Aortic Arch receptor

A

transmit to vagus N to solitary nucleus of medulla

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93
Q

Carotid sinus

A

transmits via glossopharyngeal N to solitary nucleus of medulla

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94
Q

Baroreceptor

A

Hypotension –> low arterial pressure –> low stretch –> low afferent baroreceptor firing –> high efferent sympathetic firing and low efferent parasympathetic –> vasoconstriction, HR, contractility

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95
Q

Cushing reflex

A

high ICP constricts arterioles –> cerebral ischemia –> high pCO2 and low pH –> central reflex sympathetic high in perfusion pressure –> high stretch –> peripheral reflex baroreceptor induced brady

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96
Q

Chemoreceptors

A

Peripheral- carotid and aortic bodies are stimulated by high pCO2 and low pH and O2
Central- changes in pH and pCO2 of brain interstitial fluid

97
Q

Increase capillary pressure

98
Q

increase capillary permeability

A

toxins, infection, burns

99
Q

increase interstitial fluid colloid osmotic pressure

A

lymphatic blockage

100
Q

decrease plasma oncotic pressure

A

nephrotic syndrome, liver failure, protein malnutrition

101
Q

Right to left shunt

A 
early cyanosis
maintain PDA
Truncus arteriosus (1 vessel)
Transposition (2 vessels)
Tricuspid atresia 
Tetralogy of Fallot
TAPVR
102
Q

Persistent truncus arteriosus

A

truncus arteriosus fails to divide into pulmonary trunk and aorta due to failure of aorticopulmonary septum formation
most also have VSD

103
Q

D transposition of great vessels

A

aorta leave RV and pulmonary trunk leaves LV –> separation of systemic and pulmonary circulation
not compatible with life unless have VSD, PDA, or PFO

104
Q

Tricuspid atresia

A

no tricuspid valve
hypoplastic RV
need ASD and VSD

105
Q

Tetralogy of Fallot

A

anterosuperior displacement of the infundibular septum
pulmonary infundibular stenosis, RVH (boot shpaed), overriding aorta, VSD
tet spells
squatting
associated with 22q11 syndromes

106
Q

Total anomalous pulmonary venous return

A

pulmonary V drain into right heart circulation

associated with ASD and PDA

107
Q

Ebstein anomaly

A

displacement of tricuspid valve leaflets downward into RV

associated wtih tricuspid regurgitation, accessory conduction pathways, right sided HF

108
Q

ASD

A 
defect in interatrial septum
wide fixed split S2
ostium secundum defects most common 
paradoxical emboli
Associated with Downs
109
Q

Eisenmenger syndrome

A

uncorrected left to right shunt –> high pulmonary blood flow –> remodeling of vasculature –> pulmonary arterial hypertension –> shunt becomes right to left
cause late cyanosis, clubbing and polycythemia

110
Q

Coarctation of the heart

A

arotic narrowing near insertion of ductus arteriosus
associated with bicuspid aortic valve, Turners
Hypertension in upper extremities and hypotension in lower extremities
Notched rib appearance of CXR
complications- HF, increased risk of cerebral hemorrhages, endocarditis

111
Q

Fetal alcohol syndrome

A

VSD, PDA, ASD, tetralogy of fallot

112
Q

Congenital rubella

A

PDA, pulmonary stenosis, septal defects

113
Q

Down syndrome

A

AV septal defect, VSD, ASD

114
Q

infant of diabetic mother

A

transposition of great vessels, VSD

115
Q

Marfan

A

mitral valve prolapse, thoracic AA and dissection, aortic regurgitation

116
Q

prenatal lithium

A

ebstein anomaly

117
Q

Turner

A

bicuspid aortic valve, coarctation of aorta

118
Q

Williams syndrome

A

supravalvular aortic stenosis

119
Q

22q11 syndromes

A

truncus arteriosus, tetralogy of fallot

120
Q

Hypertension

A

persistent systolic BP >130 and diastolic BP >80

increase with age, obesity, DM, physical inactivity, salt intake, alcohol, smoking, FamHx, AA

121
Q

Hypertensive urgency

A

severe >180/120 without acute end organ damage

122
Q

Hypertensive emergency

A

severe HTN with evidence of acute end organ damage

123
Q

Xanthoma

A

plaques or nodules composed of lipid laden histiocytes in skin

124
Q

Tendinous xanthoma

A

lipid deposit in tendon

Achilles

125
Q

Corneal arcus

A

lipid deposit in cornea
elderly
early in life with hypercholesteremia

126
Q

arteriosclerosis

A

hardening of arteries with wall thickening and loss of elasticity

127
Q

Arteriolosclerosis

A

affects small arteries and arterioles
hyaline- thickening of vessel walls secondary to plasma protein leak into endothelium in essential HTN or DM
hyperplastic- onion skinning with proliferation of smooth muscle cells

128
Q

Monckeberg sclerosis

A

medium sized arteries
calcifications of internal elastic lamina and media of arteries –> vascular stiffening without obstruction
pipestem appearance on X ray
does not obstruct blood flow

129
Q

atherosclerosis

A

disease of elastic arteries and large and medium sized muscular arteries
Abdominal aorta > coronary A > popliteal A > Carotid A > circle of willis
risk factors- smoking, HTN, dyslipidemia, DM, age, sex, FamHx
Angina, claudication
endothelial cell dysfunction –> macrophage and LDL accumulation –> foam cells –> fatty streaks –> smooth M migration –> ECM deposition –> plaque —> atheroma –> calcification

130
Q

Abdominal Aortic Anerurysm

A

associated with atherosclerosis
risk factors- smoking, age male, Fam Hx
palpable pulsatile ab mass

131
Q

Thoracic aortic aneurysm

A

associated with cystic medial degeneration
risk factor: HTN, bicuspid aortic valve, connective tissue disease, tertiary syphilis
May lead to aortic valve regurgitation

132
Q

Traumatic aortic rupture

A

due to trauma and deceleration injury
commonly at aortic isthmus
X ray may reveal widened mediastinus

133
Q

Aortic dissection

A

longitudinal intimal tear forming a false lumen.
Associated with HTN, bicuspid aortic valve, inherited connective tissue disorder
Can present with tearing, sudden onset chest pain radiating to back unequal BP in arms
Mediastinal widening
Type A- proximal involves ascending aorta. May result in acute aortic regurgitation or cardiac tamponade
Type B- involves only descending aorta

134
Q

Angina

A

chest pain due to ischemic myocardium secondary to coronary A narrowing or spasm, no myocyte necrosis

135
Q

Stable angina

A

secondary to atherosclerosis
exertional chest pain in classic distribution
ST depression
resolve with rest and nitro

136
Q

Vasospastic angina

A

occurs at rest secondary to coronary artery spasm
transient ST elevation
smoking is risk factor only
triggered by cocaine, alcohol, triptans
treat with CCB, nitrates and stop smoking

137
Q

Unstable angina

A

thrombosis with incomplete coronary artery occlusion
may have ST depression and T wave inversion
NO CARDIAC BIOMARKER ELEVATION
increase in frequency or intensity of chest pain or any chest pain at rest

138
Q

Coronary steal syndrome

A

distal coronary stenosis, vessels are maximally dilated at baseline
administer vasodilators –> blood is shunted toward well perfused areas –> ischmeia in myocardium perfused by stenosed vessels

139
Q

Sudden cardiac death

A

death from cardiac causes within 1 hour of onset of symptoms via lethal arrhythmia
associated with CAD, cardiomyopathy, hereditary ion channelopathies

140
Q

Chronic ischemic heart disease

A

progressive onset of HF over many years due to chronic ischemic myocardial damage

141
Q

Myocardial infarction

A

Due to rupture of coronary A atherosclerotic plaque –> acute thrombosis, increase cardiac biomarkers

142
Q

NSTEMI

A

subendocardial infarcts
subendocardium vulnerable to ischemia
ST depression

143
Q

STEMI

A

transmural infarts
full thickness of myocardial wall involved
ST elevation and Q waves

144
Q

commonly occluded coronary A

A

LAD > RCA> circumflex

145
Q

Symptoms of MI

A

diaphoresis, nausea, vomiting, severe retrosternal pain, pain in left arm or jaw, SOB, fatigue

146
Q

0-24 hour of MI

A

dark mottling
early coagulative necrosis –> cell content released into blood, edema, hemorrhage, WAVY FIBERS
reperfusion injury –> free radicals and increase calcium –> hypercontraction of myofibrils
complications –> ventricular arrhythmia, HF, cardiogenic shock

147
Q

1-3 days after MI

A

extensive coagulative necrosis, tissue surrounding infarct shows acute inflammation with neutrophils
complications –>postinfarction fibrinous pericarditis

148
Q

3-14 days after MI

A

macrophages then granulation tissue
complications –> free wall rupture (tamponade, papillary muscle rupture) –> mitral regurgitation, interventricular septal rupture due to macrophage mediated structural degradation –> left to right shunt. LV pseudoaneurysm

149
Q

2 weeks to months after MI

A

contracted scar complete

Complications –> Dressler syndrome, HF, arrhythmias, true ventricular aneurysm

150
Q

D(x) MI

A

first 6 hours - EKG –> STEMI vs NSTEMI, peaked T waves
Cardiac troponin I rises after 4 hours, peak at 24 hours and is high for 7-10 days
CKMB rises after 6-12 hours- d(x) reinfarction

151
Q

LAD infarct

152
Q

Anteroapical distal LAD

153
Q

LAD/LCX

154
Q

Lateral (LCX)

155
Q

inferior (RCA)

A

II, III, aVF

156
Q

Posterior PDA

A

V7-V9, ST depression in V1-V3 with tall R waves

157
Q

Cardiac arrhythmia

A

occurs within the first few days after MI

IMPORTANT CAUSE OF DEATH

158
Q

Postinfarction fibrinous pericarditis

A

1-3 days post MI

159
Q

Papillary muscle rupture

A

2-7 days after MI; posteromedial papillary M rupture increase risk due to single blood supple from PDA
severe mitral regurgitation

160
Q

Interventricular septal rupture

A

3-5 days after MI

macrophage mediated degradation –> VSD > high O2 saturation and pressure in RV

161
Q

Ventricular pseudoaneurysm formation

A

3-14 days post MI- free wall rupture contained by adherent pericardium or scar tissue
low CO risk of arrhythmias, embolus from mural thrombus

162
Q

Ventricular free wall rupture

A

5-14 days post MI- free wall rupture –> cardiac tamponade
LV hypertrophy and previous MI protect against free wall rupture
sudden death

163
Q

True ventricular aneurysm

A

2 weeks to several months post MI- outward bulge with contraction
associated with fibrosis

164
Q

Dressler syndrome

A

several week post MI
autoimmune phenomenon
fibrinous pericarditis

165
Q

LV failure and pulmonary edema

A

secondary to LV infarction, VSD, free wall rupture, papillary muscle rupture with mitral regurgitation

166
Q

Acute coronary syndrome treatments

A

unstable/ NSTEMI- anticoagulation, antiplatelet + ADP receptor inhibitor, B blockers, ACEi, statins. Symptom control with nitro and morphine
STEMI- + reperfusion therapy

167
Q

Dilated Cardiomyopathy

A

Most common
idiopathic or familial (TTN mut)
HF, S3 systolic regurgitatnt murmur, dilated heart, balloon appearance on CXR
T(x) Na+ restriction, ACEi, B blockers, diuretics, mineralcorticoid receptor blockers, digoxin, ICD, heart transplant
eccentric hypertrophy

168
Q

Takotsubo cardiomyopathy

A

broken heart syndrome

ventricular apical ballooning increased by sympathetic stimulation

169
Q

Hypertrophic obstructive cardiomyopathy

A

familial, AD sarcoplasmic protein mutations, HTN, Friedreich ataxia
syncope during exercise –> sudden death due to ventricular arrhythmias
S4, systolic murmur, mitral regurgitation
T(x): stop athletics, B blockers or CCB
concentric hypertrophy
asymmetric septal hypertrophy and systolic anterior motion of mitral valve –> outflow obstruction –> dyspnea

170
Q

Restrictive cardiomyopathy

A

postradiation fibrosis, loffler endocarditis, endocardial fibroelastosis, amyloidosis, sarcoidosis, hemochromatosis
thick myocardium

171
Q

Loffler endocarditis

A

associated with hypereosinophilic syndrome

eosinophils in myocardium

172
Q

Heart failure

A

cardiac pump dysfunction –> congestion and low perfusion

dyspnea, orthopnea, fatigue, S3 heart sound, rales, JVD, pitting edema

173
Q

Systolic dysfunction

A

low EF, high EDV, low contractility secondary to MI or dilated cardiomyopathy

174
Q

Diastolic dysfunction

A

preserved EF, normal EDV, low compliance

secondary to myocardial hypertrophy

175
Q

Left Heart Failure

A

orthopnea- SOB when supine
Paroxysmal nocturnal dyspnea- breathlessness awakening from sleep
pulmonary edema- high pulmonary venous pressure

176
Q

Right heart failure

A

Hepatomegaly (nutmeg liver)
JVD
peripheral edema

177
Q

Hypovolemic shock

A 
hemorrhage, dehydration, burns
skin cold and clammy
LOW preload
low CO
high afterload
Treat with IV fluids
178
Q

Cardiogenic shock

A 
Acute MI, HF, valvular dysfunction, arrhythmia
skin cold and clammy
LOW CO
high afterload
treat with inotropes, diuresis
179
Q

obstructive shock

A 
cardiac tamponade, pulmonary embolism, tension pneumothorax
skin cold and clammy
LOW CO
high afterload
treat by relieving obstruction
180
Q

Distributive shock- sepsis, anaphylaxis

A

skin warm
low preload
high CO
LOW afterload

181
Q

Distributive shock- CNS injury

A

skin Dry
low preload
low CO
LOW afterload

182
Q

Cardiac tamponade

A

compression of the heart by fluid in pericardial space
low CO
Becks triad- hypotension, distended neck veins, distant heart sounds
High HR, pulsus paradoxus

183
Q

pulsus paradoxus

A

low amplitude of systolic BP >10 during inspiration

constrictive pericarditis, obstructive pulmonary disease, tamponade

184
Q

Acute bacterial endocarditis

A

S aureus. Large vegetations on preciously normal valves.

Rapid onset

185
Q

Subacute bacterial endocarditis

A

viridan strep
smaller vegetations on congenitally abnormal or diseased valves
dental procedures
gradual onset

186
Q

Bacterial endocarditis

A

fever, new murmur, roth spots, osler nodes, janeway lesions, splinter hemorrhages
associated with glomerulonephritis, septic arterial or pulmonary emboli
(-) culutre –> coxiella burnetti, bartonella
Mitral valve most frequent
Tricuspid if IV drugs (s. aureus, pseudomonas, candida)
S. bovis- colon cancer
s- epidermidis- prosthetic valves
Native valve endocarditis –> HACEK

187
Q

Rheumatic Fever

A

pharyngeal infection via group A B hemolytic strep
Mitral > aortic&raquo_space; tricuspid
Associated with Aschoff bodies, Anitschkow cells, high anti strep O, high anti DNase B
Type 2 hypersensitivity
JONES- joint, carditis, nodules, erythema marginatum, syndeham chorea

188
Q

Syphilitic heart disease

A

tertiary
disrupt vasa vasorum of aorta with atrophy of vessel wall and dilation of aorta and valve ring
calcifications of aortic root, ascending aortic arch and thoracic aorta
tree bark appearance

189
Q

Acute pericarditis

A

sharp pain, aggravated by inspiration and relieved by sitting up and leaning forward
widespread ST segment elevation or PR depression
idiopathic, cocksakie B neoplasia, autoimmune, uremia, CV, radiation
T(x) NSAIDs, colchicine, glucocorticoids, dialysis

190
Q

Myocarditis

A

global enlargement of heart and dilation of all chambers.
dyspnea, chest pain, fever, arrhythmias
caused by viral infection, parasitic, bacterial, toxins, rheumatic fever, drugs, autoimmune disease
complications: sudden death, arrhythmias, heart block, dilated cardiomyopathy, HF, mural thrombosis with systemic emboli

191
Q

Giant cell arteritis

A 
elderly females
CAROTID A
focal granulomatous inflammation
unilateral HA, temporal A tenderness, claudication of jaw
Irreversible blindness
associated with polymyalgia rheumatica
High ESR
T(x) high dose corticosteroid to prevent blindness
192
Q

Takayasu arteritis

A

Asian females <40 years
pulseless disease, fever, night sweats, arthritis, myalgias, skin nodules, ocular disturbances
Granulomatous thickening and narrowing of aortic arch and proximal great vessels
High ESR
T(x) corticosteroids

193
Q

Buerger Disease

A

Heavy smokes, males <40 years
intermittent claudication
gangrene, autoamputation of digits, superficial nodular phlebitis
Raynaud phenomenon
Segmental thrombosing vasculitis with vein and nerve involvement
T(x) stop smoking

194
Q

Kawasaki Disease

A

Asian children <4 years
conjunctival injection, rash, adenopathy, strawberry tongue, hand foot changes, fever
Develop coronary A aneurysm, thrombosis/ rupture –> death
T(x): IVIg and aspirin

195
Q

Polyarteritis nodosa

A

middle age men
Hep B
fever, weight loss, malaise, HA, ab pain, melena, HTN, neuro problems, cutaneous eruptions, renal damage
Renal and visceral vessels, not pulmonary A
T(x): corticosteroids and cyclophosphamide

196
Q

Behcet syndrome

A

Recurrent aphthous ulcers, genital ulcers, uveitis, erythema nodosum
via HSV or parvovirus
Immune complex vasculitis
HLA B51

197
Q

Cutaneous small vessel vasculitis

A

7-10 days after medication or infection
palpable purpura, no visceral involvement
immune complex mediated leukocytoclastic vasculitis

198
Q

Eosinophilic granulomatosis with polyangiitis

A

Asthma, sinusitis, skin nodules, purpura, peripheral neuropathy
Can involve heart, GI, kidneys
granulomatous necrotizing vasculitis with eosinophilia
MPO ANCA, high IgE

199
Q

Granulomatosis with polyangiitis

A

Upper respiratory tract- perforation of nasal septum, chronic sinusitis, otitis media, mastoiditis
lower respiratory tract- hemoptysis, cough, dyspnea
Renal- hematuria, red cell casts
Focal necrotizing vasculitis + necrotizing granulomas in lung and upper airway + necrotizing glomerulonephritis
PR3 ANCA
large nodular densities on CXR
T(x)- cyclophosphamide, corticosteroids

200
Q

IgA vasculitis

A

Henoch Schnolein purpura
childhood
follow URI
palpable purpura on leg/butt +arthralgia + ab pain (intussception)
secondary to IgA immune complex deposition
Associated with IgA nephropathy
T(x): supportive

201
Q

Microscopic polyangitis

A

necrotizing vasculitis in lung, kidneys and skin
pauci immune glomerulonephritis and palpable purpura
No granulomas
MPO ANCA
T(x) cyclophosphamide, corticosteroids

202
Q

Mixed cryoglobinemia

A 
viral infection (HCV)
palpable purpura, wekness, arthralgia
peripheral neuropathy and renal disease
precipitate in cold
mixed IgG and IgM complex deposition
203
Q

Myomas

A

primary cardiac tumor in adults
in LA
ball valve obstruction in the LA
IL 6 produced –> constitutional symptoms
tumor plop is early diastole
gelatinous material, myxoma cells in glycosaminoglycans

204
Q

Rhabdomyoma

A

primary cardiac tumor of children associated with tuberous sclerosis
hamartomatous growths

205
Q

Kussmaul sign

A

high JVP on inspiration instead of decrease

may be seen with constrictive pericarditis, restrictive cardiomyopathy, RHF, massive pPE, RA or ventricular tumors

206
Q

Hereditary hemorrhagic telangiectasia

A

Osler Weber Rendu
AD disorder of blood vessels
blanching lesions on skin and mucous membranes, recurrent epistaxis, skin discoloration, arteriovenous malformations, GI bleed, hematuria.

207
Q

Primary HTN treatment

A

thiazide diuretics, ACEi, ARBs, CCB

208
Q

HTN with HF treatment

A

Diuretics, ACEi, ARBs, B blockers, aldosterone antagonists

209
Q

HTN with DM treatment

A

ACEi, ARBs, CCB, thiazide diuretics, B blockers

210
Q

HTN in asthma treatment

A

ARBs, CCB, thiazides, cardioselective B blockers

211
Q

HTN in pregnancy treatment

A

Hydralazine, labetolol, methyldopa, nifedipine

212
Q

Dihydropyridines

A

-pine
block VGCC (L-type) of cardiac and smooth muscle –> decrease muscle contractility
Dihydropyridines- HTN, angina, Raynaud
Nimodipine- subarachnoid hemorrhage
Nicardipine- HTN urgency/emergency
Adverse: gingival hyperplasia, peripheral edema, flushing, dizziness

213
Q

Non- dihydropyridines

A

diltiazem, verapamil
block VGCC (L-type) of cardiac and smooth muscle –> decrease muscle contractility
HTN, angina, a fib/flutter
Adverse: gingival hyperplasia, cardiac depression, AV block, hyperprolactinemia, constipation

214
Q

Hydralazine

A

increase cGMP –> smooth muscle relaxation, vasodilate arterioles, decrease afterload
used for severe HTN, HF, safe for pregnancy
Adverse: compensatory tachy, fluid retention, HA, angina, drug induced lupus

215
Q

Hypertensive emergency treatment

A

Nitroprusside- short acting vasodilator, increase cGMP via release of NO. Can cause CN- tox
Fenoldopam- D1 agonist –> coronary, peripheral, renal, splanchnic vasodilation. lower BP, increase natriuresis. Can cause hypotension and tachy

216
Q

Nitrates

A

Nitroglycerin, isosorbide dinitrate, isosorbide mononitrate
vasodilate by increase NO in vascular smooth muscle –> increase cGMP and smooth muscle relaxation
used for angina, acute coronary syndrome, PE
adverse: reflex tachy, hypotension, flushing, HA

217
Q

Nitrate therapy

A

decrease EDV, BP, Ejection time, MVO2

increases Contractility and HR

218
Q

B blocker therapy

A

decrease BP, ejection time, MVO2, contractility and HR

219
Q

Nitrates + B blockers

A

Lower BP and MVO2

220
Q

Ranolazine

A

inhibit late phase of inward sodium current –> decrease diastolic wall tension and O2 consumption. DOES NOT EFFECT HR or BP
used in angina refractory
Adverse: constipation, dizziness, HA, nausea

221
Q

Sacubitril

A

neprilysin inhibitor, prevent degradation of ANP and BNP, AngII, substrate P –> increase vasodilation, lower ECF volume
used in combo with valsartan to treat HFrEF
Adverse: hypotension, hyperkalemia, cough, dizziness, contra with ACEi

222
Q

HMG CoA reductase inhibitors

A

statins
lower LDL, TG, higher HDL
inhibit HMG CoA to mevalonate
Adverse: hepatotoxicity, myopathy

223
Q

Bile acid resins

A

cholestyramine, colestipol, colesevelam
lower LDL
higher HDL and TG
prevent intestinal reabsorption of bile acids
Adverse: GI upset, decreased absorption of other drugs and fat soluble vitamins

224
Q

Ezetimibe

A

lower LDL
prevent cholesterol absorption at small intestine brush border
Adverse: increase LFT and diarrhea

225
Q

Fibrates

A 
-fibrozil
lower LDL and TG
high HDL
upregulate LPL --> increase TG clearance
activate PPARa to induce HDL synthesis
Adverse: myopathy, cholesterol gallstones
226
Q

Niacin

A

low LDL and TG
high HDL
inhibit lipolysis in adipose tissue, reduce hepatic VLDL synthesis
Adverse: flushed face, hyperglycemia, hyperuricemia

227
Q

PCSK9 inhibitors

A 
-ocumab
low LDL, TG
high HDL
inactivate LDL receptor degradation --> increase LDL removal in blood stream
Adverse: myalgias, delirium, dementia
228
Q

Fish oil and marine Omega 3 FA

A

high LDL, HDL
low TG
decrease FFA delivery to liver and decrease activity of TG synthesizing enzymes
Adverse: nausea

229
Q

Digoxin

A

inhibit Na+/K+ ATPase –> inhibit Na+/Ca2+ exchanger –> increase calcium –> + inotropy –> stimulate vagus N –> decrease HR
used in HF, A fib
Adverse: cholinergic effects, blurry yellow vision, arrhythmias, AV block
contra in renal failure, hypokalemia
antidote- slowly normalize K+, cardiac pacer, anti digoxin Fab fragments, Mg2+

230
Q

Class 1A Na+ blockers

A

Quinidine, procainamide, disopyramide
Moderate Na+ block. increase AP duration, increase effective refractory period, increase QT interval
used for atrial and ventricular arrhythimias SVT and VT
Adverse: cinchonism, reversible SLE, HF, thrombocytopenia, torsades, increase QT interval

231
Q

Class 1B Na+ blockers

A 
Lidocaine, mexiletine
weak Na+ block
decrease AP duration
used in acute ventricular arrhythmias
Adverse: CNS stimulation/depression, CV depression
232
Q

Class 1C Na+ blockers

A 
Flecanide, propafenone
strong Na+ blocker
prolong ERP in AV node 
used in SVTs, a fib
Adverse: proarrhythmic contra in structural and ischemic heart disease
233
Q

Class 2 B blockers

A

-lol
Decrease SA and AV node activity by low cAMP and calcium
decrease slope of phase 4
used in SVT, ventricular rate control for a fib and flutter
Adverse: impotence, exacerbation of COPD and asthma, CV effects, sedation, dyslipidemia (metoprolol)

234
Q

Class 3 K+ blockers

A

amiodarone, ibutilide, dofetilide, sotalol
increase AP duration ERP and QT
used in a fib and flutter, V tach
Adverse: torsade de pointe
amiodarone- pulmonary fibrosis, hepatotox, hypothyroid, corneal deposits, skin deposits, neuro, constipation, CV

235
Q

Class 4 CCB

A

diltiazem verapamil
decrease conduction velocity, high ERP, PR
used to prevent nodal arrhythmias, rate control for a fib
Adverse: constipation, flushing, edema, CV

236
Q

Adenosine

A

increase K+ out of cell –> hyperpolarize the cell and decrease AV conduction
Diagnose and terminate SVT
short acting
blunted by theophyline and caffeine
Adverse: flushing. hypotension, chest pain sense of impending doom, bronchospasm

237
Q

Magnesium

A

effective in torsades de pointes and digoxin tox

238
Q

Ivabradine

A

prolong slow depolarization by inhibiting funny channels
used in chronic stable angina in patients that cannot take B blockers
Adverse: luminous phenomena.visual brightness, hypertension, brady

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