Cardiovascular Flashcards Preview

FirstAID > Cardiovascular > Flashcards

Flashcards in Cardiovascular Deck (222):
1

Acute chest pain that radiates to back?

Acute dissecting aortic aneurysm; usually initiated by an intimal tear

2

wide, fixed splitting of S2 that doesn't vary with respiration

ASD

3

What may lead to eye problems following treatment for an inferior MI (ST elevation in inferior leads)?

Inferior lead MIs are associated with bradycardia; so, pts are often given atropine to treat the bradycardia. Side effect of atropine = eye problems!

4

What artery does coronary artery occlusion most commonly occur in?

LAD = Left Anterior Descending artery
=> anterior wall MI
*LAD comes off the LCA (left main coronary artery), supplies the apex and anterior interventricular septum

5

Which coronary artery supplies the SA and AV nodes?

Majority of time --> SA and AV nodes are supplied by the RCA

6

Which coronary artery supplies the right ventricle?

Acute marginal artery (comes off the RCA)

7

Which coronary artery supplies the posterior left ventricle?

CFX = Circumflex artery (comes off the LCA)

8

PD = Posterior Descending artery is supplied by? supplies?

"Right Dominant" heart --> majority of cases (about 80%), RCA supplies the PD, which supplies the inferior part of the Left ventricle
*20% of the time, the PD arises from the CFX (Circumflex artery, which arises from the LCA)

9

Most posterior part of the heart? What may it cause if it enlarges?

-most posterior part of the heart is the Left Atrium
-If enlargement of Left Atrium --> dysphagia (d/t esophageal compression) or Hoarseness (d/t recurrent laryngeal nerve compression)

10

CO (Cardiac Output) = ?

CO = SV X HR

(CO = Stroke Volume X Heart Rate)

***note: if HR is too high --> diastolic filling is incomplete --> get decreased CO (ie ventricular tachycardia)

11

Fick Principle:

CO = (rate of O2 consumption) / (arterial O2 content - Venous O2 content)

12

MAP (mean arterial pressure) = P =?

MAP = CO X TPR
P = Q X R

*TPR = R = Total Peripheral Resistance

13

Pulse Pressure = ?

Pulse Pressure = Systolic Pressure - Diastolic Pressure

14

Pulse Pressure is proportional to?

Stroke Volume

15

Stroke Volume = ?

SV = CO/HR = EDV - ESV

16

EDV vs ESV

EDV = End-Diastolic Volume = full heart
ESV = End-Systolic Volume = empty heart (after pumping out!)

17

What maintains the CO during early stages of exercise? late stages of exercise?

*Early stages of exercise --> CO maintained by SV
*Late stages of exercise --> CO is maintained by HR

18

Which 3 factors affect Stroke Volume?
Increased SV when these factors increase/decrease?:

SV CAP:
-Contractility
-Afterload
-Preload

Increased SV when:
-Increased contractility
-Decreased afterload
-Increased Preload

19

4 factors that increase contractility (and thus increase SV):

1) Catecholamines --> increase activity of Calcium pump in Sarcomplasmic Reticulum (act on Beta-1 receptors)
2) Increased intracellular Calcium
3) Decreased extracellular Sodium (b/c decreased activity of Na+/Ca2+ exchanger, so more Calcium stay inside cell)
4) Digitalis (b/c blocks Na+/K+ ATPase, so decreased extracellular Na+ --> decreased activity of Na+/Ca2+ exchanger --> more Calcium stays in cell, so --> increased intracellular Calcium)

20

5 factors that decreased contractility (and thus decrease SV):

1) Beta-1 blockade (decreased cAMP-->decreased Protein Kinase A --> decrease intracellular Ca)
2) Heart failure (systolic dysfxn)--> decreased SV in heart failure
3) Acidosis
4) Hypoxia/Hypercapnea (decreased PO2/increased PCO2)
5) Non-dihydropyridine Ca2+ channel blockers (ie Verapamil, Diltiazem)

21

3 states in which have increased SV:

-Pregnancy (b/c increased blood volume, so increased preload)
-Exercise (b/c increased pre-load + increased catecholamines)
-Anxiety (b/c increased catecholamines)

22

4 factors that increase myocardial O2 demand:

1) increased afterload
2) increased contractility
3) increased heart rate
4) increased heart size

23

What is the preload? What states may increase preload?

Preload = Ventricular EDV
Increased preload with:
-Exercise (slightly)
-Pregnancy
-Increased blood volume (ie over-transfusion)
-Excitement (ie sympathetics)

***Preload Pumps up the heart!

24

Mean arterial pressure = ?

MAP = 2/3 diastolic pressure + 1/3 systolic pressure

25

Preload and Afterload: Which is proportional to the mean arterial pressure and total peripheral resistance? to central venous pressure?

-Central venous pressure is about equal to the preload
-Total peripheral resistance is about equal to the afterload

26

Effect of venodilators (ie Nitroglycerin) on heart?

decrease preload

27

Effect of vasodilators (ie hydralazine) on heart?

decrease afterload

28

effect of ACE-inhibitors and ARBs on heart?

decrease preload AND decrease afterload

29

How to decrease O2 demand in a heart attack? (3 ways)

-decrease afterload --> ACE inhibitors
-decrease contractility --> Beta-blockers
-decrease HR --> Beta-blockers

30

EF = Ejection Fraction = ?

What is it normally? (%)

EF = what heart can pump out / what heart can hold

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

EF is an index of ventricular contractility

EF is normally > or = 55%
-->get decreased EF is systolic heart failure

31

Preload and Afterload: Which is proportional to the mean arterial pressure and total peripheral resistance? to central venous pressure?

-Central venous pressure is about equal to the preload
-Total peripheral resistance is about equal to the afterload

32

Effect of venodilators (ie Nitroglycerin) on heart?

decrease preload

33

Effect of vasodilators (ie hydralazine) on heart?

decrease afterload

34

effect of ACE-inhibitors and ARBs on heart?

decrease preload AND decrease afterload

35

How to decrease O2 demand in a heart attack? (3 ways)

-decrease afterload --> ACE inhibitors
-decrease contractility --> Beta-blockers
-decrease HR --> Beta-blockers

36

EF = Ejection Fraction = ?

What is it normally? (%)

EF = what heart can pump out / what heart can hold

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

EF is an index of ventricular contractility

EF is normally > or = 55%
-->get decreased EF is systolic heart failure

37

delta P (pressure) = ?

delta P = Q X R

Pressure = Flow X Restistance

38

Effects of Viscosity and Radius on Resistance?

*Resistance is proportional to Viscosity (increase viscosity --> increase R)

*Resistance is inversely proportional to radius^4 (increase radius --> decrease resistance, and visa versa)

39

What is the main component that determines viscosity?

Hematocrit

40

3 states in which have increased Viscosity:

1) Polycythemia
2) Hyperproteinemic states (ie Multiple Myeloma)
3) Hereditary spherocytosis

41

S1 sound:

Mitral and Tricuspid valve closure
-loudest at mitral area

42

S2 sound:

Aortic and Pulmonary valve closure
-loudest at left sternal border

43

S3 sound:

"Ken-Tuc-Key" (key = S3) or "Lub-Dub-Ta"
-in EARLY diastole, during rapid ventricular filling phase.
-Associated with: increased filling pressures (MR, CHF), and more common in dilated ventricles
-Normal in children and pregnant women

44

When is a S3 sound considered normal?

-Children
-Pregnant women

45

S4 sound:

="atrial kick"
"Ten-Nes-See" (ten=S4) or "Ta-Lub-Dub"
-in LATE diastole
-High atrial pressure
-Associated with ventricular hypertrophy (LA has to push against stiff LV wall)

46

Mitral and Tricuspid Valves

MitraL --> Left! Bicuspid valve
Triscupid --> Right

47

Isovolumetric Contraction

Period between mitral valve closure and aortic valve opening; period of highest O2 consumption

48

Systolic Ejection

period between aortic valve opening and closing

49

Isovolumetric Relaxation

Period between aortic valve closing and mitral valve opening

50

Rapid Filling

Period just after mitral valve opens

51

Reduced Filling

Period just before mitral valve closure

52

S2 Splitting:

Aortic valve closes before pulmonic (inspiration increases this difference)

53

What may increase the difference in S2 splitting (when aortic valve closes before pulmonic)? When is S2 splitting normal? When is S2 splitting pathologic?

Inspiration
*Note: split S2 on inspiration = normal; split S2 on expiration = pathologic

54

Jugular Venous Pulse (JVP)

"At Carter's Xing Vehicles Yield"
-a wave = atrial contraction
-c wave = RV contraction (closed tricuspid bulges into atrium)
-x descent = atrial relaxation (downward displacement of closed tricuspid during ventricular contraction)
-v wave = increased RA pressure, d/t filling against closed tricuspid
-y descent = blood flow from RA to RV

55

Wide S2 splitting is associated with?

-Pulmonic stenosis
-R bundle branch block

*kind of just an exaggeration of normal splitting

56

Fixed S2 splitting is associated with?

ASD

57

Paradoxical S2 splitting is associated with?

-Aortic stenosis
-L bundle branch block

*hear pulmonic closure before aortic!

58

Systolic murmurs:

-Aortic or Pulmonic stenosis
-Mitral or Tricuspid Regurg

59

Diastolic Murmurs:

-Mitral or Tricuspid stenosis
-Aortic or Pulmonic Regurg

60

Which murmurs are worse with inspiration? Worse with expiration?

-Tricuspid = worse with inspiration (b/c increased blood in RA)
-Mitral = worse with expiration (b/c increased blood into LA)

61

Holosystolic Murmur:

-Tricuspid Regurg
-Mitral Regurg
-VSD

62

Holosystolic murmur that increases in intensity during inspiration?

-Tricuspid Regurgitation

63

Murmur that is loudest at apex, radiates toward axilla?

-Mitral Regurgitation
--> enhanced by: expiration, squatting, hand grip

64

Murmur that is loudest at tricuspid area and radiates to Right sternal border?

Tricuspid Regurgitation:
-->enhanced by inspiration

65

Pulsus parvus et tardus

pulse is weak compared to heart sounds
-Aortic stenosis

66

Bicuspid aortic valve --> what kind of murmur?

Aortic stenosis

67

Systolic ejection murmur following ejection click

Aortic stenosis
-ejection click is d/t abrupt halting of valve leaflets

68

holosystolic, harsh-sounding murmur; loudest at tricuspid area (over L sternal border in 3rd or 4th intercostal space)

VSD

69

Midsystolic click

*Mitral Prolapse
-click is d/t sudden tensing of chordae tendineae
-loudest at S2
-can predispose to infective endocarditis

70

Diastolic murmur, bounding pulses, head bobbing

-Aortic regurgitation

71

Murmur with an opening snap

Mitral Stenosis
-snap is d/t abrupt halt of leaflet motion in diastole, after rapid opening d/t fusion at leaflet tips
-enhanced by expiration

72

continuous machine-like murmur; loudest at S2

PDA

73

Speed of conduction through heart: fastest --> slowest:

Fastest "Park At Ventura Avenue" Slowest
Purkinje > Atria > Ventricles > AV node

74

inverted T wave on ECG

indicates recent MI

75

presence of U wave on ECG?

caused by hypokalemia or bradycardia

76

Conduction pathway through heart:

SA node --> atria --> AV node --> common bundle --> LAF --> Bundle branches --> Purkinje fibers --> ventricles

77

Torsades de pointes
-What can it progress to?
-What may predispose to it?

= Ventricular tachycardia; fast, wide QRS of varying amplitudes.
-Can progress to V-fib
-anything that prolongs QT interval can predispose to torsades

78

Jervell and Lange-Nielsen syndrome

-autosomal recessive
-Torsades de pointes + severe congenital sensorineural deafness

79

Drugs that can prolong QT interval (and thus predispose to Torsades de pointes)?

-Macrolides
-Antimalarials
-Haloperidol
-Risperidone (atypical antipsychotic)
-Methadone
-Protease inhibitors
-Class 1A antiarrhythmics

80

What drug can be given to treat torsades de pointes?

Magnesium!

81

WPW = Wolf-Parkinson White Syndrome

Ventricular pre-excitation syndrome - have an accessory excitation pathway from atria to ventricle that bypasses AV node; so, get early ventricular depolarization and see a Delta wave
--> may lead to SVT
--> Treat with Procainamide and Amiodarone

82

Delta wave

seen with WPW syndrome

83

Irregularly irregular ECG with no discrete P waves; see irregularly spaced QRS complexes

Atrial fibrillation (no distinct SA node; have several SA nodes acting at once, so no coordinated atrial contractions)
--> get pooling of blood in atria --> can lead to pulm embolism, stroke, SVT
*Treat with: beta blockers, Ca-channel blockers, or digoxin (plus prophylaxis against thromboembolism with warfarin)

84

Sawtooth appearance on ECG

Atrial flutter
-treat with class IA, IC or III antiarrhythmics, or beta-blockers

85

PR interval is prolonged by >200 msec on ECG

1st degree AV block
-asymptomatic

86

ECG with progressive lengthening of PR interval until a beat is "dropped" (so, have a P wave, not followed by a QRS complex)

2nd degree AV block = Mobitz type I = Wenckebach AV block
-asymptomatic

87

ECG with sudden dropped beats (QRS complexes) after a P wave; no change in PR interval prior to the dropped beat.

-Mobitz type II AV Block (2nd degree AV block)
-pathologic --> may progress to 3rd degree AV block

88

ECG with both P waves and QRS complexes, but P waves bear no relation to the QRS complexes.

-3rd degree = Complete AV block
-->atria and ventricles beat independently of one another

*Lyme disease may result in 3rd degree heart block

89

What microbiology disease may lead to 3rd degree heart block?

Lyme disease may result in 3rd degree heart block

90

ECG with completely erratic rhythm and no identifiable waves

V-fib (fatal arrhythmia without immediate CPR and defibrillation)

91

ANP = Atrial Natriuretic Peptide:

-Released from atria in response to increased blood volume and atrial pressure
-leads to generalized vascular relaxation
-lowers BP by:
-->peripheral vasodilation
-->natriuresis
-->diuresis
*contstricts efferent renal arterioles and dilates afferent arterioles (cGMP mediated) which promotes diuresis (and "escapes from aldosterone")

92

Responses to BP changes in the aortic arch? carotid sinus?

-aortic arch --> only responds to increased BP; transmits signal via vagus nerve to medulla
-Carotid sinus --> responds to increased and decreased BP; transmits signal via glossopharyngeal nerve to solitary nucleus of medulla

93

Carotid massage:

Carotid massage increases cardiac PARASYMPATHETIC tone --> get increased AV node refractory period

carotid massage --> increased pressure on carotid artery --> increased stretch --> increased afferent baroreceptor firing --> decreased HR

SO: massage--> Increased BP --> decreased HR

94

Cushing Reaction:

increased ICP --> constricts arterioles --> cerebral ischemia --> HTN (sympathetic response) --> reflex bradycardia

95

Cushing's Triad

1) HTN
2) Bradycardia
3) Respiratory depression

***get Cushing's triad when: intracranial hemorrhage with increased ICP

96

PCWP = Pulmonary Capillary Wedge Pressure (mmHg): Approximates what?

-LA pressure

97

Swan-Ganz catheter:

-used to measure PCWP (pulm capillary wedge pressure); so used to approximate LA pressure
*mechanism: venous catheter into internal jugular or subclavian vein --> SVC --> RA --> RV --> Pulm artery --> stops somewhere along here, balloon is wedged into a branch of the pulm artery; measures pressure on opposite side of ballon --> so, = pressure in LA

98

What does hypoxia do to vasculature throughout the body?

*In majority of organs: hypoxia --> vasodilation
*In pulmonary vasculature: hypoxia --> vasoconstriction (this way, only well-ventilated areas are perfused)
***so, lungs = unique in hypoxia

99

"blue babies" vs "blue kids"

*blue babies = early cyanosis; R--> L shunts (the 5 Ts)
*blue kids = late cyanosis: L--> R shunts (VSD, ASD, PDA) (then, get Eisenmenger's syndrome, eventually, leading to late cyanosis...)

100

Early Cyanosis/ R-->L shunts causes:

5 T's:
-TOF (= most common cause)
-Transposition of Great Vessels
-Truncus arteriosus
-Tricuspid atresia
-Total anomalous pulmonary venous return (TAPVR)

101

Persistent truncus arteriosus:

-failure of truncus arteriosus to divide into pulmonary trunk and aorta; so just have 1 vessel!
-causes cyanosis at birth

102

Tricuspid atresia

absent tricuspid valve, and hypoplastic RV
-cyanotic at birth
-requires both ASD + VSD for viability

103

TAPVR = Total Anomalous Pulmonary Venous Return

pulmonary veins drain into right heart circulation (similar to transposition...)
-must have a patent foramen ovale or an ASD to be viable.
-babies cyanotic at birth

104

Causes of L-->R shunts (late cyanosis)

1) VSD (most common)
2) ASD (loud S1; wide, fixed split S2)
3) PDA (machinery murmur; most close on own w/in first 24 hours; otherwise, close with indomethacin)

*L-->R shunts: VSD, ASD, PDA may lead to Eisenmenger's syndrome if not corrected

105

Eisenmenger's syndrome:

-uncorrected VSD, ASD, PDA --> causes compensatory pulmonary vascular hypertrophy --> results in progressive pulmonary hypertension

increased pulmonary resistance --> shunt reverses from L-->R to R-->L; get late cyanosis (clubbing + polycythemia)

106

Cyanosis + Clubbing (swollen finger tips) + Polycythemia:

Eisenmenger's syndrome

107

Tetralogy of Fallot

1) Pulmonary stenosis (most important determinant for prognosis)
2) RVH (causes boot-shaped heart on x-ray)
3) Overriding aorta (overrides VSD)
4) VSD

108

What causes Tetralogy of Fallot?

anterosuperior displacement of infundibular septum

109

Why do pts with TOF squat to relieve symptoms?

Squatting--> compress femoral arteries --> increased TPR--> decreased R-->L shunt and thus directs more blood from RV to lungs

110

Cause of Transposition of great vessels?

Failure of aorticopulmonary septum to spiral

111

Infantile vs Adult coarctation of the aorta:

Infantile--> preductal aortic stenosis (proximal to insertion of ductus arteriosus); assoc w/Turner's
Adult: postductal aortic stenosis; distal to ligamentum arteriosum

112

Notching of ribs

Coarctation of aorta (adult type/post-ductal)

113

Paradoxical hypertension in upper extremities; hypotension in lower extremities

Coarctation of aorta (adult type/post-ductal)

114

22q11 syndromes associated with what cardiac defects?

(ie DiGeorge syndrome)
-Truncus arteriosus
-TOF

115

Congenital rubella is associated with what cardiac defects?

-PDA
-pulmonary artery stenosis
-septal defects

116

What cardiac defect is associated with Turner's syndrome?

Coarctation of aorta (preductal/infantile type)

117

Cardiac defect associated with infants born to diabetic mothers?

Transposition of great vessels

118

Monckeberg arteriosclerosis

-calcification of MEDIA of arteries (intima not involved); usually benign
-"pipestem" arteries

119

Arteriolosclerosis

hyaline thickening of small arteries in essential HTN or DM
-hyperplastic "onion skinning" in malignant HTN

120

Atherosclerosis (what layer of arterial wall is involved?

fibrous plaques and aterhomas in INTIMA of arteries

121

Abdominal aortic aneurysms: associated with what precursor condition?

-Associated with atherosclerosis of the abdominal aorta

122

mediastinal widening on CXR

Aortic dissection (have intraluminal tear, forming a false lumen)

123

DX of MI:

-first 6 hours: ECG = gold-standard
-4 hrs - 7-10 days: Cardiac troponin (=most specific)
-CK-MB = nonspecific, but good for dx reinfarction on top of acute MI

124

most specific marker of MI and lasts longest

Cardiac troponin I (rises after 4 hours, stays elevated for 7-10 days)

125

ST elevation on ECG after MI

Transmural infacts (non-STEMI = subendocardial infarcts; get ST depression on ECG)

126

Dressler's syndrome

autoimmune process several weeks post-MI --> get fibrinous pericarditis

127

S3, balloon appearance on CXR, laterally displaced apical pulse:

-Dilated Cardiomyopathy

128

S4, increased sized of apical pulse, systolic murmur

Hypertrophic cardiomyopathy

129

Possible etiologies of Dilated Cardiomyopathy:

ABCCCD
-Alcohol (chronic)
-wet Beriberi
-Coxsackie B virus myocarditis
-Cocaine (chronic)
-Chaga's
-Doxorubicin toxicity (anti-cancer drug)
-also: hemochromatosis and peripartum cardiomyopathy

130

Most common cause of Right heart failure?

Left heart failure
*isolated R heart failure is usually d/t cor pulmonale

131

signs of Left heart failure:

-pulmonary edema (have hemosiderin-laden macrophages = heart failure cells in lungs)
-paroxysmal nocturnal dyspnea
-orthopnea (shortness of breath while supine)

132

signs of Right heart failure:

-Hepatomegaly --> nutmeg liver
-ankle, sacral edema
-Jugular venous distention

133

Valsalva meanuever effect on vasculature/murmurs:

decreases venous return
-most murmurs decrease in intensity
-increased intensity of hypertrophic cardiomyopathy murmurs

134

Hand grip effect on vasculature/murmurs:

increases systemic vascular resistance
-increases mitral regurg, VSD systolic murmurs

135

Rapid squatting effect on vasculature/murmurs:

increases venous return, increases afterload
-decreases intensity of hypertrophic cardiomyopathy murmurs

136

VSD vs Tricuspid regurgitation murmurs:

Both:
-holosystolic
-loudest at tricuspid area

Differentiate by clinical:
-newborn--> prob VSD
-adult IV drug user --> prop Tricuspid regurgitation

***also: tricuspid = worse with inspiration; VSD = not usually worsened with inspiration

137

Causes of Tricuspid regurgitation?

-endocarditis (IV drug users...)
-RV dilation
-Rheumatic fever

138

Causes of Mitral regurgitation?

-Ischemic heart disease
-Mitral valve prolapse
-LV dilation
-Rheumatic fever

139

Main causes of aortic stenosis?

-Bicuspid aortic valve
-Age-related calcification

140

Murmur that is normally benign, but can predispose to infective endocarditis:

-Mitral Prolapse
***can predispose to infective endocarditis ONLY if also have mitral regurgitation associated with it.

141

Murmurs associatd with endocarditis:

-mitral regurg and mitral stenosis
-aortic regurg and aortic stenosis
-tricuspid regurg

142

Splitting of S2 that doesn't change with inspiration?

=Fixed splitting
--> ASD

143

Roth's spots

round white spots on retina, surrounded y hemorrhage; seen in bacterial endocarditis (but, rare)

144

Janeway lesions

painless lesions on palms or soles; bacterial endocarditis

145

Osler's nodes

painful lesions on fingers or toes; bacterial endocarditis

146

splinter hemorrhages on nail bed

bacterial endocarditis

147

Signs/Symptoms of Bacterial Endocarditis (X8)

"FROM JANE"
-Fever
-Roth's spots
-Osler's nodes
-new Murmur
-Janeway lesions
-Anemia
-Nail-bed hemorrhage = splinter hemorrhages
-Emboli (Pulm embolism if Tricuspid EC; Stroke if Mitral EC)

148

Most common cause of Acute Bacterial Endocarditis? Subacute Bacterial Endocarditis?

-Acute--> S. aureus (rapid; on previously normal heart valves)
-Subacute: Viridans Strep (ie Strep sanguis, mutans) --> more insidious; on previously abnormal/diseased valves (ie mutans, after dental procedures)

149

Aschoff bodies

Area of fibrinoid necrosis/granuloma surrounded by mononuclear and multinucleated giant cells

150

Sydenham's chorea

Chorea related to Rheumatic fever
-->most common acquired chorea of childhood and only nuero manifestation of acute rheumatic fever; CNS autoimmune rxn, precipitated by GAS pharyngitis, after latency of 203 months
-->pts have increased risk for chronic rheumatic heart disease

151

Signs/Symptoms of Rheumatic Fever (X7):

"FEVERSS"
-Fever
-Erythema marginatum
-Valvular damage (vegetation and fibrosis)
-ESR elevated
-Red hot joints (migtatory polyarthritis)
-Subcutaneous nodules
-St. Vitus' dance = Sydenham's chorea

***also:
-Aschoff bodies
-Anitschkow's cells (activated histiocytes)
-Elevated ASO titers
-Antibodies to M protein

152

What type of hypersensitivity rxn is Rheumatic Fever?

Type II hypersensitivity

153

Acute pain, worse with inspiration, relieved by sitting up and leaning forward:

Acute pericarditis

154

ST elevation in ALL ECG leads?

Pericarditis

155

Friction rub

Fibrinous pericarditis (ie with Dressler's syndrome)

156

Pulsus Paradoxus

seen in cardiac tamponade
-exaggerated decrease in systolic BP during inspiration (by >10 mmHg)

157

Hypotension + increased JVD + distant heart sounds + increased HR + really decreased systolic BP during inspiration?

Cardiac tamponade

158

"Tree Bark" appearance of the aorta

seen with Tertiary Syphilis --> calcification of the aortic root and ascending aortic arch
--> tertiary syphilis disrupts vaso vasorum of the aorta
--> may result in aortic aneurysm....

159

"ball-valve" obstruction in left atrium; and multiple syncopal episodes

Myxoma = primary cardiac tumor in adults

160

primary cardiac tumor associated with tuberous sclerosis?

Rhabdomyomas
--> most frequent primary cardiac tumors in kids

161

Most common heart tumor?

Metastasis...

162

Kussmaul's sign:

increased jugular venous pressure on inspiration

163

Most common vasculitis?

Temporal/Giant Cell Arteritis

164

unilateral headache, jaw claudication, elevated ESR, mostly in elderly females:

Temporal/Giant Cell Arteritis

165

Weak upper extremity pulses, younger females (<40 yo), elevated ESR

Takayasu's arteritis

166

Vasculitis associated with Hepatitis B?

Polyarteritis nodosa

167

Which vessels are NOT affected in Polyarteritis nodosa?

Pulmonary arteries are NOT typically involved in Polyarteritis nodosa

168

1 case when kids can be given Aspirin?

Kawasaki disease (to prevent coronary aneurysms)

169

Coronary aneurysms in kids?

Kawasaki disease

170

strawberry tongue + lymphadenitis + peeling skin in kid?

Kawasaki disease

171

Vasculitis in a heavy smoker; usually male < 40 yo:

Buerger's disease

172

p-ANCA

-Microscoppic polyangitis (purpura/vasculitis + glomerulonephritis)
-Churg-Strauss syndrome

173

Vasculitis with asthma and eosinophilia?

Churg-Strauss syndrome

174

most common childhood systemic vasculitis?

-Henoch-Schonlein purpura

175

Palpable purpura on butt/legs + Arthralgia (esp knees) + GI symptoms
--> in kids, following an URI
--> IgA immune complexes

Henoch-Schonlein purpura

176

2 types of Vasculitis with immune complexes:

-Polyarteritis Nodosa
-Henoch-Scholein Purpura (IgA immune complexes)

177

Port-wine stain on face; seizures, early-onset glaucoma

Sturge-Weber Disease (congentical vascular disorder; affects capillary-sized blood vessels)

178

Strawberry and Cherry Hemangiomas:

-Both are benign capillary hemangiomas (little red lesions)
-Strawberry--> infants; regresses spontaneously at 5-8 yo
-Cherry--> Elderly (little red mole); doesn't regress; increase frequency with increase age

179

Cystic hygroma

red lesion on neck; seen with Turner syndrome

180

Red-Blue tumor under fingernails

-Glomus tumor
-->benign, but painful

181

Bacillary angiomatous (caused by? may be mistaken for?)

-benign capillary red skin papules in AIDS pts
-caused by Bartonella henselae
-may be mistaken for Kaposi's sarcoma

182

What should Beta-blockers be used cautiously in pts with DM?

beta-blockers can mask symtpoms of hypoglycemia in diabetic pts

183

first-line therapy for HTN in pregnancy?

-Hydralazine with Methyldopa

184

Hydralazine mechanism:
-Toxicity?

Vasodilates areterioles > veins
--> decreases Afterload!

*Toxicity: reflex/compensatory tachycardia; Drug-induced SLE

185

Prinzmetal's angina

--> occurs at rest, secondary to coronary artery vasospasm
--> see ST elevation on ECG

186

anti-hypertensive drug that can cause cyanide toxicity?

Nitroprusside

187

anti-hypertensive drugs that decrease Preload AND Afterload?

Nitroprusside and ACE-inhibitors/ARBs

188

Calcium Channel Blockers: Which are dihydropyridines? Non-dihydropyridines?

-Non-Dihydrogpyridines --> act directly on the heart: Verapamil and Diltiazem
-Dihydropyridines: act on vascular smooth muscle: Nifedipine, Amlodipine...
***Dihydropyridine CCBs act like nitrates: dilate veins and decrease preload
***Non-dyhydropyridine CCBs act like Beta-blockers (increase preload; decrease afterload)

189

Nitrates mechanism? Effect on preload?

Dilate veins >> arteries
-decrease preload

190

non-cardiac clinical use of nitrates?

aphrodisiac and erection enhancer

191

side effects of nitrates?

-reflex tachycardia
-throbbing headaches
-cutaneous flushing
-tolerance/"Monday disease"

192

Drugs that decrease BP that are safe in pregnancy?

-Hydralazine
-Methyldopa
-Nifedipine
-Labetolol (mixed alpha/beta blocker; anti-HTN)

193

Drug of choice to decrease LDL? Side effects?

-HMG-CoA Reductase Inhibitors = Statins
-Side effects: Hepatotoxicity, Myopathy/Rhabdomyolysis

194

Side effects of Statins?

-Hepatotoxicity (elevated LFTs)
-Myopathy/Rhabdomyolysis

195

Drug of choice to increase HDL?
Side effects?

*Niacin = Vitamin B3
*Side effects:
-red, flushed face (can combat with aspirin)
-Hyperglycemia (acanthosis nigricans)
-Hyperuricemia (may exacerbate gout)

196

What may be given to combat side effects of Niacin therapy?

Aspirin (b/c red/flushed face may be d/t PG's; so, give Aspirin to decrease PGs)

197

Which lipid-lowering drug may cause hyperglycemia and hyperuricemia?

-Niacin (Vitamin B3)

198

Drug of choice to decrease TGs?

-Fibrates
--> side effects include hepatotoxicity and myositis (so, don't give with statins, b/c exacerbate side effects)
***can also give omega-3-FAs to decrease TGs

199

Ezetimibe

Cholesterol absorption blocker (lipid-lowering drug)
-not used much, b/c may increase plaque thickness
-prevent cholesterol reabsorption at small intestine brush border

200

Cholestyramine

Bile acid resin, decreases TGs (lipid-lowering drug)
-not used much, b/c tastes bad, causes GI discomfort, decreased absorption of fat-soluble vitamins

201

2nd line therapy if LDL is still high, despite Statins?

Ezetimibe (cholesterol absorption blocker)

202

Charcoal may be used as an antidote for?

-Digoxin toxicity!

203

Best anti-arrhythmic drug post-MI?

Class IB antiarrhythmics (Lidocaine, Tocainide, Mexiletine (Phenytoin))

204

Anti-arrhythmic that's contra-indicated post-MI?

Class IC (Flecainide, Propafenone)

205

Effect of Class I antiarrhythmics on cardiac action potential and ECG?

-Decrease slope of Phase 0
*IA --> increase AP duration, increase ERP, increase QT
*IB --> decrease AP duration
*IC --> no effect on AP duration

206

Effect of Class II antiarrhythmics on cardiac Action Potential and ECG?

-decrease slope of phase 4
-increase PR interval (so slows AV conduction) --> takes longer to travel from SA node to ventricles via AV node, bundle of His, and fascicles)

207

List the Class IA antiarrhythmics:

"Double Quarter Pounder"
-Disopyramide
-Quinidine
-Procainamide

208

List the Class IB antiarrhythmics:

"Lettuce, Tomato, Mayo (Pickles)"
-Lidocaine
-Tocainide
-Mexiletine
-(Phenytoin)

209

List the Class IC antiarrhythmics:

"Fries, Please"
-Flecainide
-Propafenone

210

List the Class III antiarrhythmics:

"K IS BAD"
-Ibutilide
-Sotalol
-Bretylium
-Amiodarone
-Dofetilide

211

Anti-arrhythmics used to treat WPW syndrome?

-Procainamide (IA)
-Amiodarone (III)

212

List the Class IV antiarrhythmics

-Verapamil
-Diltiazem

213

Effect of Class II antiarrhythmics on cardiac Action Potential and ECG?

-decrease slope of phase 4
-increase PR interval (so slows AV conduction) --> takes longer to travel from SA node to ventricles via AV node, bundle of His, and fascicles)

214

List the Class IA antiarrhythmics:

"Double Quarter Pounder"
-Disopyramide
-Quinidine
-Procainamide

215

List the Class IB antiarrhythmics:

"Lettuce, Tomato, Mayo (Pickles)"
-Lidocaine
-Tocainide
-Mexiletine
-(Phenytoin)

216

List the Class IC antiarrhythmics:

"Fries, Please"
-Flecainide
-Propafenone

217

List the Class III antiarrhythmics:

"K IS BAD"
-Ibutilide
-Sotalol
-Bretylium
-Amiodarone
-Dofetilide

218

Anti-arrhythmics used to treat WPW syndrome?

-Procainamide (IA)
-Amiodarone (III)

219

List the Class IV antiarrhythmics

-Verapamil
-Diltiazem

220

child with weakened femoral pulses, systolic ejection murmur, higher BP on one arm than the other?

Coarctation of the Aorta - Infantile/Preductal type

221

Why increased coronary blood flow in aortic stenosis?

Blood flow through coronary arteries is regulated almost entirely by the metabolic requirements of the cardiac muscle. When have increased oxygen consumption by heart muscle, increased proportion of ATP is broken down to adenosine. Adenosine causes dilation of coronary arteries, which increases oxygen delivery to coronary arteries. So, in this sense, coronary blood flow increases proportionally to heart oxygen consumption.

***So, in aortic stenosis --> get increased Left Ventricular pressure --> increased oxygen consumption by Left Ventricle, because has a higher work load in pumping.

222

Capillary fluid exchange equation (Starling Force Equation):
Direction of flow?

Pnet = [(pc-pi) - (nc-ni)]
where:
pc = capillary pressure
pi = interstitial fluid pressure
nc = plasma colloid osmotic pressure
ni = interstitial fluid colloid osmotic pressure

If Pnet = positive --> net flow OUT of capillary
If Pnet = negative --> net flow IN to capillary