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USMLE Step 1 > Cardiovascular - First Aid > Flashcards

Cardiovascular - First Aid Flashcards

1
Q

Heart Embryology:

ascending aorta and pulmonary trunk

A

Truncus Arteriosus

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2
Q

Heart Embryology:

smooth parts (outflow tract) of left and right ventricles

A

Bulbus Cordis

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3
Q

Heart Embryology:

  • atrial septum
  • membranous interventricular septum
  • AV and semilunar valves
A

Endocardial Cushion

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4
Q

Heart Embryology:

trabeculated part of left and right atria

A

Primitive Atrium

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5
Q

Heart Embryology:

trabeculated part of left and right ventricles

A

Primitive Ventricle

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6
Q

Heart Embryology:

smooth part of left atrium

A

Primitive Pulmonary Vein

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7
Q

Heart Embryology:

coronary sinus

A

Left Horn of Sinus Venosus

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8
Q

Heart Embryology:

smooth part of right atrium (sinus venarum)

A

Right Horn of Sinus Venosus

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9
Q

Heart Embryology:

superior vena cava (SVC)

A
  • Right Common Cardinal Vein
  • Right Anterior Cardinal Vein
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10
Q

The _____ is the first functional organ in vertebrate embryos.

A

heart

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11
Q

The heart beats spontaneously by _____ of development.

A

week 4

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12
Q

Cardiac Looping

A
  • Primary heart tube loops to establish left-right polarity; begins in week 4 of gestation.
  • Defect in left-right Dynein (involved in L/R asymmetry) can lead to Dextrocardia, as seen in Kartagener syndrome (1° ciliary Dyskinesia).
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13
Q

​Septation of the Atria

A
  1. Septum primum grows toward endocardial cushions, narrowing foramen primum.
  2. Foramen secundum forms in septum primum (foramen primum disappears).
  3. Septum secundum develops as foramen secundum maintains right-to-left shunt.
  4. Septum secundum expands and covers most of the foramen secundum. The residual foramen is the foramen ovale.
  5. Remaining portion of septum primum forms valve of foramen ovale.
  6. Septum secundum and septum primum fuse to form the atrial septum.
  7. Foramen ovale usually closes soon after birth because of ↑ LA pressure.
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14
Q

_____ is caused by failure of septum primum and septum secundum to fuse after birth; most are left untreated. Can lead to paradoxical emboli (venous thromboemboli that enter systemic arterial circulation), similar to those resulting from an ASD.

A

Patent Foramen Ovale

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15
Q

​Septation of the Ventricles

A
  1. Muscular interventricular septum forms. Opening is called interventricular foramen.
  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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16
Q

_____ is the most common congenital cardiac anomaly.

A

Ventricular Septal Defect

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17
Q

VSD usually occurs in the _____.

A

membranous septum

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18
Q

Outflow Tract Formation

A

neural crest and endocardial cell migrations → truncal and bulbar ridges that spiral and fuse to form aorticopulmonary septum → ascending aorta and pulmonary trunk

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19
Q

Conotruncal Abnormalities Associated with
Failure of Neural Crest Cells to Migrate

A
  • Transposition of Great Vessels
  • Tetralogy of Fallot
  • Persistent Truncus Arteriosus
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20
Q

Valve Development

A
  • Aortic/Pulmonary: derived from endocardial cushions of outflow tract
  • Mitral/Tricuspid: derived from fused endocardial cushions of the AV canal
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21
Q

Valvular anomalies may be _____.

A
  • stenotic
  • regurgitant
  • atretic—tricuspid atresia
  • displaced—Ebstein anomaly
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22
Q

Fetal Circulation

A

3 Important Shunts:

  • Blood entering fetus through the umbilical vein is conducted via the ductus venosus into the IVC, bypassing hepatic circulation.
  • Most of the highly oxygenated blood reaching the heart via the IVC is directed through the foramen ovale and pumped into the aorta to supply the head and body.
  • Deoxygenated blood from the SVC passes through the RA → RV → main pulmonary artery → ductus arteriosus → descending aorta; shunt is due to high fetal pulmonary artery resistance (due partly to low O2 tension).
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23
Q

Blood in umbilical vein has a Po2 of ≈ _____ and is ≈ _____ saturated with O2.

A
  • 30 mm Hg
  • 80% O2
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24
Q

Transitional Circulation

A

At birth, infant takes a breath → ↓ resistance in pulmonary vasculature → ↑ left atrial pressure vs. right atrial pressure → foramen ovale closes (now called fossa ovalis); ↑ in O2 (from respiration) and ↓ in prostaglandins (from placental separation) → closure of ductus arteriosus.

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25
Q

_____ helps close PDA → ligamentum arteriosum (remnant of ductus arteriosus).

A

Indomethacin

Prostaglandins E1 and E2 kEEp PDA open.

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26
Q

Fetal-Postnatal Derivatives:

Median Umbilical Ligament

A

Allantois → Urachus

Urachus is part of allantoic duct between bladder and umbilicus.

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27
Q

Fetal-Postnatal Derivatives:

Ligamentum Arteriosum

A

Ductus Arteriosus

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28
Q

Fetal-Postnatal Derivatives:

Ligamentum Venosum

A

Ductus Venosus

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29
Q

Fetal-Postnatal Derivatives:

Fossa Ovalis

A

Foramen Ovale

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30
Q

Fetal-Postnatal Derivatives:

Nucleus Pulposus

A

Notochord

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31
Q

Fetal-Postnatal Derivatives:

Medial Umbilical Ligaments

A

Umbilical Arteries

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32
Q

Fetal-Postnatal Derivatives:

Ligamentum Teres Hepatis (Round Ligament)

A

Umbilical Vein

*contained in falciform ligament

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33
Q

Anatomy of the Heart

A
  • Right-Dominant Circulation (85%) = PDA arises from RCA
  • Left-Dominant Circulation (8%) = PDA arises from LCX
  • Codominant Circulation (7%) = PDA arises from both LCX and RCA
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34
Q

The SA node is commonly supplied by the _____ (blood supply independent of dominance).

A

RCA

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35
Q

The AV node is supplied by the _____.

A

PDA

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36
Q

Coronary artery occlusion most commonly occurs in the _____.

A

LAD

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37
Q

Coronary blood flow peaks in _____.

A

early diastole

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38
Q

The most posterior part of the heart is the _____. Its enlargement can cause dysphagia (due to compression of the esophagus) or hoarseness (due to compression of the left recurrent laryngeal nerve, a branch of the vagus nerve).

A

left atrium

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39
Q

Pericardium Layers

A

Outer → Inner:

  • Fibrous Pericardium
  • Parietal Layer of Serous Pericardium
  • Visceral Layer of Serous Pericardium

The pericardial cavity lies between parietal and visceral layers.

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40
Q

The pericardium is innervated by the _____.

A

phrenic nerve

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41
Q

Pericarditis can cause referred pain to the _____.

A

shoulder

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42
Q

Cardiac Output

A

CO = stroke volume (SV) × heart rate (HR)

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43
Q

Fick Principle

A
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44
Q

Mean Arterial Pressure

A

MAP = CO × total peripheral resistance (TPR)

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45
Q

MAP (at resting HR)

A

MAP (at resting HR) = ⅔ diastolic pressure + ⅓ systolic pressure

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46
Q

Pulse Pressure

A

Pulse Pressure = systolic pressure – diastolic pressure

Pulse pressure is proportional to SV, and inversely proportional to arterial compliance.

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47
Q

Stroke Volume

A

SV = end-diastolic volume (EDV) − end-systolic volume (ESV)

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48
Q

During the early stages of exercise, CO is maintained by _____.

A
  • ↑ HR
  • ↑ SV
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49
Q

During the late stages of exercise, CO is maintained by _____ only.

A

↑ HR

*SV plateaus

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50
Q

Diastole is preferentially shortened with _____ → less filling time → ↓ CO (eg. ventricular tachycardia).

A

↑ HR

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51
Q

↑ Pulse Pressure

A
  • hyperthyroidism
  • aortic regurgitation
  • aortic stiffening (isolated systolic hypertension in elderly)
  • obstructive sleep apnea (↑ sympathetic tone)
  • anemia
  • exercise (transient)
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52
Q

↓ Pulse Pressure

A
  • aortic stenosis
  • cardiogenic shock
  • cardiac tamponade
  • advanced heart failure (HF)
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53
Q

Stroke Volume is affected by _____.

A

SV CAP

  • Contractility
  • Afterload
  • Preload

A failing heart has ↓ SV (systolic and/or diastolic dysfunction)

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54
Q

↑ SV

A
  • ↑ Contractility (eg. anxiety, exercise)
  • ↑ Preload (eg. early pregnancy)
  • ↓ Afterload
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55
Q

↑ Contractility and SV

A
  • Catecholamine Stimulation via β1 Receptor:
    • Ca2+ channels phosphorylated → ↑ Ca2 entry → ↑ Ca2+-induced Ca2+ release and ↑ Ca2+ storage in sarcoplasmic reticulum
    • Phospholamban phosphorylation → active Ca2+ ATPase → ↑ Ca2+ storage in sarcoplasmic reticulum
  • ↑ intracellular Ca2+
  • ↓ extracellular Na+ (↓ activity of Na+/Ca2+ exchanger)
  • Digitalis (blocks Na+/K+ pump → ↑ intracellular Na+ → ↓ Na+/Ca2+ exchanger activity → ↑ intracellular Ca2+)
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56
Q

↓ Contractility and SV

A
  • β1-blockade (↓ cAMP)
  • HF with systolic dysfunction
  • Acidosis
  • Hypoxia/Hypercapnia (↓ Po2/ ↑ Pco2)
  • Non-Dihydropyridine Ca2+ Channel Blockers
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57
Q

Preload is approximated by _____.

A

ventricular EDV

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58
Q

Preload depends on _____.

A
  • venous tone
  • circulating blood volume
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59
Q

↓ Preload

A

Venous Vasodilators (eg. nitroglycerin)

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60
Q

Afterload approximated by _____.

A

MAP

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61
Q

Laplace’s Law

A

↑ afterload → ↑ pressure → ↑ wall tension per

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62
Q

LV compensates for ↑ afterload by _____ in order to ↓ wall tension.

A

thickening (hypertrophy)

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63
Q

↓ Afterload

A

Arterial Vasodilators (eg. hydralazine)

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64
Q

↓ Preload and Afterload

A
  • ACE Inhibitors
  • ARBs
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65
Q

Chronic Hypertension ( ↑ MAP) → _____

A

LV Hypertrophy

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66
Q

↑ Myocardial O2 Demand

A

MyoCARDial O2:

  • ↑ Contractility
  • ↑ Afterload (proportional to arterial pressure)
  • ↑ Heart Rate
  • ↑ Diameter of ventricle (↑ wall tension)
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67
Q

Cardiac wall tension follows _____.

A

Laplace’s Law

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68
Q

Wall Tension

A

Wall Tension = Pressure × Radius

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69
Q

Wall Stress

A
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70
Q

Ejection Fraction

A
  • Left Ventricular EF is an index of ventricular contractility.
  • EF is ↓ in systolic HF.
  • EF is normal in HF with preserved ejection fraction.
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71
Q

Starling Curve

A
  • Force of contraction is proportional to end-diastolic length of cardiac muscle fiber (preload).
  • ↑ contractility with catecholamines, positive inotropes (eg. digoxin).
  • ↓ contractility with loss of myocardium (eg. MI), β-blockers (acutely), non-dihydropyridine Ca2+ channel blockers, dilated cardiomyopathy.
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72
Q

Resistance, Pressure, Flow

A
  • Pressure gradient drives flow from high pressure to low pressure.
  • Compliance = ΔV/ΔP
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73
Q

_____ have the highest total cross-sectional area and the lowest flow velocity.

A

Capillaries

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74
Q

_____ account for most of TPR.

A

Arterioles

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75
Q

_____ provide most of the blood storage capacity.

A

Veins

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76
Q

Viscosity depends mostly on _____.

A

Hematocrit

  • ↑ in hyperproteinemic states (eg. multiple myeloma) and polycythemia
  • ↓ in anemia
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77
Q

Cardiac and Vascular Function Curves

A
  • Intersection of Curves = Operating Point of the Heart (ie. venous return and CO are equal)
  • Changes often occur in tandem, and may be reinforcing (eg. exercise ↑ inotropy and ↓ TPR to maximize CO) or compensatory (eg, HF ↓ inotropy → fluid retention to ↑ preload to maintain CO).
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78
Q

Inotropy

A

Changes in contractility → altered CO for a given RA pressure (preload).

  • catecholamines, digoxin ⊕, exercise
  • HF with reduced EF, narcotic overdose, sympathetic inhibition ⊝
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79
Q

Venous Return

A

Changes in circulating volume or venous tone → altered RA pressure for a given CO. Mean systemic pressure (x-intercept) changes with volume/venous tone.

  • fluid infusion, sympathetic activity ⊕
  • acute hemorrhage, spinal anesthesia ⊝
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80
Q

Total Peripheral Resistance

A

At a given mean systemic pressure (x-intercept) and RA pressure, changes in TPR → altered CO.

  • vasopressors ⊕
  • exercise, AV shunt ⊝
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81
Q

Pressure-Volume Loops

A

Phases—Left Ventricle:

  1. Isovolumetric Contraction—period between mitral valve closing and aortic valve opening; period of highest 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 opening
  5. Reduced Filling—period just before mitral valve closing
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82
Q

Cardiac Cycle

A

Phases—Left Ventricle:

  • Isovolumetric Contraction—period between mitral valve closing and aortic valve opening; period of highest O2consumption
  • Systolic Ejection—period between aortic valve opening and closing
  • Isovolumetric Relaxation—period between aortic valve closing and mitral valve opening
  • Rapid Filling—period just after mitral valve opening
  • Reduced Filling—period just before mitral valve closing
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83
Q

Heart Sounds

A
  • S1—mitral and tricuspid valve closure. Loudest at mitral area.
  • S2—aortic and pulmonary valve closure. Loudest at left upper sternal border.
  • S3—in early diastole during rapid ventricular filling phase. Associated with ↑ filling pressures (eg. mitral regurgitation, HF) and more common in dilated ventricles (but can be normal in children, young adults, and pregnant women).
  • S4—in late diastole (“atrial kick”). Best heard at apex with patient in left lateral decubitus position. High atrial pressure. Associated with ventricular noncompliance (eg. hypertrophy). Left atrium must push against stiff LV wall. Consider abnormal, regardless of patient age.
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84
Q

Jugular Venous Pulse (JVP)

A
  • a wave—atrial contraction. Absent in atrial fibrillation (AF).
  • c wave—RV contraction (closed tricuspid valve bulging into atrium).
  • x descent—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.
  • v wave—↑ right atrial pressure due to filling (“villing”) against closed tricuspid valve.
  • y descent—RA emptying into RV. Prominent in constrictive pericarditis, absent in cardiac tamponade.
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85
Q

Heart Sounds:

Normal Splitting

A
  • inspiration → drop in intrathoracic pressure → ↑ venous return → ↑ RV filling → ↑ RV stroke volume → ↑ RV ejection time → delayed closure of pulmonic valve
  • ↓ pulmonary impedance (↑ capacity of the pulmonary circulation) also occurs during inspiration, which contributes to delayed closure of pulmonic valve
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86
Q

Heart Sounds:

Wide Splitting

A
  • seen in conditions that delay RV emptying (eg. pulmonic stenosis, right bundle branch block)
  • causes delayed pulmonic sound (especially on inspiration)
  • an exaggeration of normal splitting
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87
Q

Heart Sounds:

Fixed Splitting

A
  • heard in ASD
  • ASD → left-to-right shunt → ↑ RA and RV volumes → ↑ flow through pulmonic valve such that, regardless of breath, pulmonic closure is greatly delayed
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88
Q

Heart Sounds:

Paradoxical Splitting

A
  • heard in conditions that delay aortic valve closure (eg. aortic stenosis, left bundle branch block)
  • normal order of valve closure is reversed so that P2 sound occurs before delayed A2 sound
  • on inspiration, P2 closes later and moves closer to A2, thereby “paradoxically” eliminating the split (usually heard in expiration)
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89
Q

Auscultation of the Heart

A
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90
Q

Besdside Maneuvers:

  • ↑ venous return to right atrium
  • ↑ intensity of right heart sounds
A

Inspiration

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91
Q

Besdside Maneuvers:

  • ↑ afterload
  • ↑ intensity of MR, AR, and VSD murmurs
  • ↓ hypertrophic cardiomyopathy and AS murmurs
  • MVP: later onset of click/murmur
A

Hand Grip

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92
Q

Besdside Maneuvers:

  • ↓ intensity of most murmurs (including AS)
  • ↑ intensity of hypertrophic cardiomyopathy murmur
  • MVP: earlier onset of click/murmur
A
  • Valsalva (phase II)
  • standing up (↓ preload)
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93
Q

Besdside Maneuvers:

  • ↑ venous return, preload, and afterload
  • ↓ intensity of hypertrophic cardiomyopathy murmur
  • ↑ intensity of AS, MR, and VSD murmurs
  • MVP: later onset of click/murmur
A

Rapid Squatting

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94
Q

Systolic Murmurs

A
  • Aortic/Pulmonic Stenosis
  • Mitral/Tricuspid Regurgitation
  • VSD
  • MVP
  • Hypertrophic Cardiomyopathy.
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95
Q

Diastolic Murmurs

A
  • Aortic/Pulmonic Regurgitation
  • Mitral/Tricuspid Stenosis
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96
Q

Systolic Murmurs:

  • crescendo-decrescendo systolic ejection murmur and soft S2 (ejection click may be present)
  • LV >> aortic pressure during systole
  • loudest at heart base; radiates to carotids
  • pulsus parvus et tardus
  • can lead to syncope, angina, and dyspnea on exertion
  • most commonly due to age-related calcification in older patients (> 60 years old) or in younger patients with early-onset calcification
A

Aortic Stenosis

SAD:

  • Syncope
  • Angina
  • Dyspnea on exertion
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97
Q

_____ are pulses that are weak with a delayed peak.

A

Pulsus Parvus et Tardus

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98
Q

Systolic Murmurs:

  • holosystolic, high-pitched “blowing murmur”
  • Mitral—loudest at apex and radiates toward axilla, often due to ischemic heart disease (post-MI), MVP, LV dilatation
  • Tricuspid—loudest at tricuspid area, commonly caused by RV dilatation
  • rheumatic fever and infective endocarditis can cause either
A

Mitral/Tricuspid Regurgitation

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99
Q

Systolic Murmurs:

  • late systolic crescendo murmur with midsystolic click (MC; due to sudden tensing of chordae tendineae)
  • most frequent valvular lesion
  • best heard over apex
  • loudest just before S2
  • usually benign
  • can predispose to infective endocarditis
  • can be caused by myxomatous degeneration (1° or 2° to connective tissue disease such as Marfan or Ehlers-Danlos syndrome), rheumatic fever, chordae rupture
A

Mitral Valve Prolapse

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100
Q

Systolic Murmurs:

  • holosystolic, harsh-sounding murmur
  • loudest at tricuspid area
A

Ventricular Septal Defect

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101
Q

Diastolic Murmurs:

  • high-pitched “blowing” early diastolic decrescendo murmur
  • long diastolic murmur, hyperdynamic pulse, and head bobbing when severe and chronic
  • wide pulse pressure
  • often due to aortic root dilation, bicuspid aortic valve, endocarditis, rheumatic fever
  • progresses to left HF
A

Aortic Regurgitation

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102
Q

Diastolic Murmurs:

  • follows opening snap (OS; due to abrupt halt in leaflet motion in diastole, after rapid opening due to fusion at leaflet tips)
  • delayed rumbling mid-to-late diastolic murmur (↓ interval between S2 and OS correlates with ↑ severity)
  • LA >> LV pressure during diastole
  • often a late (and highly specific) sequela of rheumatic fever
  • chronic disease can result in LA dilatation → dysphagia/hoarseness via compression of esophagus/left recurrent laryngeal nerve, respectively
A

Mitral Stenosis

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103
Q

Continuous Murmurs:

  • machine-like murmur
  • best heard at left infraclavicular area
  • loudest at S2
  • often due to congenital rubella or prematurity
A

Patent Ductus Arteriosus

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104
Q

Myocardial Action Potential

A
  • Phase 0 = rapid upstroke and depolarization—voltage-gated Na+ channels open.
  • Phase 1 = initial repolarization—inactivation of voltage-gated Na+ channels. Voltage-gated K+ channels begin to open.
  • Phase 2 = plateau—Ca2+ influx through voltage-gated Ca2+ channels balances K+ efflux. Ca2+ influx triggers Ca2+ release from sarcoplasmic reticulum and myocyte contraction.
  • Phase 3 = rapid repolarization—massive K+ efflux due to opening of voltage-gated slow K+ channels and closure of voltage-gated Ca2+ channels.
  • Phase 4 = resting potential—high K+ permeability through K+ channels.

*also occurs in bundle of His and Purkinje fibers

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105
Q

In contrast to skeletal muscle, cardiac muscle _____.

A
  • cardiac muscle action potential has a plateau, which is due to Ca2+ influx and K+ efflux
  • cardiac muscle contraction requires Ca2+ influx from ECF to induce Ca2+ release from sarcoplasmic reticulum (Ca2+-induced Ca2+ release)
  • cardiac myocytes are electrically coupled to each other by gap junctions
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106
Q

Pacemaker Action Potential

A

Occurs in the SA and AV nodes.

  • Phase 0 = upstroke—opening of voltage-gated Ca2+ channels. Fast voltage-gated Na+ channels are permanently inactivated because of the less negative resting potential of these cells. Results in a slow conduction velocity that is used by the AV node to prolong transmission from the atria to ventricles.
  • Phases 1 and 2 are absent.
  • Phase 3 = repolarization—inactivation of the Ca2+ channels and ↑ activation of K+ channels → ↑ K+ efflux.
  • Phase 4 = slow spontaneous diastolic depolarization due to If (“funny current”). If channels responsible for a slow, mixed Na+/K+ inward current; different from INa in phase 0 of ventricular action potential. Accounts for automaticity of SA and AV nodes. The slope of phase 4 in the SA node determines HR. ACh/adenosine ↓ the rate of diastolic depolarization and ↓ HR, while catecholamines ↑ depolarization and ↑ HR. Sympathetic stimulation ↑ the chance that If channels are open and thus ↑ HR.
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107
Q

Conduction Pathway

A

SA node → atria → AV node → bundle of His → right and left bundle branches → Purkinje fibers → ventricles

*left bundle branch divides into left anterior and posterior fascicles

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108
Q

_____ “pacemaker” inherent dominance with slow phase of upstroke.

A

SA Node

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109
Q

The AV node is located in the _____.

A

posteroinferior part of the interatrial septum

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110
Q

_____ delay from the AV node allows time for ventricular filling.

A

100-msec

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111
Q

Pacemaker Rates

A

SA > AV > bundle of His/Purkinje/ventricles

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112
Q

Speed of Conduction

A

Purkinje > atria > ventricles > AV node

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113
Q

Electrocardiogram

A
  • P wave—atrial depolarization, atrial repolarization is masked by QRS complex
  • PR interval—time from start of atrial depolarization to start of ventricular depolarization (normally < 200 msec)
  • QRS complex—ventricular depolarization (normally < 120 msec)
  • QT interval—ventricular depolarization, mechanical contraction of the ventricles, ventricular repolarization
  • T wave—ventricular repolarization, T-wave inversion may indicate ischemia or recent MI
  • J point—junction between end of QRS complex and start of ST segment
  • ST segment—isoelectric, ventricles depolarized
  • U wave—prominent in hypokalemia (think hyp“U”kalemia), bradycardia
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114
Q

Dysrhythmias:

  • polymorphic ventricular tachycardia
  • characterized by shifting sinusoidal waveforms on ECG
  • can progress to ventricular fibrillation (VF)
  • long QT interval predisposes to _____
  • caused by drugs, ↓ K+, ↓ Mg2+, and congenital abnormalities
A

Torsades de Pointes

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115
Q

Drug-Induced Long QT

A

ABCDE:

  • AntiArrhythmics (class IA, III)
  • AntiBiotics (eg. macrolides)
  • Anti“C”ychotics (eg. haloperidol)
  • AntiDepressants (eg. TCAs)
  • AntiEmetics (eg. ondansetron)
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116
Q

Torsades de Pointes is treated with _____.

A

Magnesium Sulfate

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117
Q

_____ is an inherited disorder of myocardial repolarization, typically due to ion channel defects; ↑ risk of sudden cardiac death (SCD) due to torsades de pointes.

A

Congenital Long QT Syndrome

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118
Q

Congenital Long QT Syndrome:

  • autosomal dominant
  • pure cardiac phenotype (no deafness)
A

Romano-Ward Syndrome

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119
Q

Congenital Long QT Syndrome:

  • autosomal recessive
  • sensorineural deafness
A

Jervell and Lange-Nielsen Syndrome

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120
Q

_____ is an autosomal dominant disorder most common in Asian males. ECG pattern of pseudo-right bundle branch block and ST elevations in V1-V3. ↑ risk of ventricular tachyarrhythmias and SCD. Prevent SCD with implantable cardioverter-defibrillator (ICD).

A

Brugada Syndrome

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121
Q

_____ is the most common type of ventricular preexcitation syndrome. Abnormal fast accessory conduction pathway from atria to ventricle
(bundle of Kent) bypasses the rate-slowing AV node → ventricles begin to partially depolarize earlier → characteristic delta wave with widened QRS complex and shortened PR interval on ECG. May result in reentry circuit → supraventricular tachycardia.

A

Wolff-Parkinson-White Syndrome

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122
Q

Dysrhythmias:

  • chaotic and erratic baseline with no discrete P waves in between irregularly spaced QRS complexes
  • irregularly irregular heartbeat
  • most common risk factors include hypertension and coronary artery disease (CAD)
  • can lead to thromboembolic events, particularly strok
  • treatment includes anticoagulation, rate control, rhythm control, and/or cardioversion
A

Atrial Fibrillation

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123
Q

Dysrhythmias:

  • a rapid succession of identical, back-to-back atrial depolarization waves
  • the identical appearance accounts for the “sawtooth” appearance of the flutter waves
  • treat like atrial fibrillation
  • definitive treatment is catheter ablation
A

Atrial Flutter

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124
Q

Dysrhythmias:

  • a completely erratic rhythm with no identifiable waves
  • fatal arrhythmia without immediate CPR and defibrillation
A

Ventricular Fibrillation

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125
Q

AV Blocks:

  • the PR interval is prolonged (> 200 msec)
  • benign and asymptomatic
  • no treatment required
A

First-Degree AV Block

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126
Q

AV Blocks:

  • progressive lengthening of PR interval until a beat is “dropped (a P wave not followed by a QRS complex)
  • usually asymptomatic
  • variable RR interval with a pattern (regularly irregular)
A

Second-Degree AV Block
Mobitz Type I (Wenckebach)

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127
Q

AV Blocks:

  • dropped beats that are not preceded by a change in the length of the PR interval (as in type I)
  • may progress to 3rd-degree block
  • often treated with pacemaker
A

Second-Degree AV Block
Mobitz Type II

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128
Q

AV Blocks:

  • the atria and ventricles beat independently of each other
  • P waves and QRS complexes not rhythmically associated
  • atrial rate > ventricular rate
  • usually treated with pacemaker
  • can be caused by Lyme disease
A

Third-Degree (Complete) AV Block

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129
Q

_____ is released from atrial myocytes in response to ↑ blood volume and atrial pressure. Acts via cGMP. Causes vasodilation and ↓ Na+ reabsorption at the renal collecting tubule. Dilates afferent renal arterioles and constricts efferent arterioles, promoting diuresis and contributing to “aldosterone escape” mechanism.

A

Atrial Natriuretic Peptide

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130
Q

_____ is released from ventricular myocytes in response to ↑ tension. Similar physiologic action to ANP, with longer half-life. _____ blood test is used for diagnosing HF (very good negative predictive value). Available in recombinant form (nesiritide) for treatment of HF.

A

B-Type (Brain) Natriuretic Peptide

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131
Q

Cardiovascular Receptors

A
  • Aortic arch transmits via vagus nerve to solitary nucleus of medulla (responds to ↓ and ↑ in BP).
  • Carotid sinus (dilated region at carotid bifurcation) transmits via glossopharyngeal nerve to solitary nucleus of medulla (responds to ↓ and ↑ in BP).
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132
Q

Cardiovascular Baroreceptors

A
  • Hypotension—↓ arterial pressure → ↓ stretch → ↓ afferent baroreceptor firing → ↑ efferent sympathetic firing and ↓ efferent parasympathetic stimulation → vasoconstriction, ↑ HR, ↑ contractility, ↑ BP. Important in the response to severe hemorrhage.
  • Carotid Massage—↑ pressure on carotid sinus → ↑ stretch → ↑ afferent baroreceptor firing → ↑ AV node refractory period → ↓ HR.
  • Component of Cushing Reflex (triad of hypertension, bradycardia, and respiratory depression)—↑ intracranial pressure constricts arterioles → cerebral ischemia → ↑ pCO2 and ↓ pH → central reflex sympathetic ↑ in perfusion pressure (hypertension) → ↑ stretch → peripheral reflex baroreceptor–induced bradycardia.
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133
Q

Cardiovascular Chemoreceptors

A
  • Peripheral—carotid and aortic bodies are stimulated by ↓ Po2 (< 60 mm Hg), ↑ Pco2, and ↓ pH of blood.
  • Central—are stimulated by changes in pH and Pco2 of brain interstitial fluid, which in turn are influenced by arterial CO2. Do not directly respond to Po2.
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134
Q

Normal Cardiac Pressures

A

Pulmonary capillary wedge pressure (PCWP; in mm Hg) is a good approximation of left atrial pressure. In mitral stenosis, PCWP > LV end diastolic pressure. PCWP is measured with pulmonary artery catheter (Swan-Ganz catheter).

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135
Q

Cardiovascular Autoregulation:

Heart

A

Local Metabolites (Vasodilatory):

  • adenosine
  • NO
  • CO2
  • ↓ O2
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136
Q

Cardiovascular Autoregulation:

Brain

A

Local Metabolites (Vasodilatory):

CO2 (pH)

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137
Q

Cardiovascular Autoregulation:

Kidneys

A
  • Myogenic Feedback
  • Tubuloglomerular Feedback
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138
Q

Cardiovascular Autoregulation:

Lungs

A

Hypoxia → Vasoconstriction

The pulmonary vasculature is unique in that alveolar hypoxia causes vasoconstriction so that only well ventilated areas are perfused. In other organs, hypoxia causes vasodilation.

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139
Q

Cardiovascular Autoregulation:

Skeletal Muscle

A

CHALK (exercise):

  • CO2
  • H+,
  • Adenosine
  • Lactate
  • K+

At Rest: sympathetic tone

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140
Q

Cardiovascular Autoregulation:

Skin

A

Sympathetic stimulation is the most important mechanism for temperature control.

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141
Q

Capillary Fluid Exchange

A

Starling Forces determine fluid movement through capillary membranes:

  • Pc = capillary pressure—pushes fluid out of capillary
  • Pi = interstitial fluid pressure—pushes fluid into capillary
  • πc = plasma colloid osmotic (oncotic) pressure—pulls fluid into capillary
  • πi = interstitial fluid colloid osmotic pressure—pulls fluid out of capillary
  • Jv = net fluid flow = Kf [(Pc − Pi) − σ(πc − πi)]
  • Kf = capillary permeability to fluid
  • σ = reflection coefficient (measure of capillary permeability to protein)
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142
Q

Capillary Fluid Exchange: Edema

A

Excess fluid outflow into interstitium is commonly caused by:

  • ↑ capillary pressure (↑ Pc; eg. HF)
  • ↓ plasma proteins (↓ πc; eg. nephrotic syndrome, liver failure, protein malnutrition)
  • ↑ capillary permeability (↑ Kf ; eg. toxins, infections, burns)
  • ↑ interstitial fluid colloid osmotic pressure (↑ πi; eg. lymphatic blockage)
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143
Q

Congenital Heart Diseases:

  • early cyanosis—“blue babies”
  • often diagnosed prenatally or become evident immediately after birth
  • usually require urgent surgical treatment and/or maintenance of a PDA
A

R → L Shunts (Cyanotic)

Right-to-Left Shunts: eaRLy cyanosis

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144
Q

Congenital CHDs

A

The 5 Ts:

  1. Truncus Arteriosus (1 vessel)
  2. Transposition of the Great Ateries (2 switched vessels)
  3. Tricuspid Atresia (3 = Tri)
  4. Tetralogy of Fallot (4 = Tetra)
  5. TAPVR (5 letters in the name)
145
Q

Congenital Heart Diseases:

  • fails to divide into pulmonary trunk and aorta due to lack of aorticopulmonary septum formation
  • most patients have accompanying VSD
A

Persistent Truncus Arteriosus

146
Q

Congenital Heart Diseases:

  • aorta leaves RV (anterior) and pulmonary trunk leaves LV (posterior) → separation of systemic and pulmonary circulations
  • not compatible with life unless a shunt is present to allow mixing of blood (eg. VSD, PDA, or patent foramen ovale)
  • due to failure of the aorticopulmonary septum to spiral
  • without surgical intervention, most infants die within the first few months of life
A

D-Transposition of Great Vessels

147
Q

Congenital Heart Diseases:

  • absence of tricuspid valve and hypoplastic RV
  • requires both ASD and VSD for viability
A

Tricuspid Atresia

148
Q

Congenital Heart Diseases:

  • caused by anterosuperior displacement of the infundibular septum
  • most common cause of early childhood cyanosis
  • pulmonary stenosis forces right-to-left flow across VSD → RVH
  • Squatting: ↑ SVR, ↓ right-to-left shunt, improves cyanosis
  • treated with early surgical correction
A

Tetralogy of Fallot

PROVe:

  • Pulmonary Infundibular Stenosis (most important determinant for prognosis)
  • Right Ventricular Hypertrophy (RVH)—boot‑shaped heart on CXR
  • Overriding Aorta
  • VSD
149
Q

Congenital Heart Diseases:

  • pulmonary veins drain into right heart circulation (SVC, coronary sinus, etc.)
  • associated with ASD and sometimes PDA to allow for right-to-left shunting to maintain CO
A

Total Anomalous Pulmonary Venous Return

150
Q

Congenital Heart Diseases:

  • characterized by displacement of tricuspid valve leaflets downward into RV, artificially “atrializing” the ventricle
  • associated with tricuspid regurgitation, accessory conduction pathways, and right-sided HF
  • can be caused by lithium exposure in utero
A

Ebstein Anomaly

151
Q

Congenital Heart Diseases:

  • acyanotic at presentation
  • cyanosis may occur years later
A

L → R Shunts (Acyanotic)

Left-to-Right shunts: “LateR” cyanosis

152
Q

Congenital Heart Diseases:

  • most common congenital cardiac defect
  • asymptomatic at birth, may manifest weeks later or remain asymptomatic throughout life
  • most self resolve
  • larger lesions may lead to LV overload and HF
  • O2 saturation ↑ in RV and pulmonary artery
A

Ventricular Septal Defect

Frequency: VSD > ASD > PDA

153
Q

Congenital Heart Diseases:

  • defect in interatrial septum
  • wide, fixed split S2
  • ostium secundum defects most common and usually an isolated finding
  • ostium primum defects rarer and usually occur with other cardiac anomalies
  • symptoms range from none to HF
  • distinct from patent foramen ovale in that septa are missing tissue rather than unfused
  • O2 saturation ↑ in RA, RV, and pulmonary artery
  • may lead to paradoxical emboli (systemic venous emboli bypass the lungs and become systemic arterial emboli)
A

Atrial Septal Defect

Frequency: VSD > ASD > PDA

154
Q

Congenital Heart Diseases:

  • in fetal period, shunt is right to left (normal)
  • in neonatal period, ↓ pulmonary vascular resistance → shunt becomes left to right → progressive RVH and/or LVH and HF
  • associated with a continuous, “machine-like” murmur
  • patency is maintained by PGE synthesis and low O2 tension
  • uncorrected lesion can eventually result in late cyanosis in the lower extremities (differential cyanosis)
A

Patent Ductus Arteriosus

Frequency: VSD > ASD > PDA

155
Q

Congenital Heart Diseases:

  • uncorrected left-to-right shunt (VSD, ASD, PDA) → ↑ pulmonary blood flow → pathologic remodeling of vasculature → pulmonary arterial hypertension
  • RVH occurs to compensate → shunt becomes right to left
  • causes late cyanosis, clubbing, and polycythemia
  • age of onset varies
A

Eisenmenger Syndrome

156
Q

Congenital Heart Diseases:

  • aortic narrowing near insertion of ductus arteriosus (“juxtaductal”)
  • associated with bicuspid aortic valve, other heart defects, and Turner syndrome
  • hypertension in upper extremities and weak, delayed pulse in lower extremities (brachial-femoral delay)
  • with age, intercostal arteries enlarge due to collateral circulation; arteries erode ribs → notched appearance on CXR
  • complications include HF, ↑ risk of cerebral hemorrhage (berry aneurysms), aortic rupture, and possible endocarditis
A

Coarctation of the Aorta

157
Q

Congenital Cardiac Defect Associations:

Fetal Alcohol Syndrome

A
  • VSD
  • PDA
  • ASD
  • TOF
158
Q

Congenital Cardiac Defect Associations:

Congenital Rubella

A
  • PDA
  • PS
  • septal defects
159
Q

Congenital Cardiac Defect Associations:

Down Syndrome

A
  • CAVSD (Endocardial Cushion Defect)
  • VSD
  • ASD
160
Q

Congenital Cardiac Defect Associations:

infant of diabetic mother

161
Q

Congenital Cardiac Defect Associations:

Marfan Syndrome

A
  • MVP
  • Thoracic Aortic Aneurysm and Dissection
  • Aortic Regurgitation
162
Q

Congenital Cardiac Defect Associations:

prenatal lithium exposure

A

Ebstein Anomaly

163
Q

Congenital Cardiac Defect Associations:

Turner Syndrome

A
  • Bicuspid Aortic Valve
  • Coarctation of Aorta
164
Q

Congenital Cardiac Defect Associations:

Williams Syndrome

A

Supravalvular Aortic Stenosis

165
Q

Congenital Cardiac Defect Associations:

22q11 Syndromes

A
  • Truncus Arteriosus
  • TOF
166
Q

Hypertension is defined as persistent _____.

A
  • Systolic BP ≥ 140 mm Hg
  • Diastolic BP ≥ 90 mm Hg
167
Q

Risk Factors for Hypertension

A
  • ↑ age
  • obesity
  • diabetes
  • physical inactivity
  • excess salt intake
  • excess alcohol intake
  • cigarette smoking
  • family history
  • African American > Caucasian > Asian
168
Q

90% of hypertension is _____ and related to ↑ CO or ↑ TPR.

A

1° (Essential)

169
Q

10% of hypertension is mostly 2° to _____.

A
  • renal/renovascular diseases such as fibromuscular dysplasia (characteristic “string of beads” appearance of renal artery)
  • atherosclerotic renal artery stenosis
  • 1° hyperaldosteronism
170
Q

Hypertension:

  • ≥ 180/≥ 120 mm Hg
  • severe hypertension without acute end-organ damage
A

Hypertensive Urgency

171
Q

Hypertension:

  • ≥ 180/≥ 120 mm Hg
  • severe hypertension with evidence of acute end-organ damage:
    • encephalopathy
    • stroke
    • retinal hemorrhages and exudates
    • papilledema
    • MI
    • HF
    • aortic dissection
    • kidney injury
    • microangiopathic hemolytic anemia
    • eclampsia
A

Hypertensive Emergency

172
Q

Hypertension predisposes to _____.

A
  • CAD
  • LVH
  • HF
  • atrial fibrillation
  • aortic dissection
  • aortic aneurysm
  • stroke
  • chronic kidney disease (hypertensive nephropathy)
  • retinopathy
173
Q

Signs of Hyperlipidemia

A
  • Xanthomas
  • Tendinous Xanthoma
  • Corneal Arcus
174
Q

Hyperlipidemia:

plaques or nodules composed of lipid-laden histiocytes in skin, especially the eyelids (xanthelasma)

175
Q

Hyperlipidemia:

lipid deposit in tendon, especially Achilles

A

Tendinous Xanthoma

176
Q

Hyperlipidemia:

  • lipid deposit in cornea
  • common in elderly (arcus senilis), but appears earlier in life with hypercholesterolemia
A

Corneal Arcus

177
Q

_____ is the hardening of arteries, with arterial wall thickening and loss of elasticity.

A

Arteriosclerosis

178
Q

Arteriosclerosis:

  • common
  • affects small arteries and arterioles
  • Two Types:
    • Hyaline—thickening of vessel walls in essential hypertension or diabetes mellitus
    • Hyperplastic—“onion skinning” in severe hypertension with proliferation of smooth muscle cells
A

Arteriolosclerosis

179
Q

Arteriosclerosis:

  • uncommon
  • affects medium-sized arteries
  • calcification of internal elastic lamina and media of arteries → vascular stiffening without obstruction
  • “pipestem” appearance on x-ray
  • does not obstruct blood flow
  • intima not involved
A

Mönckeberg Sclerosis (Medial Calcific Sclerosis)

180
Q

Arteriosclerosis:

  • very common
  • disease of elastic arteries and large- and medium-sized muscular arteries
  • caused by buildup of cholesterol plaques
A

Atherosclerosis

181
Q

Location of Atherosclerosis

A

Abdominal aorta > Coronary artery > Popliteal artery > Carotid artery

“After I workout my abs, I grab a Corona and pop my collar up to my carotid.”

182
Q

Risk Factors for Atherosclerosis:

A
  • Modifiable:
    • smoking
    • hypertension
    • dyslipidemia (↑ LDL, ↓ HDL)
    • diabetes
  • Non-Modifiable:
    • age
    • sex (↑ in men and postmenopausal women)
    • family history
183
Q

Symptoms of Atherosclerosis:

A
  • angina
  • claudication
  • can be asymptomatic
184
Q

Progression of Atherosclerosis:

A

Inflammation: endothelial cell dysfunction → macrophage and LDL accumulation → foam cell formation → fatty streaks → smooth muscle cell migration (involves PDGF and FGF), proliferation, and extracellular matrix deposition → fibrous plaque → complex atheromas

185
Q

Complications of Atherosclerosis:

A
  • aneurysms
  • ischemia
  • infarcts
  • peripheral vascular disease
  • thrombus
  • emboli
186
Q

_____ is a localized pathologic dilatation of the aorta. May cause abdominal and/or back pain, which is a sign of leaking, dissection, or imminent rupture.

A

Aortic Aneurysm

187
Q

Aortic Aneurysm:

  • associated with atherosclerosis
  • rsk factors include history of tobacco use, ↑ age, male sex, family history
  • may present as palpable pulsatile abdominal mass
  • most often infrarenal (distal to origin of renal arteries)
A

Abdominal Aortic Aneurysm

188
Q

Aortic Aneurysm:

  • associated with cystic medial degeneration
  • risk factors include hypertension, bicuspid aortic valve, connective tissue disease (eg. Marfan syndrome)
  • also associated with 3° syphilis (obliterative endarteritis of the vasa vasorum)
  • aortic root dilatation may lead to aortic valve regurgitation
A

Thoracic Aortic Aneurysm

189
Q

_____ is due to trauma and/or deceleration injury, most commonly at aortic isthmus (proximal descending aorta just distal to origin of left subclavian artery).

A

Traumatic Aortic Rupture

190
Q

_____ is the longitudinal intimal tear forming a false lumen. Associated with hypertension, bicuspid aortic valve, inherited connective tissue disorders (eg. Marfan syndrome). Can present with tearing, sudden onset chest pain radiating to the back +/− markedly unequal BP in arms. CXR shows mediastinal widening. Can result in organ ischemia, aortic rupture, death.

A

Aortic Dissection

191
Q

Aortic Dissection:

  • involves ascending aorta
  • may extend to aortic arch or descending aorta
  • may result in acute aortic regurgitation or cardiac tamponade
  • surgical treatment
A

Stanford Type A (Proximal)

Ascending

192
Q

Aortic Dissection:

  • involves only descending aorta (below ligamentum arteriosum)
  • treat medically with β-blockers, then vasodilators
A

Stanford Type B (Distal)

Below

193
Q

Ischemic Heart Disease Manifestations:

  • chest pain due to ischemic myocardium 2° to coronary artery narrowing or spasm
  • no myocyte necrosis
194
Q

Angina:

  • usually 2° to atherosclerosis (≥ 70% occlusion)
  • exertional chest pain in classic distribution (usually with ST depression on ECG)
  • resolves with rest or nitroglycerin
195
Q

Angina:

  • occurs at rest 2° to coronary artery spasm
  • transient ST elevation on ECG
  • smoking is a risk factor
  • hypertension and hypercholesterolemia are not risk factors
  • triggers include cocaine, alcohol, and triptans
  • treat with Ca2+ channel blockers, nitrates, and smoking cessation (if applicable)
A

Vasospastic (Prinzmetal or Variant)

196
Q

Angina:

  • thrombosis with incomplete coronary artery occlusion
  • +/− ST depression and/or T-wave inversion on ECG but no cardiac biomarker elevation (unlike NSTEMI)
  • ↑ in frequency or intensity of chest pain or any chest pain at rest
197
Q

Ischemic Heart Disease Manifestations:

  • distal to coronary stenosis, vessels are maximally dilated at baseline
  • administration of vasodilators (eg. dipyridamole, regadenoson) dilates normal vessels → blood is shunted toward well-perfused areas → ischemia in myocardium perfused by stenosed vessels
  • principle behind pharmacologic stress tests with coronary vasodilators
A

Coronary Steal Syndrome

198
Q

Ischemic Heart Disease Manifestations:

  • death from cardiac causes within 1 hour of onset of symptoms, most commonly due to a lethal arrhythmia (eg. VF)
  • associated with CAD (up to 70% of cases), cardiomyopathy (hypertrophic, dilated), and hereditary ion channelopathies (eg. long QT syndrome, Brugada syndrome)
  • prevent with ICD
A

Sudden Cardiac Death

199
Q

Ischemic Heart Disease Manifestations:

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

A

Chronic Ischemic Heart Disease

200
Q

Ischemic Heart Disease Manifestations:

  • most often due to rupture of coronary artery atherosclerotic plaque → acute thrombosis
  • ↑ cardiac biomarkers (CK-MB, troponins) are diagnostic
A

Myocardial Infarction

201
Q

Myocardial Infarction:

  • transmural infarcts
  • full thickness of myocardial wall involved
  • Q waves
A

ST-Segment Elevation MI (STEMI)

202
Q

Myocardial Infarction:

  • subendocardial infarcts
  • subendocardium (inner 1⁄3) especially vulnerable to ischemia
  • ST depression on ECG
A

Non-ST-Segment Elevation MI (NSTEMI)

203
Q

Commonly Occluded Coronary Arteries

A

LAD > RCA > circumflex

204
Q

Symptoms of Myocardial Infarction

A
  • diaphoresis
  • nausea
  • vomiting
  • severe retrosternal pain
  • pain in left arm and/or jaw
  • shortness of breath
  • fatigue
205
Q

Evolution of Myocardial Infarction:

  • early coagulative necrosis
  • release of necrotic cell contents into blood
  • edema, hemorrhage, wavy fibers
  • neutrophils appear.
  • reperfusion injury, associated with generation of free radicals, leads to hypercontraction of myofibrils through ↑ free calcium influx
  • ventricular arrhythmia, HF, cardiogenic shock
206
Q

Evolution of Myocardial Infarction:

  • extensive coagulative necrosis
  • tissue surrounding infarct shows acute inflammation with neutrophils
  • postinfarction fibrinous pericarditis
A

1–3 days

207
Q

Evolution of Myocardial Infarction:

  • macrophages, then granulation tissue at margins.
  • free wall rupture → tamponade
  • papillary muscle rupture → mitral regurgitation
  • interventricular septal rupture due to macrophage-mediated structural degradation
  • LV pseudoaneurysm (risk of rupture)
A

3–14 days

208
Q

Evolution of Myocardial Infarction:

  • contracted scar complete
  • Dressler syndrome, HF, arrhythmias, true ventricular aneurysm (risk of mural thrombus)
A

2 weeks to several months

209
Q

Diagnosis of Myocardial Infarction:

gold standard in the first 6 hours

210
Q

Diagnosis of Myocardial Infarction:

  • rises after 4 hours
  • peaks at 24 hr
  • ↑ for 7–10 days
  • more specific than other protein markers
A

Troponin I

211
Q

Diagnosis of Myocardial Infarction:

  • rises after 6–12 hour
  • peaks at 16–24 hr
  • predominantly found in myocardium but can also be released from skeletal muscle
  • useful in diagnosing reinfarction following acute MI because levels return to normal after 48 hours
212
Q

Diagnosis of Myocardial Infarction:

ECG Changes

A
  • ST elevation (STEMI, transmural infarct)
  • ST depression (NSTEMI, subendocardial infarct)
  • hyperacute (peaked) T waves
  • T-wave inversion
  • new left bundle branch block
  • pathologic Q waves
  • poor R wave progression (evolving or old transmural infarct)
213
Q

ECG Localization of STEMI:

V1–V2

A

Anteroseptal (LAD)

214
Q

ECG Localization of STEMI:

V3–V4

A

Anteroapical (distal LAD)

215
Q

ECG Localization of STEMI:

V5–V6

A

Anterolateral (LAD or LCX)

216
Q

ECG Localization of STEMI:

Lead I, aVL

A

Lateral (LCX)

217
Q

ECG Localization of STEMI:

Lead II, III, aVF

A

Inferior (RCA)

218
Q

ECG Localization of STEMI:

  • V7–V9
  • ST depression in V1–V3 with tall R waves
A

Posterior (PDA)

219
Q

Myocardial Infarction Complications:

  • occurs within the first few days after MI
  • important cause of death before reaching the hospital and within the first 24 hours post-MI
A

Cardiac Arrhythmia

220
Q

Myocardial Infarction Complications:

  • occurs 1–3 days after MI
  • friction rub
A

Postinfarction Fibrinous Pericarditis

221
Q

Myocardial Infarction Complications:

  • occurs 2–7 days after MI
  • posteromedial papillary muscle rupture ↑ risk due to single blood supply from posterior descending artery
  • can result in severe mitral regurgitation
A

Papillary Muscle Rupture

222
Q

Myocardial Infarction Complications:

  • occurs 3–5 days after MI
  • macrophage-mediated degradation → VSD → ↑ O2 saturation and pressure in RV
A

Interventricular Septal Rupture

223
Q

Myocardial Infarction Complications:

  • occurs 3–14 days after MI
  • contained free wall rupture
  • ↓ CO
  • risk of arrhythmia
  • embolus from mural thrombus
A

Ventricular Pseudoaneurysm Formation

224
Q

Myocardial Infarction Complications:

  • occurs 5–14 days after MI
  • causes cardiac tamponade
  • LV hypertrophy and previous MI is protective
  • acute form usually leads to sudden death
A

Ventricular Free Wall Rupture

225
Q

Myocardial Infarction Complications:

  • occurs 2 weeks to several months after MI
  • outward bulge with contraction (“dyskinesia”)
  • associated with fibrosis
A

True Ventricular Aneurysm

226
Q

Myocardial Infarction Complications:

  • occurs several weeks after MI
  • autoimmune phenomenon resulting in fibrinous pericarditis
A

Dressler Syndrome

227
Q

Myocardial Infarction Complications:

can occur 2° to LV infarction, VSD, free wall rupture, papillary muscle rupture with mitral regurgitation

A

LV Failure and Pulmonary Edema

228
Q

Treatment for Unstable Angina/NSTEMI

A
  • Anticoagulation (eg. heparin)
  • Antiplatelet Therapy (eg. aspirin)
  • ADP Receptor Inhibitors (eg. clopidogrel)
  • β-Blockers
  • ACE Inhibitors
  • Statins
  • Symptom Control:
    • Nitroglycerin
    • Morphine
229
Q

Treatment for STEMI

A
  • Reperfusion Therapy
    • most important
    • percutaneous coronary intervention preferred over fibrinolysis
  • Anticoagulation (eg. heparin)
  • Antiplatelet Therapy (eg. aspirin)
  • ADP Receptor Inhibitors (eg. clopidogrel)
  • β-Blockers
  • ACE Inhibitors
  • Statins
  • Symptom Control:
    • Nitroglycerin
    • Morphine
230
Q

Cardiomyopathies:

  • most common cardiomyopathy (90% of cases)
  • often idiopathic or familial
  • can be caused by hemochromatosis, sarcoidosis, thyrotoxicosis, and peripartum cardiomyopathy
  • leads to systolic dysfunction
  • eccentric hypertrophy (sarcomeres added in series)
A

Dilated Cardiomyopathy

231
Q

Causes of Dilated Cardiomyopathy

A

ABCCCD:

  • Alcohol abuse
  • wet Beriberi
  • Coxsackie B viral myocarditis
  • chronic Cocaine use
  • Chagas disease
  • Doxorubicin toxicity
  • hemochromatosis
  • sarcoidosis
  • thyrotoxicosis
  • peripartum cardiomyopathy
232
Q

Findings in Dilated Cardiomyopathy

A
  • HF
  • S3
  • systolic regurgitant murmur
  • dilated heart on echocardiogram
  • balloon appearance of heart on CXR
233
Q

Treatment for Dilated Cardiomyopathy

A
  • Na+ restriction
  • ACE inhibitors
  • β-blockers
  • Diuretics
  • Digoxin
  • ICD
  • heart transplant
234
Q

Cardiomyopathies:

  • dilated cardiomyopathyy
  • broken heart syndrome
  • ventricular apical ballooning likely due to increased sympathetic stimulation (eg. stressful situations)
A

Takotsubo Cardiomyopathy

235
Q

Cardiomyopathies:

  • 60–70% of cases are familial, autosomal dominant (most commonly due to mutations in genes encoding sarcomeric proteins, such as myosin binding protein C and β-myosin heavy chain)
  • causes syncope during exercise and may lead to sudden death (eg. in young athletes) due to ventricular arrhythmia
  • diastolic dysfunction ensues
  • marked ventricular concentric hypertrophy (sarcomeres added in parallel), often septal predominance
  • myofibrillar disarray and fibrosis
A

Hypertrophic Obstructive Cardiomyopathy

236
Q

Causes of Hypertrophic Obstructive Cardiomyopathy

A
  • Autosomal Dominant
  • Chronic HTN
  • Friedreich Ataxia
237
Q

Findings in Hypertrophic Obstructive Cardiomyopathy

A
  • S4
  • systolic murmur
  • MR—due to impaired mitral valve closure
238
Q

Treatment for Hypertrophic Obstructive Cardiomyopathy

A
  • cessation of high-intensity athletics
  • β-blocker
  • Non-Dihydropyridine Ca2+ Channel Blockers (eg. verapamil)
  • ICD—if patient is high risk
239
Q

Physiology of Hypertrophic Obstructive Cardiomyopathy

A

asymmetric septal hypertrophy and systolic anterior motion of mitral valve → outflow obstruction → dyspnea, possible syncope

240
Q

Cardiomyopathies:

  • can have low voltage ECG despite thick myocardium (especially in amyloidosis)
  • \diastolic dysfunction ensues
A

Restrictive/Infiltrative Cardiomyopathy

241
Q

Restrictive/Infiltrative Cardiomyopathies

A

Puppy LEASH:

  • Postradiation Fibrosis
  • Löffler Endocarditis
  • Endocardial Fibroelastosis—thick fibroelastic tissue in endocardium of young children)
  • Amyloidosis
  • Sarcoidosis
  • Hemochromatosis—although dilated cardiomyopathy is more common
242
Q

Cardiomyopathies:

  • associated with hypereosinophilic syndrome
  • histology shows eosinophilic infiltrates in myocardium
A

Löffler Endocarditis

243
Q

_____ si the clinical syndrome of cardiac pump dysfunction → congestion and low perfusion.

A

Heart Failure

244
Q

Signs and Symptoms of Heart Failure

A
  • Signs:
    • S3 heart sound
    • rales
    • jugular venous distention (JVD)
    • pitting edema
  • Symptoms:
    • dyspnea
    • orthopnea
    • fatigue
245
Q

Heart Failure:

  • reduced EF
  • ↑ EDV
  • ↓ contractility often 2° to ischemia/MI or dilated cardiomyopathy
A

Systolic Dysfunction

246
Q

Heart Failure:

  • preserved EF
  • normal EDV
  • ↓ compliance (↑ EDP) often 2° to myocardial hypertrophy
A

Diastolic Dysfunction

247
Q

Right HF most often results from _____.

248
Q

_____ refers to isolated right HF due to pulmonary cause.

A

Cor Pulmonale

249
Q

_____ ↓ mortality from heart failure.

A
  • ACE Inhibitors
  • Angiotensin II Receptor Blockers
  • β-Blockers (except in acute decompensated HF)
  • Spironolactone
250
Q

_____ relieve symptoms from heart failure.

A
  • Thiazides
  • Loop Diuretics
251
Q

_____ improve symptoms and mortality from heart failure.

A
  • Hydralazine
  • Nitrates
252
Q

Left Heart Failure:

  • shortness of breath when supine
  • ↑ venous return from redistribution of blood (immediate gravity effect) exacerbates pulmonary vascular congestion
253
Q

Left Heart Failure:

  • breathless awakening from sleep
  • ↑ venous return from redistribution of blood, reabsorption of peripheral edema, etc.
A

Paroxysmal Nocturnal Dyspnea

254
Q

Left Heart Failure:

  • ↑ pulmonary venous pressure → pulmonary venous distention and transudation of fluid
  • presence of hemosiderin-laden macrophages (“HF” cells) in lungs
A

Pulmonary Edema

255
Q

Right Heart Failure:

  • nutmeg liver
  • ↑ central venous pressure → ↑ resistance to portal flow
  • rarely, leads to “cardiac cirrhosis”
A

Hepatomegaly

256
Q

Right Heart Failure:

↑ venous pressure

A

Jugular Venous Distention

257
Q

Right Heart Failure:

↑ venous pressure → fluid transudation

A

Peripheral Edema

258
Q

_____ is the ianadequate organ perfusion and delivery of nutrients necessary for normal tissue and cellular function. Initially may be reversible but life threatening if not treated promptly.

259
Q

Shock:

  • caused by hemorrhage, dehydration, and burns
  • cold, clammy
  • ↓↓↓ PCWP (preload)
  • ↓ CO
  • ↑ SVR (afterload)
  • treated with IV fluids
A

Hypovolemic Shock

260
Q

Shock:

  • caused by acute MI, HF, valvular dysfunction, and arrhythmia
  • cold, clammy
  • ↑ or ↓ PCWP (preload)
  • ↓↓ CO
  • ↑ SVR (afterload)
  • treated with inotropes and diuresis
A

Cardiogenic Shock

261
Q

Shock:

  • caused by cardiac tamponade, pulmonary embolism, tension pneumothorax
  • cold, clammy
  • ↑ or ↓ PCWP (preload)
  • ↓↓ CO
  • ↑ SVR (afterload)
  • treated by relieving obstruction
A

Obstructive Shock

262
Q

Shock:

  • caused by sepsis and anaphylaxis
    • warm
    • ↓ PCWP (preload)
    • ↑ CO
    • ↓↓ SVR (afterload)
  • caused by CNS injury
    • dry
    • ↓ PCWP (preload)
    • ↓ CO
    • ↓↓ SVR (afterload)
  • treated with IV fluids, pressors, and epinephrine (anaphylaxis)
A

Distributive Shock

263
Q

Bacterial Endocarditis:

  • S. aureus (high virulence)
  • large vegetations on previously normal valves
  • rapid onset
264
Q

Bacterial Endocarditis:

  • Viridans Streptococci (low virulence)
  • smaller vegetations on congenitally abnormal or diseased valves
  • sequela of dental procedures
  • gradual onset
265
Q

Symptoms of Bacterial Endocarditis

A

Bacteria FROM JANE:

  • Fever—most common
  • Roth Spots—round white spots on retina
    surrounded by hemorrhage
  • Osler Nodes—tender raised lesions on finger or toe pads due to immune complex deposition
  • Murmur
  • Janeway Lesions—small, painless, erythematous lesions on palm or sole
  • Anemia
  • Nail-Bed Hemorrhage—splinter hemorrhages
  • Emboli
266
Q

Bacterial endocarditis is associated with _____.

A
  • glomerulonephritis
  • septic arterial or pulmonary emboli
267
Q

Endocarditis may be nonbacterial (marantic/thrombotic) 2° to _____.

A
  • malignancy
  • hypercoagulable state
  • lupus
268
Q

Bacterial endocarditis requires multiple blood cultures for diagnosis. If culture ⊝, it is most likely caused by _____.

A
  • Coxiella burnetti
  • Bartonella spp.
  • HACEK
    • Haemophilus
    • Aggregatibacter (formerly Actinobacillus)
    • Cardiobacterium
    • Eikenella
    • Kingella
269
Q

The _____ is most frequently involved in bacterial endocarditis.

A

Mitral Valve

270
Q

Tricuspid valve endocarditis is associated with
_____ and bacteria such as _____.

A
  • IV Drug Abuse (don’t “tri” drugs)
  • S. aureus
  • Pseudomonas
  • Candida
271
Q

Bacterial Endocarditis:

colon cancer

A

S. bovis (gallolyticus)

272
Q

Bacterial Endocarditis:

prosthetic valves

A

S. epidermidis

273
Q

_____ is a a consequence of pharyngeal infection with group A β-hemolytic streptococci. Late sequelae include rheumatic heart disease, which affects heart valves.

A

Rheumatic Fever

274
Q

Rheumatic fever affects the _____ valves.

A

Mitral > Aortic >> Tricuspid

*high-pressure valves are affected the most

275
Q

Rheumatic fever presents with mitral _____.

A
  • Mitral Regurgitation—early lesion
  • Mitral Stenosis—late lesion
276
Q

Rheumatic fever is associated with _____.

A
  • Aschoff Bodies (granuloma with giant cells)
  • Anitschkow Cells (enlarged macrophages with ovoid, wavy, rod-like nucleus)
  • ↑ Antistreptolysin O (ASO) titers
277
Q

Pathogenesis of Rheumatic Fever

A
  • immune mediated (type II hypersensitivity)
  • not a direct effect of bacteria
  • antibodies to M protein cross-react with self antigens (molecular mimicry)
278
Q

Findings in Rheumatic Fever

A

J♥NES (major criteria):

  • Joint (migratory polyarthritis)
  • ♥ (carditis)
  • Nodules in Skin (subcutaneous)
  • Erythema Marginatum (evanescent rash with ring margin)
  • Sydenham Chorea
279
Q

Treatment and prophylaxis for rheumatic fever is _____.

A

Penicillin

280
Q

_____ is the inflammation of the pericardium. Commonly presents with sharp pain, aggravated by inspiration, and relieved by sitting up and leaning forward. Often complicated by pericardial effusion . Presents with friction rub.

A

Acute Pericarditis

281
Q

ECG changes in acute pericarditis include _____.

A
  • widespread ST-segment elevation
  • PR depression
282
Q

Acute pericarditis is caused by _____.

A
  • idiopathic (most common; presumed viral)
  • confirmed infection (eg. coxsackievirus B)
  • neoplasia
  • autoimmune (eg. SLE, rheumatoid arthritis)
  • uremia
  • cardiovascular (acute STEMI or Dressler syndrome)
  • radiation therapy
283
Q

_____ is the inflammation of myocardium → global enlargement of heart and dilation of all chambers. Major cause of SCD in adults < 40 years old. Presentation highly variable, can include dyspnea, chest pain, fever, arrhythmias (persistent tachycardia out of proportion to fever is characteristic).

A

Myocarditis

284
Q

Causes of Myocarditis

A
  • Viral—Adenovirus, Coxsackie B, Parvovirus B19, HIV, HHV-6, lymphocytic infiltrate with focal necrosis highly indicative of viral myocarditis
  • Parasitic—Trypanosoma cruzi, Toxoplasma gondii
  • Bacterial—Borrelia burgdorferi, Mycoplasma pneumoniae
  • Toxins—carbon monoxide, black widow venom
  • Rheumatic Fever
  • Drugs—Doxorubicin, Cocaine
  • Autoimmune—Kawasaki disease, sarcoidosis, SLE, polymyositis/dermatomyositis
285
Q

Complications of Myocarditis

A
  • sudden death
  • arrhythmias
  • heart block
  • dilated cardiomyopathy
  • HF
  • mural thrombus with systemic emboli
286
Q

_____ is the compression of the heart by fluid (eg. blood, effusions in pericardial space) → ↓ CO. Equilibration of diastolic pressures in all 4 chambers.

A

Cardiac Tamponade

287
Q

Findings in Cardiac Tamponade

A
  • Beck Triad
    • hypotension
    • distended neck veins
    • distant heart sounds
  • ↑ HR
  • pulsus paradoxus
  • ECG shows low-voltage QRS and electrical alternans (due to “swinging” movement of heart in large effusion)
288
Q

_____ is the ↓ in amplitude of systolic BP by > 10 mm Hg during inspiration. Seen in cardiac tamponade, asthma, obstructive sleep apnea, pericarditis, croup.

A

Pulsus Paradoxus

289
Q

_____ occurs when 3° syphilis disrupts the vasa vasorum of the aorta with consequent atrophy of vessel wall and dilatation of aorta and valve ring. May see calcification of aortic root, ascending aortic arch, and thoracic aorta. Leads to “tree bark” appearance of aorta. Can result in aneurysm of ascending aorta or
aortic arch, aortic insufficiency.

A

Syphilitic Heart Disease

290
Q

Vasculitides:

Large-Vessel Vasculitis

A
  • Giant Cell (Temporal) Arteritis
  • Takayasu Arteritis
291
Q

Vasculitides:

  • large-vessel vasculitis
  • usually elderly females
  • unilateral headache (temporal artery), jaw claudication
  • may lead to irreversible blindness due to ophthalmic artery occlusion
  • associated with polymyalgia rheumatica
  • most commonly affects branches of carotid artery
  • focal granulomatous inflammation
  • ↑ ESR
  • treated with high-dose corticosteroids prior to temporal artery biopsy to prevent blindness
A

Giant Cell (Temporal) Arteritis

292
Q

Vasculitides:

  • large-vessel vasculitis
  • usually Asian females < 40 years old
  • “pulseless disease” (weak upper extremity pulses), fever, night sweats, arthritis, myalgias, skin nodules, ocular disturbances
  • granulomatous thickening and narrowing of aortic arch and proximal great vessels
  • ↑ ESR
  • treated with corticosteroids
A

Takayasu Arteritis

293
Q

Vasculitides:

Medium-Vessel Vasculitis

A
  • Polyarteritis Nodosa
  • Kawasaki Disease (Mucocutaneous Lymph Node Syndrome)
  • Buerger Disease (Thromboangiitis Obliterans)
294
Q

Vasculitides:

  • medium-vessel vasculitis
  • usually middle-aged men
  • Hepatitis B seropositivity in 30% of patients
  • fever, weight loss, malaise, headache
  • GI: abdominal pain, melena
  • hypertension, neurologic dysfunction, cutaneous eruptions, renal damage
  • typically involves renal and visceral vessels, not pulmonary arteries
  • transmural inflammation of the arterial wall with fibrinoid necrosis
  • different stages of inflammation may coexist in different vessels
  • innumerable renal microaneurysms and spasms on arteriogram
  • treat with with corticosteroids, cyclophosphamide
A

Polyarteritis Nodosa

295
Q

Vasculitides:

  • medium-vessel vasculitis
  • Asian children < 4 years old
  • conjunctival injection, rash (polymorphous → desquamating), adenopathy (cervical), strawberry tongue (oral mucositis), hand-foot changes (edema, erythema), fever
  • may develop coronary artery aneurysms
  • thrombosis or rupture can cause death
  • treated with IV immunoglobulin and aspirin
A

Kawasaki Disease (Mucocutaneous Lymph Node Syndrome)

CRASH and burn.

  • Conjunctival injection
  • Rash (polymorphous → desquamating)
  • Adenopathy (cervical)
  • Strawberry tongue (oral mucositis)
  • Hand-foot changes (edema, erythema)
  • fever
296
Q

Vasculitides:

  • medium-vessel vasculitis
  • heavy smokers, males < 40 years old
  • intermittent claudication may lead to gangrene, autoamputation of digits, superficial nodular phlebitis
  • Raynaud phenomenon is often present
  • segmental thrombosing vasculitis with vein and nerve involvement
  • treated with smoking cessation
A

Buerger Disease (Thromboangiitis Obliterans)

297
Q

Vasculitides:

Small-Vessel Vasculitis

A
  • Granulomatosis with Polyangiitis (Wegener)
  • Microscopic Polyangiitis
  • Behçet Syndrome
  • Eosinophilic Granulomatosis with Polyangiitis (Churg-Strauss)
  • Immunoglobulin A Vasculitis
298
Q

Vasculitides:

  • small-vessel vasculitis
  • Upper Respiratory Tract: perforation of nasal septum, chronic sinusitis, otitis media, mastoiditis
  • Lower Respiratory Tract: hemoptysis, cough, dyspnea
  • Renal: hematuria, red cell casts
  • Triad:
    • focal necrotizing vasculitis
    • necrotizing granulomas in the lung and upper airway
    • necrotizing glomerulonephritis
  • PR3-ANCA/c-ANCA G (anti-proteinase 3)
  • CXR: large nodular densities
  • treated with cyclophosphamide, corticosteroids
A

Granulomatosis with Polyangiitis (Wegener)

299
Q

Vasculitides:

  • small-vessel vasculitis
  • necrotizing vasculitis commonly involving lung, kidneys, and skin with pauci-immune glomerulonephritis and palpable purpura
  • presentation similar to granulomatosis with polyangiitis but without nasopharyngeal involvement
  • no granulomas.
  • MPO-ANCA/p-ANCA H (antimyeloperoxidase)
  • treated with cyclophosphamide, corticosteroids
A

Microscopic Polyangiitis

300
Q

Vasculitides:

  • small-vessel vasculitis
  • high incidence in Turkish and eastern Mediterranean descent
  • recurrent aphthous ulcers, genital ulcerations, uveitis, erythema nodosum
  • can be precipitated by HSV or parvovirus
  • flares last 1–4 weeks
  • immune complex vasculitis
  • associated with HLA-B51
A

Behçet Syndrome

301
Q

Vasculitides:

  • small-vessel vasculitis
  • asthma, sinusitis, skin nodules or purpura, peripheral neuropathy (eg. wrist/foot drop)
  • can also involve heart, GI, kidneys (pauciimmune glomerulonephritis)
  • granulomatous, necrotizing vasculitis with eosinophilia
  • MPO-ANCA/p-ANCA, ↑ IgE level
A

Eosinophilic Granulomatosis with Polyangiitis (Churg-Strauss)

302
Q

Vasculitides:

  • small-vessel vasculitis
  • Henoch-Schönlein Purpura
  • most common childhood systemic vasculitis
  • often follows URI
  • Classic Triad:
    • Skin: palpable purpura on buttocks/legs
    • arthralgias
    • GI: abdominal pain (associated with intussusception)
  • vasculitis 2° to IgA immune complex deposition
  • associated with IgA nephropathy (Berger disease)
A

Immunoglobulin A Vasculitis

303
Q

The most common heart tumor is a _____.

A

Metastasis

304
Q

Cardiac Tumors:

  • most common 1° cardiac tumor in adults
  • 90% occur in the atria (mostly left atrium)
  • described as a “ball valve” obstruction in the left atrium (associated with multiple syncopal episodes)
  • may auscultate early diastolic “tumor plop” sound
  • Histology:
    • gelatinous material
    • myxoma cells immersed in glycosaminoglycans
305
Q

Cardiac Tumors:

  • most frequent 1° cardiac tumor in children (associated with tuberous sclerosis)
  • Histology: hamartomatous growths
A

Rhabdomyomas

306
Q

_____ shows ↑ in JVP on inspiration instead of a normal ↓. May be seen with constrictive pericarditis, restrictive cardiomyopathies, right atrial or ventricular tumors.

A

Kussmaul Sign

inspiration → negative intrathoracic pressure not transmitted to heart → impaired filling of right ventricle → blood backs up into vena cava → JVD

307
Q

_____ is also known as Osler-Weber-Rendu syndrome. Inherited disorder of blood vessels.

Findings:

  • blanching lesions (telangiectasias) on skin and mucous membranes
  • recurrent epistaxis
  • skin discolorations
  • arteriovenous malformations (AVMs)
  • GI bleeding
  • hematuria
A

Hereditary Hemorrhagic Telangiectasia

308
Q

Hypertension Treatment:

Primary (Essential) Hypertension

A
  • Thiazide Diuretics
  • ACE Inhibitors
  • Angiotensin II Receptor Blockers (ARBs)
  • Dihydropyridine Ca2+ Channel Blockers
309
Q

Hypertension Treatment:

Hypertension with Heart Failure

A
  • Diuretics
  • ACE Inhibitors
  • ARBs
  • β-Blockers (compensated HF)
  • Aldosterone Antagonists

β-blockers must be used cautiously in decompensated HF and are contraindicated in cardiogenic shock. In HF, ARBs may be combined with the neprilysin inhibitor sacubitril.

310
Q

Hypertension Treatment:

Hypertension with Diabetes Mellitus

A
  • ACE Inhibitors
  • ARBs
  • Ca2+ Channel Blockers
  • Thiazide Diuretics
  • β-Blockers

ACE inhibitors/ARBs are protective against diabetic nephropathy.

311
Q

Hypertension Treatment:

Hypertension in Asthma

A
  • ARBs
  • Ca2+ Channel Blockers
  • Thiazide Diuretics
  • Selective β-Blockers

Avoid nonselective β-blockers to prevent β2‑receptor–induced bronchoconstriction. Avoid ACE inhibitors to prevent confusion between drug or asthma-related cough.

312
Q

Hypertension Treatment:

Hypertension in Pregnancy

A

He likes my neonate.

  • Hydralazine
  • Labetalol
  • Methyldopa
  • Nifedipine
313
Q

Calcium Channel Blockers

A
  • Amlodipine
  • Clevidipine
  • Nicardipine
  • Nifedipine
  • Nimodipine (dihydropyridines, act on vascular
  • smooth muscle)
  • Diltiazem
  • Verapamil (non-dihydropyridines, act on heart)
314
Q

Hypertension Treatment:

block voltage-dependent L-type calcium channels of cardiac and smooth muscle → ↓ muscle contractility

A

Calcium Channel Blockers

  • Vascular Smooth Muscle
    • Amlodipine = Nifedipine > Diltiazem > Verapamil
  • Heart
    • Verapamil > Diltiazem > Amlodipine = Nifedipine (verapamil = ventricle)
315
Q

Calcium Channel Blockers:

  • hypertension
  • angina (including Prinzmetal)
  • Raynaud phenomenon
A

Dihydropyridines (except Nimodipine)

316
Q

Calcium Channel Blockers:

subarachnoid hemorrhage (prevents cerebral vasospasm)

A

Nimodipine

317
Q

Calcium Channel Blockers:

hypertensive urgency or emergency

A
  • Nicardipine
  • Clevidipine
318
Q

Calcium Channel Blockers:

  • hypertension
  • angina
  • atrial fibrillation/flutter
A

Non-Dihydropyridines

319
Q

Adverse Effects of Calcium Channel Blockers

A
  • Non-Dihydropyridine: cardiac depression, AV block, hyperprolactinemia, constipation, gingival hyperplasia
  • Dihydropyridine: peripheral edema, flushing, dizziness.
320
Q

Hypertension Treatment:

  • ↑ cGMP → smooth muscle relaxation
  • vasodilates arterioles > veins; afterload reduction
  • used in severe hypertension (particularly acute), HF (with organic nitrate)
  • safe to use during pregnancy
  • frequently coadministered with a β-blocker to prevent reflex tachycardia
  • causes compensatory tachycardia (contraindicated in angina/CAD), fluid retention, headache, angina, SLE-like syndrome
A

Hydralazine

321
Q

Hypertensive emergency is treated with _____.

A
  • Clevidipine
  • Fenoldopam
  • Labetalol
  • Nicardipine
  • Nitroprusside
322
Q

Hypertensive Emergency:

  • short acting
  • ↑ cGMP via direct release of NO
  • can cause cyanide toxicity (releases cyanide)
A

Nitroprusside

323
Q

Hypertensive Emergency:

  • Dopamine D1 receptor agonist—coronary, peripheral, renal, and splanchnic vasodilation
  • ↓ BP, ↑ natriuresis
  • also used postoperatively as an antihypertensive
  • can cause hypotension and tachycardia
A

Fenoldopam

324
Q

Nitrates

A
  • Nitroglycerin
  • Isosorbide Dinitrate
  • Isosorbide Mononitrate
325
Q

Hypertension Treatment:

  • vasodilate by ↑ NO in vascular smooth muscle → ↑ in cGMP and smooth muscle relaxation
  • dilate veins >> arteries, ↓ preload
  • angina, acute coronary syndrome, pulmonary edema
  • causes reflex tachycardia (treat with β-blockers), hypotension, flushing, headache,
  • “Monday Disease”
    • industrial exposure
    • development of tolerance for the vasodilating action during the work week and loss of tolerance over the weekend → tachycardia, dizziness, headache upon reexposure
  • contraindicated in right ventricular infarction
326
Q

Antianginal Therapy

A

Goal is reduction of myocardial O2 consumption (MVO2) by ↓ 1 or more of the determinants of MVO2: end-diastolic volume, BP, HR, contractility.

327
Q

Antianginal Therapy:

  • ↓ End-Diastolic Volume
  • ↓ Blood Pressure
  • no effect on Contractility
  • ↑ Heart Rate—reflex response
  • ↓ Ejection Time
  • ↓ MVO2
328
Q

Antianginal Therapy:

  • no effect or ↑ End-Diastolic Volume
  • ↓ Blood Pressure
  • ↓ Contractility
  • ↓ Heart Rate
  • ↑ Ejection Time
  • ↓ MVO2
A

β-Blockers

329
Q

Antianginal Therapy:

  • no effect or ↓ End-Diastolic Volume
  • ↓ Blood Pressure
  • little/no effect on Contractility
  • no effect or ↓ Heart Rate
  • little/no effect on Ejection Time
  • ↓↓ MVO2
A

Nitrates + β-Blockers

330
Q

Cardiac Drugs:

  • inhibits the late phase of sodium current thereby reducing diastolic wall tension and oxygen consumption
  • does not affect heart rate or contractility
  • used in angina refractory to other medical therapies
  • causes constipation, dizziness, headache, nausea, QT prolongation
A

Ranolazine

331
Q

Cardiac Drugs:

  • selective PDE-3 inhibitor
  • Cardiomyocytes:
    • ↑ cAMP accumulation → ↑ Ca2+ influx → ↑ inotropy and chronotropy
  • Vascular Smooth Muscle:
    • ↑ cAMP accumulation → inhibition of MLCK activity → general vasodilation
  • short-term use in acute decompensated HF
  • causes arrhythmias and hypotension
332
Q

Lipid-Lowering Agents

A
  • HMG-CoA Reductase Inhibitors
    • Lovastatin
    • Pravastatin
  • Bile Acid Resins
    • Cholestyramine
    • Colestipol
    • Colesevelam
  • Ezetimibe
  • Fibrates
    • Gemfibrozil
    • Bezafibrate
    • Fenofibrate
  • Niacin (Vitamin B3)
  • PCSK9 Inhibitors
    • Alirocumab
    • Evolocumab
333
Q

Lipid-Lowering Agents:

  • ↓↓↓ LDL
  • ↑ HDL
  • ↓ TGs
  • inhibit conversion of HMGCoA to mevalonate, a cholesterol precursor
  • ↓ mortality in CAD patients
  • causes hepatotoxicity (↑ LFTs), myopathy (esp. when used with fibrates or niacin)
A

HMG-CoA Reductase Inhibitors

  • Lovastatin
  • Pravastatin
334
Q

Lipid-Lowering Agents:

  • ↓↓ LDL
  • slightly ↑ HDL
  • slightly ↑ TGs
  • prevent intestinal reabsorption of bile acids
  • liver must use cholesterol to make more
  • causes GI upset, ↓ absorption of other drugs and fat-soluble vitamins
A

Bile Acid Resins

  • Cholestyramine
  • Colestipol
  • Colesevelam
335
Q

Lipid-Lowering Agents:

  • ↓↓ LDL
  • ↑/— HDL
  • ↓/— TGs
  • prevents cholesterol absorption at small intestine brush border
  • rarely ↑ LFTs
  • causes diarrhea
336
Q

Lipid-Lowering Agents:

  • ↓ LDL
  • ↑ HDL
  • ↓↓↓ TGs
  • upregulate LPL → ↑ TG clearance
  • activates PPAR-α to induce HDL synthesis
  • causes myopathy (↑ risk with statins), cholesterol gallstones (via inhibition of cholesterol 7α-hydroxylase)
A

Fibrates

  • Gemfibrozil
  • Bezafibrate
  • Fenofibrate
337
Q

Lipid-Lowering Agents:

  • ↓↓ LDL
  • ↑↑ HDL
  • ↓ TGs
  • inhibits lipolysis (hormonesensitive lipase) in adipose tissue
  • reduces hepatic VLDL synthesis
  • causes red, flushed face, which is ↓ by NSAIDs or long-term use
  • causes hyperglycemia and hyperuricemia
A

Niacin (Vitamin B3)

338
Q

Lipid-Lowering Agents:

  • ↓↓↓ LDL
  • ↑ HDL
  • ↓ TGs
  • inactivation of LDL-receptor degradation, increasing amount of LDL removed from bloodstream
  • causes myalgias, delirium, dementia, other neurocognitive effects
A

PCSK9 Inhibitors

  • Alirocumab
  • Evolocumab
339
Q

Cardiac Drugs:

  • cardiac glycoside
  • direct inhibition of Na+/K+ ATPase → indirect inhibition of Na+/Ca2+ exchanger
  • ↑ [Ca2+]i → positive inotropy
  • stimulates vagus nerve → ↓ HR
  • used in HF (↑ contractility) and atrial fibrillation (↓ conduction at AV node and depression of SA node)
340
Q

Adverse Effects of Digoxin

A
  • can lead to hyperkalemia, which indicates poor prognosis
  • Cholinergic:
    • nausea, vomiting, diarrhea, blurry yellow vision (think van Gogh), arrhythmias, AV block
  • ↑ Toxicity:
    • renal failure (↓ excretion)
    • hypokalemia (permissive for digoxin binding at K+-binding site on Na+/K+ ATPase)
    • drugs that displace digoxin from tissue-binding sites
    • ↓ clearance (eg. verapamil, amiodarone, quinidine)
341
Q

Antidote to Digoxin

A
  • slowly normalize K+
  • cardiac pacer
  • Anti-Digoxin Fab Fragments
  • Mg2+
342
Q

Antiarrhythmics:

  • slow or block (↓) conduction (especially in depolarized cells)
  • ↓ slope of phase 0 depolarization
  • state dependent (selectively depress tissue that is frequently depolarized [eg. tachycardia])
A

Class I (Sodium Channel Blockers)

343
Q

Class IA Antiarrhythmics

A

The Queen Proclaims Diso’s pyramid.

  • Quinidine
  • Procainamide
  • Disopyramide
344
Q

Antiarrhythmics:

  • sodium channel blocker
  • ↑ AP duration, ↑ effective refractory period (ERP) in ventricular action potential, ↑ QT interval, some potassium channel blocking effects
  • used in both atrial and ventricular arrhythmias, especially re-entrant and ectopic SVT and VT
  • causes cinchonism (headache, tinnitus with quinidine), reversible SLE-like syndrome (procainamide), HF (disopyramide), thrombocytopenia, torsades de pointes due to ↑ QT interval
345
Q

Class IB Antiarrhythmics

A

I’d Buy Liddy’s Mexican Tacos.

  • Lidocaine
  • MexileTine
346
Q

Antiarrhythmics:

  • sodium channel blocker
  • ↓ AP duration
  • preferentially affect ischemic or depolarized Purkinje and ventricular tissue
  • Phenytoin can also fall into this category
  • used in acute ventricular arrhythmias (especially post-MI), digitalis-induced arrhythmias
  • best in post-MI
  • causes CNS stimulation/depression and cardiovascular depression
347
Q

Class IC Antiarrhythmics

A

“Can I have Fries, Please.”

  • Flecainide
  • Propafenone
348
Q

Antiarrhythmics:

  • sodium channel blocker
  • significantly prolongs ERP in AV node and accessory bypass tracts
  • no effect on ERP in Purkinje and ventriculartissue.
  • minimal effect on AP duration
  • used in SVTs, including atrial fibrillation
  • used only as a last resort in refractory V
  • is proarrhythmic, especially post-MI (contraindicated)
  • contraindicated in structural and ischemic heart disease
349
Q

Class II Antiarrhythmics

A

β-Blockers

  • Metoprolol
  • Propranolol
  • Esmolol
  • Atenolol
  • Timolol
  • Carvedilol
350
Q

Antiarrhythmics:

  • decrease SA and AV nodal activity by ↓ cAMP, ↓ Ca2+ currents
  • suppress abnormal pacemakers by ↓ slope of phase 4
  • AV node is particularly sensitive → ↑ PR interval
  • used in SVT, ventricular rate control for atrial fibrillation and atrial flutter
  • causes impotence, exacerbation of COPD and asthma, cardiovascular effects (bradycardia, AV block, HF), CNS effects (sedation, sleep alterations)
  • may mask the signs of hypoglycemia
  • cause unopposed α1-agonism if given alone for pheochromocytoma or cocaine toxicity
  • overdose is treated with saline, atropine, glucagon
A

Class II (β-Blockers)

  • Esmolol—very short acting
  • Metoprolol—dyslipidemia
  • Propranolol—exacerbate vasospasm in Prinzmetal angina
351
Q

Class III Antiarrhythmics

A

Potassium Channel Blockers

AIDS:

  • Amiodarone
  • Ibutilide
  • Dofetilide
  • Sotalol
352
Q

Antiarrhythmics:

  • ↑ AP duration, ↑ ERP, ↑ QT interval
  • used in atrial fibrillation, atrial flutter, and ventricular tachycardia (amiodarone, sotalol)
A

Class III (Potassium Channel Blockers)

  • Sotalol—torsades de pointes, excessive β blockade
  • Ibutilide—torsades de pointes
353
Q

Antiarrhythmics:

  • potassium channel blocker
  • causes pulmonary fibrosis, hepatotoxicity, hypothyroidism or hyperthyroidism (40% iodine by weight), acts as hapten (corneal deposits, blue/gray skin deposits resulting in photodermatitis), neurologic effects, constipation, cardiovascular effects (bradycardia, heart block, HF)
  • remember to check PFTs, LFTs, and TFTs befire using
  • is lipophilic and has class I, II, III, and IV effects
A

Amiodarone

354
Q

Class IV Antiarrhythmics

A

Calcium Channel Blockers

  • Verapamil
  • Diltiazem
355
Q

Antiarrhythmics:

  • ↑ conduction velocity, ↓ ERP, ↓ PR interval
  • prevention of nodal arrhythmias (eg, SVT), rate control in atrial fibrillation
  • causes constipation, flushing, edema, and cardiovascular effects (HF, AV block, sinus node depression)
A

Class IV (Calcium Channel Blockers)

356
Q

Antiarrhythmics:

  • ↑ K+ out of cells → hyperpolarizing the cell and ↓ ICa, decreasing AV node conduction
  • drug of choice in diagnosing/terminating certain forms of SVT
  • very short acting (~ 15 sec)
  • effects blunted by theophylline and caffeine (both are _____ receptor antagonists)
  • adverse effects include flushing, hypotension, chest pain, sense of impending doom, and bronchospasm
357
Q

Antiarrhythmics:

  • torsades de pointes
  • digoxin toxicity
358
Q

Cardiac Drugs:

  • selective inhibition of funny sodium channels (If), prolonging slow depolarization phase (phase 4)
  • ↓ SA node firing → negative chronotropic effect without inotropy, reduces cardiac O2 requirement
  • used in chronic stable angina in patients who cannot take β-blockers
  • used in chronic HF with reduced ejection fraction
  • causes luminous phenomena/visual brightness, hypertension, and bradycardia
A

Ivabradine

USMLE Step 1 (18 decks)

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