Cardiovascular - First Aid

Question 1

Heart Embryology:

ascending aorta and pulmonary trunk

Answer 1

Truncus Arteriosus

Question 2

Heart Embryology:

smooth parts (outflow tract) of left and right ventricles

Answer 2

Bulbus Cordis

Question 3

Heart Embryology:

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

Answer 3

Endocardial Cushion

Question 4

Heart Embryology:

trabeculated part of left and right atria

Answer 4

Primitive Atrium

Question 5

Heart Embryology:

trabeculated part of left and right ventricles

Answer 5

Primitive Ventricle

Question 6

Heart Embryology:

smooth part of left atrium

Answer 6

Primitive Pulmonary Vein

Question 7

Heart Embryology:

coronary sinus

Answer 7

Left Horn of Sinus Venosus

Question 8

Heart Embryology:

smooth part of right atrium (sinus venarum)

Answer 8

Right Horn of Sinus Venosus

Question 9

Heart Embryology:

superior vena cava (SVC)

Answer 9

• Right Common Cardinal Vein
• Right Anterior Cardinal Vein

Question 10

The _____ is the first functional organ in vertebrate embryos.

Answer 10

heart

Question 11

The heart beats spontaneously by _____ of development.

Answer 11

week 4

Question 12

Cardiac Looping

Answer 12

• 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).

Question 13

​Septation of the Atria

Answer 13

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.

Question 14

_____ 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.

Answer 14

Patent Foramen Ovale

Question 15

​Septation of the Ventricles

Answer 15

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.

Question 16

_____ is the most common congenital cardiac anomaly.

Answer 16

Ventricular Septal Defect

Question 17

VSD usually occurs in the _____.

Answer 17

membranous septum

Question 18

Outflow Tract Formation

Answer 18

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

Question 19

Conotruncal Abnormalities Associated with
Failure of Neural Crest Cells to Migrate

Answer 19

• Transposition of Great Vessels
• Tetralogy of Fallot
• Persistent Truncus Arteriosus

Question 20

Valve Development

Answer 20

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

Question 21

Valvular anomalies may be _____.

Answer 21

• stenotic
• regurgitant
• atretic—tricuspid atresia
• displaced—Ebstein anomaly

Question 22

Fetal Circulation

Answer 22

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).

Question 23

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

Answer 23

• 30 mm Hg
• 80% O₂

Question 24

Transitional Circulation

Answer 24

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.

Question 25

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

Answer 25

Indomethacin Prostaglandins **E**₁ and **E**₂ k**EE**p PDA open.

Question 26

Fetal-Postnatal Derivatives: Median Umbilical Ligament

Answer 26

Allantois → Urachus Urachus is part of allantoic duct between bladder and umbilicus.

Question 27

Fetal-Postnatal Derivatives: Ligamentum Arteriosum

Answer 27

Ductus Arteriosus

Question 28

Fetal-Postnatal Derivatives: Ligamentum Venosum

Answer 28

Ductus Venosus

Question 29

Fetal-Postnatal Derivatives: Fossa Ovalis

Answer 29

Foramen Ovale

Question 30

Fetal-Postnatal Derivatives: Nucleus Pulposus

Answer 30

Notochord

Question 31

Fetal-Postnatal Derivatives: Medial Umbilical Ligaments

Answer 31

Umbilical Arteries

Question 32

Fetal-Postnatal Derivatives: Ligamentum Teres Hepatis (Round Ligament)

Answer 32

Umbilical Vein \*contained in falciform ligament

Question 33

Anatomy of the Heart

Answer 33

* 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

Question 34

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

Answer 34

RCA

Question 35

The AV node is supplied by the \_\_\_\_\_.

Answer 35

PDA

Question 36

Coronary artery occlusion most commonly occurs in the \_\_\_\_\_.

Answer 36

LAD

Question 37

Coronary blood flow peaks in \_\_\_\_\_.

Answer 37

early diastole

Question 38

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).

Answer 38

left atrium

Question 39

Pericardium Layers

Answer 39

Outer → Inner: * Fibrous Pericardium * Parietal Layer of Serous Pericardium * Visceral Layer of Serous Pericardium The pericardial cavity lies between parietal and visceral layers.

Question 40

The pericardium is innervated by the \_\_\_\_\_.

Answer 40

phrenic nerve

Question 41

Pericarditis can cause referred pain to the \_\_\_\_\_.

Answer 41

shoulder

Question 42

Cardiac Output

Answer 42

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

Question 43

Fick Principle

Answer 43

Question 44

Mean Arterial Pressure

Answer 44

MAP = CO × total peripheral resistance (TPR)

Question 45

MAP (at resting HR)

Answer 45

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

Question 46

Pulse Pressure

Answer 46

Pulse Pressure = systolic pressure – diastolic pressure Pulse pressure is proportional to SV, and inversely proportional to arterial compliance.

Question 47

Stroke Volume

Answer 47

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

Question 48

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

Answer 48

* ↑ HR * ↑ SV

Question 49

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

Answer 49

↑ HR \*SV plateaus

Question 50

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

Answer 50

↑ HR

Question 51

↑ Pulse Pressure

Answer 51

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

Question 52

↓ Pulse Pressure

Answer 52

* aortic stenosis * cardiogenic shock * cardiac tamponade * advanced heart failure (HF)

Question 53

Stroke Volume is affected by \_\_\_\_\_.

Answer 53

**SV CAP** * Contractility * Afterload * Preload A failing heart has ↓ SV (systolic and/or diastolic dysfunction)

Question 54

↑ SV

Answer 54

* ↑ Contractility (eg. anxiety, exercise) * ↑ Preload (eg. early pregnancy) * ↓ Afterload

Question 55

↑ Contractility and SV

Answer 55

* 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⁺)

Question 56

↓ Contractility and SV

Answer 56

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

Question 57

Preload is approximated by \_\_\_\_\_.

Answer 57

ventricular EDV

Question 58

Preload depends on \_\_\_\_\_.

Answer 58

* venous tone * circulating blood volume

Question 59

↓ Preload

Answer 59

Venous Vasodilators (eg. nitroglycerin)

Question 60

Afterload approximated by \_\_\_\_\_.

Answer 60

MAP

Question 61

Laplace’s Law

Answer 61

↑ afterload → ↑ pressure → ↑ wall tension per

Question 62

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

Answer 62

thickening (hypertrophy)

Question 63

↓ Afterload

Answer 63

Arterial Vasodilators (eg. hydralazine)

Question 64

↓ Preload and Afterload

Answer 64

* ACE Inhibitors * ARBs

Question 65

Chronic Hypertension ( ↑ MAP) → \_\_\_\_\_

Answer 65

LV Hypertrophy

Question 66

↑ Myocardial O₂ Demand

Answer 66

Myo**CARD**ial O_²: * ↑ **C**ontractility * ↑ **A**fterload (proportional to arterial pressure) * ↑ Heart **R**ate * ↑ **D**iameter of ventricle (↑ wall tension)

Question 67

Cardiac wall tension follows \_\_\_\_\_.

Answer 67

Laplace’s Law

Question 68

Wall Tension

Answer 68

Wall Tension = Pressure × Radius

Question 69

Wall Stress

Answer 69

Question 70

Ejection Fraction

Answer 70

* Left Ventricular EF is an index of ventricular contractility. * EF is ↓ in systolic HF. * EF is normal in HF with preserved ejection fraction.

Question 71

Starling Curve

Answer 71

* 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.

Question 72

Resistance, Pressure, Flow

Answer 72

* Pressure gradient drives flow from high pressure to low pressure. * Compliance = ΔV/ΔP

Question 73

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

Answer 73

Capillaries

Question 74

\_\_\_\_\_ account for most of TPR.

Answer 74

Arterioles

Question 75

\_\_\_\_\_ provide most of the blood storage capacity.

Answer 75

Veins

Question 76

Viscosity depends mostly on \_\_\_\_\_.

Answer 76

Hematocrit * ↑ in hyperproteinemic states (eg. multiple myeloma) and polycythemia * ↓ in anemia

Question 77

Cardiac and Vascular Function Curves

Answer 77

* 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).

Question 78

Inotropy

Answer 78

Changes in contractility → altered CO for a given RA pressure (preload). * catecholamines, digoxin ⊕, exercise * HF with reduced EF, narcotic overdose, sympathetic inhibition ⊝

Question 79

Venous Return

Answer 79

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 ⊝

Question 80

Total Peripheral Resistance

Answer 80

At a given mean systemic pressure (x-intercept) and RA pressure, changes in TPR → altered CO. * vasopressors ⊕ * exercise, AV shunt ⊝

Question 81

Pressure-Volume Loops

Answer 81

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

Question 82

Cardiac Cycle

Answer 82

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

Question 83

Heart Sounds

Answer 83

* _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.

Question 84

Jugular Venous Pulse (JVP)

Answer 84

* _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.

Question 85

Heart Sounds: Normal Splitting

Answer 85

* 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

Question 86

Heart Sounds: Wide Splitting

Answer 86

* 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

Question 87

Heart Sounds: Fixed Splitting

Answer 87

* 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

Question 88

Heart Sounds: Paradoxical Splitting

Answer 88

* 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)

Question 89

Auscultation of the Heart

Answer 89

Question 90

Besdside Maneuvers: * ↑ venous return to right atrium * ↑ intensity of right heart sounds

Answer 90

Inspiration

Question 91

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

Answer 91

Hand Grip

Question 92

Besdside Maneuvers: * ↓ intensity of most murmurs (including AS) * ↑ intensity of hypertrophic cardiomyopathy murmur * MVP: earlier onset of click/murmur

Answer 92

* Valsalva (phase II) * standing up (↓ preload)

Question 93

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

Answer 93

Rapid Squatting

Question 94

Systolic Murmurs

Answer 94

* Aortic/Pulmonic Stenosis * Mitral/Tricuspid Regurgitation * VSD * MVP * Hypertrophic Cardiomyopathy.

Question 95

Diastolic Murmurs

Answer 95

* Aortic/Pulmonic Regurgitation * Mitral/Tricuspid Stenosis

Question 96

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

Answer 96

Aortic Stenosis **SAD**: * **S**yncope * **A**ngina * **D**yspnea on exertion

Question 97

\_\_\_\_\_ are pulses that are weak with a delayed peak.

Answer 97

Pulsus Parvus et Tardus

Question 98

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

Answer 98

Mitral/Tricuspid Regurgitation

Question 99

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

Answer 99

Mitral Valve Prolapse

Question 100

Systolic Murmurs: * holosystolic, harsh-sounding murmur * loudest at tricuspid area

Answer 100

Ventricular Septal Defect

Question 101

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

Answer 101

Aortic Regurgitation

Question 102

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

Answer 102

Mitral Stenosis

Question 103

Continuous Murmurs: * machine-like murmur * best heard at left infraclavicular area * loudest at S2 * often due to congenital rubella or prematurity

Answer 103

Patent Ductus Arteriosus

Question 104

Myocardial Action Potential

Answer 104

* _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

Question 105

In contrast to skeletal muscle, cardiac muscle \_\_\_\_\_.

Answer 105

* 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

Question 106

Pacemaker Action Potential

Answer 106

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 I_f (“funny current”). If channels responsible for a slow, mixed Na⁺/K⁺ inward current; different from I_Na 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 I_f channels are open and thus ↑ HR.

Question 107

Conduction Pathway

Answer 107

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

Question 108

\_\_\_\_\_ “pacemaker” inherent dominance with slow phase of upstroke.

Answer 108

SA Node

Question 109

The AV node is located in the \_\_\_\_\_.

Answer 109

posteroinferior part of the interatrial septum

Question 110

\_\_\_\_\_ delay from the AV node allows time for ventricular filling.

Answer 110

100-msec

Question 111

Pacemaker Rates

Answer 111

SA \> AV \> bundle of His/Purkinje/ventricles

Question 112

Speed of Conduction

Answer 112

Purkinje \> atria \> ventricles \> AV node

Question 113

Electrocardiogram

Answer 113

* _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

Question 114

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

Answer 114

Torsades de Pointes

Question 115

Drug-Induced Long QT

Answer 115

**ABCDE**: * Anti**A**rrhythmics (class IA, III) * Anti**B**iotics (eg. macrolides) * Anti“**C**”ychotics (eg. haloperidol) * Anti**D**epressants (eg. TCAs) * Anti**E**metics (eg. ondansetron)

Question 116

Torsades de Pointes is treated with \_\_\_\_\_.

Answer 116

Magnesium Sulfate

Question 117

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

Answer 117

Congenital Long QT Syndrome

Question 118

Congenital Long QT Syndrome: * autosomal dominant * pure cardiac phenotype (no deafness)

Answer 118

Romano-Ward Syndrome

Question 119

Congenital Long QT Syndrome: * autosomal recessive * sensorineural deafness

Answer 119

Jervell and Lange-Nielsen Syndrome

Question 120

\_\_\_\_\_ 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).

Answer 120

Brugada Syndrome

Question 121

\_\_\_\_\_ 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.

Answer 121

Wolff-Parkinson-White Syndrome

Question 122

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

Answer 122

Atrial Fibrillation

Question 123

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

Answer 123

Atrial Flutter

Question 124

Dysrhythmias: * a completely erratic rhythm with no identifiable waves * fatal arrhythmia without immediate CPR and defibrillation

Answer 124

Ventricular Fibrillation

Question 125

AV Blocks: * the PR interval is prolonged (\> 200 msec) * benign and asymptomatic * no treatment required

Answer 125

First-Degree AV Block

Question 126

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)

Answer 126

Second-Degree AV Block Mobitz Type I (Wenckebach)

Question 127

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

Answer 127

Second-Degree AV Block Mobitz Type II

Question 128

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

Answer 128

Third-Degree (Complete) AV Block

Question 129

\_\_\_\_\_ 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.

Answer 129

Atrial Natriuretic Peptide

Question 130

\_\_\_\_\_ 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.

Answer 130

B-Type (Brain) Natriuretic Peptide

Question 131

Cardiovascular Receptors

Answer 131

* 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).

Question 132

Cardiovascular Baroreceptors

Answer 132

* 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.

Question 133

Cardiovascular Chemoreceptors

Answer 133

* 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.

Question 134

Normal Cardiac Pressures

Answer 134

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).

Question 135

Cardiovascular Autoregulation: Heart

Answer 135

Local Metabolites (Vasodilatory): * adenosine * NO * CO₂ * ↓ O₂

Question 136

Cardiovascular Autoregulation: Brain

Answer 136

Local Metabolites (Vasodilatory): CO₂ (pH)

Question 137

Cardiovascular Autoregulation: Kidneys

Answer 137

* Myogenic Feedback * Tubuloglomerular Feedback

Question 138

Cardiovascular Autoregulation: Lungs

Answer 138

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.

Question 139

Cardiovascular Autoregulation: Skeletal Muscle

Answer 139

**CHALK** (exercise): * **C**O₂ * **H**⁺, * **A**denosine * **L**actate * **K**⁺ At Rest: sympathetic tone

Question 140

Cardiovascular Autoregulation: Skin

Answer 140

Sympathetic stimulation is the most important mechanism for temperature control.

Question 141

Capillary Fluid Exchange

Answer 141

Starling Forces determine fluid movement through capillary membranes: * P_c = capillary pressure—pushes fluid out of capillary * P_i = interstitial fluid pressure—pushes fluid into capillary * π_c = plasma colloid osmotic (oncotic) pressure—pulls fluid into capillary * π_i = interstitial fluid colloid osmotic pressure—pulls fluid out of capillary * J_v = net fluid flow = K_f [(P_c − P_i) − σ(π_c − π_i)] * K_f = capillary permeability to fluid * σ = reflection coefficient (measure of capillary permeability to protein)

Question 142

Capillary Fluid Exchange: Edema

Answer 142

Excess fluid outflow into interstitium is commonly caused by: * ↑ capillary pressure (↑ P_c; eg. HF) * ↓ plasma proteins (↓ π_c; eg. nephrotic syndrome, liver failure, protein malnutrition) * ↑ capillary permeability (↑ K_f ; eg. toxins, infections, burns) * ↑ interstitial fluid colloid osmotic pressure (↑ π_i; eg. lymphatic blockage)

Question 143

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

Answer 143

R → L Shunts (Cyanotic) **R**ight-to-**L**eft Shunts: ea**RL**y cyanosis

Question 144

Congenital CHDs

Answer 144

The **5 T**s: 1. **T**runcus Arteriosus (**1** vessel) 2. **T**ransposition of the Great Ateries (**2** switched vessels) 3. **T**ricuspid Atresia (**3** = Tri) 4. **T**etralogy of Fallot (**4** = Tetra) 5. **T**APVR (**5** letters in the name)

Question 145

Congenital Heart Diseases: * fails to divide into pulmonary trunk and aorta due to lack of aorticopulmonary septum formation * most patients have accompanying VSD

Answer 145

Persistent Truncus Arteriosus

Question 146

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

Answer 146

D-Transposition of Great Vessels

Question 147

Congenital Heart Diseases: * absence of tricuspid valve and hypoplastic RV * requires both ASD and VSD for viability

Answer 147

Tricuspid Atresia

Question 148

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

Answer 148

Tetralogy of Fallot **PROV**e: * **P**ulmonary Infundibular Stenosis (most important determinant for prognosis) * **R**ight Ventricular Hypertrophy (RVH)—boot‑shaped heart on CXR * **O**verriding Aorta * **V**SD

Question 149

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

Answer 149

Total Anomalous Pulmonary Venous Return

Question 150

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

Answer 150

Ebstein Anomaly

Question 151

Congenital Heart Diseases: * acyanotic at presentation * cyanosis may occur years later

Answer 151

L → R Shunts (Acyanotic) **L**eft-to-**R**ight shunts: “**L**ate**R**” cyanosis

Question 152

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

Answer 152

Ventricular Septal Defect Frequency: VSD \> ASD \> PDA

Question 153

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)

Answer 153

Atrial Septal Defect Frequency: VSD \> ASD \> PDA

Question 154

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)

Answer 154

Patent Ductus Arteriosus Frequency: VSD \> ASD \> PDA

Question 155

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

Answer 155

Eisenmenger Syndrome

Question 156

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

Answer 156

Coarctation of the Aorta

Question 157

Congenital Cardiac Defect Associations: Fetal Alcohol Syndrome

Answer 157

* VSD * PDA * ASD * TOF

Question 158

Congenital Cardiac Defect Associations: Congenital Rubella

Answer 158

* PDA * PS * septal defects

Question 159

Congenital Cardiac Defect Associations: Down Syndrome

Answer 159

* CAVSD (Endocardial Cushion Defect) * VSD * ASD

Question 160

Congenital Cardiac Defect Associations: infant of diabetic mother

Answer 160

* TGA * VSD

Question 161

Congenital Cardiac Defect Associations: Marfan Syndrome

Answer 161

* MVP * Thoracic Aortic Aneurysm and Dissection * Aortic Regurgitation

Question 162

Congenital Cardiac Defect Associations: prenatal lithium exposure

Answer 162

Ebstein Anomaly

Question 163

Congenital Cardiac Defect Associations: Turner Syndrome

Answer 163

* Bicuspid Aortic Valve * Coarctation of Aorta

Question 164

Congenital Cardiac Defect Associations: Williams Syndrome

Answer 164

Supravalvular Aortic Stenosis

Question 165

Congenital Cardiac Defect Associations: 22q11 Syndromes

Answer 165

* Truncus Arteriosus * TOF

Question 166

Hypertension is defined as persistent \_\_\_\_\_.

Answer 166

* Systolic BP ≥ 140 mm Hg * Diastolic BP ≥ 90 mm Hg

Question 167

Risk Factors for Hypertension

Answer 167

* ↑ age * obesity * diabetes * physical inactivity * excess salt intake * excess alcohol intake * cigarette smoking * family history * African American \> Caucasian \> Asian

Question 168

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

Answer 168

1° (Essential)

Question 169

10% of hypertension is mostly 2° to \_\_\_\_\_.

Answer 169

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

Question 170

Hypertension: * ≥ 180/≥ 120 mm Hg * severe hypertension without acute end-organ damage

Answer 170

Hypertensive Urgency

Question 171

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

Answer 171

Hypertensive Emergency

Question 172

Hypertension predisposes to \_\_\_\_\_.

Answer 172

* CAD * LVH * HF * atrial fibrillation * aortic dissection * aortic aneurysm * stroke * chronic kidney disease (hypertensive nephropathy) * retinopathy

Question 173

Signs of Hyperlipidemia

Answer 173

* Xanthomas * Tendinous Xanthoma * Corneal Arcus

Question 174

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

Answer 174

Xanthomas

Question 175

Hyperlipidemia: lipid deposit in tendon, especially Achilles

Answer 175

Tendinous Xanthoma

Question 176

Hyperlipidemia: * lipid deposit in cornea * common in elderly (arcus senilis), but appears earlier in life with hypercholesterolemia

Answer 176

Corneal Arcus

Question 177

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

Answer 177

Arteriosclerosis

Question 178

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

Answer 178

Arteriolosclerosis

Question 179

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

Answer 179

Mönckeberg Sclerosis (Medial Calcific Sclerosis)

Question 180

Arteriosclerosis: * very common * disease of elastic arteries and large- and medium-sized muscular arteries * caused by buildup of cholesterol plaques

Answer 180

Atherosclerosis

Question 181

Location of Atherosclerosis

Answer 181

Abdominal aorta \> Coronary artery \> Popliteal artery \> Carotid artery “After I workout my **ab**s, I grab a **Corona** and **pop** my collar up to my **carotid**.”

Question 182

Risk Factors for Atherosclerosis:

Answer 182

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

Question 183

Symptoms of Atherosclerosis:

Answer 183

* angina * claudication * can be asymptomatic

Question 184

Progression of Atherosclerosis:

Answer 184

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

Question 185

Complications of Atherosclerosis:

Answer 185

* aneurysms * ischemia * infarcts * peripheral vascular disease * thrombus * emboli

Question 186

\_\_\_\_\_ 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.

Answer 186

Aortic Aneurysm

Question 187

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)

Answer 187

Abdominal Aortic Aneurysm

Question 188

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

Answer 188

Thoracic Aortic Aneurysm

Question 189

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

Answer 189

Traumatic Aortic Rupture

Question 190

\_\_\_\_\_ 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.

Answer 190

Aortic Dissection

Question 191

Aortic Dissection: * involves ascending aorta * may extend to aortic arch or descending aorta * may result in acute aortic regurgitation or cardiac tamponade * surgical treatment

Answer 191

Stanford Type A (Proximal) **A**scending

Question 192

Aortic Dissection: * involves only descending aorta (below ligamentum arteriosum) * treat medically with β-blockers, then vasodilators

Answer 192

Stanford Type B (Distal) **B**elow

Question 193

Ischemic Heart Disease Manifestations: * chest pain due to ischemic myocardium 2° to coronary artery narrowing or spasm * no myocyte necrosis

Answer 193

Angina

Question 194

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

Answer 194

Stable

Question 195

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)

Answer 195

Vasospastic (Prinzmetal or Variant)

Question 196

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

Answer 196

Unstable

Question 197

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

Answer 197

Coronary Steal Syndrome

Question 198

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

Answer 198

Sudden Cardiac Death

Question 199

Ischemic Heart Disease Manifestations: progressive onset of HF over many years due to chronic ischemic myocardial damage

Answer 199

Chronic Ischemic Heart Disease

Question 200

Ischemic Heart Disease Manifestations: * most often due to rupture of coronary artery atherosclerotic plaque → acute thrombosis * ↑ cardiac biomarkers (CK-MB, troponins) are diagnostic

Answer 200

Myocardial Infarction

Question 201

Myocardial Infarction: * transmural infarcts * full thickness of myocardial wall involved * Q waves

Answer 201

ST-Segment Elevation MI (STEMI)

Question 202

Myocardial Infarction: * subendocardial infarcts * subendocardium (inner 1⁄3) especially vulnerable to ischemia * ST depression on ECG

Answer 202

Non-ST-Segment Elevation MI (NSTEMI)

Question 203

Commonly Occluded Coronary Arteries

Answer 203

LAD \> RCA \> circumflex

Question 204

Symptoms of Myocardial Infarction

Answer 204

* diaphoresis * nausea * vomiting * severe retrosternal pain * pain in left arm and/or jaw * shortness of breath * fatigue

Question 205

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

Answer 205

0–24 hr

Question 206

Evolution of Myocardial Infarction: * extensive coagulative necrosis * tissue surrounding infarct shows acute inflammation with neutrophils * postinfarction fibrinous pericarditis

Answer 206

1–3 days

Question 207

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)

Answer 207

3–14 days

Question 208

Evolution of Myocardial Infarction: * contracted scar complete * Dressler syndrome, HF, arrhythmias, true ventricular aneurysm (risk of mural thrombus)

Answer 208

2 weeks to several months

Question 209

Diagnosis of Myocardial Infarction: gold standard in the first 6 hours

Answer 209

ECG

Question 210

Diagnosis of Myocardial Infarction: * rises after 4 hours * peaks at 24 hr * ↑ for 7–10 days * more specific than other protein markers

Answer 210

Troponin I

Question 211

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

Answer 211

CK-MB

Question 212

Diagnosis of Myocardial Infarction: ECG Changes

Answer 212

* 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)

Question 213

ECG Localization of STEMI: V₁–V₂

Answer 213

Anteroseptal (LAD)

Question 214

ECG Localization of STEMI: V₃–V₄

Answer 214

Anteroapical (distal LAD)

Question 215

ECG Localization of STEMI: V₅–V₆

Answer 215

Anterolateral (LAD or LCX)

Question 216

ECG Localization of STEMI: Lead I, aVL

Answer 216

Lateral (LCX)

Question 217

ECG Localization of STEMI: Lead II, III, aVF

Answer 217

Inferior (RCA)

Question 218

ECG Localization of STEMI: * V₇–V₉ * ST depression in V₁–V₃ with tall R waves

Answer 218

Posterior (PDA)

Question 219

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

Answer 219

Cardiac Arrhythmia

Question 220

Myocardial Infarction Complications: * occurs 1–3 days after MI * friction rub

Answer 220

Postinfarction Fibrinous Pericarditis

Question 221

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

Answer 221

Papillary Muscle Rupture

Question 222

Myocardial Infarction Complications: * occurs 3–5 days after MI * macrophage-mediated degradation → VSD → ↑ O₂ saturation and pressure in RV

Answer 222

Interventricular Septal Rupture

Question 223

Myocardial Infarction Complications: * occurs 3–14 days after MI * contained free wall rupture * ↓ CO * risk of arrhythmia * embolus from mural thrombus

Answer 223

Ventricular Pseudoaneurysm Formation

Question 224

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

Answer 224

Ventricular Free Wall Rupture

Question 225

Myocardial Infarction Complications: * occurs 2 weeks to several months after MI * outward bulge with contraction (“dyskinesia”) * associated with fibrosis

Answer 225

True Ventricular Aneurysm

Question 226

Myocardial Infarction Complications: * occurs several weeks after MI * autoimmune phenomenon resulting in fibrinous pericarditis

Answer 226

Dressler Syndrome

Question 227

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

Answer 227

LV Failure and Pulmonary Edema

Question 228

Treatment for Unstable Angina/NSTEMI

Answer 228

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

Question 229

Treatment for STEMI

Answer 229

* 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

Question 230

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)

Answer 230

Dilated Cardiomyopathy

Question 231

Causes of Dilated Cardiomyopathy

Answer 231

**ABCCCD**: * **A**lcohol abuse * wet **B**eriberi * **C**oxsackie B viral myocarditis * chronic **C**ocaine use * **C**hagas disease * **D**oxorubicin toxicity * hemochromatosis * sarcoidosis * thyrotoxicosis * peripartum cardiomyopathy

Question 232

Findings in Dilated Cardiomyopathy

Answer 232

* HF * S3 * systolic regurgitant murmur * dilated heart on echocardiogram * balloon appearance of heart on CXR

Question 233

Treatment for Dilated Cardiomyopathy

Answer 233

* Na+ restriction * ACE inhibitors * β-blockers * Diuretics * Digoxin * ICD * heart transplant

Question 234

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

Answer 234

Takotsubo Cardiomyopathy

Question 235

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

Answer 235

Hypertrophic Obstructive Cardiomyopathy

Question 236

Causes of Hypertrophic Obstructive Cardiomyopathy

Answer 236

* Autosomal Dominant * Chronic HTN * Friedreich Ataxia

Question 237

Findings in Hypertrophic Obstructive Cardiomyopathy

Answer 237

* S4 * systolic murmur * MR—due to impaired mitral valve closure

Question 238

Treatment for Hypertrophic Obstructive Cardiomyopathy

Answer 238

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

Question 239

Physiology of Hypertrophic Obstructive Cardiomyopathy

Answer 239

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

Question 240

Cardiomyopathies: * can have low voltage ECG despite thick myocardium (especially in amyloidosis) * \diastolic dysfunction ensues

Answer 240

Restrictive/Infiltrative Cardiomyopathy

Question 241

Restrictive/Infiltrative Cardiomyopathies

Answer 241

**P**uppy **LEASH**: * **P**ostradiation Fibrosis * **L**öffler Endocarditis * **E**ndocardial Fibroelastosis—thick fibroelastic tissue in endocardium of young children) * **A**myloidosis * **S**arcoidosis * **H**emochromatosis—although dilated cardiomyopathy is more common

Question 242

Cardiomyopathies: * associated with hypereosinophilic syndrome * histology shows eosinophilic infiltrates in myocardium

Answer 242

Löffler Endocarditis

Question 243

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

Answer 243

Heart Failure

Question 244

Signs and Symptoms of Heart Failure

Answer 244

* Signs: * S3 heart sound * rales * jugular venous distention (JVD) * pitting edema * Symptoms: * dyspnea * orthopnea * fatigue

Question 245

Heart Failure: * reduced EF * ↑ EDV * ↓ contractility often 2° to ischemia/MI or dilated cardiomyopathy

Answer 245

Systolic Dysfunction

Question 246

Heart Failure: * preserved EF * normal EDV * ↓ compliance (↑ EDP) often 2° to myocardial hypertrophy

Answer 246

Diastolic Dysfunction

Question 247

Right HF most often results from \_\_\_\_\_.

Answer 247

Left HF

Question 248

\_\_\_\_\_ refers to isolated right HF due to pulmonary cause.

Answer 248

Cor Pulmonale

Question 249

\_\_\_\_\_ ↓ mortality from heart failure.

Answer 249

* ACE Inhibitors * Angiotensin II Receptor Blockers * β-Blockers (except in acute decompensated HF) * Spironolactone

Question 250

\_\_\_\_\_ relieve symptoms from heart failure.

Answer 250

* Thiazides * Loop Diuretics

Question 251

\_\_\_\_\_ improve symptoms and mortality from heart failure.

Answer 251

* Hydralazine * Nitrates

Question 252

Left Heart Failure: * shortness of breath when supine * ↑ venous return from redistribution of blood (immediate gravity effect) exacerbates pulmonary vascular congestion

Answer 252

Orthopnea

Question 253

Left Heart Failure: * breathless awakening from sleep * ↑ venous return from redistribution of blood, reabsorption of peripheral edema, etc.

Answer 253

Paroxysmal Nocturnal Dyspnea

Question 254

Left Heart Failure: * ↑ pulmonary venous pressure → pulmonary venous distention and transudation of fluid * presence of hemosiderin-laden macrophages (“HF” cells) in lungs

Answer 254

Pulmonary Edema

Question 255

Right Heart Failure: * nutmeg liver * ↑ central venous pressure → ↑ resistance to portal flow * rarely, leads to “cardiac cirrhosis”

Answer 255

Hepatomegaly

Question 256

Right Heart Failure: ↑ venous pressure

Answer 256

Jugular Venous Distention

Question 257

Right Heart Failure: ↑ venous pressure → fluid transudation

Answer 257

Peripheral Edema

Question 258

\_\_\_\_\_ 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.

Answer 258

Shock

Question 259

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

Answer 259

Hypovolemic Shock

Question 260

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

Answer 260

Cardiogenic Shock

Question 261

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

Answer 261

Obstructive Shock

Question 262

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)

Answer 262

Distributive Shock

Question 263

Bacterial Endocarditis: * *S. aureus* (high virulence) * large vegetations on previously normal valves * rapid onset

Answer 263

Acute

Question 264

Bacterial Endocarditis: * Viridans Streptococci (low virulence) * smaller vegetations on congenitally abnormal or diseased valves * sequela of dental procedures * gradual onset

Answer 264

Subacute

Question 265

Symptoms of Bacterial Endocarditis

Answer 265

Bacteria **FROM JANE**: * **F**ever—most common * **R**oth Spots—round white spots on retina surrounded by hemorrhage * **O**sler Nodes—tender raised lesions on finger or toe pads due to immune complex deposition * **M**urmur * **J**aneway Lesions—small, painless, erythematous lesions on palm or sole * **A**nemia * **N**ail-Bed Hemorrhage—splinter hemorrhages * **E**mboli

Question 266

Bacterial endocarditis is associated with \_\_\_\_\_.

Answer 266

* glomerulonephritis * septic arterial or pulmonary emboli

Question 267

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

Answer 267

* malignancy * hypercoagulable state * lupus

Question 268

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

Answer 268

* *Coxiella burnetti* * *Bartonella* spp. * HACEK * *Haemophilus* * *Aggregatibacter* (formerly *Actinobacillus*) * *Cardiobacterium* * *Eikenella* * *Kingella*

Question 269

The _____ is most frequently involved in bacterial endocarditis.

Answer 269

Mitral Valve

Question 270

Tricuspid valve endocarditis is associated with \_\_\_\_\_ and bacteria such as \_\_\_\_\_.

Answer 270

* IV Drug Abuse (don’t “**tri**” **drugs**) * *S. aureus* * *Pseudomonas* * *Candida*

Question 271

Bacterial Endocarditis: colon cancer

Answer 271

*S. bovis (gallolyticus)*

Question 272

Bacterial Endocarditis: prosthetic valves

Answer 272

*S. epidermidis*

Question 273

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

Answer 273

Rheumatic Fever

Question 274

Rheumatic fever affects the _____ valves.

Answer 274

Mitral \> Aortic \>\> Tricuspid \*high-pressure valves are affected the most

Question 275

Rheumatic fever presents with mitral \_\_\_\_\_.

Answer 275

* Mitral Regurgitation—early lesion * Mitral Stenosis—late lesion

Question 276

Rheumatic fever is associated with \_\_\_\_\_.

Answer 276

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

Question 277

Pathogenesis of Rheumatic Fever

Answer 277

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

Question 278

Findings in Rheumatic Fever

Answer 278

**J♥NES** (major criteria): * **J**oint (migratory polyarthritis) * **♥** (carditis) * **N**odules in Skin (subcutaneous) * **E**rythema Marginatum (evanescent rash with ring margin) * **S**ydenham Chorea

Question 279

Treatment and prophylaxis for rheumatic fever is \_\_\_\_\_.

Answer 279

Penicillin

Question 280

\_\_\_\_\_ 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.

Answer 280

Acute Pericarditis

Question 281

ECG changes in acute pericarditis include \_\_\_\_\_.

Answer 281

* widespread ST-segment elevation * PR depression

Question 282

Acute pericarditis is caused by \_\_\_\_\_.

Answer 282

* 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

Question 283

\_\_\_\_\_ 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).

Answer 283

Myocarditis

Question 284

Causes of Myocarditis

Answer 284

* _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

Question 285

Complications of Myocarditis

Answer 285

* sudden death * arrhythmias * heart block * dilated cardiomyopathy * HF * mural thrombus with systemic emboli

Question 286

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

Answer 286

Cardiac Tamponade

Question 287

Findings in Cardiac Tamponade

Answer 287

* 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)

Question 288

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

Answer 288

Pulsus Paradoxus

Question 289

\_\_\_\_\_ 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.

Answer 289

Syphilitic Heart Disease

Question 290

Vasculitides: Large-Vessel Vasculitis

Answer 290

* Giant Cell (Temporal) Arteritis * Takayasu Arteritis

Question 291

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

Answer 291

Giant Cell (Temporal) Arteritis

Question 292

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

Answer 292

Takayasu Arteritis

Question 293

Vasculitides: Medium-Vessel Vasculitis

Answer 293

* Polyarteritis Nodosa * Kawasaki Disease (Mucocutaneous Lymph Node Syndrome) * Buerger Disease (Thromboangiitis Obliterans)

Question 294

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

Answer 294

Polyarteritis Nodosa

Question 295

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

Answer 295

Kawasaki Disease (Mucocutaneous Lymph Node Syndrome) **CRASH** and **burn**. * **C**onjunctival injection * **R**ash (polymorphous → desquamating) * **A**denopathy (cervical) * **S**trawberry tongue (oral mucositis) * **H**and-foot changes (edema, erythema) * **fever**

Question 296

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

Answer 296

Buerger Disease (Thromboangiitis Obliterans)

Question 297

Vasculitides: Small-Vessel Vasculitis

Answer 297

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

Question 298

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

Answer 298

Granulomatosis with Polyangiitis (Wegener)

Question 299

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

Answer 299

Microscopic Polyangiitis

Question 300

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

Answer 300

Behçet Syndrome

Question 301

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

Answer 301

Eosinophilic Granulomatosis with Polyangiitis (Churg-Strauss)

Question 302

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)

Answer 302

Immunoglobulin A Vasculitis

Question 303

The most common heart tumor is a \_\_\_\_\_.

Answer 303

Metastasis

Question 304

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

Answer 304

Myxoma

Question 305

Cardiac Tumors: * most frequent 1° cardiac tumor in children (associated with tuberous sclerosis) * Histology: hamartomatous growths

Answer 305

Rhabdomyomas

Question 306

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

Answer 306

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

Question 307

\_\_\_\_\_ 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

Answer 307

Hereditary Hemorrhagic Telangiectasia

Question 308

Hypertension Treatment: Primary (Essential) Hypertension

Answer 308

* Thiazide Diuretics * ACE Inhibitors * Angiotensin II Receptor Blockers (ARBs) * Dihydropyridine Ca²⁺ Channel Blockers

Question 309

Hypertension Treatment: Hypertension with Heart Failure

Answer 309

* 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.

Question 310

Hypertension Treatment: Hypertension with Diabetes Mellitus

Answer 310

* ACE Inhibitors * ARBs * Ca²⁺ Channel Blockers * Thiazide Diuretics * β-Blockers ACE inhibitors/ARBs are protective against diabetic nephropathy.

Question 311

Hypertension Treatment: Hypertension in Asthma

Answer 311

* 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.

Question 312

Hypertension Treatment: Hypertension in Pregnancy

Answer 312

**H**e **l**ikes **m**y **n**eonate. * Hydralazine * Labetalol * Methyldopa * Nifedipine

Question 313

Calcium Channel Blockers

Answer 313

* Amlodipine * Clevidipine * Nicardipine * Nifedipine * Nimodipine (dihydropyridines, act on vascular * smooth muscle) * Diltiazem * Verapamil (non-dihydropyridines, act on heart)

Question 314

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

Answer 314

Calcium Channel Blockers * Vascular Smooth Muscle * Amlodipine = Nifedipine \> Diltiazem \> Verapamil * Heart * Verapamil \> Diltiazem \> Amlodipine = Nifedipine (**verapamil** = **ventricle**)

Question 315

Calcium Channel Blockers: * hypertension * angina (including Prinzmetal) * Raynaud phenomenon

Answer 315

Dihydropyridines (except Nimodipine)

Question 316

Calcium Channel Blockers: subarachnoid hemorrhage (prevents cerebral vasospasm)

Answer 316

Nimodipine

Question 317

Calcium Channel Blockers: hypertensive urgency or emergency

Answer 317

* Nicardipine * Clevidipine

Question 318

Calcium Channel Blockers: * hypertension * angina * atrial fibrillation/flutter

Answer 318

Non-Dihydropyridines

Question 319

Adverse Effects of Calcium Channel Blockers

Answer 319

* _Non-Dihydropyridine_: cardiac depression, AV block, hyperprolactinemia, constipation, gingival hyperplasia * _Dihydropyridine_: peripheral edema, flushing, dizziness.

Question 320

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

Answer 320

Hydralazine

Question 321

Hypertensive emergency is treated with \_\_\_\_\_.

Answer 321

* Clevidipine * Fenoldopam * Labetalol * Nicardipine * Nitroprusside

Question 322

Hypertensive Emergency: * short acting * ↑ cGMP via direct release of NO * can cause cyanide toxicity (releases cyanide)

Answer 322

Nitroprusside

Question 323

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

Answer 323

Fenoldopam

Question 324

Nitrates

Answer 324

* Nitroglycerin * Isosorbide Dinitrate * Isosorbide Mononitrate

Question 325

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

Answer 325

Nitrates

Question 326

Antianginal Therapy

Answer 326

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

Question 327

Antianginal Therapy: * ↓ End-Diastolic Volume * ↓ Blood Pressure * no effect on Contractility * ↑ Heart Rate—reflex response * ↓ Ejection Time * ↓ MVO₂

Answer 327

Nitrates

Question 328

Antianginal Therapy: * no effect or ↑ End-Diastolic Volume * ↓ Blood Pressure * ↓ Contractility * ↓ Heart Rate * ↑ Ejection Time * ↓ MVO₂

Answer 328

β-Blockers

Question 329

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

Answer 329

Nitrates + β-Blockers

Question 330

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

Answer 330

Ranolazine

Question 331

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

Answer 331

Milrinone

Question 332

Lipid-Lowering Agents

Answer 332

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

Question 333

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)

Answer 333

HMG-CoA Reductase Inhibitors * Lovastatin * Pravastatin

Question 334

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

Answer 334

Bile Acid Resins * Cholestyramine * Colestipol * Colesevelam

Question 335

Lipid-Lowering Agents: * ↓↓ LDL * ↑/— HDL * ↓/— TGs * prevents cholesterol absorption at small intestine brush border * rarely ↑ LFTs * causes diarrhea

Answer 335

Ezetimibe

Question 336

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)

Answer 336

Fibrates * Gemfibrozil * Bezafibrate * Fenofibrate

Question 337

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

Answer 337

Niacin (Vitamin B3)

Question 338

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

Answer 338

PCSK9 Inhibitors * Alirocumab * Evolocumab

Question 339

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)

Answer 339

Digoxin

Question 340

Adverse Effects of Digoxin

Answer 340

* 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)

Question 341

Antidote to Digoxin

Answer 341

* slowly normalize K⁺ * cardiac pacer * Anti-Digoxin Fab Fragments * Mg²⁺

Question 342

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])

Answer 342

Class I (Sodium Channel Blockers)

Question 343

Class IA Antiarrhythmics

Answer 343

The **Queen** **Proc**laims **Diso**’s **pyramid**. * **Quin**idine * **Proc**ainamide * **Disopyramid**e

Question 344

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

Answer 344

Class IA

Question 345

Class IB Antiarrhythmics

Answer 345

**I**’d **B**uy **Lid**dy’s **Mexi**can **T**acos. * **Lid**ocaine * **Mexi**le**T**ine

Question 346

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

Answer 346

Class IB

Question 347

Class IC Antiarrhythmics

Answer 347

“**C**an **I** have **F**ries, **P**lease.” * **F**lecainide * **P**ropafenone

Question 348

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

Answer 348

Class IC

Question 349

Class II Antiarrhythmics

Answer 349

β-Blockers * Metoprolol * Propranolol * Esmolol * Atenolol * Timolol * Carvedilol

Question 350

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

Answer 350

Class II (β-Blockers) * Esmolol—very short acting * Metoprolol—dyslipidemia * Propranolol—exacerbate vasospasm in Prinzmetal angina

Question 351

Class III Antiarrhythmics

Answer 351

Potassium Channel Blockers **AIDS**: * **A**miodarone * **I**butilide * **D**ofetilide * **S**otalol

Question 352

Antiarrhythmics: * ↑ AP duration, ↑ ERP, ↑ QT interval * used in atrial fibrillation, atrial flutter, and ventricular tachycardia (amiodarone, sotalol)

Answer 352

Class III (Potassium Channel Blockers) * Sotalol—torsades de pointes, excessive β blockade * Ibutilide—torsades de pointes

Question 353

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

Answer 353

Amiodarone

Question 354

Class IV Antiarrhythmics

Answer 354

Calcium Channel Blockers * Verapamil * Diltiazem

Question 355

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)

Answer 355

Class IV (Calcium Channel Blockers)

Question 356

Antiarrhythmics: * ↑ K⁺ out of cells → hyperpolarizing the cell and ↓ I_Ca, 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

Answer 356

Adenosine

Question 357

Antiarrhythmics: * torsades de pointes * digoxin toxicity

Answer 357

Mg²⁺

Question 358

Cardiac Drugs: * selective inhibition of funny sodium channels (I_f), 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

Answer 358

Ivabradine