Cardiovascular Flashcards

Question

Derivative of allantosis

Answer 1

becomes the urachus, which is part of the allantoic duct between bladder and umbilicus. The umbilicus becomes the median umbilical ligament.

Answer 2

Ligamentum arteriosum

Answer 3

Ligamentum venosum

Answer 4

Fossa ovalis

Answer 5

nucleus pulposus

Answer 6

Medial umbilical ligaments

Answer 7

Ligamentum teres hepatis. It is contained in falciform ligament.

Answer 8

There are two main coronary arteries, the left coronary artery (LCA) and right coronary artery (RCA). Coronary blood flow peaks in early diastole.

Answer 9

LCA originates from the left aortic sinus and bifurcates into: LAD (left anterior descending) artery, which gives off superficial (diagonal) and multiple deep (septal perforator) branches. LCX (left circumflex) artery

Answer 10

RCA originates from right aortic sinus and splits into: Right marginal branch. PDA (posterior descending artery). SA nodal artery

Answer 11

The artery that supplies the posterior descending artery (PDA) determines the coronary dominance: Right dominant: the RCA supplies the PDA (85% of population). Left dominant: the LCX (Left circumflex branch of LCA) supplies the PDA (8% of population). Co-dominant: the PDA arises from both the LCX and the RCA (7% of population)

Answer 12

The Left Circumflex Branch (LCX) of the Left Coronary Artery (LCA) supplies: Posterolateral wall of left ventricle and anterolateral papillary muscle

Answer 13

The Left anterior descending branch (LAD) of the left coronary artery (LCA): Anterior wall of left ventricle, anterior 2/3 of the interventricular septum, anterolateral papillary muscle. This is the most common site for occlusion.

Answer 14

In most people, the right coronary artery (RCA) supplies: Right atrium and ventricle (inferior walls), left ventricle (diaphragmatic surface), posterior 1/3 of the interventricular septum, SA node, and AV node (in right-dominant individuals). Infarct may cause nodal dysfunction (bradycardia or heart block).

Answer 15

The posterior descending/interventricular artery (PDA) supplies: Posterior 1/3 of interventricular septum, posterior walls of ventricles, and posteromedial papillary muscle

Answer 16

the most posterior part of the heart is the left atrium; 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).

Answer 17

CO = SV x HR. Whereby: CO = cardiac output, SV = stroke volume. SV is a function of contractility and preload. HR = heart rate. Using Fick’s principle: CO = (VO2) / (Ca – Cv) Whereby: CO = cardiac output, VO2 = oxygen consumption (ml/min), Ca = oxygen content of arterial blood, Cv = oxygen content of mixed venous blood. During the early stages of exercise, CO is maintained by an increase in HR only (SV plateaus). Diastole is preferentially shortened with an increase in HR, leading to a decrease in filling time, decreasing CO (eg ventricular tachycardia).

Answer 18

MAP = CO x TPR. Technically, MAP = (CO x TPR) + CVP. However, CVP is usually quite low compared to MAP, so this can be approximated as MAP = CO x TPR. MAP = mean arterial pressure; TPR = total peripheral resistance; CVP = central venous pressure. MAP ≈ diastolic pressure + 1/3 pulse pressure or, alternatively, MAP ≈ 2/3 diastolic pressure + 1/3 systolic pressure

Answer 19

Pulse pressure = systolic pressure – diastolic pressure. Pulse pressure is directly proportional to stroke volume. A higher stroke volume, such as in aortic regurgitation, will exhibit a high pulse pressure (high systolic and low diastolic measurements). An increase in pulse pressure occurs in hyperthyroidism, aortic regurgitation, aortic stiffening (isolated systolic hypertension in the elderly), obstructive sleep apnea (an increase in sympathetic tone), exercise (transient). A decrease in pulse pressure is seen in aortic stenosis, cardiogenic shock, cardiac tamponade, advanced heart failure.

Answer 20

SV=end-diastolic volume (EDV) - end stystolic volume (ESV). Stroke volume is affected by contractility, afterload, and preload (SV CAP). There is an increase of SV with an increase in contractility (eg anxiety, exercise, and pregnancy), an increase in preload, and a decrease in afterload. A failing heart has a decrease in SV (systolic and/or diastolic dysfunction).

Answer 21

Contractility is the intrinsic ability of cardiac muscle to develop force at a given muscle length. Also know as inotropism. Contractility is related to the intracellular Ca2+ concentration and can be estimated using the ejection fraction (stroke volume/end-diastolic volume). An increased HR leads to an increase in action potential frequency. This leaves less time for the Na/K ATPase to pump Na out of the cell and the Na/Ca exchanger becomes less effective. As a result, more Ca enters the myocardial cells during the plateau and more Ca is released from the sarcoplasmic reticulum, resulting in greater myocardial contractility. Cardiac glycosides (digitalis) -> increase the force of contraction by inhibiting Na+, K+-ATPase in the myocardial membrane. An increase in intracellular Na+ leads to decreased activity of the Na+-Ca2+ exchanger which is responsible for bringing sodium ions into the cell and removing Ca2+. This leads to increased Ca2+ and thus increased contractility. Contractility (and SV) decrease with beta 1 blockade (a decrease in cAMP), HF with systolic dysfunction, acidosis, hypoxia/hypercapnia (a decrease in PO2/an increase in PCO2), non-dihydropyridine Ca channel blockers.

Answer 22

Myocardial O2 demand increases with an increase in contractility, afterload (proportional to arterial pressure), heart rate, diameter of ventricle (increase in wall tension).

Answer 23

Wall tension=(pressure x radius)/(2 x wall thickness).

Answer 24

Preload is approximated by ventricular EDV. It depends on venous tone and circulating blood volume. vEnodilators (eg nitroglycerin) decreases prEload.

Answer 25

Afterload is approximated by MAP. An increase in afterload causes there to be an increase in pressure, which increases wall tension. LV compensates for an increase in afterload by thickening (hypertrophy) in order to decrease wall tension. vAsodilators (eg hydrAlAzine) decrease Afterload (Arterial). ACE inhibitors and ARBs decrease both preload and afterload. Chronic hypertension (an increase in MAP) causes LV hypertrophy.

Answer 26

EF=SV/EDV=(EDV-ESV)/EDV. Left ventricular EF is an index of ventricular contractility. Normal EF is greater than 55%. EF decreases in systolic HF. EF is normal in diastolic HF.

Answer 27

The Starling curve describes the increase in cardiac output (or stroke volume) in response to increase in venous return/preload or end-diastolic volume. The Starling Curve is based on a length – tension relationship. Increased end diastolic volume causes an increased ventricular fiber length, with resultant increase in developed tension/pressure. Up and left shift of Starling curve (increase in contractility): Increased HR (due to exercise, etc.); Sympathetic stimulation or ß1 sympathomimetic agonists; Increased intracellular calcium. Downward shift of the Starling curve is caused by negative inotropes such as beta blockers (carvedilol, metoprolol) and calcium channel blockers (verapamil, diltiazem). Congestive heart failure shifts the Starling curve down and to the right.

Answer 28

ΔP = Q*R, where P = pressure, Q = blood flow, R = resistance. Flow (Q) remains constant, so the equation can be rearranged to: Q = ΔP/R. (In this case, ΔP represents the difference in arterial blood pressure before and after the arterioles.) Since flow is constant, ΔP must increase when resistance increases

Answer 29

TR=R1+R2+R3...

Answer 30

1/TR=1/R1+1/R2+1/R3...

Answer 31

The cardiac function curve depicts the Frank-Starling relationship for the ventricle, and shows that cardiac output is a function of end-diastolic volume. The vascular function (venous return) curve depicts the relationship between blood flow through the vascular system (venous return) and right atrial pressure. When combining the cardiac output and venous return curves the intersection is known as the equilibrium, or steady state point. This is the operating point of the heart.

Answer 32

Positive inotropic agents result in a shift of the curve to a higher cardiac output and a correspondingly lower right atrial pressure. Negative inotropic agents or pathological conditions such as heart failure lead to decreased cardiac output and a higher right atrial pressure.

Answer 33

Changes in blood volume or venous capacitance change the venous return curve, and causes an increase in both cardiac output and right atrial pressure. An increase in blood volume or decrease in venous capacitance, such as a transfusion or exercise, increase mean systemic pressure, shifting the venous return curve to the right. A new equilibrium point is reached, and both cardiac output and right atrial pressure are increased. A decrease in blood volume or increase in venous capacitance, such as hemorrhage, decrease mean systemic pressure, and the venous return curve shifts to the left. At the new equilibrium point both cardiac output and right atrial pressure are decreased.

Answer 34

Changes in total peripheral resistance alter both curves simultaneously, however the mean systemic pressure remains constant. Increasing total peripheral resistance causes a decrease in both the cardiac output and venous return curves. A counterclockwise rotation of the venous return curve occurs. The increased total peripheral resistance leads to decreased venous return as the blood is retained on the arterial side. A downward shift of the cardiac output curve is a result of increased aortic pressure (increased afterload) as the heart has to pump against a higher pressure. Decreasing total peripheral resistance causes an increase in both cardiac output and venous return. A clockwise rotation of the venous return curve occurs. Decreased total peripheral resistance results in more blood being able to flow back to the heart from the arterial side. An upward shift of the cardiac output curve is caused by the decreased aortic pressure (decreased afterload).

Answer 35

Isovolumetric contraction (3 to 5). At point 3, the cycle is at end diastole with the mitral valve closed; LV has been filled by the EDV. The ventricles begin contraction when the mitral valve closes and before the aortic valve opens (point 5), the period of highest O2 consumption.

Answer 36

Systolic ejection (5 to 7). At point 5, aortic valve opens and the total stroke volume is ejected into the aorta. The ventricle volume decreases, but the ventricular pressure continues to increase until near the very end of this phase. At point 7 , the pressure drop causes the aortic valve to close. The width of the pressure-volume loop is measured graphically to represent the stroke volume. The volume remaining in the LV at point 7 is end systolic volume.

Answer 37

Isovolumetric relaxation (7 to 1). After point 7, the ventricle begins to relax. Since all the valves are closed again, the ventricular volume is constant (isovolumetric) in this phase.

Answer 38

Ventricular filling (1 to 3). At point 1, the mitral valve opens and the filling of the ventricles begins. Initially, a rapid filling period begins which is followed by a reduced filling.

Answer 39

Increased preload leads to an increase in ventricular end-diastolic volume and results from increased venous return. This, in turn, results in an increase in stroke volume based on the Frank-Starling relationship. Since increased preload causes increased stroke volume, this results in an increased width of the pressure-volume loop.

Answer 40

Increased afterload requires the ventricle to pump against a higher pressure, decreasing stroke volume. This decreased stroke volume leaves more blood left in the heart after each contraction, and results in an increase in end-systolic volume. The decrease in stroke volume from increased afterload is reflected in decreased width and increased height of the pressure–volume loop.

Answer 41

With increased contractility the ventricle is able to develop greater tension than usual during systole, causing an increase in stroke volume. This results in a decrease in end-systolic volume.

Answer 42

The cardiac cycle is the process of cardiac filling and ejection, and is often visualized with electrocardiography or jugular venous pressure readings. Atrial systole is the activation of the atria, pumping atrial blood into the ventricles. Isovolumetric ventricular contraction happens when the ventricles contract before the aortic and pulmonic valves open; it is the period of highest O2 consumption. Rapid ventricular ejection is the period of ventricular contraction after the aortic and pulmonic valves have opened, when the ventricles are ejecting blood into the pulmonic and systemic circulations. Reduced ventricular ejection follows rapid ventricular ejection and results from decreased ventricular volume. This follows the length-tension relationship described by the Frank-Starling equation, where contraction strength is directly related to the load; therefore, a decreased volume would translate into a decreased load, which means less contraction strength and reduced ventricular ejection. Isovolumetric ventricular relaxation is the period between the aortic valve closing and the mitral valve opening. Rapid ventricular filling happens when the atrial pressure equals the ventricular pressure. It starts when the mitral and tricuspid valves open.

Answer 43

The first heart sound (S1) is the sound of the atrioventricular (tricuspid and mitral) valves closing; it occurs at the beginning of isovolumetric ventricular contraction.

Answer 44

The second heart sound (S2) is the sound of the aortic and pulmonic valves closing. Normally, the aortic valve closes before the pulmonic, which may result in “splitting” of the second heart sound, typically during inspiration.

Answer 45

The third heart sound (S3) results from blood sloshing against the ventricular walls during the middle third of diastole. In children and pregnant women the third heart sound may be normal. In adults it is associated with increased filling pressure from a dilated ventricle, and is considered pathological.

Answer 46

The fourth heart sound (S4) is a low frequency diastolic sound that occurs during the late diastolic filling phase (the atrial kick). It results from an atrial kick filling a ventricle with decreased compliance, often seen in left ventricular hypertrophy. S4 is heard before S1. It is sometimes heard in the elderly due to a stiff ventricle. When loud, it is indicative of a pathological state, generally a hypertrophic left ventricle. The trough is where the aortic valve closed, and the following "bump" in pressure results from aortic pressure recoil against a closed aortic valve. This bump is also known as the dicrotic wave.

Answer 47

“a” wave — increase in right atrial pressure during atrial contraction (i.e., atrial systole). Absent “a” wave is characteristic of atrial fibrillation due to a lack of coordinated atrial contraction

Answer 48

“c” wave — increase in right atrial pressure during right ventricular isovolumic systole (contraction); due to bulging of the tricuspid valve into the right atrium.

Answer 49

“x” descent — decrease in right atrial pressure following the peak of the “c” wave due to atrial relaXation. Absent “x” descent — tricuspid regurgitation. Backflow of blood into the right atrium during systole prevents relaxation of right atrial pressure. (may see a positive wave)

Answer 50

“v” wave — increase in right atrial pressure during late ventricular systole due to right atrial filling against a closed tricuspid valve. Peak of “v” wave usually corresponds with (or occurs just after) the T wave on EKG.

Answer 51

“y” descent — decrease in right atrial pressure following the peak of the “v” wave; due to tricuspid valve opening and right atrium emptYing

Answer 52

Inspiration causes a drop in intrathoracic pressure, increasing venous return. This causes an increase in RV filling, which increases RV stroke volume. This increases RV ejection time and delayed closure of pulmonic valve. A decrease in pulmonary impedance (an increase in capacity of the pulmonary circulation) also occurs during inspiration, which contributes to delayed closure of pulmonic valve.

Answer 53

This is seen on conditions that delay RV emptying (eg pulmonic stenosis, right bundle branch block). Delay in RV emptying causes delayed pulmonic sound (regardless of breath). It is an exaggeration of normal splitting

Answer 54

It is seen in ASD. ASD leads to left to right shunt, which increase RA and RV volumes, causing there to be an increase in flow through the pulmonic valve such that, regardless of breath, pulmonic closure is greatly delayed.

Answer 55

It is seen in conditions that delay aortic valve closure (eg aortic stenosis, left bundle branch block). This causes a reversal of the normal order of valve closure is reversed so that P2 sound occurs before delated A2 sound. Therefore on inspiration, P2 closes later and moves closer to A2, thereby paradoxically eliminating the split.

Answer 56

The aortic valve is best heard in the 2nd intercostal space at the upper right sternal border. Systolic murmur: aortic stenosis, aortic valve sclerosis. Diastolic murmur: aortic regurgitation (heard best at left lower sternal border at third and fourth intercostal spaces)

Answer 57

The pulmonic valve is best hears in the 2nd intercostal space at the upper left sternal border. Systolic ejection murmur: pulmonic stenosis. Flow murmur: atrial septal defect. Diastolic murmur: pulmonic regurgitation. ASD commonly presents with a pulmonary flow murmur (an increase flow through pulmonary valve) and a diastolic rumble (an increase flow across tricupsid); blood flow across the actual ASD does not cause a murmur because there is no significant pressure gradient. The murmur later progresses to a louder diastolic murmur of pulmonic regurgitation from dilation of the pulmonary artery.

Answer 58

The tricuspid valve is best heard at the lower left sternal border. Pansystolic murmur: tricuspid regurgitation, ventricular septal defect. Diastolic murmur: tricuspid stenosis, atrial septal defect

Answer 59

The mitral valve is best heard in the 5th intercostal space at the left midclavicular line. Systolic murmur: mitral regurgitation. Diastolic murmur: mitral stenosis

Answer 60

It increases venous return to right atrium. It increases the intensity of right heart sounds.

Answer 61

It increases afterload. It increases the intensity of MR, AR, and VSD murmurs. It decreases hypertrophic cardiomyopathy murmurs. MVP will have a later onset of click/murmur.

Answer 62

This decreases preload. It decreases intensity of most murmurs (including AS). It increases the intensity of hypertrophic cardiomyopathy murmur. It will also cause an earlier onset of click/murmur of MVP.

Answer 63

This increases venous return and preload. This decreases the intensity of hypertrophic cardiomyopathy murmur. It also increases the intensity of AS murmur. It also causes there to be a later onset of click/murmur of MVP.

Answer 64

includes aortic/pulmonic stenosis, mitral/tricuspid regurgitation, VSD, and MVP.

Answer 65

includes aortic pulmonic regurgitation, mitral/tricuspid stenosis.

Answer 66

Aortic stenosis causes a pansystolic crescendo-decrescendo murmur heard loudest in the second intercostal space at the right sternal border, which often radiates to the carotid arteries or can be auscultated at the clavicles. The murmur increases in intensity with maneuvers that increase preload (e.g. leg-raising) and decreases in intensity with maneuvers that decrease preload (e.g. Valsalva) or increase afterload (e.g. isometric hand-squeezing). Aortic stenosis is associated with an S4 heart sound. Physical exam may reveal pulsus parvus et tardus (weak peripheral pulses with a maximal intensity peak that is late relative to the heartbeat) due to the slowed emptying of left ventricle to the systemic circulation. It can lead to Syncope, Angina, and Dyspnea on exertion (SAD). It is often due to age related calcification or early-onset calcification of bicuspid aortic valve.

Answer 67

Holosystolic, high-pitched "blowing murmur". It is the loudest at the apex and radiates toward the axilla. MR is often due to ischemic heart disease (post-MI), MVP, LV dilation. It can also be caused by rheumatic fever and infective endocarditis.

Answer 68

Holosystolic, high-pitched "blowing murmur". It is the loudest at the tricuspid area and radiates to the right sternal border. TR is commonly caused by RV dilatation. It can also be caused by rheumatic fever and infective endocarditis.

Answer 69

On auscultation a mid-to-late systolic click which varies with maneuvers (earlier with decreased left ventricular end-diastolic volume (LVEDV), later with increased LVEDV) and a soft late systolic murmur of mitral regurgitation are appreciated that is the loudest right before S2. Standing and valsalva decrease preload, reducing the LVEDV and relieving the cordae tendinae of some tension. This makes the click occur earlier in systole. Squatting increases preload, augmenting the LVEDV and placing greater tension on the cordae tendinae. This makes the click occur later in systole. It is the most frequent valvular lesion. It is usually benign but can predispose to infective endocarditis. It can be caused by myxomatous degneration (primary or secondary to connective tissue disease such as Marfan or Ehlers-Danlos syndrome), rheumatic fever, chordae rupture.

Answer 70

Holosystolic, harsh sounding murmur. Loudest at the tricuspid.

Answer 71

Aortic regurgitation causes a high-pitched diastolic murmur, often with a blowing quality, beginning immediately after A2. It may decrescendo or persist throughout diastole, and is enhanced by the patient leaning forward and holding his breath at end-expiration. There is a long diastolic murmur and signs of hyperdynamic pulse when severe and chronic. It is often due to aortic root dilation, bicuspid aortic valve, endocarditis, rheumatic fever. It can progress to left HF.

Answer 72

On auscultation a low-pitched diastolic rumble with an opening snap (due to abrupt halt in leaflet motion in diastole, after rapid opening due to fusion of leaflet tips) just after the second heart sound is heard best at the fourth intercostal space, midclavicular line, with the patient in left lateral decubitus position. The time between the opening snap and the second heart sound decreases as the stenosis becomes more severe. Patients may have a loud first heart sound by comparison. LA pressure is much greater than LV pressure during diastole. It often occurs secondary to rheumatic fever. Chronic MS can result in LA dilation.

Answer 73

A patent ductus arteriosus has a classic “machine-like” continuous murmur that distinguishes it from other heart conditions. It is loudest at S2. It is often due to congenital rubella or prematurity. It is best heard at the left infraclavicular area.

Answer 74

Action potentials in myocytes in ventricles, atria, and Purkinje fibers have 5 phases named Phase 0 to 4. These cell types have a resting membrane potentials of about -90 mV. The resting membrane potential is determined by conductance to K+ and it approaches the K+ equilibrium potential.

Answer 75

Phase 0 is the upstroke of the action potential. It is caused by an increase in Na+ conductance. Fast voltage gated Na+ channels open (Na+ influx) and the membrane potential approaches the Na+ equilibrium potential.

Answer 76

Phase 1 is the initial repolarization. Na channels have a decrease in conductance, and voltage gated K+ channels begin to open. Activation of voltage gated K+ channels results in transient repolarization that explains the small dip before the plateau. This occurs before the calcium channels open.

Answer 77

Phase 2 is the plateau of the action potential. It is caused by an increased Ca2+ conductance through L type voltage gated Ca2+ channels, balanced by an K+ efflux through leaky K+ channels. Ca2+ flows into the cell and K+ flows out. Ca2+ influx induces Ca2+ release from the sarcoplasmic reticulum causing myocyte contraction.

Answer 78

Phase 3 is the rapid repolarization. It is caused by a massive K+ efflux due to the opening of voltage-gated slow K+ channels and closure of voltage-gated Ca2+ channels. Subsequent large outward K+ current hyperpolarizes the membrane.

Answer 79

Phase 4 is the resting membrane potential. Inward and outward currents are equal again, and membrane potential approaches K+ equilibrium potential again.

Answer 80

Cardiac muscle action potential has a plateau, which is due to Ca influx and K efflux; myocyte contraction occurs due to Ca induced Ca release from the sarcoplasmic reticulum. Cardiac nodal cells spontaneously depolarize during diastole, resulting is automaticity due to If channels (funny current channels responsible for a slow mixed Na/K inward current). Cardiac myocytes are electrically coupled to wach other by gap junctions.

Answer 81

Action potential in SA and AV nodes differ from the ventricular action potential. They have only 3 phases. Phase 1 and Phase 2 are not present in the SA/AV node action potentials

Answer 82

Phase 0 – upstroke of action potential. Opening of slow voltage gated Ca channels. This differs from ventricular action potential, which has a fast upstroke that is dependent on Na current. The slower conduction velocity allows AV node time to transmit action potential from atria to ventricles. This delay allows the atria time to empty before ventricles contract.

Answer 83

Phase 3 – repolarization. Ca channels are inactivated which result in a K efflux from activation of K channels

Answer 84

Phase 4 – slow depolarization. Accounts for the pacemaker automaticity. In pacemaker cells, phase 4 of the action potential is characterized by spontaneous depolarization due to increased inward Na conductance, known as the pacemaker (“funny”) current. The funny current controls the rate of spontaneous activity of sinoatrial myocytes and hence the cardiac rate. In contrast to phase 4 of pacemaker action potentials, phase 4 of ventricular cardiomyocyte (ie, nonpacemaker) action potentials is characterized by K equilibrium, with no spontaneous inward Na conductance.

Answer 85

Atrial depolarization. Atrial repolarization is masked by QRS complex.

Answer 86

It is the time from start of atrial depolarization to start of ventricular depolarization (normally less then 200 msec).

Answer 87

The QRS complex represents ventricular depolarization, which is normally

Answer 88

The QT interval represents ventricular depolarization, mechanical contraction of the ventricles, and ventricular repolarization and is affected by serum Ca2+ levels: Hypocalcemia prolongs the QT interval. Hypercalcemia shortens the QT interval

Answer 89

The T wave marks ventricular repolarization. T-wave inversion may indicate recent MI.

Answer 90

The junction between the end of QRS complex and start of ST segment.

Answer 91

The ST segment is isoelectric in a normal heart since it represents a period where the ventricles are depolarized and there are no currents towards the leads of the ECG.

Answer 92

It is caused by hypokalemia and bradycardia

Answer 93

From highest speed to lowest: Purkinje, atria, ventricles, and AV node.

Answer 94

SA, than AV, than bundle of his/purkinje/ventricles.

Answer 95

SA node to atria to AV node to commun bundle to bundle branches, to fasicles to purkinje fibers to ventricles.

Answer 96

SA node is the pacemaker due to inherent dominance with slow phase of upstroke.

Answer 97

AV node is located in the posterioinferior part of the interatrial septum. Blood supply usually from RCA. 100 msec delay allows time for ventricular filling.

Answer 98

Polymorphic ventricular tachycardia characterized by shifting sinusoidal waveforms on ECG. It can progress to ventricular fibrillation. Long GT interval predisposes to torsades de pointes. It can be caused by drugs, a decrease in K, a decrease in Mg, or other abnormalities. Treament includes magnesium sulfate. Drugs that prolong QT (ABCDE): AntiArrhythmics (Class IA, III), AntiBiotics (e.g., macrolides), Anti"C"ychotics (e.g., haloperidol), AntiDepressants (e.g., TCAs), and AntiEmetics (e.g., ondansetron)

Answer 99

An inherited disorder of myocardial repolarization, typically due to ion channel defects. There is an increase risk of sudden cardiac death due to torsade de pointes. Types include Romano Ward and syndrome Jervell and Lange-Nielsen syndrome.

Answer 100

A congenital long QT syndrome. It is autosomal dominant, pure cardiac phenotype (no deafness).

Answer 101

A congenital long QT syndrome. It is autosomal recessive with sensorineural deafness.

Answer 102

Brugada syndrome is a genetic disorder of cardiac sodium channels that leads to an increased risk of ventricular tachyarrhythmias and sudden cardiac death. Brugada syndrome is an autosomal dominant disorder most common in Asian males. ST segment elevation >2mm in >1 of V1-V3 followed by a negative T wave is the only ECG abnormality that is potentially diagnostic in Brugada syndrome. The only proven therapy for Brugada syndrome is an implantable cardioverter-defibrillator (ICD).

Answer 103

Wolff-Parkinson-White syndrome is a pre-excitation syndrome wherein an extra conduction pathway/accessory pathway (aka the bundle of Kent) leads to arrhythmias marked by the characteristic delta wave with shortened PR interval on ECG. Symptoms range from asymptomatic, to palpitations and vague complaints, to sudden death from tachyarrhythmias that prevent ventricular filling. Wolff-Parkinson White syndrome is diagnosed by ECG with a: Shortened PR interval; Widened QRS complex; Delta wave (which signifies early ventricular depolarization).

Answer 104

Chaotic and erratic baseline (irregularly irregular) with no discrete P waves in between irregularly spaced QRS complexes. It is associated with hypertension, coronary artery disease (CAD), rheumatic heart disease, binge drinking (holiday heart), HG, valvular disease, hyperthyroidism. It can result in atrial stasis and lead to cardioembolic events. Treatment includes antithrombotic therapy (eg warfarin), rate control (beta-blockers, non-dihydropyridine Ca channel blocker, digoxin), rhythm control (class Ic or III antiarrhythmics), and/or cardioversion (pharmacological or electrical).

Answer 105

A rapid succession of identical, back to back atrial depolarization waves. The identical appearance accounts for the sawtooth appearance of the flutter waves. Management similar to atrial fibrillation (rate contol, anticoagulation, cardioversion). Definitive treatment is catheter ablation.

Answer 106

A completely erratic rhythm with no identifiable waves. Fatal arrhythmia without immediate CPR and defibrillation.

Answer 107

The PR interval is prolonged (over 200 msec). It is benign and asymptomatic. No treatment is required.

Answer 108

There are progressive lengthening of PR interval until a beat is dropped (a P wave is not followed by QRS complex). It is usually asymptomatic. Variable RR interval with a pattern (regularly irregular).

Answer 109

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. It is often treated with a pacemaker.

Answer 110

The atria and ventricles beat independently of each other. Both P waves and QRS complexes are present, although the P waves bear no relation to the QRS complexes. Atrial rate is faster than ventricular rate. It is usually treated with pacemaker. Lyme disease can result in 3rd degree heart block.

Answer 111

It is released from atrial myocytes in response to an increase in blood volume and atrial pressure. It acts via cGMP. It causes vasodilation and a decrease in Na reabsorption at the renal collecting tubule. It dilates afferent renal arterioles and constricts efferent arterioles, promoting diuresis and contributing to aldosterone escape mechanism.

Answer 112

It is released from ventricular myocytes in response to increase tension. There are similar physiologic action to ANP, with longer half life. BNP blood test used for diagnosing HF (very good negative predictive value). It is available in recombinant form (nesiritide) for treatment of HF.

Answer 113

The two important peripheral locations of baroreceptors in the body are the carotid sinus and the aortic arch. The aortic arch contains both baroreceptors and chemoreceptors, while the carotid sinus contains just baroreceptors. The carotid body is the other location of the peripheral chemoreceptors. The receptors in the aortic arch transmit information via the vagus nerve and those in the carotid sinus via the glossopharyngeal nerve. They both go to the solitary nucleus of the medulla.

Answer 114

The purpose of a “carotid massage” is to decrease heart rate (HR). This is a vagal response to increasing pressure on the carotid sinus, which leads to: Increased stretch; Increased baroreceptor firing; Increased AV node refractory period; and Decreased HR

Answer 115

The Cushing reflex is a physiologic response to increased intracranial pressure. The 3 responses are: Increased blood pressure; Bradycardia; Respiratory depression. During the Cushing reflex, the increased intracranial pressure causes compression of cerebral arterioles and cerebral ischemia (increased cerebral PCO2). This leads to an increase in sympathetic stimulation in order to increase perfusion pressure (blood pressure). The baroreceptors sense this increased BP and induce bradycardia.

Answer 116

The chemoreceptors in the carotid and aortic bodies respond to: Decreased PO2 (less than 60 mmHg, primary stimulus), Increased PCO2, Decreased blood pH. In response to a decrease in PO2 as seen in respiratory arrest or circulatory shock, firing of peripheral chemoreceptors leads to an increase in sympathetic firing and decrease in parasympathetic output. This is in contrast to local mediators of blood pressure where low PO2 leads to vasodilation. This induces the following cardiovascular responses: Vasoconstriction, Increased sympathetic outflow to the heart, Increased arterial pressure

Answer 117

Normal inferior vena cava and right atrial pressure is less than 5 mmHg.

Answer 118

Normal right ventricular pressure is ~ 25/5 mmHg.

Answer 119

The normal mean pulmonary artery pressure is ~ 25/10 mmHg. Pulmonary hypertension occurs when the mean pulmonary artery pressure is ≥ 25 mmHg at rest.

Answer 120

Normal left atrial pressure is less than 12. PCWP approximates left atrial pressure. It should be measured at end expiration, since this is the closest to zero intrathoracic pressure. In mitral stenosis, pulmonary capillary wedge pressure is greater than left ventricular diastolic pressure.

Answer 121

Normal left ventricular pressure is ~ 130/10 mmHg.

Answer 122

Normal aortic pressure is ~ 130/90 mmHg.

Answer 123

Local metabolites (vasodilatory): adenosine, NO, CO2, a decrease in O2.

Answer 124

Local metabolites (vasodilatory): CO2 (pH)

Answer 125

myogenic and tubuloglomerular feedback

Answer 126

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

Answer 127

Local metabolites during exercise include lactate, adenosine, K, H, and CO2. At rest, it is regulated by sympathetic tone.

Answer 128

Sympathetic stimulation is the most important mechaism for temperature control.

Answer 129

Starling forces determine fluid movement through the capillary membranes. Capillary pressure (Pc) pushes fluid out of the capillary. Interstitial fluid pressure (Pi) pushes fluid into the capillary. Plasma colloid osmotic pressure (PIc) pulls fluid into the capillary. Interstitial fluid colloid osmotic pressure (PIi) pull fluid out of capillary. Net fluid flow (Jc)= Kf[(Pc-Pi)-zeta(PIc-PIi)]. Where Kf=permeability of capillary to fluid, zeta=permeability of capillary to protein.

Answer 130

Occurs when there is excess fluid outflow into interstitium commonly caused by an increase in capillary pressure (eg heart failure), a decrease in plasma proteins (eg nephrotic syndrome or liver failure), increase in capillary permeability (eg toxins, infections, burns), an increase in interstitial fluid colloid osmotic pressure (eg lymphatic blockage).

Answer 131

These cause early cyanosis (blue babies). It is often diagnosed prenatally or become evident immediately after birth. It usually require urgent surgical correction and/or maintenance of a PDA. The 5 T's: truncus arteriosus (1 vessel), transposition (2 switched vessels), tricuspid atresia (3=tri), tetralogy of Fallot (4=tetra), and TAPVR (5 letters in the name).

Answer 132

Causes right to left shunt and "blue baby". The truncus arteriosus fails to divide into pulmonary trunk and aorta due to a lack of aorticopulmonary septum formation. Most patients will have an accompanying VSD.

Answer 133

Causes right to left shunt and "blue baby". The aorta leaves the RV (anteriorly) and the pulmonary trunk leaves the LV (posteriorly) causes there to be a separation of systemic and pulmonary circulation. It is not compatible with life unless a shunt is present to allow mixing of blood (eg VSD, PDA or patent foramen ovale). It is due to failure of the aorticopulmonary septum to spiral. Without surgical intervention, most infants will die within the first few months of life.

Answer 134

Causes right to left shunt and "blue baby". It is the absence of tricuspid valve and hypoplastic RV. It requires both an ASD and a VSD for viability.

Answer 135

Causes right to left shunt and "blue baby". It is caused by anterosuperior displacement of the infundibular septum. It is the most common cause of early childhood cyanosis. The four parts include: 1. Pulmonary infundibular stenosis (the most important determinant for prognosis), 2. Right ventricular hypertrophy (RVH), which creates a boot shaped heart on CXR, 3. Overriding aorta, 4. VSD. (PROVe) The pulmonary stenosis forces a right to left flow across the VSD, leading to early cyanotic "tet spells" and RVH. Squatting increase systemic vascular resistance, thereby decreasing right to left shunt and improves cyanosis. Treatment is early surgical correction.

Answer 136

Causes right to left shunt and "blue baby". It is due to pulmonary veins draining into right side of heart circulation (SVC, coronary sinus, etc). It is associated with ASD and sometimes PDA to allow for right to left shunting to maintain cardiac output.

Answer 137

It causes late cyanosis (blue kids). In order of highest to lowest frequency: VSD, ASD, PDA. Right to Left shunts=eaRLy cyanosis. Left to Right shunts= LateR cyanosis.

Answer 138

It is a left to right shunt causing late cyanosis (blue kids). It is the most common congenital cardiac defect. It is asymptomatic at birth, but may manifest weeks later or remain asymptomatic throughout life. Most self resolve. Larger lesions may lead to LV overload and HF.

Answer 139

It is a left to right shunt causing late cyanosis (blue kids). It is due to a defect in interatrial septum. It causes a loud S1 and a wide fixed split S2. Ostium secundum defects are the most common and usually occur as an isolated finding. Ostium primum defects are rarer, yet usually occur with other cardiac anomalies. Symptoms range from none to HF. It is distinct from patent foramen ovale in that septa are missing tissue rather than unfused.

Answer 140

In the fetal period, shunting from right to left is normal. In the neonatal period, a decrease in lung resistance causes shunting to switch to left to right, which can cause progressive RVH and/or LVH and HF. It is associated with a continuous machine like murmur. Patency is maintained by PGE synthesis and low O2 tension. Uncorrected PDA can eventually result in late cyanosis in the lower extremities (differential cyanosis). Indomethacin (ENDomethacin) ends patency of PDA. PGE KEEps it open (which may be necessary to sustain life in conditions such as transposition of the great vessels). PDA is normal in utero and normally closes only after birth.

Answer 141

Uncorrected left to right shunt (VSD, ASD, PDA) can lead to an increase in pulmonary blood flow causing pathologic remodeling of vasculature, which leads to pulmonary arterial hypertension. RVH occurs to compensate and eventually shunt switches from right to left. It causes late cyanosis, clubbing, and polycythemia. Age of onset varies.

Answer 142

Aortic narrowing near insertion of ductus arteriosus (juxtaductal). It is associated with bicuspid aortic valve, other heart defects, and Turner syndrome. It can cause hypertension in the upper extremities and weak, delayed pulse in the lower extremities (brachial femoral delay). With age, collateral arteries erode ribs (notched appearance on CXR).

Answer 143

VSD, PDA, ASDm tetralogy of Fallot

Answer 144

Septal defects, PDA, pulmonary artery stenosis

Answer 145

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

Answer 146

Transposition of great vessels.

Answer 147

MVP, thoracic aortic aneurysm and dissection, aortic regurgitation.

Answer 148

Ebstein anomaly

Answer 149

Bicuspid aortic valve and coarctation of aorta

Answer 150

Supravalvular aortic stenosis

Answer 151

Truncus arteriosus and tetralogy of fallot

Answer 152

It is defines as persistent systolic BP over 140 and/or diastolic BP over 90 mmHG. 90% of hypertension is primary (essential) and related to increase in cardiac output or total peripheral resistance. The remaining 10% is moslty secondary to renal/renovascular disease (eg fibromuscular dysplasia, usually found in younger women) and primary hyperaldosteronism.

Answer 153

Increase in age, obesity, diabetes, physical inactivity, excess salt intake, excess alcohol intake, family history, blacks more than whites more than Asians.

Answer 154

Severe hypertension (above 180/120) without acute end organ damage.

Answer 155

Severe hypertension (above 180/120) with evidence of acute end organ damage (eg encephalopathy, stroke, retinal hemorrhages and exudates, papilledema, MI, HF, aortic dissection, kidney injury, microangiopathic hemolytic anemia, eclampsia.

Answer 156

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

Answer 157

Renal arterial hyalinosis on PAS stain

Answer 158

renal artery stenosis, can cause secondary hypertension. Renal artery have a string of beads appearance.

Answer 159

Plaques or nodules composed of lipid laden histiocytes in skin, especially in the eyelids (xanthelasma). Seen with hyperchylomicronemia

Answer 160

Lipid deposit in tendon, especially Achilles. Seen with familial hypercholesterolemia

Answer 161

Lipid deposit in cornea. It is common in elderly (arcus snilis), but appears earlier in life in hypercholestrolemia.

Answer 162

Hardening of arteries, with arterial wall thickening and loss of elasticity.

Answer 163

A type of arteriosclerosis. It is common, affects small arteries and arterioles. Two types: hyaline (thickening of vessel walls in essential hypertension or diabetes mellitus) and hyperplastic (onion skinning: in severe hypertension with proliferation of smooth muscle cells).

Answer 164

A type of arteriosclerosis. It is uncommon It affects medium sized arteries. Calcification of elastic lamina of arteries causes vascular stiffening without obstruction. Pipestem appearance on x-ray. It does not obstruct blood flow; intima is not involved.

Answer 165

It is very common. Disease of elastic arteries and large and medium sized muscular arteries; a form of arteriosclerosis caused by buildup of cholesterol plaques.

Answer 166

Modifiable risk factors include smoking, hypertension, hyperlipidemia, diabetes. Nonmodifiable risk factors include age, sex, (increased in men and postmenopausal women), family history.

Answer 167

Inflammation plays a major role in pathogenesis. Endothelial cell dysfunction causes macrophage and LDL accumulation, causing foam cell formation, creating fatty streaks. Smooth muscle cells than migrate (involving PDGF and FGF), which proliferate and increase extracellular matrix deposition. This creates a fibrous plaque, which creates a complex artheroma.

Answer 168

Aneurysms, ischemia, infarcts, peripheral vascular disease, thrombus, emboli.

Answer 169

From most common to least: abdominal aorta, coronary artery, popliteal artery, carotid artery.

Answer 170

Angina, claudication, but can be asymptomatic.

Answer 171

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

Answer 172

It is associated with atherosclerosis. Risk factors include history of tobacco use, increased age, male sex, family history. It may present as palpable pulsatile abdominal mass.

Answer 173

It is associated with cystic medial degeneration. Risk factors include hypertension, bicuspid aortic valve, connective tissue disease (eg marfan syndrome). Also historically associated with tertiary syphilis (obliterative endarteritis of the vasa vasorum).

Answer 174

Longitudinal intimal tear forming a false lumen. It is associated with hypertension, bicuspid aortic valve, inherited connective tissue disorders (eg Marfan syndrome). It can present with tearing chest pain, with sudden onset, radiating to the back with or without markedly unequal BP in arms. CXR shows mediastinal widening. It can result in rupture, pericardial tamponade, and death. There are two types: Stanford type A (proximal) and Stanford type B (distal)

Answer 175

Stanford type A (proximal) involves Ascending aorta. It may extend to aortic arch or descending aorta. Treatment is surgery.

Answer 176

Stanford type B (distal) involves the descending aorta and/or aortic arch. No ascending aorta involvement. Treat medically with beta-blockers, then vasodilators.

Answer 177

Chest pain due to ischemic myocardium secondary to coronary artery narrowing or spasm. No myocyte necrosis.

Answer 178

It is usually secondary to atherosclerosis, exertional chest pain in classic distribution (usually with ST depression on ECG), resolving with rest or nitroglycerin

Answer 179

It occurs at rest secondary to atherosclerosis. There is exertional chest pain in classic distribution (usually with ST depression on ECG). Known triggers include tobacco, cocaine, and triptans but trigger is often unknown. Treat with Ca channel blockers, nitrates, and smoking cessation (if applicable).

Answer 180

Thrombosis with incomplete coronary artery occlusion. It occurs with or without ST depression and.or T wave inversion on ECG but no cardiac biomarker elevation (unlike NSTEMI). There is an increase in frequency or intensity of chest pain or any chest pain at rest.

Answer 181

It occurs distal to coronary stenosis, vessels are maximally dilated at baseline. Administration of vasodilators (eg dipyridamole, regadenoson) dilates normal vessels and shunts blood toward well-perfused areas causes a decrease flow and ischemia in poststenotic region. This is the principle behind pharmacologic stress tests.

Answer 182

Most often due to acute thrombosis due to rupture of coronary artery athersclerotic plaque. If transmural, ECG may show ST elevations (STEMI). If it is subendocardial, ECG may show ST depressions (NSTEMI). Cardiac biomarkers are diagnostic.

Answer 183

Death from cardia causes within 1 hour of onset of symptoms, most commonly due to a lethal arrhythmia eg ventricular fibrillation). It is associated with CAD (up to 70% of cases), cardiomyopathy (hypertrophic, dilated), and hereditary ion channelopathies (eg long QT syndrome, Brugada syndrome).

Answer 184

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

Answer 185

From most common to least: LAD, RCA, circumflex

Answer 186

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

Answer 187

There are no gross and microscopic changes visible in this time period. Complications include arrhythmia, HF, and cardiogenic shock.

Answer 188

Visible grossly, there is visibly an occluded artery with infarct, appearing as dark mottling or pale with tetrazolium stain. Microscopically, there is early coagulative necrosis, release of necrotic cell contents into blood. There is also edema, hemorrhage, wavy fibers.. Neutrophils appear at this time. Reperfusion injury may cause contraction bands (due to free radical damage). Complications at this time include arrhythmia, HF, cardiogenic shock.

Answer 189

Grossly there is hyperemia (an excess of blood in the vessels). Microscopically, there is extensive coagulative necrosis. Tissue surrounding infarct shows acute inflammation with neutrophils. Complications at this point include postinfarction fibrinous pericarditis.

Answer 190

Grossly, there is a hyperemic border, central yellow-brown softening with maximally yellow and soft by 10 days. Microscopically, there are macrophages then granulation tissue at margins. Complications at this time include free wall rupture, leading to tamponade. Papillary muscle rupture can also occur leading to mitral regurgitation. Interventicular septal rupture due to macrophage mediated structural degradation is also possible. There is also a risk of LV pseudoaneurysm, which runs the risk of rupture.

Answer 191

Grossly, there are recanalized artery with gray-white tissue. Microscopically, the contracted scar is complete. Complications at this time includes Dressler syndrome, HF, arrhythmias, true ventricular aneurysm (risk of mural thrombus).

Answer 192

In the first 6 hours, ECG is the gold standar. Cardiac troponin I rises after four hours and is increased for 7-10 days. It is more specific than other protein markers. CK-MB rises after 6-12 hours and is predominantly found in myocardium but can also be released from skeletal muscle. It is useful in diagnosing reinfarction following acute MI because levels return to normal after 48 hours. ECG changes can include ST elevation (STEMI, transmural infarct), ST depression (NSTEMI, subendocardial infarct), hyperacute (peaked) T waves, T wave inversion, new left bundle branch block, and pathologic Q waves or poor R wave progression (evolving or old transmural infarct).

Answer 193

It effects the entire wall. There is necrosis. ST elevation on ECG and Q waves.

Answer 194

It is due to ischemic necrosis of less than 50% of ventricle wall. The subendocardium especially vulnerable to ischemia. There is ST depression on ECG.

Answer 195

Elevated or Q waves V1-V2

Answer 196

Elevated or Q waves V3-V4

Answer 197

Elevated or Q waves V5-V6

Answer 198

Elevated or Q waves I, aVL

Answer 199

Elevated or Q waves II, III, aVF (inFerior)

Answer 200

Cardiac arrhythmia is an important cause of death before reaching the hospital. It is common in the first few days. LV failure and pulmonary edema. Cardiogenic shock (large infarct has a higher risk of mortality). Ventricular free wall rupture, which can lead to cardiac tamponade. Papillary muscle rupture, which can lead to severe mitral regurgitation. Interventricular septum rupturem which can cause VSD. The greatest risk is about 3-14 days post MI (as with rupture). True ventricular aneurysm is an outward bulge during contraction (dyskinesia), associated with fibrosis and arises two weeks to several months after MI. Postinfarction fibrinous pericarditis causes a friction rub 1-3 days post MI.

Answer 201

An autoimmune phenomenon resulting in fibrinous pericarditis (several weeks post MI)

Answer 202

Anticoagulation (eg heparin), antiplatelet therapy (eg aspirin plus clopidogrel), beta blockers, ACE inhibitors, statins. Symptoms control with nitroglycerin and morphine.

Answer 203

In addition to treatment for NSTEMI, reperfusion therapy is the most important (percutaneous coronary intervention preferred over fibrinolysis).

Answer 204

It is the most common cardiomyopathy (90% of cases). It is often idiopathic or familial. Other etiologies include chronic Alcohol abuse, wet Beriberi, Coxsackie B virus myocarditis, chronic Cocaine use, Chagas disease, Doxorubicin toxicity, hemochromatosis, sarcoidosis, peripartum cardiomyopathy (ABCCCD). Findings include HF, S3, systolic regurgitant murmur, dilated heart on echocardiogram, balloon appearance of heart on echocardiogram, balloon appearance of heart on CXR. Treatment includes NA restriction, ACE inhibitors, beta-blockers, diuretics, digoxin, ICD, heart transplant. Systolic dysfunction ensues. Eccentric hypertrophy (sarcomeres added in series).

Answer 205

60-70% of cases are familial, autosomal dominant (commonly a beta-myosin heavy-chain mutation). It can be associated with Friedreich ataxia. It causes syncope during exercise and may lead to sudden death in young athletes due to ventricular arrhythmia. Findings include S4, systolic murmur. There may be mitral regurgitation due to impaired mitral valve closure. Treatment includes cessation of high intensity athletics, use of beta blocker or non dihydropyridine Ca channel blockers (eg verapamil). ICD if patient is high risk. Diastolic dysfunction ensures. There is marked ventricular hypertrophy, often septal predominance. Myofibrillar disarray and fibrosis. Obstructive hypertrophic cardiomyopathy (subset) causes asymmetric septal hypertrophy and systolic anterior motion of mitral valve, causing outflow obstruction, leading to dyspnea and possible syncope.

Answer 206

Major causes include sarcoidosis, amyloidosis, postradiation fibrosis, endocardial fibroelastosis (thick fibroelatic tissue in endocardium of young children). Loffler syndrome (endomyocardial fibrosis with a prominent eosinophilic infiltrate), and hemochromatosis (dilated cardiomyopathy can also occur). Diastolic dysfunction ensures. It can have low voltage ECG despite thick myocardium (especially amyloid).

Answer 207

Clinical syndrome of cardiac pump dysfunction causing congestion and low perfusion. Symptoms include dyspnea, orthopnea, fatigue. Signs include rales, JVD, pitting edema. Systolic dysfunction causes reduced EF, increase EDV. There is a decrease in compliance often secondary to myocardial hypertrophy. Right HF most often results from left HF. Isolated right HF is usually due to cor pulmonale. ACE inhibitors or angiotensin II receptor blockers (except in acute decompensated HF), and spironolactone decreases mortality. Thiazide or loop diuretics are used mainly for symptomatic relief. Hydralazine with nitrate therapy improves both symptoms and mortality in select patients.

Answer 208

Seen with left heart failure. Shortness of breath when supine. An increase in venous return from redistribution of blood (immediate gravity effect) exacerbates pulmonary vascular congestion.

Answer 209

Seen with left heart failure. Brathless awakening from sleep. An increase in venous return from redistribution of blood and reabsorption of edema, etc.

Answer 210

Seen with left heart failure. Increase in pulomonary venous pressure causes pulmonary venous distention and transudation of fluid. Presence of hemosiderin laden macrophages (HF cells) in lungs.

Answer 211

Seen with right heart failure. An increase in central venous pressure causes increase resistance to portal flow. Rarely, leads to cardiac cirrhosis.

Answer 212

Seen with right heart failure. Increase in venous pressure

Answer 213

Seen with right heart failure. An increase in venous pressure causes fluid transudation.

Answer 214

It is caused by hemorrhage, dehydration, and burns. Skin is cold and clammy. CVP (preload) in greatly decreased. Cardiac output is decreased. SVR (afterload) is increased. Treatment includes IV fluids.

Answer 215

It is caused by acute MI, HF, valvular dysfunction, arrhythmia. Skin is cold and clammy. CVP (preload) is increased. Cardiac output is greatly decreased. SVR (afterload) is increased. Treatment is inotropes, diuresis.

Answer 216

It is caused by cardiac tamponade, PE. Skin is cold and clammy. CVP (preload) is increased. Cardiac output is greatly decreased. SVR (afterload) is increased. Treatment is relief of obstruction.

Answer 217

It is caused by sepsis, CNS injury, anaphylaxis. Skin is warm and dry. CVP (preload) is decreased. Cardiac output is increased. SVR (afterload) is greatly decreased. Treatment includes pressors and IV fluids.

Answer 218

SIRS (Systemic Inflammatory Response Syndrome) is a clinical condition related to sepsis characterized by dysregulated inflammatory response to an infectious or noninfectious process. A patient must meet two or more of the following criteria to be diagnosed with SIRS: HR over 90 bpm; Temperature below 36°C (96.8°F) or over 38°C (100.4°F); WBC count below 4,000 cells/mm3 or over 12,000 cells/mm3 or 10% bandemia; Respiratory rate over 20 or PaCO2 below 32 mmHg.

Answer 219

Presentation includes fever (most common symptom), new murmur, Roth spots (round white spots on the retina surrounded by hemorrhage), Osler nodes (tender raised lesions on finger pads and toe pads), Janeway lesions (small painless, erthematous lesions on palm or sole), glomerulonephritis, septic arterial or pulmonary emobli, splinter hemorrhages on nail bed. (Bacteria FROM JANE: Fever, Roth spots, Osler nodes, Murmur, Janeway lesions, Anemia, Nail bed hemorrhage, and emboli.). Multiple blood cultures are necessary for diagnosis. Mitral valve is most frequently involved.

Answer 220

S. aureus (high virulence). There is rapid onset. There are large vegetations on previously normal valves.

Answer 221

Viridans streptococci (low virulence). There are smaller vegetations on congenitally abnormal or diseased valves. It can be a sequela of dental procedures. It has a gradual onset.

Answer 222

S. bovis (gallolyticus)

Answer 223

S. epidermidis

Answer 224

It can be marantic/thrombotic, secondary to malignancy, hypercoagulable state, or lupus.

Answer 225

It is associated tricuspid valve endocarditis (don't tri drugs). It is associated with S. aureus, Pseudomonas, and Candida.

Answer 226

Most likely Coxiella burnetii, Bartonella spp., HACEK (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella).

Answer 227

It is a consequence of pharyngeal infection with group A beta-hemolytic streptococci. Late sequelae include rheumatic heart disease, which affects heart valves (from most common to least: mitral, aortic, tricuspid (high pressure valves are the most affected). Early lesion causes mitral valve regurgitation; late lesion causes mitral stenosis. It is associated with Aschoff bodies (granuloma with giant cells), Anitschkow cells (enlarged macrophages with ovoid, wavy, rod-like nucleus), increased anti-streptolysin O (ASO) titers. It is immune mediated (type II hypersensitivity) and not due to a direct effect of bacteria. Antibodies to M protein cross-react with self antigens (molecular mimicry). Treatment/ prophylaxis includes penicillin. Jones criteria includes: Joint (migratory polyarthritis), o=heart (carditis), Nodules in skin (subcutaneous), Erythema marginatum, Sydenham chorea.

Answer 228

It commonly presents with sharp pain, aggravated by inspiration, and relieved by sitting up and leaning forward. It presents with friction rub. ECG changes include widespread ST-segment elevation and/or PR depression. Causes include idiopathic (most common and is presumed to be viral), confirmed infection (eg Coxsackievirus), neoplasia, autoimmune (eg SLE, rheumatoid arthritis), uremia, cardiovascular (acute STEMI or Dressler syndrome), radiation therapy.

Answer 229

Compression of heart by fluid (eg blood, effusions) in pericardial space, which decreases cardiac output. Equilibration of diastolic pressure in all four chambers. Findings include Beck triad (hypotension, distended neck veins, distant heart sounds), increase in heart rate, pulsus paradoxus. ECG shows low-voltage QRS and electrical alternans (due to swinging movement of heart in large effusion).

Answer 230

A decrease in amplitude of systolic BP by more than 10 mmHg during inspiration. Seen in cardiac tamponade, asthma, obstructive sleep apnea, pericarditis, croup.

Answer 231

Tertiary syphilis disrupts the vasa vasorum of the aorta with consequent atrophy of vessel wall and dilation of aorta and valve ring. There may be calcification of aortic root and ascending aortic arch. It leads to tree bark appearance of aorta. It can result in aneurysm of ascending aorta or aortic arch, aortic insufficiency.

Answer 232

The most common heart tumor is a metastasis.

Answer 233

A cardiac tumor. It is the most common primary cardiac tumor in adults. 90% occur in the atria (mostly left atrium). Myxomas are usually described as a ball valve obstruction in the left atrium (associated with multiple syncopal episodes). There may be an early diastolic "tumor plop" sound on auscultation.

Answer 234

Most frequent primary cardiac tumor in children. It is associated with tuberous sclerosis.

Answer 235

An increase in JVP on inspiration instead of a normal decrease. Inspiration creates negative intrathoracic pressure that does not get transmitted to heart, causing impaired filling of right ventricle. This causes blood to back up into venae cavae, causing JVD. It may be seen with constrictive pericarditis, restrictive cardiomyopathies, right atrial or ventricular tumors.

Answer 236

A rare blood vessel malignancy typically occurring in the head, neck, and breast areas. It is usually seen in elderly, on sun exposed areas. It is associated with radiation therapy and chronic postmastectomy lymphedema. Hepatic angiosarcoma is associated with vinyl chloride and arsenic exposures. It is very aggressive and difficult to resent due to delay in diagnosis.

Answer 237

Benign capillary skin papules found in AIDS. It is caused by Bartonella henselae infections. Frequently mistaken for Kaposi sarcoma, but has neutrophilic infiltrate.

Answer 238

Benign capillary hemangioma of the elderly. It does not regress. Frequency increases with age.

Answer 239

Cavernous lymphangioma of the neck. It is associated with turner syndrome.

Answer 240

Benign, painful, red-blue tumor under fingernails. It arises from modified smooth muscle cells of the thermoregulatory glomus body.

Answer 241

Endothelial malignancy that is most commonly found in the skin, but also in the mouth, GI tract, and respiratory tract. It is associated with HHV-8 and HIV. It is frequently mistaken for bacillary angiomatosis, but has lymphocytic infiltrate.

Answer 242

Polypoid capillary hemangioma that can ulcerate and bleed. It is associated with trauma and pregnancy.

Answer 243

Benign capillary hemangioma of infancy. It appears in the first few weeks of life (1/200 births). It grows rapidly and regresses spontaneously by 5-8 years.

Answer 244

A decrease in blood flow to the skin due to arteriolar (small vessel) vasospasm in response to cold or stress causing a color change from white (ischemia) to blue (hypoxia) to red (reperfusion). It occurs most often in the fingers and toes. It is called Raynaud disease when it is primary (idiopathic) and Raynaud syndrome when secondary to a disease process such as mixed connective tissue disease, SLE, or CREST (limited form of systemic sclerosis) syndrome. Treat with Ca channel blockers.

Answer 245

A large vessel vasculitis. Giant cell (temporal) arteritis is a granulomatous large vessel vasculitis involving superficial temporal and ophthalmic arteries. Giant cell arteritis occurs most often in females over the age of 50. Symptoms of giant cell arteritis include temporal headache, jaw claudication, and blindness in the ipsilateral eye due to ophthalmic artery vasculitis. Giant cell arteritis is commonly associated with polymyalgia rheumatica, which is characterized by muscle and joint pain, and normal serum creatine kinase. A common laboratory finding in giant cell arteritis includes an increased ESR and is used as a screening test. Treatment of giant cell arteritis consists of corticosteroids. Must be done PRIOR to temporal artery biopsy to prevent vision loss. Diagnosis of Temporal (Giant Cell) arteritis is made by biopsy, which reveals inflamed vessel wall with giant cells and intimal fibrosis. Lesions are segmental, requiring biopsy of a long segment of a vessel and a negative result does not rule out the disease.

Answer 246

A large vessel vasculitis. Takayasu arteritis, also known as pulseless disease, is a granulomatous large vessel vasculitis involving aortic arch vessels. Takayasu arteritis occurs most often in young Asian women and children. Symptoms of Takayasu arteritis include an absent upper extremity pulse, discrepancy in blood pressure between the arms (over 10 mm Hg), night sweats, arthritis, myalgias, skin nodules, visual defects, and stroke. Treatment of Takayasu arteritis consists of corticosteroids.

Answer 247

A medium vessel vasculitis. Polyarteritis nodosa is a segmental transmural necrotizing vasculitis of medium-sized muscular arteries (does not involve arterioles, capillaries, or venules). Destruction of arterial media and internal elastic lamina. Ongoing/recurrent insults lead to lesions of different ages. Results in aneurysmal nodules, which may rupture. These give a "string of pearls" appearance during imaging that is sometimes seen in polyarteritis nodosa. Frequency of arterial involvement in polyarteritis nodosa from highest to lowest: Kidney, Heart, Liver, GI. Hepatitis B infection in 30% of these patients with polyarteritis nodosa. In addition to HBV, HCV and hairy cell leukemia are associated with polyarteritis nodosa.

Answer 248

No association with ANCAs: p-ANCA (perinuclear antineutrophil cytoplasmic antibodies) may be either absent or present; it is not diagnostic. If it is present, it most often indicates small-vessel disease. Dx depends on imaging: arteriograms showing microaneurysms in small/medium arteries of abdominal organs.

Answer 249

S/Sx due to ischemia and infarction of affected organs: Kidney – renal failure, Coronary – ischemic heart disease, acute myocardial infarction, GI – abdominal pain, nausea, bloody diarrhea, Musculoskeletal – arthritis, myalgia, arthralgia, CNS – eye and skin complaints. Remember in PAN the Pulmonary vessels Are Not affected. Pulmonary vasculature is spared in polyarteritis nodosa.

Answer 250

A medium vessel vasculitis. Kawasaki disease is a necrotizing medium-sized vessel vasculitis involving coronary arteries. Kawasaki disease most often occurs Asian children under the age of 4. Kawasaki disease is the leading cause of acquired heart disease in children in developed countries. Signs and symptoms of Kawasaki disease can be remembered with the mnemonic, CRASH and burn: Conjunctival injection, Rash, Adenopathy (cervical), Strawberry tongue (oral mucositis), Hand-foot changes (edema, erythema on palms and soles), Fever (burn). 2 sequelae of coronary artery aneurysms in Kawasaki disease are: Rupture, Thrombosis, leading to myocardial infarction. Treatment of Kawasaki disease consists of intravenous immunoglobulins and aspirin. Corticosteroids are indicated only when two courses of intravenous immunoglobulins are unsuccessful.

Answer 251

A medium vessel vasculitis. Buerger disease (thromboangiitis obliterans) is a medium-sized vessel vasculitis with digital vessel thrombosis and damage to neurovascular compartment. Buerger disease most commonly occurs in male smokers between the ages of 25 and 50 (usually under the age of 40). Physical symptoms involve the lower extremities in the majority of the cases, and are characterized by ischemic ulcers or gangrene of the foot and toes. Amputation resulting from ischemia and gangrene is a common complication. Physical symptoms involve the upper extremities in 40-50% of the cases that are characterized by upper limb ischemia with ulceration and gangrene and Raynaud phenomenon. Since Buerger disease is highly associated with smoking, the first-line treatment for most patients is smoking cessation.

Answer 252

A small vessel vasculitis. Henoch Schönlein Purpura is the most common systemic vasculitis in children. Henoch Schönlein Purpura is a small vessel vasculitis characterized by IgA, C3, and immune complex deposition in blood vessels. Diagnosis of Henoch Schönlein Purpura can be confirmed with a renal biopsy demonstrating mesangial IgA deposition on immunofluorescence. In ~ 50% of cases of Henoch Schönlein Purpura, the patient (usually a child) will have a recent history of a upper respiratory infection. Patients with Henoch Schönlein Purpura commonly present with: Palpable purpura on buttocks and/or legs; Arthralgias; Abdominal pain and bleeding; Hematuria due to IgA nephropathy

Answer 253

A small vessel vasculitis. Granulomatosis with polyangiitis (previously known as Wegener's granulomatosis) is a small vessel granulomatous vasculitis that affects the: Upper respiratory tract (i.e. nose, sinuses); Lower respiratory tract (i.e. lung); Kidney. Granulomatosis with polyangiitis symptoms include necrotizing granulomas in kidney, upper and lower respiratory tract that can be seen as large nodular densities on chest X-ray. Granulomatosis with polyangiitis in the upper respiratory tract produces symptoms that include chronic sinusitis, otitis media, and mastoiditis and lesions that include nasopharynx-saddle nose deformity and collapsed trachea. Granulomatosis with polyangiitis in the lower respiratory tract produces symptoms that include hemoptysis, cough, and dyspnea and lesions that include cavitating nodular lesions. Complications of Granulomatosis with polyangiitis are infarctions in the lungs and crescentic glomerulonephritis in the kidneys. Patients with granulomatosis with polyangiitis are often positive for c-ANCA (PR3-ANCA) antibodies. Treatment of Granulomatosis with polyangiitis involves corticosteroids and cyclophosphamide.

Answer 254

A small vessel vasculitis. Eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome) can be distinguished from polyarteritis nodosa by the presence of granulomas as well as the abundance of eosinophils. Eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome) is MPO-ANCA (p-ANCA) positive. The 6 diagnostic criteria: presence of 4 of the following 6 is both sensitive (85%) and specific (over 99%) for eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome): Asthma (wheezing, expiratory rhonchi), Paranasal sinusitis, Eosinophilia (eosinophil count over 10% on peripheral smear—vs. normal eosinophil count of 1-3%). Migratory pulmonary infiltrates on chest x-ray (“migratory” because these infiltrates may be transient and may appear to move to different locations on serial imaging examinations). Extravascular accumulations of eosinophils—confirmed on tissue biopsy of skin or nasal polyp. Neuropathy (poly or mono) (usually peripheral neuropathy causing pain/anesthesia/parathesia in hands and feet)

Answer 255

A small vessel vasculitis. Microscopic polyangiitis is a small vessel necrotizing vasculitis that affects capillaries, arterioles, and venules. Unlike polyarteritis nodosa, all lesions are at the same stage of inflammation and unlike in granulomatosis with polyangiitis (Wegener), granulomatous inflammation is absent. Microscopic polyangiitis is MPO-ANCA (p-ANCA) positive in over 70% of patients. The most common clinical manifestations of microscopic polyangiitis are: Constitutional symptoms (weight loss, fevers, malaise, joint and muscle aches); Kidney inflammation (necrotizing glomerulonephritis); Skin lesions (most commonly palpable purpura of the lower extremities); Peripheral nerve damage (mononeuritis multiplex: damage to two or more separate peripheral nerves); Lung involvement (pulmonary capillaritis leading to alveolar hemorrhage)

Answer 256

Thiazide diuretics, ACE inhibitors, angiotensin II receptor blockers (ARBs), dihydropyridine Ca channel blockers.

Answer 257

Diuretics, ACE inhibitors/ ARBs, beta blockers (compensated HF), aldosterone antagonists. Beta blockers must be used cautiously in decompensated HF and are contraindicated in cardiogenic shock.

Answer 258

ACE inhibitors/ ARBs (they are protective against diabetic nephropathy), Ca channel blockers, thiazide diuretics, beta blockers.

Answer 259

Hydralazine, labetalol, methyldopa, nifedipine

Answer 260

Ca channel blocker, dihydropyridine, acts on vascular smooth muscle

Answer 261

Ca channel blocker, dihydropyridine, acts on vascular smooth muscle. It is used to trat hypertensive urgency or emergency.

Answer 262

Ca channel blocker, dihydropyridine, acts on vascular smooth muscle

Answer 263

Ca channel blocker, dihydropyridine, acts on vascular smooth muscle

Answer 264

Ca channel blocker, dihydropyridine, acts on vascular smooth muscle. It is used to treat subarachnoid hemorrhage by preventing cerebral vasospasm.

Answer 265

Ca channel blocker, non-dihydropyridines, acts on heart

Answer 266

Ca channel blocker, non-dihydropyridines, acts on heart

Answer 267

Block voltage dependent L type calcium channels of cardiac and smooth muscle causing a decrease in muscle contractility.

Answer 268

Vascular smooth muscle effectiveness from highest to lowest: amlodipine=nifedipine, diltiazem, verapamil. They are, except for nimodipine, used to treat hypertension, angina (including Prinzmetal), Raynaud phenomenon.

Answer 269

Effectiveness on heart highest to lowest: verapmil, dilitiazem, amlodipine=nifedipine (Verapamil=Ventricle). They are used to trat hypertension, angina, atrial fibrillation/flutter.

Answer 270

Cardiac depression, AV block (non-dihydropyridines), peripheral edema, flushing, dizziness, hyperprolactinemia (verapamil), constipation, gingival hyperplasia.

Answer 271

Increases cGMP causing smooth muscle relaxation. Vasodilates arterioles more than veins. Reduces afterload.

Answer 272

Severe hypertension (particularly acute), HF (with organic nitrate). Safe to use during pregnancy. Frequently coadministered with a beta blocker to prevent reflex tachycardia.

Answer 273

Compensatory tachycardia (contraindicated in angina/CAD), fluid retention, headache, angina. Lupus like syndrome.

Answer 274

Drugs include clevidipine, fenoldopam, labetalol, nicradipine, nitroprusside.

Answer 275

Short acting, increases cGMP via direct release of NO. It can cause cyanide toxicity (releases cyanide).

Answer 276

Dopamine D1 receptor agonist, causes coronary, peripheral, renal , and splanchnic vasodilation. Decreases BP and increases natriuresis.

Answer 277

Vasodilate by increasing NO in vascular smooth muscle by causing an increase in cGMP and smooth muscle relaxation. It dilates veins much more than arteries. Decreases preload.

Answer 278

Angina, acute coronary syndrome, pulmonary edema.

Answer 279

Reflex tachycardia (treat with beta-blockers), hypotension, flushing, headache, Monday disease with industrial exposure (development of tolerance for the vasodilating action during the work weekend loss of tolerance over the weekend causing tachycardia, dizziness, headache upon reexposure).

Answer 280

The objective of anginal therapy is to decrease myocardial oxygen demand/consumption and/or increase coronary blood flow. This can be achieved by: Decreasing HR (heart rate); Decreasing contractility; Decreasing end-diastolic volume; Decreasing blood pressure (proportional to afterload). Partial beta agonists are contraindicated in angina.

Answer 281

It decreases end diastolic volume, decreases blood pressure, no effect on contratility, increases heart rate (reflex response), decrease ejection time, and decreased MVO2.

Answer 282

It decreases or has no effect on end diastolic volume, decreases blood pressure, decreases contratility, decreases heart rate, increase ejection time, and decreased MVO2. Verapamil is similar to beta blockers in effect.

Answer 283

It decreases or has no effect on end diastolic volume, decreases blood pressure, little or no effect on contratility, decreases or no effect on heart rate, little or no ejection time, and greatly decreased MVO2.

Answer 284

Cardiac glycosides are generally used to treat congestive heart failure and atrial fibrillation.

Answer 285

Digitalis inhibits the Na+/K+ ATPase by competing with K+ for binding to the extracellular alpha subunit. Inhibition of Na-K-ATPase leads to increased intracellular Na+ in myocytes, which indirectly slows down extrusion of Ca2 via Na/Ca2 pump. This leads to intracellular Ca2+ and more stored Ca2+ in sarcoplasmic reticulum, thereby increasing the amount of Ca2+ released by each subsequent action potential which increases contractility (i.e. increased force of contraction for a given preload). Digitalis stimulates the vagus nerve, thereby reducing heart rate. This has an anti-arrhythmic effect.

Answer 286

Digoxin is extracted from Digitalis lanata plant. Binds to extracellular α subunit of Na/K ATPase in myocytes. Shorter half life (1-2 days) compared to digitoxin. Eliminated by kidney, so there is a longer half-life in patients with kidney failure. Digitoxin is eliminated in the liver, unlike digoxin. Digitoxin has a longer half life (5-7 days) compared to digoxin

Answer 287

Toxicities of cardiac glycosides include: Anorexia, Nausea, Cholinergic effects which include disorientation, and visual effects (halos), Cardiac arrhythmias. EKG changes ( ST depression, T wave inversion, scooping of the ST segments, decreases QT, and increases PR interval) are not a sign of toxicity, rather it is expected and called the digitalis effect. Risks of Toxicity increased by: Renal failure (only in digoxin); Hypokalemia from diuretics (digoxin competes with K+ for the same binding site on Na+/K+ ATPase); Hypomagnesemia; Quinidine, Amiodarone. Combination therapy with calcium channel blockers (especially Verapamil). Hyperkalemia indicates a poor prognosis in patient with digoxin toxicity.

Answer 288

Antidote to toxicity (use the mnemonic “LAMPP”): Lidocaine, Anti-dig Fab fragments, Magnesium for treatment of hypomagnesemia, Potassium for treatment of hypokalemia before administration of digoxin, Phenytoin for arrhythmias that do not respond to lidocaine

Answer 289

Statins competitively and reversibly inhibit HMG-CoA reductase, the rate-limiting enzyme in cholesterol synthesis. HMG-CoA reductase catalyzes the conversion of HMG-CoA to mevalonate. Inhibition of HMG-CoA reductase results in: Impaired hepatic cholesterol synthesis; Increased hepatic LDL receptor expression (A compensatory response to the reduced intracellular hepatocyte cholesterol); Serum LDL is reduced due to increased hepatic LDL uptake. Statins have the following effects on blood lipids: greatly decreases LDL (greatest decrease), increases HDL (minimal effect), decreases Triglycerides. Side effects of statins include: Myopathy/rhabdomyolysis, which is particularly common when used in combination with fibrates or niacin; Hepatotoxicity which can manifest with elevated LFTs

Answer 290

Fibrates are the most effective agents in reducing triglycerides. Four examples of fibrates are: Gemfibrozil, Clofibrate, Bezafibrate, Fenofibrate. Mechanism: activation of nuclear transcription factor PPAR alpha leads to upregulation of lipoprotein lipase. This causes increased clearance of triglyceride rich lipoproteins and increased HDL synthesis. LDL is slightly decreased. HDL is slightly increased. Triglycerides are greatly decreased. Side effects of fibrates include myopathy/rhabdomyolysis, which is particularly common when used in combination with statins, and cholesterol gallstones

Answer 291

In adipose tissue, niacin inhibits hormone-sensitive lipase, which catalyzes the the lipolysis of triglycerides. This reduces the availability of free fatty acids for hepatic triglyceride synthesis. In the liver, niacin also reduces the hepatic production of VLDL, which ultimately reduces LDL levels. Niacin has the following effects on lipids: greatly decreases LDL, greatly increases HDL, decreases Triglycerides. Niacin is the most effective antilipid for elevating serum HDL levels. Side effects of niacin include: Flushed red face (treat with preadministration of aspirin), Hyperglycemia (acanthosis nigricans), Hyperuricemia (exacerbates gout).

Answer 292

Bile acid resins include: Cholestyramine, Colestipol, Colesevelam. The mechanism of bile acid resins is as follows: 1. Positively-charged bile acid resins bind negatively-charged bile acids, forming a complex. 2. These complexes are excreted in stool, depleting the pool of bile acids (> 95% of bile acids are normally reabsorbed). 3. Hepatic synthesis of bile-acids increases, depleting hepatic cholesterol (bile acids are made from cholesterol). 4. Hepatocytes increase expression of LDL receptors. 5. Serum LDL is reduced due to increased hepatic LDL uptake. Side effects of bile acid resins include: GI discomfort (constipation, diarrhea, and flatulence), Malabsorption of fat-soluble vitamins and drugs. Since increased levels of bile acids can irritate skin and cause pruritus, bile acid resins can be used to treat pruritus in liver failure because they deplete bile acid reserves.

Answer 293

Ezetimibe is an inhibitor of dietary cholesterol absorption in small intestine brush border. Ezetimibe reduces LDL levels as monotherapy and can be combined with statins for further LDL reduction. Side effects of ezetimibe include: Hepatotoxicity (rare), which manifests as increased LFTs and diarrhea.

Answer 294

Slow or block (decreases) conduction, especially in depolarized cells. It decreases the slope of phase O depolarization. They are state dependent and selectively depress tissue that is frequently depolarized (eg tachycardia).

Answer 295

Class 1A anti-arrhythmic, sodium channel blocker. Causes cinchonism (headache and tinnitus)

Answer 296

Class 1A anti-arrhythmic, sodium channel blocker. Causes reversible SLE-like syndrome

Answer 297

Class 1A anti-arrhythmic, sodium channel blocker. Can cause heart failure

Answer 298

Quinidine, Procainamide, Discopyramide. The Queen Proclaims Disco's Pyramid.

Answer 299

It increases AP duration, thereby increasing effective refractory period (ERP) in ventricular action potential. On ECG, QT is prolonged.

Answer 300

Used for both atrial and ventricular arrhythmias, especially re-entrant and ectopic SVT and VT.

Answer 301

Cinchonism (headache, tinnitus with quinidine), reversible SLE-like syndrome (procainamide), heart failure (disopyramide), thrombocytopenia, torsades de pointes due to an increase in QT interval.

Answer 302

class 1B anti-arrhythmic, sodium channel blocker

Answer 303

class 1B anti-arrhythmic, sodium channel blocker

Answer 304

Lidocaine and mexiletine. I'd Buy Liddy's Mexican Tacos.

Answer 305

It decreases AP duration. It preferentially affect ischemic or depolarized Purkinje and ventricular tissue. Phenytoin can also fall into the IB category.

Answer 306

Used to treat acute ventricular arrhythmias (especially post MI), digitalis induced arrhythmias. IB is the Best post MI.

Answer 307

CNS stimulation/depression, cardiovascular depression.

Answer 308

class 1C anti-arrhythmic, sodium channel blocker

Answer 309

class 1C anti-arrhythmic, sodium channel blocker

Answer 310

Flecainide, Propafenone. Can I have Fries Please.

Answer 311

It significantly prolongs effective refractory period in AV node and accessory bypass tracts. There is no effect on ERP in Purkinje and ventricular tissue. There is a minimal effect on AP duration.

Answer 312

They are used to treat SVTs, including atrial fibrillation. It is only used as a last resort in refractory ventricular tachycardia.

Answer 313

It is proarrhythmic, especially post-MI (contraindicated). IC is Contraindicated in structural and ischemic heart disease.

Answer 314