Cardio Flashcards

Question

Transposition of the great vessels

Answer 1

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 irst few months of life.

Answer 2

Absence of tricuspid valve and hypoplastic RV; requires both ASD and VSD for viability. Tricuspid atresia is a form of congenital heart disease whereby there is a complete absence of the tricuspid valve. Therefore, there is an absence of right atrioventricular connection. This leads to a hypoplastic (undersized) or absent right ventricle. This defect is contracted during prenatal development, when the heart does not finish developing. It causes the heart to be unable to properly oxygenate the rest of the blood in the body. Because of this, the body does not have enough oxygen to live, so other defects must occur to maintain blood flow. ⭐️Because of the lack of an A-V connection, an atrial septal defect (ASD) must be present to fill the left ventricle with blood. Also, since there is a lack of a right ventricle there must be a way to pump blood into the pulmonary arteries, and this is accomplished by a ventricular septal defect (VSD). The causes of Tricupsid atresia are unknown.[1]

Answer 3

Caused by anterosuperior displacement of the infundibular septum. Most common cause of early childhood cyanosis 1. Pulmonary infundibular stenosis (most important determinant for prognosis) 2. Right ventricular hypertrophy (RVH)—boot-shaped heart on CXR 3. Overriding aorta 4. VSD Pulmonary stenosis forces right-to-left flow across VSD > RVH, “tet spells” (often caused by crying, fever, and exercise due to exacerbation of RV outlow obstruction). PROVe. Squatting: increases SVR, decreases right-to-left shunt, improves cyanosis. Treatment: early surgical correction.

Answer 4

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 5

Characterized by displacement of tricuspid valve lealets downward into RV, artiicially “atrializing” the ventricle. Associated with tricuspid regurgitation and right heart failure. Can be caused by lithium exposure in utero.

Answer 6

Acyanotic at presentation; cyanosis may occur years later. Frequency: VSD > ASD > PDA. Right-to-Left shunts: eaRLy cyanosis. Left-to-Right shunts: “LateR” cyanosis.

Answer 7

Most common congenital cardiac defect. Asymptomatic at birth, may manifest week later or remain asymptomatic throughout life. Most self resolve; larger lesions may lead to LV overload and HF. O2 saturation increase in RV and pulmonary artery

Answer 8

Defect in interatrial septum; loud S1; wide, fixed split S2. Ostium secundum defects most common and usually occur as isolated findings; ostium primum defects rarer yet 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 increases in RA, RV, and pulmonary artery. May lead to paradoxical emboli (systemic VENOUS emboli use ASD to bypass lungs and become systemic arterial emboli).

Answer 9

In fetal period, shunt is right to left (normal). In neonatal period, decrease 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 PDA can eventually result in late cyanosis in the lower extremities (differential cyanosis). Endomethacin” (indomethacin) ends patency of PDA; PGE keeps ductus Going (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 10

Uncorrected left-to-right shunt (VSD, ASD, PDA) > increase pulmonary blood flow > pathologic remodeling of vasculature > pulmonary arterial hypertension. RVH occurs to compensate > shunt becomes right to left. Causes late cyanosis, clubbing D , and polycythemia. Age of onset varies.

Answer 11

Infantile: Preductal coarctation - (Turner Syndrome, FA p585) - constriction is proximal to the DA. Before birth, blood flows through the DA to the descending aorta for distribution to the lower body. Collaterals DO NOT NEED develop in utero. For this reason, preductal coarctation can be life-threating in neonate. Cyanosis from birth immediately symptomatic Adult: there is no PDA, the coarctation is after the major branches of the aorta so intercostals have to form. Blood can't flow well so instead more are forced out into the major branches leading to hypertension in upper extremities and hypotension in lower extremities. Intercostals will try to bypass the coarctation and lead to rib notching. The renals are in the hypotense region so they think there is hypotension and activate the RAAS. ______________________________ FA: 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 collateralcirculation; arteries erode ribs > notched appearance on CXR. Complications include HF, risk of cerebral hemorrhage (berry aneurysms), aortic rupture, and possible endocarditis.

Answer 12

Aortic arch derivatives 1st: Part of maxillary artery (branch of external carotid). 1st arch is maximal 2nd: Stapedial artery and hyoid artery. Second = Stapedial 3rd: Common Carotid artery and proximal part of internal Carotid artery C is 3rd letter of alphabet ``` 4th: On left, aortic arch; on right, proximal part of right subclavian artery. 4th arch (4 limbs) -systemic ``` 🌈6th: Proximal part of pulmonary arteries and (on left only) ductus arteriosus *6th arch = pulmonary and pulmonary -to systemic shunt (ductus arteriosus *Right recurrent laryngeal nerve loops around right subclavian artery 4th Left recurrent laryngeal nerve loops around aortic arch distal to ductus arteriosus

Answer 13

C. inferior vena cava

Answer 14

E. sixth aortic arch - ductus arteriosus

Answer 15

1) Right-dominant circulation=85%; defined by which artery supplies the PDA - supplies posterior 1/3 of interventricular septum, AV node and posterior wall of ventricles 2) SA and AV node usually supplied by RCA 3) Coronary artery occlusion most commonly occurs in the LAD 4) Left atrium enlargement can cause dysphagia (compression of the esophagus) or hoarseness (compression of the left recurrent laryngeal nerve, a branch of the vagus).

Answer 16

Phase 0 = Rapid upstroke – Voltage-gated (VG) Na+ channel open. Phase 1 = Initial repolarization – inactivation of VG Na+ channels. VG K+ channel begins to open. Phase 2 = Plateau – Ca2+ influx through VG 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 VG slow K+ channels and closure of VG Ca2+ channels. Phase 4 = Resting potential – high K+ permeability through K+ channels

Answer 17

1. CO = SV x HR (ml or L/min) 2. SV = EDV-ESV 3. EF = SV/EDV normal is >55% 4. Wall tension = (Pressure x radius)/(2 x thickness) 5. MAP = CO x TPR (aka SVR), MAP = 2/3 diastolic + 1/3 systolic 6. Resistance - viscocity x length / radius ^4 7. Fick's principle: CO = (rate of O2 consumption)/ (arterial O2 content − venous O2 content 8. Pulse pressure = systolic pressure – diastolic pressure *Pulse pressure is proportional to SV, inversely proportional to * arterial compliance.

Answer 18

1. Phosphorylation of Ca2+ channels causes the Ca2+ channels to remain open ⏱longer. - increase contractility with increase intracellular calcium 2. Phosphorylation of proteins in the SR enhances release of Ca2+. - increase contractility with increase intracellular calcium 3. Phosphorylation of myosin increases myosin ATPase which increases the speed of cross-bridge cycling. 4. Phosphorylation of Ca2+ pumps in the SR increases the speed of calcium re-uptake, and relaxation.

Answer 19

The sodium-calcium exchanger (often denoted NCX) removes calcium from cells, using the electrochemical gradient of sodium (Na+). Calcium out, sodium in. When the exchanger works poorly, calcium accumulates in the myocyte leading to enhanced contractility. First of all digitalis increases inotropy and SV. It does this not by directly affecting the NCX. Digitalis competes with K+ for binding to the Na+/K+ ATPase. (Potassium in, sodium out) Therefore hypokalemia increases risk of drug toxicity. Therefore sodium builds up intracellularly and the NCX can't bring sodium in and calcium out so calcium builds intracellularly

Answer 20

increased by Contractility, Afterload, heart Rate, and ventricular Diameter

Answer 21

D. Radius increases by the 3rd root of volume assuming the LV is a sphere

Answer 22

Cardiomyocytes grow in both length and width by addition of sarcomeres. Physiological stimulation (such as pregnancy or endurance training) can induce eccentric hypertrophy. Here sarcomeres are added to increase length but cellular width also increases somewhat. Physiologic concentric hypertrophy is seen in isometric exercise training, such as weight-lifting (increase in sarcomere width only). Pathologic eccentric hypertrophy features increases in sarcomere but cells shrink in width (e.g. valvular regurgitation). Pathologic concentric hypertrophy arises in chronic hypertension or aortic stenosis.

Answer 23

B> concentric because wall tension would decrease

Answer 24

D. Systemic vascular resistance. During exercise, muscle tissue receives up to 85% of blood flow due to vasodilation of muscle vascular beds. In most vascular beds, the SNS causes vasoconstriction via a1 adrenergic receptors. The notable exception is the muscle bed where b2 adrenergic receptors predominant. These receptors when bound by catecholamines cause vasodilation.

Answer 25

Increased pulse pressure in... -hyperthyroidism, -aortic regurgitation (drops diastolic because blood has another route), -aortic stiffening (arteriosclerosis in elderly - can't absorb pressure -exercise (transient) increases BP and decreases SVR) -obstructive sleep apnea (increases sympathetic tone) Decreased pulse pressure in - aortic stenosis, - cardiogenic shock, - cardiac tamponade - advanced heart failure (HF).

Answer 26

Hydrostatic pressure - is about fluid movement OUT Osmotic pressure - is about solute concentration drawing fluid IN Net filtration pressure, the higher it is, the higher the movement OUT of capillaries

Answer 27

1) Increased capillary pressure (increased Pc, heart failure) 2) Decreased plasma proteins (decreased πc, nephrogenic syndrome, liver failure) 3) Increased capillary permeability (increased Kf, toxins, infections, burns) 4) Increased interstitial fluid colloid osmotic pressure (increased π lymphatic blockage)

Answer 28

S1- mitral and tricuspid valve closure. Loudest at mitral area S2- aortic and pulmonary valve closure. Loudest at left upper sternal border S3 (abnormal)- in early diastole during rapid ventricular filling phase. Associated with increased filling pressures (e.g. CHF) and more common in dilated ventricles. Can be normal in children and pregnant women. S4 (abnormal)(“atrial kick”) – in late diastole. High atrial pressure. Associated with ventricular hypertrophy. Left atrium must push against stiff LV wall. - "stiff noncompliant ventricle during left atrial contraction).

Answer 29

Normal splitting – Inspiration > drop in intrathoracic pressure > increased venous return to the RV > increased RV stroke volume and ejection time > delayed closure of pulmonic valve (P2). Also decreased pulmonary impedance and therefore increased capacity of the pulmonary circulation Wide splitting –Delay in RV emptying causes delayed P2 (regardless of breath but especially on inspiration). An exaggeration of normal splitting. -Right bundle branch block, pulmonary stenosis Fixed splitting – Left to right shunt, increased RA and RV volume, regardless of breath. P2 will always be greatly delayed. *Atrial septal defect Paradoxical splitting – Delay in LV emptying. Normal order of valve closure is reversed so that P2 sound occurs before delayed A2 sound. -left bundle branch -aortic stenosis Therefore on inspiration, P2 closes later and moves closer to A2, thereby “paradoxically” eliminating the split (usually heard in expiration).

Answer 30

[Systolic] Holosystolic, high-pitched “blowing murmur.” Mitral—loudest at apex and radiates toward axilla. MR is often due to ischemic heart disease (post-MI), mitral valve prolapse, LV dilatation. Acute: endocarditis, papillary muscle rupture, trauma, chordal rupture) Chronic: myxomatous, RF, healed endocarditis, radiation) Tricuspid—loudest at tricuspid area. TR commonly caused by RV dilatation. Rheumatic fever and infective endocarditis can cause either MR or TR. ``` Aortic stenosis (AS): Crescendo-decrescendo systolic ejection murmur (ejection click may be present). LV >> aortic pressure during systole. Loudest at heart base; radiates to carotids. “🌌Pulsus parvus et tardus”—pulses are weak with a delayed peak. Can lead to Syncope, Angina, and Dyspnea on exertion (SAD). Most commonly due to agerelated calcification in older patients (> 60 years old) or in younger patients with early-onset calcification of bicuspid aortic valve. ``` VSD Loudest at tricuspid area with a L to R shunt. Harsh holosystolic murmur in physical exam. Mitral Valve prolapse (MVP) 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 31

C. The patient has mitral stenosis resulting in LA enlargement and pressure on the L recurrent laryngeal nerve (see arrow). This is Ortner’s syndrome

Answer 32

1. Aortic stenosis 2. Aortic regurg 3. Mitral stenosis 4. Mitral regurg

Answer 33

Phase 0= Upstroke- VG Ca2+ channels open. VG Na+ channels are inactivated at less negative resting voltage. Phase 1 and 2 = absent Phase 3= inactivation of the Ca2+ channels and increase activation of the K+ channels resulting in K+ efflux Phase 4= slow spontaneous diastolic depolarization due to If (“funny current”). If channels responsible for a slow, mixed Na+/K+ inward current; different from INa in phase 0 of ventricular action potential. Accounts for automaticity of SA and AV nodes. The slope of phase 4 in the SA node determines HR. ACh/adenosine decrease the rate of diastolic depolarization and decrease HR, while catecholamines increase depolarization and increase HR. Sympathetic stimulation increase the chance that If channels are open and thus increase HR.

Answer 34

1st degree – PR interval is prolonged (>200 msec). Benign and asymptomatic. No treatment required. 2nd degree -Mobitz type I (Wenckebach)- Progressive lengthing of the PR interval until a beat is “dropped”. Usually asymptomatic -Mobitz Type II – Dropped beats that are not preceded by a change in length of the PR interval (as in type I). May progress to 3rd- degree block. Often treated with pacemaker. (one beat drop 2) 3rd degree (complete) –Both P waves and QRS complexes are present, although the P waves bear no relation to the QRS complexes. The atrial rate is faster than ventricular rate. Usually treated with pacemaker. Lyme disease and MIs are causes.

Answer 35

Baroreceptor Reflex Aortic arch transmits via CN X. Carotid sinus transmits via CN IX. High BP activates baroreceptor activity, which the solitary nucleus integrates and then activates the PSNS (and inhibits the SNS) to slow heart rate and reduce BP Low BP reduces baroreceptor activity, which the solitary nucleus integrates and activates the SNS (and inhibits the PSNS) to increase HR and increase BP

Answer 36

This is a patient with paroxysmal supraventricular tachycardia (PSVT), the most common paroxysmal tachycardia. PSVT typically results from a re-entrant impulse traveling through slowly and rapidly conducting segments of the AV node. Simple treatments include maneuvers that increase cardiac PSNS tone, such as carotid sinus massage and the Valsalva maneuver. The PSNS primarily functions to slow the heart rate by slowing conduction through the AV node, which is specifically beneficial for this arrhythmia because it abolishes the re-entrant circuit and the arrhythmia.

Answer 37

1. 💦Bladder outlet obstruction/smooth muscle constriction aka urinary retention. 2. Mydriasis - ciliary body contracts 3. Increased intraocular pressure - reduces reuptake of aqueous humor, acute angle closure glaucoma.

Answer 38

They affect pancreatic beta cells and also inhibition of insulin release They also decrease production of aqueous humor. Alpha 2, always think blocking release.

Answer 39

Contractility (and SV) increase with: -Catecholamine stimulation via β1 receptor: -Ca2+ channels phosphorylated > increased Ca2+ entry > increased Ca2+-induced Ca2+ release and increased Ca2+ storage in sarcoplasmic reticulum -Phospholamban phosphorylation > active Ca2+ ATPase > increased Ca2+ storage in sarcoplasmic reticulum - a protein that negatively regulates SERCA, increasing the uptake and storage of calcium in SR -increased intracellular Ca2+ -decreased extracellular Na+ (decreased activity of Na+/Ca2+ exchanger) -Digitalis (blocks Na+/K+ pump > increased intracellular Na+ > decreased Na+/Ca2+ exchanger activity > increased intracellular Ca2+) Contractility and SV decrease with: -β1-blockade (decreased cAMP) -HF with systolic dysfunction -Acidosis -Hypoxia/hypercapnia (decrease Po2/ increase Pco2) - Non-dihydropyridine Ca2+ channel blockers

Answer 40

- Natriuresis | - Vascular smooth muscle relaxation (renal splanchnic)

Answer 41

Endothelium dependent vasoregulation - Dilation: NO, Prostacyclin - Endothelin: strongest vasoconstrictor substances Antihypertrophic properties -inhibition of vascular smooth muscle cells proliferation and migration Modulation of immune response -resist WBC adhesion and attachment Anticoagulant, antithrombotic, profibrinolytic function - heparan sulfate - thrombomodulin

Answer 42

1. damage to endothelium (large,medium sized muscular arteries especially at bifurcations) - disturbed shear features low flow, flow reversal and an altered EC phenotype and behavior - high EC turnover, poor alignment, inflammatory genes, high permeability, oxidative stress (ROS), prothrombotic - prostacyclin and NO decreased 2. LDL oxidation 3. Scavenger receptor - macrophages take up oxidized LDL becoming foam cell 4. Oxidized LDL and damage signals expression of adhesion molecules, monocyte attachment, transmigration, monocyte activation into more macrophages. 5. Cell necrosis leaves a lipid pool 6. Macrophage cytokines stimulate smooth muscle cells migration and replication, matrix synthesis eventually forming fibrous cap. 7. Active macrophages eventually weaken the plaque cap, exposure of matrix to platelets and mural thrombus formation.

Answer 43

Female (45, XO) Short stature (if untreated; preventable with growth hormone therapy), ovarian dysgenesis (streak ovary), shield chest, bicuspid aortic valve, coarctation (femoral < brachial pulse), lymphatic defects (result in webbed neck or cystic hygroma; lymphedema in feet, hands) horseshoe kidney. Most common cause of 1° amenorrhea. No Barr body. Menopause before menarche. decrease estrogen leads to increase LH, FSH. Sometimes due to mitotic error - mosaicism (eg, 45,XO/46,XX). Pregnancy is possible in some cases (IVF, exogenous estradiol-17β and progesterone). Congenital defect: Bicuspid aortic valve, coarctation of aorta, dissection of aorta Most girls and women with Turner syndrome have normal intelligence. Developmental delays, nonverbal learning disabilities, and behavioral problems are possible, although these characteristics vary among affected individuals.

Answer 44

Cardiac myocyte [camp] - decreased JGA cell [camp] decreased Vascular smooth muscle [cAMP] no change

Answer 45

Diabetes mellitus

Answer 46

Ventricular septal defect Membranous interventricular septum

Answer 47

elevated serum troponins and ST elevation -not: t wave inversion, ST depression, Q waves

Answer 48

A defect in atrial septum.

Answer 49

Epinephrine: first line for anaphalactic shock

Answer 50

Hemorrhage - really low left atrium pressure.

Answer 51

paradoxically split S2

Answer 52

Tetralogy of Fallot | Subvalvular pulmonic stenosis

Answer 53

Serum transaminases

Answer 54

Clopidogrel

Answer 55

Hybernating myocardium is myocardium that is hypokinetic due to longstanding severe ischemia, but has viability and wall motion improves after revascularization.

Answer 56

Papillary muscle disfunction from ischemia can cause mitral regurgitation which would produce a pansystolic murmer.

Answer 57

Positive test: • 1mm of horizontal or downsloping ST-segment depression • Markedly positive: • Fall in systolic blood pressure, ventricular arrhythmias, >2mm ST segment depression, ischemic changes within 3 minutes or lasting more than 5 minutes after the end of exercise, or patient exercise<2 minutes

Answer 58

Effects of warfarin on protein C synthesis

Answer 59

increase in IP3

Answer 60

Decreased gastrointestinal absorption of cholesterol

Answer 61

Norepinephrine.

Answer 62

``` Stage A: high risk for HF without structural heart disease or symptoms  Hypertension  Atherosclerotic heart disease  Diabetes  Obesity  Metabolic syndrome  Family history of cardiomyopathy ``` ``` Stage B: Structural heart disease without the development of HF  Prior myocardial infarction  Depressed LV ejection fraction  Left ventricular hypertrophy  Asymptomatic valvular heart disease ``` Stage C: Structural heart disease with current or prior symptoms (heart failure syndrome) ``` Stage D Heart Failure End-stage HF Refractory symptoms requiring special intervention:  Inotropes  LVAD  Transplant  Hospice ```

Answer 63

1. Tachypnea and diaphoresis during feeds 2. Easy fatigability 3.   Irritability 4.   Decreased volume of feeds 5. Poor weight gain •  “Failure to thrive”

Answer 64

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). Pericardium consists of 3 layers (from outer to inner): 􀂃 Fibrous pericardium 􀂃 Parietal layer of serous pericardium 􀂃 Visceral layer of serous pericardium Pericardial cavity lies between parietal and visceral layers. Pericardium innervated by phrenic nerve. Pericarditis can cause referred pain to the shoulder.

Answer 65

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

Answer 66

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—increased 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.

Answer 67

1. increase intensity of right heart sounds 2. increase intensity of MR, AR, and VSD murmurs decrease hypertrophic cardiomyopathy and AS, mitral valve prolapse later onset of click/murmur 3. decrease intensity of most murmurs (including AS) due to decreased preload- increase intensity of hypertrophic cardiomyopathy murmur MVP: earlier onset of click/murmur 4. decrease intensity of hypertrophic cardiomyopathy murmur increase intensity of AS, MR, and VSD murmurs MVP: later onset of click/murmur

Answer 68

[Diastolic] -Aortic regurgitation (AR) 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. [Mitral stenosis (MS)] 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 (decreased interval between S2 and OS correlates with increased severity). LA >> LV pressure during diastole. Often a late (and highly specific) sequela of rheumatic fever. Chronic MS can result in LA dilatation. Continuous PDA Continuous machine-like murmur. Loudest at S2. Often due to congenital rubella or prematurity. Best heard at left infraclavicular area

Answer 69

First degree AV block Diagnosis:  PR Interval > 200 msec with one to one relationship between P waves and QRS complexes  Mechanism: -Slowing of conduction in the AV node  Etiology: -Increased Parasympathetic Tone, Medications that slow AV Nodal conduction, AV nodal Ischemia -Chronic degenerative disease, Inferior Myocardial infarction  Clinical Presentation: -Elderly - Beta-blockers, Calcium channel blockers, Digitalis  Treatment: - Usually no treatment, avoid drugs that will further impair AV conduction Mobitz Type 1 2nd degree (Wenckebach):  Diagnosis: -Intermittent failure of AV conduction with some p waves not followed by QRS complex, constant P to P intervals and prolongation of the PR interval before block  Mechanism: -Impaired conduction in the AV Node with intermittent block  Etiology: Increased Parasympathetic Tone, Medications that slow AV Nodal conduction, AV nodal Ischemia, inflammation  Clinical Presentation: - Inferior MI, Lyme myocarditis, congenital AV block , post OHS - Trained Athlete, Beta-blockers, Calcium channel blockers  Treatment: -Usually reversible with removing medications or with time - May need atropine, isoproterenol or temporary pacing Mobitz Type 2: 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 70

``` Dilated cardiomyopathy (DCM) is a condition in which the heart's ability to pump blood is decreased because the heart's main pumping chamber, the left ventricle, is enlarged and weakened. In some cases, it prevents the heart from relaxing and filling with blood as it should. decreases contractility and leads to lower ejection fraction and possibly heart failure ```

Answer 71

Procainamide

Answer 72

Slow conduction and unidirectional block

Answer 73

It binds to open and inactivated sodium channels. Primarily inactivated sodium channels which are found in ischemic tissue due to the inability of Na/K ATPase to hyperpolarize the cell.

Answer 74

Mitral stenosis, likely pathogenesis is immune mediated valve damage.

Answer 75

P2 in accentuated

Answer 76

Adenosine AV nodal reentrant tachycardia - it opens AV noe potassium channels causing hyperpolarization.

Answer 77

This is aortic stenosis A2 is after P2 and upon inspiration its paradoxical because they are closer Congenital anomaly of the valve - bicuspid -fixed stenosis prevents the augmentation of cardiac output

Answer 78

Metoprolol

Answer 79

Papillary muscle rupture - decrease afterload

Answer 80

Left ventricular systolic dysfunction. Left sternal border murmur that increases with inspiration: Tricuspid valve regurg - increase with inspiration - increases preload, more going through the right sided valves, which fits with right heart failure - can't empty properly, the heart gets bigger, it stretches the annulus of the valve so it doesn't close properly. The most common cause of right heart failure is?

Answer 81

Atrioventricular nodal reentrant tachycardia.

Answer 82

Polymorphic ventricular tachycardia, characterized by shifting sinusoidal waveforms on ECG; can progress to ventricular fibrillation (VF). Long QT interval predisposes to torsades de pointes. Caused by drugs, decrease K+, decrease Mg2+, congenital abnormalities. Treatment includes magnesium sulfate. ``` Drug-induced long QT (ABCDE): AntiArrhythmics (class IA, III) AntiBiotics (eg, macrolides) Anti“C”ychotics (eg, haloperidol) AntiDepressants (eg, TCAs) AntiEmetics (eg, ondansetron) Torsades de pointes = twisting of the points ```

Answer 83

Inherited disorder of myocardial repolarization, typically due to ion channel defects; increase risk of sudden cardiac death (SCD) due to torsades de pointes. Includes: - Romano-Ward syndrome—autosomal dominant, pure cardiac phenotype (no deafness). - Jervell and Lange-Nielsen syndrome— autosomal recessive, sensorineural deafness.

Answer 84

Autosomal dominant disorder most common in Asian males. ECG pattern of 👾pseudo-right bundle branch block and ST elevations in V1-V3. increase risk of 👾ventricular tachyarrhythmias and SCD. PreventSCD with implantable cardioverter-defibrillator (ICD). EKG - type 1, coved type ST segment elevation, type 2 - saddle back type ST elevation

Answer 85

Atrial fibrillation: chaotic and erratic baseline with no discrete P waves in between irregularly spaced QRS complexes - loss of "a" wave. Irregularly irregular heartbeat - think Afib. Most common risk factors include hypertension and coronary artery disease (CAD). Ag, valvular heart disease, congestive heart failure. -enlarged atrium R or L. Can lead to thromboembolic events, particularly stroke. Treatment includes anticoagulation, rate control, rhythm control, and/or cardioversion. Atrial Flutter - 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. Ventricular Fibrillation - A completely erratic rhythm with no identifiable waves. Fatal arrhythmia without immediate CPR and defibrillation.

Answer 86

Atrial natriuretic peptide: Released from atrial myocytes in response to increased blood volume and atrial pressure. Acts via cGMP. Causes vasodilation and decrease Na+ reabsorption at the renal collecting tubule. Dilates afferent renal arterioles and constricts efferent arterioles, promoting diuresis and contributing to “aldosterone escape” mechanism. B-type (brain) natriuretic peptide Released from ventricular myocytes in response to increased tension. Similar physiologic action to ANP, with longer half-life. BNP blood test used for diagnosing HF (very good negative predictive value). Available in recombinant form (nesiritide) for treatment of HF.

Answer 87

Mnemonic: CO2, H+, Adenosine, Lactate, K+ (CHALK) Heart: Local metabolites (vasodilatory): adenosine, NO, CO2, decreased O2 Brain: Local metabolites (vasodilatory): CO2 (pH) Kidneys: Myogenic and tubuloglomerular feedback Lungs: Hypoxia causes vasoconstriction Skeletal muscle Local metabolites during exercise: lactate, adenosine, K+, H+, CO2 At rest: sympathetic tone *Note: 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 88

1. Fetal alcohol syndrome - VSD, PDA, ASD, tetralogy of Fallot 2. Congenital rubella - PDA, pulmonary artery stenosis, septal defects 3. Down Syndrome -AV septal defect (endocardial cushion defect), VSD, ASD 4. Diabetic mother - transposition of the great vessels 5. Marfan Syndrome -MVP, thoracic aortic aneurysm and dissection, aortic regurgitation 6. Prenatal lithium exposure - Ebstein anomaly 7. Turner Syndrome - Bicuspid aortic valve, coarctation of aorta 8. Williams syndrome - Supravalvular aortic stenosis 9. 22q11 syndrome - Truncus arteriosus, tetralogy of Fallot

Answer 89

90% of hypertension is 1° (essential) and related to increased CO or increased TPR. Remaining 10% mostly 2° to renal/renovascular disease (eg, fibromuscular dysplasia [which has characteristic “string of beads” appearance of renal artery], atherosclerosis) and 1° hyperaldosteronism. Hypertensive urgency—severe (≥ 180/≥ 120 mm Hg) hypertension without acute end-organ damage. Hypertensive emergency—severe hypertension 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: seizures that occur during a woman's pregnancy or shortly after giving birth.). PREDISPOSES TO CAD, LVH, HF, atrial fibrillation; aortic dissection, aortic aneurysm; stroke; chronic kidney disease (hypertensive nephropathy); retinopathy.

Answer 90

Takotsubo cardiomyopathy: “broken heart syndrome”—ventricular apical ballooning likely due to increased sympathetic stimulation (s t re s s f u l sit u at ion s). _________________________ Post-menopausal women  Can mimic ACS  Chest pain, diffuse T-wave inversions, + Troponin  Echo, cardiac cath – LV gram  LV function normalizes over days or weeks

Answer 91

. (has sign of infection, hypotension, maybe she is bleeding. and age of cardiovascular risk (maybe cardiac event) ``` Before PE DD: •  Hypovolemic Shock –  Bleeding –  Inadequate fluid resuscita>o ``` • Cardiogenic Shock –  MI, arrythmia, pulmonary embolu •  Distributive Shock –  Sepsis _________________________ Significant PE findings -febrile -skin is warm pink and well perfused, -no JVD -lungs are clear (suggesting that its not a cardiogenic shock) -normal S1,S2, no S3/S4 , not a primary problem with the heart -that leaves us with septic shock or hypovolemic shock so this must be septic shock.

Answer 92

Clinical features of pericardial tamponade Hypotension Muffled HS JV distension (due to impaired filling) + tachycardia pulsus paradoxus

Answer 93

Cardiogenic shock

Answer 94

``` Hypovolemic: Caused by: hemmorhage, dehydration, burns. Skin - cold and clammy PCWP- really low CO - low SVR - high Treatment: IV fluid ``` ``` Cardiogenic: Caused by Acute MI, HF, vavlular dyfunction, arrhythmia Skin - cold clammy - Preload can be increased or decreased CO- REALLY LOW SVR - high Treatment: inotropes, diuretics ``` ``` Obstructive: Caused by cardiac tamponade, pulmonary embolism, tension pneumothorax, Skin -cold, clammy PCWP can be increased or decreased CO - REALLY LOW Treatment: relieve obstruction ``` ``` Distributive: Caused by sepsis, anaphylaxis, Skin- warm PCWP - low CO - high SVR - REALLY LOW Tx- IV fluids, pressors ``` ``` caused by CNS injury Skin - dry PCWP - low CO- low SVR - REALLY low HR - slow** Tx- IV fluids, pressors ```

Answer 95

``` Sulfa drugs, Hydralazine, Isoniazid, Procainamide, Phenytoin, Etanercept Methyl-dopa ```

Answer 96

Most common cardiomyopathy (90% of cases). Often idiopathic or familial. Other etiologies include chronic Alcohol abuse, wet Beriberi, Coxsackie B viral myocarditis, chronic Cocaine use, Chagas disease, Doxorubicin toxicity, hemochromatosis, sarcoidosis, peripartum cardiomyopathy. Findings: HF, S3, systolic regurgitant murmur, dilated heart on echocardiogram, balloon appearance of heart on CXR. Treatment: Na+ restriction, ACE inhibitors, β-blockers, diuretics, digoxin, ICD, heart transplant. Systolic dysfunction ensues. Eccentric hypertrophy A (sarcomeres added in series). ABCCCD.

Answer 97

Slowest conduction: 1. AV node - .05, 40-55 bpm 2. Ventricular myocardium - .3 - 1.0, no beats 3. atrial myocardium - 1.0-1.2, no beats 4. Bundle of his - 1.2 - 2.0, 25-40 bpm 5. Bundle branches/Purkinje network - 2.0-4.0, 25-40 bpm.

Answer 98

``` Left: [symptoms]- -Dyspnea -Orthopnes -PND -Fatigue ``` ``` [physical findings] -Tachycardia/Tachypnea -Rales -Cheyne-Stokes -S3 gallop (Systolic Dysfunction) - S4 gallop (diastolic dysfunction) ________________ Right: [symptoms] -Peripheral edema -RUQ discomfort -Decreased appetite ``` [physical findings] - Jugular venous distension - Hepatomegaly - Peripheral edema - Ascites

Answer 99

LQT1 - decreased outward potassium - AD and AR LQT2 - decreased outward potassium AD only LQT3 (sodium channel) - increased inward sodium AD only Inherited disorder of myocardial repolarization, typically due to ion channel defects; increase risk of sudden cardiac death (SCD) due to torsades de pointes. Includes: 1. Romano-Ward syndrome—autosomal dominant, pure cardiac phenotype (no deafness). 2Jervell and Lange-Nielsen syndrome— autosomal recessive, sensorineural deafness. 3. Autosomal dominant disorder most common in Asian males. ECG pattern of pseudo-right bundle branch block and ST elevations in V1-V3. Increase risk of ventricular tachyarrhythmias and SCD. Prevent SCD with implantable cardioverter-deibrillator (ICD).

Answer 100

B - radial to femoral pulse delay this is a coarctation of the aorta - notching will occur before or after the PDA - the differential cyanosis will only occur if coarctation is before the open ductus, if there was no open ductus there would be no flow for infants because no intercostals

Answer 101

Likely a bicupsid aorta. B. Ascending aortic dilatation - bicuspid aorta is associated with higher rates of aortic stenosis, aortic dissection and aortic aneurysm.

Answer 102

Marfan syndrome—[AD]!! connective tissue disorder affecting skeleton, heart, and eyes. FBN1 gene mutation on chromosome 15 results in defective fibrillin, a glycoprotein that forms a sheath around elastin. Findings: tall with long extremities; pectus carinatum (more speciic) or pectus excavatum; hypermobile joints; long, tapering fingers and toes (arachnodactyly); cystic medial necrosis of aorta; bicuspid aorta, aortic incompetence and dissecting aortic aneurysms; loppy mitral valve. Subluxation of lenses, typically upward and temporally.

Answer 103

All of the above. A.  Weak or absent left carotid pulse B.  Wide pulse pressure - no hypovolemic shock because you aren't losing blood volume, but it can rupture. Diastolic drops - 40% will have aortic regurgitation - the head bobbing, pulsation in the capillary beds of finger (quinckes), the huge differential in pressure causes the headbobbing (systolic + low diastolic) C.  Early diastolic decrescendo murmur D.  Weak or absent left brachial pulse E.  All of the above

Answer 104

A. most common cause is degenerative *B. screening for this disorder is cost effective C. below the renals usually D. likely caused by just hypertension and atherosclerosis and inflammation

Answer 105

Syndromic connective tissue disorders - Marfan Syndrome: fibrillin - Ehlers-Danlos (vascular): type III pro-collagen - Loeys-Dietz Syndrome: TGF-beta receptor - Turner syndrome: XO

Answer 106

* *thoracic is acquired - mostly degenerative (hypertension, smoking, atherosclerosis) - acquired infection (SYPHILIS, arteritis of the vasovasorum within the media) Often asymptomatic -most common presenting symptom is pain - acute will imply and impending rupture or dissection {Aortic} -environmental risk is more important as dissection is more likely degenerative -smoking, COPD, prior aneurysm, CAD, hypertension -hereditary disorders (Marfan, E-D), genetics -usually asymptomatic until rupture - symptoms can include back, flank, abdominal or groin pain, occassionally compressive symptoms, PE- unreliable but you can find a pulsatile abdominal mass in the epigastric region [rupture] -abdominal or back pain plus low blood pressure -ruptured AAA - groin pain, syncope, paralysis and flank mass- rupture of AAA has 80% mortality -Physical signs; hypotension, cold clammy extremities, other signs of shock - it takes time to get septic shock but this is very acute FA Associated with cystic medial degeneration. Risk factors include hypertension, bicuspid aortic valve, connective tissue disease (eg, Marfan syndrome). Also historically associated with 3° syphilis (obliterative endarteritis of the vasa vasorum). Aortic root dilatation may lead to aortic valve regurgitation.

Answer 107

Look for signs of arterial insufficiency - absent or diminished pulses * **-atrophy of calf muscles ) bilateral because occlusion in one is leading to lack of exercise entirely - disease of distal superficial femoral artery is most common! - male erectile dysfunction - (aortoiliac area, pain in thigh and buttocks - thickened toe nails - (not predictive sign)- loss of hair below the knees) - thin, shiny skin (venous disease skin gets thicken, hemosideron deposition) - non-healing wounds - **dependent rubor - ischemia interferes with normal autonomic autoregulation of arterioles so they no longer constrict in the presence of pressure (turn pale when press skin) - dependent because if you lift the leg then it turns white

Answer 108

``` [Hypovolemic] Caused by: hemmorhage, dehydration, burns, trauma Skin - cold and clammy PCWP- really low - low preload CO - low SVR - HIGH Treatment: IV fluid ``` **Look for narrow pulse pressure >750 mL of blood loss, systolic BP is normal and becomes reduced Diastolic BP is increased because you have severe narrowing of blood vessels -cardiac compliance is normal or low

Answer 109

``` Distributive: Caused by sepsis, anaphylaxis, Skin- warm PCWP - low, low filling pressures NO JVD CO - high - decreased MAP tho because of volume depletion Contractility - low SVR - REALLY LOW **warm, dry skin, pink Tx- IV fluids, pressors ``` SEPTIC SHOCK - profound (vasoplegic shock) vasodilation and permeability (disrupted cell-cell contacts) + decreased perfusion in periphery despite increased vasopressors -initiated by danger signals - pathogen associated molecular patterns, recognized leading to robust inflammatory response NEUROGENIC SHOCK - sympathetic tone secondary to spinal cord injury ANAPHYLACTIC SHOCK - histamine, leukotriene C4, prostaglandin D2 release cause profound vasodilation

Answer 110

``` Cardiogenic: Caused by Acute MI, HF, vavlular dyfunction, arrhythmia Skin - cold clammy - Preload can be increased or decreased *YES JVD CO- REALLY LOW SVR - high -vasoconstriction Low MAP - low SV Treatment: inotropes, diuretics ``` * leading cause of death for patients with acute MI - primary pump failure: myocardial infarction (>40% ventricle) - cardiomyopathy (fulminant myocarditis, dilated cardiomyopathy) - rhythm disturbance, valvular heart disease pathophysiology 1. coronary occlusion/myocardial ischemia 2. profound depression of myocardial contractility 3. reduced cardiac output 4. low blood pressure * *5. worsening coronary insufficiency (perfusion of coronaries depends on pressure in aortic root so if pressure falls, worse perfusion) Findings: 1. Hypotension and low cardiac output - tachycardia, faint pulses 2. hypoperfusion: agitation, disorientation, or lethargy - cool, clammy, cyanotic extremities - oliguria (low urine output) 3. congestion: elevation of jugular venous pressure, pulmonary rales, third heart sounds.

Answer 111

``` Obstructive: Caused by cardiac tamponade, pulmonary embolism (increased afterload), tension pneumothorax, Skin -cold, clammy PCWP can be increased or decreased [*YES JVD] Filling pressures are HIGH PVR is HIGH CO - REALLY LOW Treatment: relieve obstruction -IMPAIRED venous return to R or l ventricle ``` Clinical features of pericardial tamponade (1. hypotension, 2. muffled HS, 3. JV distension - Beck's triad) 4. * *look for PULSUS PARADOXUS: an abnormally large decrease in systolic blood pressure and pulse wave amplitude during inspiration. The normal fall in pressure is less than 10 mmHg. 5. ELECTRICAL ALTERNANS - alternating QRS morphology. The heart is floating in a sac so the vector is shifting all the time ``` Mechanism of pulsus paradoxus: with -increased venous return to right side of the heart > there is no change to the volume of the left ventricle, the reason for this is because the right ventricle is complaint, when there is volume around the pericardial sac, the pressure is on the walls of both ventricles. The right ventricle is not compliant as the excess volume comes into it then, the only complaint area that is not really feeling the pressure is the septum which pushes into the left and impedes the blood filling the LV from the pulmonary circulation, LV volume declines, drop in LV pressure worsens. _________________________________ Tension pneumothorax: Clinical features 1. Absent breath sounds 2. Jugular Venous distension 3. Tracheal deviation -CVP is high (no muffled heart sounds unlike tamponode) ```

Answer 112

Contraction: 1. action potential reaches Smooth MUSCLE CELL > membrane depolarization 2. L-type voltage gated calcium channel > influx 3. Increased intracellular calcium 4. Calcium binds to CALMODULIN 5. Ca2+-calmodulin activate MYOSIN LIGHT CHAIN KINASE (MLCK) 6. MLCK phosphorylates light chains in myosin heads and increases myosin ATPase activity 7. active myosin crossbridges slide along actin and create muscle tension Relaxation 1. Agonist binds to receptor on ENDOTHELIAL CELL (acetylcholine, bradykinin) 2. increased calcium 3. NO synthase active > (L-arginine to NO) 4. NO quickly diffuses into the smooth muscle cell 5. NO converts GTP > cGMP 6. cGMP activates MYOSIN-LIGHT Chain phosphatase (MLCP) relaxation

Answer 113

Answer 1. (D) The patient is quickly going into shock after trauma. So-called shock lung, with diffuse alveolar damage, is common in this situation. Infarction of the liver is uncommon because of this organ’s dual blood supply. Basal ganglia hemorrhages are more typical of hypertension, not hypotension with shock. Passive congestion is less likely because of the diminished blood volumes and tissue perfusion that occur in shock. Gangrene requires much longer to develop and is not a common complication of shock.

Answer 114

Answer 2. (A) Atherosclerosis is thought to result from a form of endothelial injury and the subsequent chronic inflammation and repair of the intima. All risk factors; including smoking, hyperlipidemia, and hypertension, cause biochemical or mechanical injury to the endothelium. Formation of foam cells occurs after the initial endothelial injury. Although lipoprotein receptor alterations can occur in some inherited conditions, these account for only a fraction of cases of atherosclerosis, and other lifestyle conditions do not affect their action. Inhibition of LDL oxidation should diminish atheroma formation. Vasomotor tone does not play a major role in atherogenesis.

Answer 115

3. (B) CRP is an acute phase reactant that increases in response to inflammation. It causes endothelial cell activation, promotes thrombosis, and increases leukocyte adhesiveness in developing atheromas. Since atherogenesis is partly an inflammatory process, the CRP is an independent predictor of cardiovascular risk. PR3 is one type of antineutrophil cytoplasmic autoantibody (ANCA) associated with some vasculitides such as microscopic polyangiitis. Cryoglobulins may be found with some forms of immune complex mediated vasculitis. The ESR (“sed rate”) is a very non-specific indicator of inflammation and therefore the internists’ least favorite test; the ESR is best known to be markedly elevated with giant cell arteritis. Though platelets play a role in atheroma formation, the actual number of platelets is not a predictor of atherogenesis.

Answer 116

4. (B) This patient has essential hypertension (no obvious cause for his moderate hypertension). Renal retention of excess sodium, which is thought to be important in initiating this form of hypertension, leads to increased intravascular fluid volume, increase in cardiac output, and peripheral vasoconstriction. Increased catecholamine secretion (as can occur in pheochromocytoma), gene defects in aldosterone metabolism, and renal artery stenosis all can cause secondary hypertension. Hypertension secondary to all causes is much less common, however, than essential hypertension. Increased production of atrial natriuretic factor reduces sodium retention and reduces blood volume.

Answer 117

C) Abdominal aneurysms are most often related to underlying atherosclerosis. This patient has multiple risk factors for atherosclerosis, including diabetes mellitus, hypertension, and smoking. When the aneurysm reaches this size, there is a significant risk of rupture. An aortic dissection is typically a sudden, life-threatening event with dissection of blood out of the aortic lumen, typically into the chest, without a pulsatile mass. The risk factors for atherosclerosis and hypertension underlie aortic dissection. An arteriovenous fistula can produce an audible bruit on auscultation. Glomus rumors are usually small peripheral masses. Polyarteritis nodosa can produce small microaneurysms in small arteries. Takayasu arteritis typically involves the aortic arch and branches in children. Thromboangiitis obliterans (Buerger disease) is a rare condition with occlusion of the muscular arteries of the lower extremities in smokers.

Answer 118

.6. (A) Prolonged fever, heart murmur, mild splenomegaly, and splinter hemorrhages suggest a diagnosis of infective endocarditis. The valvular vegetations with infective endocarditis are friable and can break off and embolize. The time course of weeks suggests a “subacute” form of bacterial endocarditis resulting from infection with a less virulent organism, such as Streptococcus viridans. Trypanosoma cruzi and coxsackievirus B are causes of myocarditis. Candida is not a common cause of infective endocarditis, but may be seen in immunocompromised patients. Tuberculosis involving the heart most often manifests as pericarditis. Pseudomonas is more likely to cause an acute form of bacterial endocarditis that worsens over days, not weeks; this organism is more common as a nosocomial infection or in injection drug users.

Answer 119

Answer 7. (A) In the period immediately after coronary thrombosis, arrhythmias are the most important complication and can lead to sudden cardiac death. It is believed that, even before ischemic injury manifests in the heart, there is greatly increased electrical irritability. Pericarditis and rupture occur several days later. An aneurysm is a late complication of healing of a large transmural infarction; a mural thrombus may fill an aneurysm and become a source of emboli. If portions of the coronary thrombus break off and embolize, they enter smaller arterial branches in the distribution already affected by ischemia.

Answer 120

Answer 8. (C) These findings indicate a floppy mitral valve, a condition that usually is asymptomatic. When symptomatic, it can cause fatigue, chest pain, and arrhythmias. Pulmonic stenosis is most often a congenital heart disease. Valvular vegetations suggest endocarditis, and a murmur is likely to be heard with infective endocarditis causing valvular insufficiency. A patent ductus arteriosus causes a shrill systolic murmur. Tricuspid regurgitation is accompanied by a rumbling systolic murmur.

Answer 121

.Answer 9. (E) Cyanosis at this early age suggests a right-to-left shunt; truncus arteriosus, transposition of the great arteries, and tetralogy of Fallot are the most common causes of cyanotic congenital heart diseases. The cerebral lesion suggests an abscess as a consequence of septic embolization from infective endocarditis, which can complicate congenital heart disease. Atrial septal defect, patent ductus arteriosus, and ventricular septal defect initially lead to left-to- right shunts. Coarctation is not accompanied by a shunt and cyanosis. In most cases, a bicuspid valve is asymptomatic until adulthood, and there is no shunt.

Answer 122

0-1 day: 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 increase of free calcium influx COmplications: ventricular arrhythmia, cardiogenic shock 1-3 days: extensive coagulative necrosis, tissue surrounding infarct shows acute inflammation with neutrophils. Complications: postinfarction fibrinous pericarditis 3-14 days - 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). ``` 2 weeks to several months -contracted scar complete -Dressler syndrome, HF, arrhythmias, true ventricular aneurysm (risk of mural thrombus). ```

Answer 123

Answer 10. (C) The kinetics of creatine kinase (CK), CK-MB, and troponin I elevations after a myocardial infarction (MI) are important. 6-12 hrs after an MI, peaks at about 16 to 24 hours, and return to normal within 48 hours. Troponin I levels begin to increase at 4 hours but remain elevated for 7 to 10 days. Total CK activity is a sensitive marker for myocardial injury in the first 24 to 48 hours. CK-MB offers more specificity, but not more sensitivity. Myocardial rupture occurs 5 to 7 days after myocardial necrosis. This patient had an MI on the day of the shoulder pain. When he saw the physician on day 3, the CK levels had returned to normal, but troponin I levels remained elevated. Three days later, the infarct ruptured

Answer 124

In the first 6 hours, ECG is the gold standard. Cardiac troponin I rises after 4 hours (peaks at 24 hr) and is increase for 7–10 days; more speciic than other protein markers. CK-MB rises after 6–12 hours (peaks at 16–24 hr) and is 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. Large MIs lead to greater elevations in troponin I and CK-MB. Exact curves vary with testing procedure. 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 125

Classically seen in tertiary syphilis which causes endarteritis of the vasa vasorum in the adventitia resulting in luminal narrowing, decreased flow and atrophy of the vessel wall. Results in a "TREE BARK" appearance of aorta The major complication is dilation of the aortic valve root resulting in aortic valve insufficiency. oTher complications include compression of the mediastinal structures like the airway or esophagus and thombosis + emboli

Answer 126

BELOW the renal arteries, ABOVE the aortic bifurcation Primarily due to atherosclerosis, classically seen in male smokers >60 yrs resulting in atrophy and weakness of the wall. Pulsatile abdominal mass that grows with time Major complication is rupture, specially when >5 cm in diameter, presents with triad of hypotension, pulsatil mass and flank pain. Other complications include compression of local structures (ureter and thrombosis/embolism

Answer 127

1. Hyaline arteriolosclerosis with benign HT or diabetes 2. Hyperplastic arteriolosclerosis with malignant HT Hyaline arteriolosclerosis is caused by proteins leaking into the vessel wall producign vascular thickening. Results in reduced vessel caliber with end organ ischemia, classically produces glomerular scarring (arteriolonephrosclerosis that slowly progresses to chronic renal failure Benign HTN is mild or moderate, clinicall silent vessels and organs are damaged slowly over time. Hyperplastic arteriolosclerosis involves thickening of vessel wall by hyperplasia of the smooth muscle (onion skin appearance). consequence of malignant hypertension. Results in reduced vessel caliber with end organ ischemia. May lead to fibrinoid necrosis of the vessel wall with hemorrhage. classically causes acute renal failure with characteristic flea bitten appearance. Malignant HTN is severe elevation in bp >180/120 - presents with acute end organ damage (acute renal failure, headache and papilledema and is a medical emergency.

Answer 128

Normal: Less than 120/80 mm Hg; Elevated: Systolic between 120-129 AND diastolic less than 80; Stage 1: Systolic between 130-139 OR diastolic between 80-89; Stage 2: Systolic at least 140 or diastolic at least 90 mm Hg; Hypertensive crisis: Systolic over 180 and/or diastolic over 120, with patients needing prompt changes in medication if there are no other indications of problems, or immediate hospitalization if there are signs of organ damage.

Answer 129

``` Dressler syndrome (autoimmune-mediated post-MI fibrinous pericarditis, 2 weeks to several months after acute episode) ```

Answer 130

Endothelial malignancy most commonly of the skin, but also mouth, GI tract, and respiratory tract. Associated with HHV-8 and HIV. Rarely mistaken for bacillary angiomatosis, but has lymphocytic infiltrate. Presents as purple patches plaques and nodules on the skin. May also involve visceral organs. Classically seen in older eastern european males, AIDs, and transplant recipients.

Answer 131

malignant proliferation of the endothelail cells, highly aggressive. Common sites include skin breast and liver. Liver angiosarcoma is associated with exposure to polyvinyl cholride, arsenic and thorotrast. FA: Rare blood vessel malignancy typically occurring in the head, neck, and breast areas. Usually in elderly, on sun-exposed areas. Associated with radiation therapy and chronic postmastectomy lymphedema. Hepatic angiosarcoma associated with vinyl chloride and arsenic exposures. Very aggressive and difficult to resect due to delay in diagnosis.

Answer 132

The pulmonary nodules are due to septic emboli breaking off from the tricuspid. Most likely pathogen is S. aureus Prosthetic valves are better It doesn't cause stenosis, it causes regurg pulmonary nodules are form the platelets Answer: stroke symptoms can occur in these patients

Answer 133

``` Fever (most common symptom), new murmur Roth spots (round white spots on retina surrounded by hemorrhage A ), Osler nodes (tender raised lesions on inger or toe pads due to immune complex deposition), -Janeway lesions (small, painless, erythematous lesions on palm or sole) glomerulonephritis, septic arterial or pulmonary emboli, splinter hemorrhages on nail bed. Multiple blood cultures necessary for diagnosis. Acute—S aureus (high virulence). Large vegetations on previously normal valves. Rapid onset. ``` ``` Subacute—viridans streptococci (low virulence). Smaller vegetations on congenitally abnormal or diseased valves. Sequela of dental procedures. Gradual onset. ``` ``` S bovis (gallolyticus) is present in colon cancer, S epidermidis on prosthetic valves. Endocarditis may also be nonbacterial (marantic/thrombotic) 2° to malignancy, hypercoagulable state, or lupus. ``` Mitral valve is most frequently involved. Tr i cuspid valve endocarditis is associated with IV drug abuse (don’t “tri” drugs). A ssociated with S aureus, Pseudomonas, and Candida. Culture ⊝; most likely Coxiella burnetii, Bartonella spp., HACEK (Haemophilus, Aggregatibacter (formerly Actinobacillus), Cardiobacterium, Eikenella, Kingella) ♥ Bacteria FROM JANE ♥: Fever Roth spots Osler nodes Murmur Janeway lesions Anemia Nail-bed hemorrhage Emboli

Answer 134

Viral myocarditis - most common cause

Answer 135

This is acute rheumatic fever Damage at this stage can affect all layers of the heart.

Answer 136

Description is of Acute viral pericarditis - or idiopathic Heart is constantly being compresssed, Y descent is when fluid leaves into the ventricles but you can only have more filling if there is space. B. absent y descent. - Prominent V wave indicates tricuspid regurg. - Prominant X and Y descents are indicative of restrictive pericarditis - square root sign is also show on pericardial constriction - inspiratory increase in JVP - they should decrease because you increase more filling of the heart, if JVP increases, that is mostly seen in pericardial constriction.

Answer 137

Midsystolic murmur. "I was doing some Kaplan questions and realized there is a discrepancy between first aid and our lectures slides/lilly. For ASD, our slides say it causes a systolic murmur on the upper left sternal boarder due to increased flow across the pulmonic valves. However, in first aid it says there is a middiastolic murmur at the left lower sternal boarder due to increased flow across the tricuspid valve. I read Lilly and it mentions it is possible to have both murmurs. However, in regard to the exam and STEP, which murmur should we more so associate with it?" A: Probably the most important thing to know about ASDs is that Patients with ASDs can have a murmur The murmur is NOT caused by the flow of blood through the ASD- why? The low velocity shunt flow across the ASD (due to the low pressure differential between the left and right atria) produces insufficient turbulence for a murmur to be heard So what causes the murmur that you can hear? It is the increased volume of blood presented to the right side of the heart that causes a FLOW murmur across the right-side valves-especially the pulmonic valve during systole. You would therefore expect: #1 A midsystolic pulmonary flow or ejection murmur, resulting from the increased blood flow across the pulmonic valve, is found in 90% of a large cohort of ASD patients. Up-to-date says that "the characteristic cardiac findings of an ASD include a midsystolic pulmonary flow or ejection murmur accompanied by a fixed split second heart sound" The above is what I would consider most important- that being said; you CAN also hear a tricuspid flow murmur in diastole if you listen VERY carefully😊 as described below! A middiastolic murmur of low to medium frequency due to high flow across the tricuspid valve may also be heard with careful auscultation- (meaning it is not easy to hear) and patients need to have a larger left-to-right shunt for that to be present

Answer 138

Inlammation of the pericardium. Commonly presents with sharp pain (can refer to shoulder), aggravated by inspiration, and relieved by sitting up and leaning forward. Often complicated by pericardial effusion. Presents with: -pericardial friction rub "sandpaper" (with 3 components, ventricular systole, diastolic filling and atrial contraction). -ECG changes include WIDEspread ST-segment elevation and/or PR depression. -Fever Causes include idiopathic (most common; presumed viral), conirmed infection (eg, Coxsackievirus, adenovirus, echovirus), neoplasia, autoimmune (eg, SLE, rheumatoid arthritis), uremia, cardiovascular (acute STEMI or Dressler syndrome), radiation therapy.

Answer 139

A consequence of pharyngeal infection with group A β-hemolytic streptococci. Late sequelae include rheumatic heart disease, which affects heart valves—mitral > aortic >> tricuspid (high-pressure valves affected most). Early lesion is mitral valve regurgitation; late lesion is mitral stenosis. Associated with Aschoff bodies (granuloma with giant cells [blue arrows in A ]), Anitschkow cells (enlarged macrophages with ovoid, wavy, rod-like nucleus [red arrow in A ]), q anti- streptolysin O (ASO) titers. Immune mediated (type II hypersensitivity); not a direct effect of bacteria. Antibodies to M protein cross-react with self antigens (molecular mimicry). Treatment/prophylaxis: penicillin.

Answer 140

Compression of the heart by luid (eg, blood, effusions [arrows in A ] in pericardial space) p r CO. Equilibration of diastolic pressures in all 4 chambers. Findings: Beck triad (hypotension, distended neck veins, distant heart sounds), q HR, pulsus paradoxus. ECG shows low-voltage QRS and electrical alternans (due to “swinging” movement of heart in large effusion). Pulsus paradoxus—r in amplitude of systolic BP by > 10 mm Hg during inspiration. Seen in cardiac tamponade, asthma, obstructive sleep apnea, pericarditis, croup.

Answer 141

3° syphilis disrupts the vasa vasorum of the aorta with consequent atrophy of vessel wall and dilatation of aorta and valve ring. May see calciication 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 insuficiency. Classically the cause of thoracic aorta aneurysm leading to dilation of the aortic root.

Answer 142

Streptococcus bovis Gram ⊕ cocci, colonizes the gut. S gallolyticus (S bovis biotype 1) can cause bacteremia and *subacute endocarditis and is associated with colon cancer. Bovis in the blood = cancer in the colon.

Answer 143

Peripheral arterial disease A: dependent rubor in left leg Left superficial femoral artery

Answer 144

-wavy myofibrils and contraction bands at infarct edges

Answer 145

Constrictive pericarditis Early diastolic knock on cardiac auscultation

Answer 146

Multiple cavitating pulmonary nodules on chest x ray Tricuspid vegetation from endocarditis. `

Answer 147

Holosystolic murmur at the apex radiating to the axilla. Migratory polyarthritis

Answer 148

Disarray of the cardiomyocytes with fibrosis Metoprolol

Answer 149

-impaired left ventricular filling

Answer 150

Alcohol Murmur results from dilation of the valve annulus

Answer 151

Continuous murmur over the midback Bicuspid aortic valve

Answer 152

increasing venous capacitance

Answer 153

Intimal tear in the ascending aorta

Answer 154

In the Congenital Heart Defects lecture slide below, it says that ASD closure is contraindicated once Eisenmenger’s is present – could you elaborate on why that is? So there are two thoughts to why this is so, and I will tell you that up-to-date says it is a "complex decision" so these patients should be referred to specialists. Clearly-- "contraindicated" may not be a 100% hard and fast rule. That being said, let's explore the possibilities. #1 most people with ASDs DO NOT get eisenmenger's (10%)- it is more common in VSD (50%) and PDA (almost all these patients will get Eisenmengers if the PDA is not ID and closed). With ASD, the larger volume of blood entering in to the pulmonary circulation results in pulmonary arteriole remodeling and can induce pulmonary hypertension which is- for all intensive purposes- identical to idiopathic pulmonary hypertension- In the RV, concentric hypertrophy develops as the RV works against the pressure load and as the pulmonary HTN worsens, the load on the ventricle will worsen and the ventricle will dilate. Symptoms of RH failure can occur. In addition, the worsening pulmonary HTN results in a continued increase in RV pressure causing a R to L shunt to occur (central cyanosis and clubbing can occur). When R to L shunt occurs- it indicates that the pulmonary HTN is severe and likely to be irreversible. At this point then, it is associated with significantly reduced life expectancy of the patients, regardless of the mode of therapy. In other words, the thinking is that surgery will not reverse the damage at this point and really offers no benefit to the patient. Moreover, there is a school of thought that maintaining the intraatrial communication provides a mechanism to maintain the cardiac output at the expense of desaturation, and there may be some benefit to this.

Answer 155

``` NO - decrease endothelin - increases H+ - decreases Oxygen - increases Adenosine - decreases Prostaglandins - decreases ```

Answer 156

- small left atrium and ventricle - ascending aorta is hypoplastic - aortic and mitral valves are atretic Two requirements 1. PDA to ensure adequate systemic perfusion from RV to aorta 2. Nonrestrictive atrial septal defect to ensure adequate mixing of oxygenatd and deoxygenated blood

Answer 157

There is asymmetric hypertrophy of the left ventricular wall in HOCM, typically affecting the septum- the wall of the ventricle is stiff and this impairs filling- there can also be a component of dynamic obstruction to flow caused by the anterial MV leaflet- so you can have LVH and can get left atrial enlargement as well. With restrictive CM- the diagnosis does not require you to have thickened walls- both ventricles are affected by the infiltrative process, both ventricles will have trouble filling, and in this case- BOTH atria will be dilated leading to "owl eye" appearance on echocardiography

Answer 158

Dissections are associated with hypertension as an initial physical finding- because essential HTN is a risk factor for AD to begin with - in addition, dissection causes pain which leads to increased catecholamines. Hypotension is an ominous finding early on- indicating a catastrophic dissection- dissection of the coronaries, pericardium or a leak.

Answer 159

The reason that dependent rubor occurs is that there is autonomic dysfunction caused by the severe ischemia- so that when the leg is dependent- the dermal arterioles do not constrict in response to the increased hydrostatic pressure. When a leg is elevated (any leg) above the heart- you should have enough blood flow to the extremity to be able to overcome the effect of gravity- but with severe ischemia- the stenosis creates such low pressure that the blood can't be pumped against gravity and the extremity perfusion will be significantly impaired. In patients with lighter skin tone, the extremity will appear white, with darker skin tone, the capillary refill will be poor.

Answer 160

1. AL amyloid – Most common type – Igg light chain produced by clonal population of plasma cells in bone marrow – Multi-organ infiltration – Up to 50% have cardiac involvement – 5% have cardiac involvement alone – Age > 50, male 2:1

Answer 161

A & C are correct .

Answer 162

Inferior vena cava (IVC) compression is common in women during the third trimester of pregnancy. The large uterus compresses the IVC, decreasing venous return to the heart. This reduction in preload reduces stroke volume, thus reducing cardiac output. Recall that mean arterial pressure = cardiac output × total peripheral resistance; an acute decrease in either of these parameters will reduce blood pressure. Pregnant women can avoid this problem by placing a pillow under their right side or by lying on their left side to remove the weight of the gravid uterus from the IVC.

Answer 163

This girl has Takayasu arteritis, a large-vessel vasculitis usually found in women <40 years of age of Asian descent. It is characterized by a thickening of the aortic arch and/or the proximal great vessels. The most prominent feature is weak pulses in the upper extremities. Complications of untreated late-stage Takayasu include aortic aneurysms and typically involve the aortic arch. This leads to narrowing, or possible obliteration, of the major arteries associated with the aortic arch. Treatment involves high doses of oral prednisone that are tapered over many months as the clinician and patient agree to minimize the adverse effects of corticosteroids.

Answer 164

Posterior descending artery This patient most likely suffered from acute mitral regurgitation secondary to rupture of the posterior papillary muscle. The anterior and posterior papillary muscles anchor the chordae tendineae, which prevent the cusps of the mitral valve from being forced into the left atrium. An occlusion of the posterior descending artery can lead to an infarction of the posterior papillary muscle and subsequent rupture of the muscle several days later. Patients will present with a sudden onset of pulmonary edema and frequently cardiogenic shock. The anterior papillary muscle is supplied by both the left anterior descending artery and the left circumflex artery. Because of its dual blood supply, the anterior papillary muscle is less likely to rupture after a MI. Furthermore, the patient’s initial MI involved the posterior aspect of the myocardium

Answer 165

Sigmoid colon The inferior mesenteric artery (IMA) originates from the aorta inferior to the renal arteries and superior to the bifurcation of the aorta into the common iliac arteries. The IMA supplies blood to the distal one-third of the transverse colon, descending and sigmoid colons, and the upper portion of the rectum. The IMA may sometimes be sacrificed during an infrarenal aortic aneurysm repair rather than being reattached to a healthy segment of aorta. Usually there is enough collateral flow to the hindgut from the superior mesenteric artery and the hypogastric arteries that the loss of the IMA does not result in costep

Answer 166

Disruption of the vasovasorum Syphilitic aortitis is characterized by obliterative endarteritis of the vasa vasorum of the tunica media. This disruption of the vasa vasorum can lead to an aneurysm, typically involving the ascending aorta, and is a manifestation of the tertiary stage of the disease. Syphilitic aneurysms are often complicated by atherosclerosis. The patient’s skin lesions are likely “gummas” of tertiary syphilis, which appear as fibrous nodules on the skin surface. Less commonly, these lesions can be ulcerative.

Answer 167

Kawasaki disease, a vasculitis of unknown etiology that is hypothesized to be an infectious or autoimmune response (ie, molecular mimicry). The major symptoms include a 1-high fever of more than five days’ duration, 2-bilateral conjunctivitis, 3-lip fissures, 4-strawberry tongue, 5-palmar and plantar desquamation, 6-cervical lymphadenopathy. Minor criteria may include elevated acute phase reactants, leukocytosis, thrombocytosis, and mild elevation of liver function test results. The most important complication of Kawasaki disease is the development of coronary artery aneurysms, which can result in MI. IV immunoglobulin and aspirin is the appropriate therapy.

Answer 168

-decreased barroreceptor firing in the carotid sinus, The carotid sinus baroreceptor sends an afferent signal via the glossopharyngeal nerve to the medulla, which in turn responds by increasing sympathetic outflow. This results in systemic vasoconstriction, increased heart rate, increased contractility, and increased blood pressure. The baroreceptor located in the aortic arch responds only to an increase in blood pressure.

Answer 169

Gq - activates phospholipase C, increasing IP3 and calcium, DAG alpha1, M1, M3 Gi - inhibition of adenylate cyclase (decrease cAMP) - alpha2, M2, D2 Gs - stimulation of adenylate cyclase (increase cAMP) - beta1, beta2, D1