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Clin Medicine > Harrison > Flashcards

Harrison Flashcards

1
Q

General exam of a pt with suspected heart disease

A

Vitals
Skin color (cyanosis, pallor, jaundice)
Clubbing
Edema
Evidence of decreased perfusion (cool and diaphoresis skin)
Hypertensive changes in optic fundi
Abdomen for hepatomegaly, ascites, or aaa
Ankle brachial index (systolic bp at angle divided by arm systolic )

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2
Q

Carotid pulsus parvus

A

Weak upstroke due to decreased stroke volume (hypovolemia, LV failure, aortic or mitral stenosis

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3
Q

Carotid pulsus tardus

A

Delayed upstroke (aortic stenosis)

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4
Q

Carotid bounding (hyperkinetic pulse)

A

Hyperkinetic circulation, aortic regurgitaiton, pda, marked vasodilation

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5
Q

Carotid pulsus bisferiens

A

Double systolic pulsation (aortic regurgitation, hypertrophic cardiomyopathy)

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6
Q

Carotid pulsus alternans

A

Regular alteration in pulse pressure amplitude (severe LV dysfunction)

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7
Q

Carotid pulsus paradoxes

A

Exaggerated inspiration fall (>10mmHg) in systolic bp (pericardial tamponade, severe obstructive lung disease)

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8
Q

Jugular venous pulsation

A

Jugular venous distention develops in right sided heart failure, constrictive pericarditis, pericardial tamponade, obstruction of SVC

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9
Q

JVP normally falls with inspiration but may rise (___ sign) with __ ___

A

Kussmaul

Constrictive pericarditis

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10
Q

Abnormalities in examination with JVP

A

Large a waveL tricuspid stenosis, pulmonic stenosis, atrioventricular dissociation (right atrium contracts against closed tricuspid valve)

Large v wave: ricuspid regurgitaiton, ASD

Steep y descent: constrictive pericarditis

Slow y descent : TS

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11
Q

Large a wave

A

Tricuspid stenosis, pulmonic stenosis, atrioventricular dissociation (right atrium contracts against closed tricuspid valve)

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12
Q

Large v wave

A

Tricuspid regurgitation, ASD

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13
Q

Steep y descent

A

Constrictive pericarditis

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14
Q

Slow y decent

A

TS

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15
Q

Precordial palpation

A

Cardiac apical impulse is normally localized at the 5th intercostal space, midclavicular line. Abnormalities include

Forceful apical thrustL left ventricular hypertrophy

Lateral and downward displacement of apex impulse: left ventricular dilation

Prominent presystolic impulseL HTN, aortic stenosis, hypertrophic cardiomyopathy

Double systolic apical impulse: hypertrophic cardiomyopathy
Sustained lift at lower left sternal borderL right ventricular hypertrophy

Dyskinesia (outward bulge) impulse: ventricular aneurysm, large dyskinesia area post MI, cardiomyopathy

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16
Q

Forceful apical thrust

A

Left ventricular hypertrophy

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17
Q

Lateral and downward displacement of apex impulse

A

Left ventricular dilation

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18
Q

Prominent presystolic impulse

A

HTN, aortic stenosis, hypertrophic cardiomyopathy

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19
Q

Double systolic apical impulse

A

Hypertrophic cardiomyopathy

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20
Q

Sustained lift at lower left sternal border

A

Right ventricular hypertrophy

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21
Q

Dyskinesia (outward bulge) impulse

A

Ventricular aneurysm, large dyskinesia area post MI, cardiomyopathy

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22
Q

S1 loud

A

Mitral stenosis, short PR, hyperkinetic heart, thin chest wall

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23
Q

S1 soft

A

Long PR interval, heart failure, mitral regurgitation, thick chest wall, pulmonary embolism

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24
Q

S1

A

First heart sound

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25
Q

S2

A

Second heart sound

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26
Q

A2

A

Aortic component of the second heart sound

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27
Q

P2

A

Pulmonic component of the second heart sound

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28
Q

ASD with _ of S2

A

Splitting

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29
Q

RBBB S2

A

Wide splitting

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30
Q

S2 left BBB

A

Reversed or paradoxical splitting

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31
Q

Pulmonary HTN S2

A

Narrow splitting

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32
Q

Normally A2 precedes P2 and splitting increases with inspiration; abnormalities include
S2

A

Widened plotting: RBBB, PS, mitral regurgitation

Fixed splitting : atrial septal defect

Narrow splitting: pulmonary HTN

Paradoxical splitting (splitting narrows with inspiration): aortic stenosis, left BBB, heart failrue

Loud A2:: systemic HTN

Soft A2:aortic stenosis

Loud P2: pulmonary arterial HTN

Soft P2: pulmonic stenosis

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33
Q

S3

A

Low pitched , heard best with bell of stethoscope at apex, following S2; normal in kids ; after age 30-35 indicated LV failure or volume overload

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34
Q

S4

A

Low pitched, heard best with bell at apex, preceding S1; reflects atrial contraction into a non compliant ventricle; found in AS, HTN, hypertrophic cardiomyopathy, and CAD

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35
Q

Opening snap

A

High pitched; follows S2 , ESRD at lower left sternal border and apex in MS; the more severe the MS, the shorter the S2-OS interval

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36
Q

Ejection clicks

A

High pitched sounds following S1 typically loudest at left sternal border;observed in dilation of aortic rot or pulmonary artery, congenital AS or PS; when due to the latter, click decreases with inspiration

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37
Q

Midsystolic clicks

A

At lower left sternal border and apex, often followed by late systolic murmur in MVP

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38
Q

Systolic murmur

A

Crescendo decrescendo ejection type or pan systolic or late systolic

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39
Q

Right sided murmurs increase with ____

A

Inspiration

Tricuspid regurgitation

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40
Q

Ejection type murmur

A

Aortic outflow tract

Aortic valve stenosis

Hypertrophic obstructive cardiomyopathy

Aortic flow murmur

Pulmonary outflow tract

Pulmonic valve stenosis

Pulmonic flow murmur

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41
Q

Holosystolic

A

Mitral regurgitation

Tricuspid regurgitation

Ventricular septal defect

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42
Q

Late systolic murmu

A

Mitral or tricuspid valve prolapse

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43
Q

Early diastolic murmur

A

Aortic valve regurgitation

Pulmonic valve regurgitation

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44
Q

Mid to late diastolic murmu

A

Mitral or tricuspid stenosis

Flow murmur across mitral or tricuspid valves

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45
Q

Continuous distaolic murmur

A

PDA

Coronary AV fistula

Ruptured sinus of valsava aneurysm

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46
Q

Effect of respiration on heart murmur and sounds

A

Systolic murmurs due to TR or pulmonic blood flow through a normal or stenosis valve and diastolic murmurs of TS or PR generally increase with inspiration, as do right sided S3 and S4. Left sided murmurs and sounds usually are louder during expiration, as in the pulmonic ejection sound

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47
Q

Valsava maneuver effect on heart murmur and sound

A

Most murmurs decrease in length and intensity. Two exceptions are systolic murmur of HCM, which usually becomes much louder, and that of MVP, which becomes longer and often louder. Following release of the valsava maneuver, right sided murmurs tend to control intensity earlier than lef sided murmurs

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48
Q

Effect of after VPM or AF on murmurs and heart sounds

A

Murmurs originating at normal or stenosis semilunar valves increase int he cardiac cycle following a VPB or in the cycle after a long cycle length in AF. By contrast, systolic murmurs due to AV valve regurgitation either do not change, diminish (papillary msucle dysfunction) or become shorter (MVP)

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49
Q

Positional changes on murmurs and heart sounds

A

Standing-most murmurs diminish , two exceptions are murmur of HCM, which becomes louder and that of MVP which lengthens and often is intensified.

Squatting-most murmurs become louder, but those of HCM and MVP usually soften and may disappear.

Passive leg raising usually produces the same result

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50
Q

Exercise and heart murmurs and sounds

A

Murmurs due to blood flow across normal or obstructed valves (PS MS) become louder with both isotonic and submaximal isometric (handgrip) exercise. Murmurs of MR, VSD, and AR also increase with handgrip exercise. However the murmur of HCM often decreases with near maximum handgrip exercise. Left sided S4 and S3 are often accentuated by exercise, particularly when due to ischemic heart disease

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51
Q

Early diastolic murmurs

A

Begin immediately after S2, are high pitched, and are usually caused by aortic or pulmonary regurgitation

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52
Q

Mid to late diastolic murmurs

A

Low pitched, heard best with bell of stethoscope; observed in MS or TS; less commonly due to atrial myxoma

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53
Q

Continuous diastolic murmur

A

Present in systole and diastole (envelops s2); found in PDA and sometimes in coarctation of aorta; less common causes are systemic or coronary AV fistula, aortopulmonary septal defect, ruptured aneurysm of sinus of valsava

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54
Q

ECG

A

Ok

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55
Q

Each horizontal box time

A

.04 s

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56
Q

HR

A

300/large boxes (each 5 mm apart) between QRS.

Or divide 1500 by number of small boxes (1 mm apart)

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57
Q

Sinus rhythm

A

Present if every p wave is followed by a QRS, PR interval >.12, every QRS is preceded by a p wave, and the p wave is upright in leads I II and III

-if not arrhythmia!

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58
Q

Mean axis normal

A

If QRS is positive in limb leads I and II

*otherwise find limb lead in which QRS I’d most isoelectric (R=S). The mean axis is perpendicular to that lead.

If the QRS is positive in that perpendicular lead, then mean axis is in the direction of that lead

If negative then mean axis points directly away from that lead

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59
Q

Left axis deviation

A

More negative than -30

Occurs in diffuse left ventricular disease, inferior MI, and in left antigen hemiblock (small R , deep S in leads II, III, AVF)

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60
Q

Right axis deviation (>90%)

A

Occurs in right ventricular hypertrophy (R>S in V1) and left posterior hemiblock (small Q and tall R in leads II, III, and AVF). Mild right axis deviation is common in thin, healthy individuals ( up to110)

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61
Q

Short interval PR (.12-.2 s)

A

Short: preexcitation syndrome (look for slurred QRS upstroke due to delta wave)

Nodal rhythm (inverted P in AVF)

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62
Q

Long PR >.2

A

First degree atrioventricular AV block

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63
Q

Widened QRS .06-.1 s

A

Ventricular premature beats

BBB: right RsR’ in V1, deep S in V6) and left RR in V6)

Toxic levels of certain drugs (flecainide, propafenone, quinidine)

Severe hypokalemia

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64
Q

Prolonged QT

A

Congenital, hypokalemia, hypocalcemia (class IA and class III Antiarrhythmics, tricyclics)

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65
Q

Right atrium hypertrophy

A

P wave> 2.5 mm in lead II

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66
Q

Left atrium hypertrophy

A

P biphasic (positive, then negative) in V1, with terminal negative force wider than .04 s

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67
Q

Right ventricle hypertrophy

A

R>S in V1 and R in V1>5 mm; deep S in V6; right axis deviation

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68
Q

Left ventricle hypertrophy

A

S in V1 plus R in V5 or V6>35 mm or R in aVL

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69
Q

Infarction and ecg

A

Following acute ST elevation MI without successful reperfusion:

pathological Q waves >.04 s and >35% of total QRS height

Acute non ST segment elevation MI shows ST-T changes in these leads without Q wave development. A number of conditions can cause Q waves

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70
Q

ST wave elevation

A

Acute MI, coronary spasm, pericarditis, LV aneurysm, brigade pattern (RBBB with ST elevation in V1-V2)

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71
Q

ST depression

A

Digitalis effect, strain (due to ventricular hypertrophy), ischemic, or nontransmural MI

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72
Q

Tall peaked T

A

Hyperkalemia, acute MI

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73
Q

Inverted T

A

Non Q wave MI, ventricular strain pattern, drug effect, hypokalemia, hypocalcemia, increased intracranial pressure

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74
Q

Echo

A

Visualizes heart in real time with ultrasound

Doppler recordings noninvasively assess hemodynamics and abnormal flow patterns.

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75
Q

What compromises echo

A

COPD, thick chest wall, narrow intercostal spaces

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76
Q

Etiology mitral stenosis

A

Most commonly rheumatic, although history of acute rheumatic fever is now uncommon; rare causes include congenital MS and calcification of the mitral annulus with extension onto the leaflets

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77
Q

History mitral stenosis

A

Symptoms most commonly begin in the fourth decade, but MS often causes severe disability at earlier ages in developing nations. Rincipal symptoms are dyspnea and pulmonary edema precipitated by exertion, excitement , fever, anemia, tachycardia, pregnancy, sexual intercourse

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78
Q

Indication pacemaker

A

Unstable below AV node or at AV

1st degree AC don’t need pacing

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79
Q

PE mitral stenosis

A

Right ventricular lift

Palpable S1

Opening snap follows A2 by .06-.12 s

OS-A2 interval inversely proportional to severity of obstruction.

Diastolic rumbling murmur with presystolic accentuation when in sinus rhythm. Duration of murmur correlated with severity of obstruction

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80
Q

Complciations MS

A

Hemoptysis, pulmonary embolism, pulmonary infection, systemic embolization; endocarditis is uncommon in pure MS

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81
Q

ECG mitral stenosis

A

A fib
Left atrial enlargement when sinus rhythm is present (sinus means there is p wave)

Right axis deviation and RV hypertrophy in the presence of pulmonary HTN

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82
Q

CXR mitral stenosis

A

Shows LA and RV enlargement and kerley B lines

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83
Q

Echo MS

A

Most useful test!

Shows reduced separation, calcification and thickening of valve leaflets and subvalvular apparatus and LA enlargement.

Doppler flow recordings provide estimation of transvavlular gradient, mitral valve area, and degree of pulmonary HTN

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84
Q

Treat MS

A

Prophylaxis for recurrent rheumatic fever(penicillin)

In presence of dyspnea, sodium restriction and oral diuretic therapy; beta blockers, rate limiting calcium channel antagonists (verampamil or dilitazem) or digoxin to slow ventricular rate in AF,

Warfarin if history of thromboembolism.

For AF of recent onset, consider conversions to sinus rhythm, ideally 3 weeks of anticoagulation

Mitral valvotoms in presence of symptoms and mitral orifice <1.5 cm

Uncomplicated-percutaneous balloon valvuloplasty unless not feasible then surgical valvotomy

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85
Q

Etiology mitral regurgitation

A

MVP, rheumatic heart disease, ischemic heart disease with papillary muscle dysfunction, LV dilation of any cause, mitral annular calcification, hypertrophic cardiomyopathy, infective endocarditis, congenital

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86
Q

Clinical mitral regurgitation

A

Fatigue, weakness, and exertional dyspnea.

PE-sharp low volume upstroke of carotid arterial pulse, LV lift, S1 diminished: wide splitting of S2
S3 common
Loud HOLOsystolic murmur at the apex (less holosystolic in acute severe MR) a Nd often a brief early-mid-diastolic murmur due to increased treansvalvular flow

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87
Q

Inferior wall MI

A

Can be epigastric and stomach-GI SYMPTOMS espicially if has risks of CAD

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88
Q

Echo mitral regurgitaiton

A

Enlarged LA, hyperdynamic LV, identifies mechanism of MR, Doppler analysis helpful in diagnosis and assessment of severity of MR and degree of pulmonary HTN

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89
Q

When treat type I AV

A

Only if symptomatic

Type II is usually sympatomatic *usually distal AV-if distal no bajk up mechanisms (bundle brancha rea will have syncope and stuff)

If SA down there are back up mechanisms

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90
Q

Treat mitral regurgitaiton

A

For severe/decompen, treat as for heart failure.

IV vasodilator (nitroprusside) are beneficial for acute , severe MR. anticoagulation is indicated int he presence of A fib

Chronic primary MR-sutiglca treatment -valve repair of replacement if pt has symptoms or evidence of progressive LV dysfunction (LVEF<60% or end systolic diameter by echo>400)

Operation should be carried out before development of chronic heart failure symptoms. Patients with functional ischemic MR may require coronary artery revasculartization along with valve repair. Functional nonischemic MR due to LV enlargement with impaired contractile function should be treated with aggressive heart failure therapies and consideration fo cardiac resynchronization therapy

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91
Q

MVP etiology

A

Most commonly idiopathic; may accompany marfan, Helmer’s Danilo’s syndome

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92
Q

Pathology MVP

A

Redundant mitral valve tissue with myxedematous degeneration and elongated chordate tendinae

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93
Q

Clinical MVP

A

Females
Most asymptomatic

Potential symptoms-vague chest pain and supraventricular and ventricular arrhythmias.

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94
Q

Most important complication MVP

A

MR

Rarely-systemic emboli from platelet fibrin deposits on valve. Sudden death is very rare

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95
Q

PE MVP

A

Mid to late systolic clicks followed by late systolic murmur at the apex ; exaggeration by valsava maneuver, reduced by squatting and isometric exercise

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96
Q

Grouped beating

A

Not 3rd degree!! Means some association …

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97
Q

Echo MVP

A

Shows posterior displacement of one or both mitral leaflets late in systole

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98
Q

Treat MVP

A

Asymptomatic-reassured

Bb may lessen chest discomfort and palpitations

Prophylaxis for infective endocarditis is indicated only if prior history of endocarditis.

Valve repair or replacement for patients with severe mitral regurgitation

Asprin or anticoagulants for patients with history of TIA or embolization

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99
Q

Etiology aortic stenosis

A

Most common as

  1. Degenerative calcification of a congenitally bicuspid valve
  2. chronic deterioration and calcification of a trileaflet valve
  3. Rheumatic disease (almost always associated with rheumatic mitral valve disease)
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100
Q

Symptoms aortic stenosis

A

Exertional dyspnea, angina, and syncope are cardinal symptoms; they occur late, after years of obstruction and aortic valve area <1

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101
Q

PE aortic stenosis

A

Weak and delayed (parvus et tardus) arterial pulses with carotid thrill.

A2 soft or absent; S4 common

Crescendo-decrescendo systolic murmur, often with systolic thrill.

Murmur is typically loudest at second right intercostal space, with radiation to carotids and sometimes to the apex (gallavardin effect)

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102
Q

ECG aortic stenosis

A

Often shows LV hypertrophy but not useful for predicting gradient

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103
Q

Echocardiogram aortic stenosis

A

Shows LV hypertrophy, calcification and thickening of aortic valve cusps with reduced systolic opening. Dilation and reduced contraction of LV indicate poor prognosis. Doppler quantitative systolic gradient and allows calculation of valve area

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104
Q

Treat aortic stenosis

A

Avoid strenuous activity in severe AS, even if in asymptomatic phase

Treat heart failure in standard fashion but use vasodilator with caution in patients with advanced disease

Valve replacement is indicated in adults with symptoms resulting from AS and hemodynamic evidence of severe obstruction

Transcatheter aortic valve implantation (TAVI) is an alternative approach for patients at excessive or prohibitive surgical risk

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105
Q

Etiology aortic regurgitation

A

Valvular: rheumatic (espicially if rheumatic mitral disease is present), bicuspid valve, endocarditis.

Dilated aortic root: dilation due to cystic medial necrosis, aortic dissection, ankylosis spondylitis, syphilis

Three fourths of patients are male

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106
Q

Clinical manifestations aortic regurgitation

A

Exertional dyspnea and awareness of forceful heartbeat, angina pectoris ,and signs of LV failure

Wide pulse pressure, water hammer pulse, capillary pulsation (Quinckes sign), A2 soft or absent, S3 may be present.

Blowing, decrescendo diastolic murmur along LEFT STERNAL BORDER(along right sternal border when due to aortic dilation).

In acute sever AR< the pulse pressure is typically not widened and the diastolic murmur is often short (only in early diastole) and soft

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107
Q

Echo aortic regurgitaiton

A

LA enlargement, LV enlargement, high frequency diastolic fluttering of mitral valve. Failure of coarctation of aortic valve leaflets may be present. Doppler studies useful in direction and quantification fo AR

Cardiac MRU helpful is echo inadequate

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108
Q

Treat aortic regurgitation

A

Standard therapy for LV failure.
Vasodilator (ACE or long acting nifedipine) are recommended if HTN present.

Avoid bb which prolong diastolic filling

Surgical valve replacement should be carried out in patients with severe AR when symptoms develop or in asymptomatic puts with LV dysfunction (LVEF<50% , end systolic diameter>50 mm, or LV diastolic dimension>65 mm) by imaging studies

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109
Q

Etiology tricuspid stenosis

A

Usually rheumatic; most common in females; almost invariably associated with MS

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110
Q

Clinical manifestations tricuspid stenosis

A

Hepatomegaly, ascites, edema, jaundice, JVD with slow y descent.

Diastolic rumbling murmur along left sternal border increased by inspiration with loud presystolic component.

Right atrial and SVC enlargement on x ray.

Doppler echo demonstrates thickened valve and impaired separation fo leaflets and provides estimate of transvalvular gradient

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111
Q

Treat tricuspid stenosis

A

Surgery if severe with valvular repair or replacement

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112
Q

Etiology tricuspid regurgitation

A

Usually functional and secondary to marked RV dilation of any cause and often associated with pulmonary HTN

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113
Q

Clinical manifestations tricuspid regurgitation

A

Severe RV failure, with edema,heptomegaly, and prominent v waves in JV pulse with rapid y descent. Systolic murmur along lower left sternal edge is increased by inspiration. Doppler echo confirms diagnosis and estimates severity

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114
Q

How treat 3rd degree AV block

A

Pacemaker

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115
Q

Treat tricuspid regurgitaiton

A

Intensive diuretic therapu when right sided heart failrue signs are present

In severe cases (absence of severe pulmonary HTN), surgical treatment consists of tricuspid annuloplasty or valve replacement

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116
Q

Early recognition an dimmediate treatment of acute ST segment elevation MI (STEMI) are essential. How diagnose

A

Characteristic history, ECG< and serum cardiac markers

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117
Q

Symptoms STEMI

A

Chest pain similar to angina but more intense and persistent; not fully relieved by rest or NO, often accompanied by nausea, sweating, apprehension.

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118
Q

What percent MI clinically silent

A

25%

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119
Q

PE STEMI

A

Pallor, diaphoresis, tachycardia, S4, dyskinesia cardiac impulse may be present. If CHF exists, rales and S3 are present. JVD is common in right ventricular infarction

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120
Q

JVD is common in what infarction

A

Right ventricular

121
Q

ECG STEMI

A

ST elevation,followed (if acute reperfusion is not acheived) by T wave inversion, then Q wave development over several hours

122
Q

Cardiac biomarkers STEMI

A

Troponin T Troponin I-highly specific
Elevated for 7-10 days

CK rise 4-8 h, peaks 24, normal 48-72

CK-MD more specific but may also be elevated with myocarditis or after electrical cardioversion

123
Q

When measure cardiac biomarkers

A

At presntation , 6-9 h later, and then 12-24 h

124
Q

Many p less QRS

A

AV dissociation

3rd degree AV

125
Q

Echo STEMI

A

Detects infarct associated regional wall motion abnormalities (but cannot distinguish acute MI from a previous myocardial scar)

Also useful in detecting RV infarction, LV aneurysm, and LV thrombus.

126
Q

MRI with delayed gadolinium enhancement echo STEMI

A

Accurately indicates regions of infarction , but is technically difficult to obtain in acutely ill patients

127
Q

Initial STEMI

A
  1. Quickly identify if patient is candidate for reperfusion therapy
  2. Relive pain
  3. Prevent/treat arrhythmias and mechanical complications
128
Q

BBB

A

V1 up

V2 down

Also have to look at QRS Edith if more than 120 it is complete

If less than 120 but above 110 it is incomplete block

80-110 normal QRS width 2 small squares-normal

RBBB-left depolarize first

129
Q

Treat STEMI

A

Asprin

History, ECG to identify STEMI (>1 mm ST elevation in two contiguous limb leads , <2 mm ST elevation in two contiguous precondition leads, or new LBBB) and appropriated of reperfusion therapy (percutaneous coronary intervention or IV fibrinolytic agent), which reduces infarct size, LV dysfunction and mortality

Primary PCI generally more effective than fibrinolytic and is preferred at experienced centers capable of performing the procedure rapidly espicially when diagnosis is in doubt , cardiogenic shock is present, bleeding risk is increased, or symptoms have been present for >3 hours

Proceed with IV PCI is not available . Door to needle time should be <30 min . 1-3 hour treatment most beneficial but still ok if 12 hours or developed new q waves

130
Q

Most anterior and posterior chamber

A

Ant-RV so VI most anterior lead

Post-LA, V6 which is at apex (LV Forces)

131
Q

R Sif chest pain or ST elevation persists >90 min after fibrinolytic

A

R +
S-referral for rescue PCI. Coronary angiography after fibrinolysis should also be considered for pets with recurrent angina or high risk features including extensive ST elevation, signs of heart failure (rales, S3, jugular venous distention, left ventricular ejection fraction <35%) or systolic bp <100

132
Q

Additional treat STEMI

A

Hospitalize in CCU with continuous ECG monitoring

IV line for emergency arrhythmia tratment

Pain control-morphine sulfate

Oxygen

Mild sedation

Soft diet and stool softeners

B blockers . Consider IV if HTN otherwise PO

Anticoagulants-continuous full dose IV heparin or LMWH followed by warfarin for patients with high risk of thromboembolism . Warfarin if used done for 3-6 months

Antiplatelets

ACE inhibtiors continued indefinitely use ARB if cant ACE

Aldosterone antagonist-if LVEF<40 and either symptomatic heart failure or diabetes donor use in patients with advanced renal insuffiency or hyperkalemia

Serum magnesium measured and depleted if necessary to reduce risk of arrhythmias

133
Q

Complications STEMI

A

Ventricular arrhythmias

Ventricular tachycardia

V fib

Accelerated idioventricular rhythm

Supraventricular arrhythmias

Bradyarrhythmias and AV block

Heart failrue

134
Q

Ventricular arrhythmias

A

Isolated ventricular premature beats

Precipitating factors should be corrected (hypoxemia, acidosis, hypokalemia, hypomagnesemia, CHF,arrhythmogenic drugs)

Routine bb diminishes ventricular ectopic. Other in hostpital antiarrhythmic therapu should be reversed for patients with sustained ventricular arrhythmias

135
Q

Ventricular tachycardia

A

If hemodynamically unstable, perform immediate electrical countershock (unsynchroniced discharfe of 200-300 J or 50% less if using biphasic device) if hemodynamically tolerated, use IV amiodarone (bolus of 150 mg over 10 min, then infusion of 1 mg/min for 6 hr then .5 mg/min)

136
Q

Ventricular fibrillation

A

Requires immediate defibillationg (200-400 J). If unsuccessful, initiate cardiopulmonary resuscitation (CPR) and standard resuscitative measures. Ventricular arrhythmias that appear several days of weeks following MI often reflect pump failure and may warrant invasive electrophysiologic study and implantation of a cardioverter defibrillator)

137
Q

Accelerated idioventricular rhythma

A

Wide QRS complex, regular rhythm, rate 60-100 b/min is common and usually benign; if it causes hypotension, treat with atropine

138
Q

Supraventricular arrhythmias

A

Sinus tachycardia may result from heart failure, hypoxemia, pain, fever, pericarditis, hypovolemia, administered to reduce myocardial oxygen demand .

Other supraventricular arrhythmias (paroxysmal supraventricular tachycardia, a flutter and fibrillation) are often secondary to heart failure. If hemodynamically unstable, proceed with electrical cardioversion. In absence of acute heart failure, suppressive alternative include beta blockers, verapamil or dilitazem

139
Q

Bradyarrhythmias and AV block

A

In inferior MI, usually represent heightened vagal tone or discrete AV nodal ischemia. If hemodynamically compromised (CHF, hypotension, emergence of ventricular arrhythmias), give atropine.

If no response , use temporary external or trasvenous pacemaker.

Isoproterenol should be avoided

In anterior MI, AV conduction defects usually reflect extensive tissue necrosis. Consider temporary external or transvenous pacemaker for

  • complete heart block
  • mobitz II
  • new I fasciculus block (LBBB RBBB+left anterior hemiblock, RBBB + left posterior hemiblock)
  • any bradyarrhythmia associated with hypotension or CHF
140
Q

Heart failure

A

CHF may result from systolic pump dysfunction, increased LV diastolic stiffness and/or acute mechanical complications

141
Q

Symptoms STEMI

A

Dyspnea
Orthopnea
Tachycardia

142
Q

Exam STEMI

A

JVD
S3 S4 gallop
Pulmonary rales
Systolic murmur if acute mitral regurgitation or ventricular septal defects has developed

143
Q

Treat heart failure

A

Initial-diuretics, inhaled O2 and vasodilator, particularly nitrates, digitalis not helpful

Diuretic, vasodilator and inotropy therapy guided invasive hemodynamic monitoring , particularly in patients with accompanying hypotension.

144
Q

Pulmonary capillary wedge

A

PCW 15-20 mmHg

In absence of hypotension, PCW>20 mmHg is treated with diuretic plus vasodilator therapu or nitroprusside and tirated to optimize bp, PCW, and systemic vascular resistance

145
Q

SVR

A

Mean arterial pressure-mean RA pressure)x 80/CO

146
Q

Normal SVR

A

900-1350

147
Q

If PCW >20 and hypotension

A

Evaluate for VSD or acute mitral regurgitation, consider dobutamine , but beware of drug induced ventricular ectopic or tachycardia

148
Q

Heart failrue after stabilization on parenteral vasodilator therapy, oral therapy follows with an ACE inhibitor or an ARB.

A

Consider addition of long term aldosterone antagonist to ACE inhibitor if LVEF<40% of symptomatic heart failrue or diabetes are present do not use if renal insuffiency or hyperkalemia are present

149
Q

Cardiogenic shock

A

Severe LV failure with hypotension , elevated PCW, cardiac index <2.2 L/min.m^2), accompanied by oliguria, peripheral vasoconstriction, dulled sensorium, and metabolic acidosis

150
Q

Treat cardiogenic shock

A

Swan ganz catheter and intraarterial bp monitoring are not always essential but may be helpful ; aim for mean PCW of 18-20 mmHg with adjustment of volume (diuretics or infusion) as needed

Vasopressin and/or intraaortic balloon counterpulsation may be necessary to maintain systolic bp>90 mmHg and reduce PCW.

Administer high conc O2 by mask; if pulmonary edema coexists, consider bilateral positive airway pressure or intubation and mechanical ventilation.

151
Q

What do if cardiogenic shock develops within 36 hours of acute STEMI

A

Reperfusion by PCI or CABG may markedly improve LV function

152
Q

Hypotension

A

May also result form right ventricular MI, which should be suspected in inferior or posterior MI, if JVD and elevation of right heart pressures predominate; right sided ECG leads typically show ST elevation, and echocardiography may confirm diagnosis.

153
Q

Treat hypotension

A

Volume infusion.

154
Q

Acute mechanical complications

A

Ventricular septal rupture and acute mitral regurgitaiton due to papilalry msucle ischemia/infarct develop during the first week following MI and are characterized by sudden onset of CHF and new systolic murmur.

Echo and Doppler interrogation can confirm presence of these complications. PCW tracings may show large v waves in either condition, but oxygen step up as the catheter is advanced from right atrium to right ventricle suggests septal rupture.

155
Q

Acute medical therapy for acute mechanical complications

A

Vasodilator therapy, intraaortic balloon pump may be required to maintain CO. Mechanical correction is the definitive therapy. Acute ventricular free wall rupture presents with sudden loss of bp, pulse, and consciousness, while ECG shows an intact rhythm (pulseless electrical activity) emergent surgical repair is crucial and mortality is high.

156
Q

Pericarditis

A

Characterized by pleuritis, positional pain and pericardial rub

Atrial arrhythmias are common; must be distinguished from recurrent angina. Often responds to asprin

Anticoagulants should be avoided when pericarditis is suspected to avoid development of pericardial bleeding/tamponade

157
Q

Ventricular aneurysm

A

Localized bulge of LV chamber due to INFARCTED myocardium.

True aneurysm-scar tissue and do not rupture. However complicatiosn include CHF, ventricular arrhythmias and thrombus

158
Q

How confirm a ventricular aneurysm

A

Echo or left ventriculography

159
Q

What is a thrombus is within the aneurysm or large aneurysmal segment due to anterior MI

A

Warrants consideration of oral anticoagulation with warfarin for 3-6 months

160
Q

PSEUDOANEURYSM

A

Form of cardiac rupture contained by local area of pericardium and organized thrombus; direct communication with the LV cavity is rpesent; surgical repair usually necessary to prevent rupture

161
Q

Recurrent angina

A

Usually associated with transient ST-T wave changes; signals high incidence of reinfarction; when it occurs in early post MI period, proceed directly to coronary arteriography, to identify those who would benefit from revascularization

162
Q

What do if patient already undergone coronary angiography and PCI, submaximal exercise testing should be performed prior to or soon after discharge. A positive test in certain subgroups (angina at a low workload, a large region of provovable ischemia, or provicable ischemia with reduced LVEF)

A

Need for cath to myocardium at risk of recurrent infarction.

Bb for at least 2 years following unless contraindicated

Continue oral antiplatelet agents

If LVEF<40% an ACE or ARC should used indefinitely

Consider addition of aldosterone antagonist

163
Q

How modify cardiac risk factors

A

Smoking, control HTN, diabetes, and serum lipids and pursue graduated exercise

164
Q

Unstable angina and non st elevation MI

A

Acute coronary syndromes with similar mechanisms , clinical presentations and treatment strategies

165
Q

Clinical presentation Unstable angina

A
  1. New onset of severe angina
  2. Angina at rest or with minimal activity,
  3. Recent increase in frequency and intensity of chronic angina
166
Q

Presntation NSTEMI

A

Symptoms identical to STEMI the two are differentiated by ECG findings

167
Q

PE UA and NSTEMI

A

May be normal or include diaphoresis, pale cool skin, tachycardia, S4 basilar rales

If large region of ischemia, may demonstrate S3, hypotension

168
Q

NSTEMI US electrocardiograph

A

May include ST depression and/or T wave inversion; unlike STMI there is no Q wave development

169
Q

Cardiac biomarkers

  • mitral stenosis can cause bienlargement of atrium cardiomyopathy and amyloid
  • see wide and notched
  • if unilateral not as wide p
A

Cardiac specific troponin s (specific and sensitive markers of myocardial necrosis) and CK-MB (less sensitive marker) are elevated in NSTEMI. Small troponin elevations may also occur in patients with CHF, myocarditis, or pulmonary embolism

170
Q

Treat NSTEMI US : step 1

A

Appropriate triage based on likelihood of CAD and acute coronary syndrome as well a s identification of higher risk patients

Patients with low likelihood of active ischemia are initially monitored by serial ECG and serum cardiac biomarkers, and for recurrent chest discomfort; if these are negative, stress testing can be used for further therapeutic planning

Therapy for UA/NSTEMI is directed
1. Against the inciting intracoronary thrombus, and 2. Toward restoration of balance between myocardial oxygen supply and demand. Patients with the highest risk scores benefit the msot from aggressive interventions

171
Q

Antithrombic therapies for NSTEMI UA

A

Asprin

Platelet P2Y12 receptor antagonist , clopidogrel

Anticoagulant : UFH, factor Xa inhibitor findaparinux, direct thrombin inhibitor bivalirudin,

For high risk patients who undergo PCI, consider IV GP IIb/IIIa antagonist (tirofiban)

172
Q

Aortic stenosis-earlier LVHantiischemic therapies

A

Nitroglycerin

If chest discomfort persists after three doses given 5 min apart, consider IV nitroglycerin
Do not use nitrates in pots with recent use or systolic bp <100. Do not sue nitrates in patients with recent use of phosphodiesterase 5 inhibitors for ED

Bb. Use verampamil or dilitazem if contraindicated if LV contractile function is not impaired

173
Q

Additional recommendations NSTEMI

A

Admit to unit with continuous ECG monitoring, initially with bed rest

Consider morphine sulfate for refractory chest discomfort

Add HMG-CoA reductase inhibitor and consider ACE

174
Q

Invasive vs conservative strangely

A

In highest risk patients, an early invasive strategy improves outcomes. In lower risk patients, angiography can be deferred but should be pursued if myocardial ischemia recurs spontaneously or is provoked by stress testing

175
Q

Long term management UA NSTEMI

A

Stress importance of smoking cessation, achieving optimal weight, diet low in saturated and trans fats, regular exercise, these principles can be reinforced by encouraging pt to enter cardiac rehabilitation program

Continue asprin, a P2Y12 receptor antagonist , bb , high dose statin and ACE inhibitor or angiotensin receptor blocker (espicially if HTN or diabetic or LV ejection fraction is reduced

176
Q

Class I recommendations f or use of an early invasive strategy

A

Recurrent angina.ischemia at rest or minimal exertion despite anti ischemic therapy

Elevation cardiac TNT or TnI

New ST segment depression

CHF symptoms, rales or worsening mitral regurgitation

Positive stress test

LVEF

177
Q

Chronic stable angina

A

Angina pectoris, the msot common clinical manifestation of CAD , results from an imbalance between myocardial O2 supply and demand, msot often due to atherosclerotic coronary artery obstruction. Other major conditions that upset this balance and result in angina include aortic valve disease, hypertrophic cardiomyopathy, and coronary artery spasm

178
Q

Symptoms chronic stable angina

A

Angina is typically associated with exertion or emotional upset; relieved quickly by rest or nitroglycerin. Major risk factors are cigarette smoking, HTN, hypercholesterolemia (increase LDL, decrease HDL), diabetes, obesity, and family history of CAD before age 55

179
Q

PE chronic stable angina

A

often normal; arterial bruits or retinal vascular abnormalities suggest generalized atherosclerosis; s4 common. During acute angina episode, other signs may appear:
Eg: an s4 diaphoresis, rales, and a transient murmur of mitral regurgitation due to papillary msucle ischemia

180
Q

ECG chronic stable angina

A

May be normal between angina episodes or show old infarction.. during angina, ST and T wave abnormalities typically appear (ST segment depression reflects subendocardial ischemia; ST segment elevation may reflect acute infarction or transient coronary artery spasm). Ventricular arrhythmias frequently accompany acute ischemia

181
Q

Stress testing chronic stable angina

A

Enhances diagnosis CAD

Exercise on treadmill or bicycle until target heart rate is acheived or pt becomes symptomatic or develops diagnostic ST segment changes.

Can even add radionuclide, echo, MRI to increase sensitivity and specificity

182
Q

Who should not do exercise testing

A

Acute MI, unstable angina, severe aortic stenosis.

In this case can do pharmacological stress with IV dipyridamole, adenosine, regadenoson, or dobutamine with radionucleoide or echo

183
Q

What is most specific for LBB on baseline ECG diagnosis

A

Adenosine or dipyridamole radionuclide imagining

184
Q

Coronary arteriography

A

Definitive test for assessing severity of CAD

185
Q

Indications for coronary arteriography

A
  1. Angina refractory to medical therapy
  2. Markedly positive exercise test (>2 mm ST segment depression, onset of ischemia at low workload, or ventricular tachycardia of hypotension with exercise) suggestive of left main or three vessel disease
  3. Recurrent angina or positive exercise test after MI
  4. To assess for coronary artery spasm
  5. To evaluate patients with perplexing chest pain in whom noninvasive tests are not diagnostic
186
Q

General treatment for stable angina

A

Identify and treat risk factors: mandatory cessation of smoking; treatment of diabetes, HTN, lipid disorders; advocate a diet low in saturated fat and trans fats

Correct exacerbating factors contributing to angina: morbid obesity, CHF, anemia, hyperthyroidism

Reassurance and pt education

187
Q

Drugs for chronic stable angina

A

Sublingual nitroglycerin ; may be repeated at 5 min ntervals; warn puts of possible headache or light headedness; teach prophylactic use of TNG proper to activity that regularly evokes angina

If chest pain persists for>10 min despite 2-3 TNG, patient should report promptly to nearest medical facility for evaluation of possible acute coronary syndrome

188
Q

Long term suppression of angina

A

Long acting nitrates

Bb

Calcium antagonists

Ranolazine

Asprin

Add ACE inhibitor in pt with CAD and LV ejection fraction <40% , HTN< diabetes, or chronic kidney disease

189
Q

Percutaneous Coronary Intervention (PCI)

A

Balloon dilation, usually with intracoronary stent implantation performed on anatomically suitable stenosis of native vessels and bypass grafts which is more effective than medical therapy for relief of angina

190
Q

Who should not have PCO

A

Asymptomatic or mildly symptomatic individuals

191
Q

Efficacy PCI

A

95% good after.
Restenosis develops in 30-45% following balloon dilation alone, in 20% after bare metal stenting, but in only <10% after drug elating stent implantation.

Late stent thrombosis may occur rarely in pets with DES; it is diminished by prolonged antiplatelet therapy (asprin indefinitely)

192
Q

Coronary artery bypass graft

A

Appropriately used for angina refractory to medical therapy or when the latter is not tolerated or if severe CAD is present . In type 2 diabetics with multivessel CAD, CABG plus optimal medical therapy is superior to medical therapy alone in prevention of major coronary events

193
Q

Advantages of percutaneous revascularization

A

Less invasive

Shorter hospital stay

Lower initial cost

Effective in relieving symptoms

194
Q

Disadvantages percutaneous coronary revascularization

A

Restenosis requiring repeat procedure

Possible incomplete revascularization

Limited to specific anatomic subsets

195
Q

Advantages coronary artery bypass grafting

A

Lower rate of recurrent angina

Ability to achieve complete revascularization

196
Q

Disadvantages with coronary artery bypass grafting

A

Cost

Risk of a repeat procedure due to late graft closure

Morbidity and mortality of major surgery

197
Q

Prinzmetal variant angina

A

Intermittent focal spasm of coronary artery; often associated with atherosclerotic lesion near site of spasm. Chest discomfort is similar to angina but more severe and occurs typically at rest, with transient ST segment elevation. May develop acute infarction or malignant arrhythmias during spasm induced ischemia

198
Q

Evaluation prinzmetal

A

ECG for ST elevation during discomfort

Confirm with angiography using provocative (IV acetylcholine) testing

199
Q

Primary treatment prinzmetal variant angina

A

Long acting nitrates and calcium antagonists.

200
Q

Who has better prognosis in prinzmetal

A

In patients with anatomically normal coronary arteries than in those with fixed coronary stenosis

201
Q

Heart failure and Cor pulmonale

A

Ok

202
Q

Heart failure and Cor pulmonale

A

Abnormality of cardiac structure and/or function restulgin in clinical symptoms and signs,hospitalizations, poor quality of liger and shortened survival.it is important to identify the underlying nature of cardiac disease and the factors that precipitate acute CHF

203
Q

Underlying cardiac diseases of heart failure and Cor pulmonale

A
  1. States that depress systolic ventricular function with reduced ejection fraction (HFrEF eg CAD, dilated cardiomyopathies, valvular disease, congenital heart disase
  2. States of heart failrue with preserved ejection fraction (HFpEF eg restrictive cardiomyopathies, hypertrophic cardiomyopathy, fibrosis, endomyocardial disorders) also termed diastolic failure
204
Q

Acute precipitating factors heart failure and Cor pulmonale

A

Excessive Na intake

Noncompliance with heart failure medications

Acute MI

Exacerbation of HTN

Acute arhythmias

Infections and/or fever

Pulmonary embolism

Anemia

Thyrotoxicosis

Pregnancy

Acute myocarditis or infective endocarditis

Certain drugs (NSAIDS, verampamil)

205
Q

Symptoms heart failure Cor pulmonale

A

Inadequate perfusion of peripheral tissues (fatigue) and elevated intracardiac filling pressures (dyspnea, orthopnea, paroxysmal nocturnal dyspnea ,peripheral edema

206
Q

PE heart failure and Cor pulmonale

A

JVD, S3 (in HFrEF/volume overload), pulmonary congestion (rales, dullness over pleural effusion), peripheral edema, hepatomegaly and ascites. Sinus tachycardia is common

In parties with HFpEF, S4 is often present

207
Q

Lab heart Paiute and Cor pulmonale

A

CXRcardiomegaly, pulmonary vascular redistribution, interstitial edema, pleural effusions.

Left ventricular systolic and diastolic dysfunction can be assessed by echo with Doppler, and EF calculated or estimated . In addition, echo can identify underlying valvular , pericardial or congenital heart disease, and regional wall motion abnormalities typical of CAD

Cardiac MR-assess ventricular structure, mass, volumes, and. Can help determine cause of heart failure

Measure B type natiuretic peptide (BNP) or N terminal pro-BNP differentiates cardiac from pulmonary causes of dyspnea (elevated in former)

208
Q

Conditions that mimic CHF

A

Pulmonary disease

Other causes of peripheral edema

209
Q

Treat heart failure goal

A

Symptomatic relied, prevention of adverse cardiac remodeling and prolonging survival.

Mainly with ACE inhibitors and bb for HFrEF once symptoms develop

210
Q

How control excess fluid retention in CHF

A

Dietary Na restriction

Diuretics: loop diuretics which you can combine with thiazide or metolazone for augmented effect

211
Q

Weight goal of diuresis

A

Loss of 1-1.5 kg/d a day

212
Q

Ace inhibitors and CHF

A

Recommended as standard initial CHF. They prolong life in patients with symptomatic CHF, delay the onset of CHF in patients with asymptomatic LV dysfunction, and lower mortality when begun soon after acute MI

213
Q

AE ACE inhibitors

A

Hypotension so start at lowest dose

214
Q

What use if ACE inhibitor intolerant(cough or angioedema)

A

ARB

215
Q

What is patient develops renal insuffiency and hyperkalemia on ACE inhibitor

A

Hydralazine plus an oral nitrate

216
Q

Beta blockers CHF

A

Administered in gradually augmented dose to improve symptoms and prolong survival in HF and reduced EF<40%. Begin at low doses and increase gradually (carvedill)

217
Q

Aldosterone antagonist CHF

A

Added to standard therapy in patients with advanced heart failure reduces mortality. Such therapy should be considered in patients with class II-IV heart failure symptoms and LVEF<35%.

218
Q

Why use caution when use aldosterone antagonist with ACE I or ARB

A

Hyperkalemia

219
Q

Digoxin CHF: why may is be used in CHF

A
  1. Marked systolic dysfunction and (LV dilation low EF, S3)

2. Heart failure with a fib

220
Q

Does digoxin prolong survival in HF

A

No but reduces hospitalizations

221
Q

When is digoxin not indicated in HF

A

CHF due to pericardial diseas, restrictive cardiomyopathy, or mitral stenosis (unless AF is present).

222
Q

Contraindication digoxin

A

Contraindicated in hypertrophic cardiomyopathy and in patient with AV conduction blocks

223
Q

Dosing digoxin

A

Depends on age, weight ,and renal function and can be guided by measurement of serum digoxin level (maintain <1 GN/ml)

224
Q

Digitalis toxicitycause

A

May be precipitated by hypokalemia, hypoxemia, hypercalcemia, hypomagnesemia, hypothyroidism, or MI

225
Q

Early signs of digitalis toxicity

A

Anorexia, nausea, lethargy

226
Q

Cardiac toxicity digitalis toxicity

A

Includes ventricular and supraventricular dysrhythmias and all depress of AV bloc. A

227
Q

What do at first sign of digitalis toxicity

A

Discontinue the drug: maintain serum K concentration between 4 and 5 molecules/L.

228
Q

What trat bradyarrhythmias and AV block from digitalis toxicity

A

Atropine or pacemaker

229
Q

How trat massive digitalis overdose

A

Antibodies

230
Q

Combination or oral vasodilator (hydralazine an disosorbide dinitrate for HF

A

May be of benefit for chronic administration in patients intolerant of ACE inhibtiors and ARBS ANS is also beneficial as part of standard therapy, alone with ACE inhibitos and bb, in african Americans with class II-IV feast failure

231
Q

Ivabradine

A

An inhibitor of AS node If current, has been shown to reduce hospitalizations and cardiovascular endpoints in heart failure and was recently approved for that purpose. Second line agent that can be prescribed with left ventricular EF >35% , in sinus rhythm with HR >70 bpm, already on maximally tolerated bb dose or have a contraindication to bb use

232
Q

Nitroprusside CHF

A

Potent vasodilator for patients with markedly elevated systemic vascular resistance.

233
Q

MOA nitroprusside

A

Metabolized to thiocyanate, which is excreted via the kidneys.

234
Q

How avoid thiocyanate toxicity

A

Follow thiocyanate levels in patients with renal dysfunction or if administered for >2 days.

235
Q

IV nesiritide

A

A purified preparation of BNP, is a vasodilator that reduces pulmonary capillary wedge pressure in arteries with acute decompensated CHF , ut has neutral effects on mortality or sense of dyspnea.

236
Q

When consider IV nesiritide

A

Refractory heart failure

237
Q

IV inotropy agent’s HF

A

Given to hospital patients for refractory symptoms or acute exacerbation of CHF to augment cardiac output.

238
Q

Contraindication IV inotropy patients

A

Hypertrophic cardiomyopathy

239
Q

Dobutamine

A

Augments CO without significant peripheral vasoconstriction or tachycardia

240
Q

Dopamine

A

Low dose-facilitates diuresis

High dose-positive inotropy effects; peripheral vasoconstriction

241
Q

Million each

A

Non sympathetic positive inotropy and vasodilator. The above vasodilator and inotropy agents may be used together for additive effect

242
Q

Can you use the vasodilator and inotropy agents together

A

Yup for additive effect

243
Q

Intima aproach to treat acute decompensated HF can rely on what

A

Patients hemodynamic profile based on clinical examination and if necessary invasive hemodynamic monitoring

244
Q

Warm and dry: symptomsdue to conditions other than heart failrue

A

Treat underlying condition

245
Q

Warm and wet:

A

Treat with diuretic and vasodilator

246
Q

Cold and wet

A

Treat with IV vasodilators and inotropy agents

247
Q

Cold and dry

A

If low filling pressure (PCW<12 mmHg) confirmed, consider trial of volume depletion

248
Q

When consider implantable cardioverter defibrillator prophylactivally for class II-III heart failure and LVEF120ms

A

35%

249
Q

When consider cardiac transplantation

A

Patients with severe disease and very limited, short term expected survival who meet stringent criteria,

250
Q

Patients with diastolic HF are treated with salt restriction and diuretics

A

BB and ACE inhibtiors May be of benefit in blunting neurohormonal activation

251
Q

Cor pulmonale

A

RV enlargement and/or altered function resulting from primary lung disease; leads to RV hypertrophy and eventually RV failure

252
Q

Etiologies Cor pulmonale

A

Pulmonary parenchymal or airway disease leading to hypoxemia vasoconstriction: COPD, CF, bronchiectasis

Diseases of the pulmonary vasculature: recurrent pulmonary emboli, pulmonary arterial hypertension, vasculitis, sickle cell

Inadequate mechanical ventilation (chronic hypoventilation),. Kyphoscloiosis, neuromuscular disorders, marked abesity, sleep apnea

253
Q

Symptoms Cor pulmonale

A

Depend on underlying disorder but include dyspnea, cough, fatigue, and sputum production (in parenchymal disease)

254
Q

PE Cor pulmonale

A

Tachypnea, RV impulse along left sternal border, loud P2, right sided S4, cyanosis, clubbing are late findings.

If RV failure develops, elevated jugular venous pressure, hepatomegaly with ascite , pedal edema; murmur of tricuspid regurgitation is common

255
Q

ECG Cor pulmonale

A

RV hypertrophy and RA enlargement ; tachyarrhythmias are common

256
Q

CXR Cor pulmonale

A

RV and pulmonary artery enlargement

If PAH present, tapering of the pulmonary artery branches

257
Q

Chest CT Cor pulmonale

A

Emphysema, interstitial lung disease, and acute pulmonary embolism

258
Q

V/Q scan

A

Reliable for diagnosis of thromboemboli.

259
Q

PLT Cor pulmonale

A

characterize intrinsic pulmonary disease

260
Q

Echo Cor pulmonale

A

RV hypertrophy; LV function typically normal

RV systolic pressure can be estimated from Doppler measurement of tricuspid regurgitation flow.

If imaging is difficult bc of air in distended lungs, RV volume and wall thickness can be evaluatd by MRI

261
Q

Right heart cath

A

Can confirm presence of pulmonary HTN and exclude left heart failure as cause

262
Q

Goal of treating Cor pulmonale

A

Aimed at underlying pulmonary disease and may include bronchodilators, antibiotics, oxygen administration and non invasive mechanical ventilation. For patients with PAH, pulmonary vasodilator therapy may be beneficial to reduce RV afterload

263
Q

IF RV failure is present in Cor pulmonale treatment

A

Low sodium diet and diuretics; digoxin is of uncertain benefit and must be administered cautiously (toxicity increased du to hypoxemia, hypercapnia, acidosis) loop diuretics must also be used with care to prevent significant metabolic alkalosis that blunts respiratory drive

264
Q

Shock

A

Condition of severe impairment of tissue perfusion leading to cellular injury and dysfunction. Rapid recognition and treatment are essential to prevent irreversible organ damage and death.

265
Q

Atrial tachycardia respond to adenosine?

A

No justventricular tachy

266
Q

Hypovolemia shock

A

Hemorrhage

Intravascular volume depletion

Internal sequestration

267
Q

Cardiogenic shock

A

Myopathic (acute MI, fulminant myocarditis)

Mechanical (acute MR, VSD..)

Arrhythmic

268
Q

Extracardiac obstructive shock

A

Pericardial tamponade

Massive pulmonary embolism

Tension pneumothorax

269
Q

Distributive shock

A

Sepsis

Toxic overdoses

Anaphylaxis

Neurogenic

Endocrinologist

270
Q

Clinical manifestations shock

A

Hypotension, tachycardia, tachypnea, pallor, restlessness, and altered sensorium

Signs of intense peripheral vasoconstriction, with weak pulses and cole clammy extremities. In distributive shock, vasodilation predominates and extremities are warm

Oliguria and metallic acidosis common

Acute lung injury and acute respiratory distress syndrome (ARDS) with noncardiogenic pulmonary edema, hypoxemia and diffuse pulmonary infiltrates

271
Q

How treat shock

A

Obtain history for underlying causes, including cardiac disease, recent fever or infection leading to sepsis, drug effects, conditions leading to pulmonary embolism, and potential sources of bleeding

272
Q

PE shock

A

Jugular veins flat and oligemic

JVD suggests cardiogenic shock ; JVD in presence of paradoxical pulse may reflect cardiac tamponade

Check for asymmetry of pulses (aortic dissection)

Check for asymmetry of pulses (aortic dissection)

Assess for HF , murmurs of aortic stenosis, acute mitral or aortic regurgitation, and VSD.

Tenderness or rebound in ab mya indicate peritonitis

High pitched bowel sounds-intestinal obstruction

Get stool guanaco to rule out GI bleeding

273
Q

Sepsis

A

Fever chills, skin lesions may suggest specific pathogens in septic shock

274
Q

Petechiae or purpura

A

Neisseria meningitidis of haemophilus influenza

275
Q

Ecthyma gangrenosum

A

Pseudomonas aeruginosa

276
Q

Generalized erythroderma

A

Toxic shock from staph aureus or strep pyogenes

277
Q

Acid base shock

A

Respiratory alkalosis precedes metabolic acidosis

278
Q

What do if sepsis suspected

A

Draw blood cultures, perform urinalysis and obtain gram stain and cultures of sputum, urine, and other suspected sites

279
Q

ECG sepsis

A

With MI or acute arrhythmia

280
Q

Chest x ray shock

A

Heart failure, tension pneumothorax, pneumonia

281
Q

Echo shock

A

Cardiac tamponade, left/right ventricular dysfunction, aortic dissection

282
Q

CVP or pulmonary capillary wedge

A

Pressure measurements may be necessary to distinguish between different categories of shock: mean PCW<6 mmHg suggests oligemic or distributive shock;

PCW>20 mmHg suggests left ventricular failure

CO is decreased inc radiogenic and oligemic shock and usually increased initially in septic shock

283
Q

Bradyarrhythmias arise from what

A

Failure of impulse initiation (SA node dysfunction)

Impaired electrical conduction (AV blocke

284
Q

SA node dysfunction etiology

A

Intrinsic (degenerative, ischemic),or rare. Mutations in Na channel or pacemaker current genes) or extrinsic (drugs, sutomonmic dysfunction)

285
Q

Symptoms of bradycardia

A

Fatigue weakness, lightheaded ness, syncope and/or episodes of associated tachycardia in patients with sick sinus syndrome

286
Q

Diagnose bradyarrhythmias SA node

A

Examine ECG for evidence of sinus bradycardia (sinus rhythm<60 b/min) or failure of rate to increase with exercise, since pauses, or exit block. In patients with SSS< periods of tachycardia (a fib/flut) occur).

Prolonged ECG monitoring aids in identifying these abnormalities. Invasive electrophysiologic testing is rarely necessary

287
Q

Treat SA node dysfunction

A

Remove or treat extrinsic causes such as contributing dugs or hypothyroidism. Otherwise, symptoms of bradycardia respond to permanent pacemaker placement. In SSS , treat assoicated a fib or flutter as indicated

288
Q

AV block

A

Impaired conduction from atria to ventricles may be structural and permanent or reversible (autonomic, metabolic, drug related)

289
Q

First degree block

A

Prolonged, constant PR interval (>.2 s). May be normal or secondary to increased vagal tone or drugs treatment not usually required

290
Q

Second degree block types

A

Mobitz I mobit

Mobitz II

291
Q

Mobitz I

A

Narrow QRS, progressive increase in PR interval until a ventricular beat is dropped, then sequence is repeated.

292
Q

When see mobitz I

A

Drug intoxication (digitalis, bb), increased vagal tone, inferior MI

293
Q

Treat mobitz I

A

No therapy required; if symptomatic, use atropine or temporary pacemaker

294
Q

Mobitz II

A

Fixed PR interval with occasional dropped beats in 2:1, 3:1, 4:1 pattern; the QRS complex is usually wide.

295
Q

When see Morbitz II

A

MI degenerative conduction system disease; more serious than mobitz I-may progress suddenly to complete AV block; permanent pacemaker is indicated

296
Q

Third degree block

A

Complete failure of conduction from atria to ventricles; atria and ventricles depolarize independently.

297
Q

Why get 3rd degree block

A

MI, digitalis toxicity, or degenerative conduction system disease.

298
Q

Treat third degree complete AV block

A

Permanent pacemaker is usually indicated, except when reversible (drug related or appear only transiently in MI without associatioed bundle branch block)

Clin Medicine (28 decks)

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