Harrison Flashcards
General exam of a pt with suspected heart disease
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 )
Carotid pulsus parvus
Weak upstroke due to decreased stroke volume (hypovolemia, LV failure, aortic or mitral stenosis
Carotid pulsus tardus
Delayed upstroke (aortic stenosis)
Carotid bounding (hyperkinetic pulse)
Hyperkinetic circulation, aortic regurgitaiton, pda, marked vasodilation
Carotid pulsus bisferiens
Double systolic pulsation (aortic regurgitation, hypertrophic cardiomyopathy)
Carotid pulsus alternans
Regular alteration in pulse pressure amplitude (severe LV dysfunction)
Carotid pulsus paradoxes
Exaggerated inspiration fall (>10mmHg) in systolic bp (pericardial tamponade, severe obstructive lung disease)
Jugular venous pulsation
Jugular venous distention develops in right sided heart failure, constrictive pericarditis, pericardial tamponade, obstruction of SVC
JVP normally falls with inspiration but may rise (___ sign) with __ ___
Kussmaul
Constrictive pericarditis
Abnormalities in examination with JVP
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
Large a wave
Tricuspid stenosis, pulmonic stenosis, atrioventricular dissociation (right atrium contracts against closed tricuspid valve)
Large v wave
Tricuspid regurgitation, ASD
Steep y descent
Constrictive pericarditis
Slow y decent
TS
Precordial palpation
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
Forceful apical thrust
Left ventricular hypertrophy
Lateral and downward displacement of apex impulse
Left ventricular dilation
Prominent presystolic impulse
HTN, aortic stenosis, hypertrophic cardiomyopathy
Double systolic apical impulse
Hypertrophic cardiomyopathy
Sustained lift at lower left sternal border
Right ventricular hypertrophy
Dyskinesia (outward bulge) impulse
Ventricular aneurysm, large dyskinesia area post MI, cardiomyopathy
S1 loud
Mitral stenosis, short PR, hyperkinetic heart, thin chest wall
S1 soft
Long PR interval, heart failure, mitral regurgitation, thick chest wall, pulmonary embolism
S1
First heart sound
S2
Second heart sound
A2
Aortic component of the second heart sound
P2
Pulmonic component of the second heart sound
ASD with _ of S2
Splitting
RBBB S2
Wide splitting
S2 left BBB
Reversed or paradoxical splitting
Pulmonary HTN S2
Narrow splitting
Normally A2 precedes P2 and splitting increases with inspiration; abnormalities include
S2
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
S3
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
S4
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
Opening snap
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
Ejection clicks
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
Midsystolic clicks
At lower left sternal border and apex, often followed by late systolic murmur in MVP
Systolic murmur
Crescendo decrescendo ejection type or pan systolic or late systolic
Right sided murmurs increase with ____
Inspiration
Tricuspid regurgitation
Ejection type murmur
Aortic outflow tract
Aortic valve stenosis
Hypertrophic obstructive cardiomyopathy
Aortic flow murmur
Pulmonary outflow tract
Pulmonic valve stenosis
Pulmonic flow murmur
Holosystolic
Mitral regurgitation
Tricuspid regurgitation
Ventricular septal defect
Late systolic murmu
Mitral or tricuspid valve prolapse
Early diastolic murmur
Aortic valve regurgitation
Pulmonic valve regurgitation
Mid to late diastolic murmu
Mitral or tricuspid stenosis
Flow murmur across mitral or tricuspid valves
Continuous distaolic murmur
PDA
Coronary AV fistula
Ruptured sinus of valsava aneurysm
Effect of respiration on heart murmur and sounds
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
Valsava maneuver effect on heart murmur and sound
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
Effect of after VPM or AF on murmurs and heart sounds
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)
Positional changes on murmurs and heart sounds
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
Exercise and heart murmurs and sounds
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
Early diastolic murmurs
Begin immediately after S2, are high pitched, and are usually caused by aortic or pulmonary regurgitation
Mid to late diastolic murmurs
Low pitched, heard best with bell of stethoscope; observed in MS or TS; less commonly due to atrial myxoma
Continuous diastolic murmur
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
ECG
Ok
Each horizontal box time
.04 s
HR
300/large boxes (each 5 mm apart) between QRS.
Or divide 1500 by number of small boxes (1 mm apart)
Sinus rhythm
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!
Mean axis normal
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
Left axis deviation
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)
Right axis deviation (>90%)
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)
Short interval PR (.12-.2 s)
Short: preexcitation syndrome (look for slurred QRS upstroke due to delta wave)
Nodal rhythm (inverted P in AVF)
Long PR >.2
First degree atrioventricular AV block
Widened QRS .06-.1 s
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
Prolonged QT
Congenital, hypokalemia, hypocalcemia (class IA and class III Antiarrhythmics, tricyclics)
Right atrium hypertrophy
P wave> 2.5 mm in lead II
Left atrium hypertrophy
P biphasic (positive, then negative) in V1, with terminal negative force wider than .04 s
Right ventricle hypertrophy
R>S in V1 and R in V1>5 mm; deep S in V6; right axis deviation
Left ventricle hypertrophy
S in V1 plus R in V5 or V6>35 mm or R in aVL
Infarction and ecg
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
ST wave elevation
Acute MI, coronary spasm, pericarditis, LV aneurysm, brigade pattern (RBBB with ST elevation in V1-V2)
ST depression
Digitalis effect, strain (due to ventricular hypertrophy), ischemic, or nontransmural MI
Tall peaked T
Hyperkalemia, acute MI
Inverted T
Non Q wave MI, ventricular strain pattern, drug effect, hypokalemia, hypocalcemia, increased intracranial pressure
Echo
Visualizes heart in real time with ultrasound
Doppler recordings noninvasively assess hemodynamics and abnormal flow patterns.
What compromises echo
COPD, thick chest wall, narrow intercostal spaces
Etiology mitral stenosis
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
History mitral stenosis
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
Indication pacemaker
Unstable below AV node or at AV
1st degree AC don’t need pacing
PE mitral stenosis
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
Complciations MS
Hemoptysis, pulmonary embolism, pulmonary infection, systemic embolization; endocarditis is uncommon in pure MS
ECG mitral stenosis
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
CXR mitral stenosis
Shows LA and RV enlargement and kerley B lines
Echo MS
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
Treat MS
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
Etiology mitral regurgitation
MVP, rheumatic heart disease, ischemic heart disease with papillary muscle dysfunction, LV dilation of any cause, mitral annular calcification, hypertrophic cardiomyopathy, infective endocarditis, congenital
Clinical mitral regurgitation
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
Inferior wall MI
Can be epigastric and stomach-GI SYMPTOMS espicially if has risks of CAD
Echo mitral regurgitaiton
Enlarged LA, hyperdynamic LV, identifies mechanism of MR, Doppler analysis helpful in diagnosis and assessment of severity of MR and degree of pulmonary HTN
When treat type I AV
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
Treat mitral regurgitaiton
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
MVP etiology
Most commonly idiopathic; may accompany marfan, Helmer’s Danilo’s syndome
Pathology MVP
Redundant mitral valve tissue with myxedematous degeneration and elongated chordate tendinae
Clinical MVP
Females
Most asymptomatic
Potential symptoms-vague chest pain and supraventricular and ventricular arrhythmias.
Most important complication MVP
MR
Rarely-systemic emboli from platelet fibrin deposits on valve. Sudden death is very rare
PE MVP
Mid to late systolic clicks followed by late systolic murmur at the apex ; exaggeration by valsava maneuver, reduced by squatting and isometric exercise
Grouped beating
Not 3rd degree!! Means some association …
Echo MVP
Shows posterior displacement of one or both mitral leaflets late in systole
Treat MVP
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
Etiology aortic stenosis
Most common as
- Degenerative calcification of a congenitally bicuspid valve
- chronic deterioration and calcification of a trileaflet valve
- Rheumatic disease (almost always associated with rheumatic mitral valve disease)
Symptoms aortic stenosis
Exertional dyspnea, angina, and syncope are cardinal symptoms; they occur late, after years of obstruction and aortic valve area <1
PE aortic stenosis
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)
ECG aortic stenosis
Often shows LV hypertrophy but not useful for predicting gradient
Echocardiogram aortic stenosis
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
Treat aortic stenosis
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
Etiology aortic regurgitation
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
Clinical manifestations aortic regurgitation
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
Echo aortic regurgitaiton
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
Treat aortic regurgitation
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
Etiology tricuspid stenosis
Usually rheumatic; most common in females; almost invariably associated with MS
Clinical manifestations tricuspid stenosis
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
Treat tricuspid stenosis
Surgery if severe with valvular repair or replacement
Etiology tricuspid regurgitation
Usually functional and secondary to marked RV dilation of any cause and often associated with pulmonary HTN
Clinical manifestations tricuspid regurgitation
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
How treat 3rd degree AV block
Pacemaker
Treat tricuspid regurgitaiton
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
Early recognition an dimmediate treatment of acute ST segment elevation MI (STEMI) are essential. How diagnose
Characteristic history, ECG< and serum cardiac markers
Symptoms STEMI
Chest pain similar to angina but more intense and persistent; not fully relieved by rest or NO, often accompanied by nausea, sweating, apprehension.
What percent MI clinically silent
25%
PE STEMI
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
JVD is common in what infarction
Right ventricular
ECG STEMI
ST elevation,followed (if acute reperfusion is not acheived) by T wave inversion, then Q wave development over several hours
Cardiac biomarkers STEMI
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
When measure cardiac biomarkers
At presntation , 6-9 h later, and then 12-24 h
Many p less QRS
AV dissociation
3rd degree AV
Echo STEMI
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.
MRI with delayed gadolinium enhancement echo STEMI
Accurately indicates regions of infarction , but is technically difficult to obtain in acutely ill patients
Initial STEMI
- Quickly identify if patient is candidate for reperfusion therapy
- Relive pain
- Prevent/treat arrhythmias and mechanical complications
BBB
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
Treat STEMI
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
Most anterior and posterior chamber
Ant-RV so VI most anterior lead
Post-LA, V6 which is at apex (LV Forces)
R Sif chest pain or ST elevation persists >90 min after fibrinolytic
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
Additional treat STEMI
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
Complications STEMI
Ventricular arrhythmias
Ventricular tachycardia
V fib
Accelerated idioventricular rhythm
Supraventricular arrhythmias
Bradyarrhythmias and AV block
Heart failrue
Ventricular arrhythmias
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
Ventricular tachycardia
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)
Ventricular fibrillation
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)
Accelerated idioventricular rhythma
Wide QRS complex, regular rhythm, rate 60-100 b/min is common and usually benign; if it causes hypotension, treat with atropine
Supraventricular arrhythmias
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
Bradyarrhythmias and AV block
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
Heart failure
CHF may result from systolic pump dysfunction, increased LV diastolic stiffness and/or acute mechanical complications
Symptoms STEMI
Dyspnea
Orthopnea
Tachycardia
Exam STEMI
JVD
S3 S4 gallop
Pulmonary rales
Systolic murmur if acute mitral regurgitation or ventricular septal defects has developed
Treat heart failure
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.
Pulmonary capillary wedge
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
SVR
Mean arterial pressure-mean RA pressure)x 80/CO
Normal SVR
900-1350
If PCW >20 and hypotension
Evaluate for VSD or acute mitral regurgitation, consider dobutamine , but beware of drug induced ventricular ectopic or tachycardia
Heart failrue after stabilization on parenteral vasodilator therapy, oral therapy follows with an ACE inhibitor or an ARB.
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
Cardiogenic shock
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
Treat cardiogenic shock
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.
What do if cardiogenic shock develops within 36 hours of acute STEMI
Reperfusion by PCI or CABG may markedly improve LV function
Hypotension
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.
Treat hypotension
Volume infusion.
Acute mechanical complications
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.
Acute medical therapy for acute mechanical complications
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.
Pericarditis
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
Ventricular aneurysm
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
How confirm a ventricular aneurysm
Echo or left ventriculography
What is a thrombus is within the aneurysm or large aneurysmal segment due to anterior MI
Warrants consideration of oral anticoagulation with warfarin for 3-6 months
PSEUDOANEURYSM
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
Recurrent angina
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
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)
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
How modify cardiac risk factors
Smoking, control HTN, diabetes, and serum lipids and pursue graduated exercise
Unstable angina and non st elevation MI
Acute coronary syndromes with similar mechanisms , clinical presentations and treatment strategies
Clinical presentation Unstable angina
- New onset of severe angina
- Angina at rest or with minimal activity,
- Recent increase in frequency and intensity of chronic angina
Presntation NSTEMI
Symptoms identical to STEMI the two are differentiated by ECG findings
PE UA and NSTEMI
May be normal or include diaphoresis, pale cool skin, tachycardia, S4 basilar rales
If large region of ischemia, may demonstrate S3, hypotension
NSTEMI US electrocardiograph
May include ST depression and/or T wave inversion; unlike STMI there is no Q wave development
Cardiac biomarkers
- mitral stenosis can cause bienlargement of atrium cardiomyopathy and amyloid
- see wide and notched
- if unilateral not as wide p
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
Treat NSTEMI US : step 1
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
Antithrombic therapies for NSTEMI UA
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)
Aortic stenosis-earlier LVHantiischemic therapies
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
Additional recommendations NSTEMI
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
Invasive vs conservative strangely
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
Long term management UA NSTEMI
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
Class I recommendations f or use of an early invasive strategy
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
Chronic stable angina
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
Symptoms chronic stable angina
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
PE chronic stable angina
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
ECG chronic stable angina
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
Stress testing chronic stable angina
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
Who should not do exercise testing
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
What is most specific for LBB on baseline ECG diagnosis
Adenosine or dipyridamole radionuclide imagining
Coronary arteriography
Definitive test for assessing severity of CAD
Indications for coronary arteriography
- Angina refractory to medical therapy
- 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
- Recurrent angina or positive exercise test after MI
- To assess for coronary artery spasm
- To evaluate patients with perplexing chest pain in whom noninvasive tests are not diagnostic
General treatment for stable angina
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
Drugs for chronic stable angina
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
Long term suppression of angina
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
Percutaneous Coronary Intervention (PCI)
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
Who should not have PCO
Asymptomatic or mildly symptomatic individuals
Efficacy PCI
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)
Coronary artery bypass graft
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
Advantages of percutaneous revascularization
Less invasive
Shorter hospital stay
Lower initial cost
Effective in relieving symptoms
Disadvantages percutaneous coronary revascularization
Restenosis requiring repeat procedure
Possible incomplete revascularization
Limited to specific anatomic subsets
Advantages coronary artery bypass grafting
Lower rate of recurrent angina
Ability to achieve complete revascularization
Disadvantages with coronary artery bypass grafting
Cost
Risk of a repeat procedure due to late graft closure
Morbidity and mortality of major surgery
Prinzmetal variant angina
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
Evaluation prinzmetal
ECG for ST elevation during discomfort
Confirm with angiography using provocative (IV acetylcholine) testing
Primary treatment prinzmetal variant angina
Long acting nitrates and calcium antagonists.
Who has better prognosis in prinzmetal
In patients with anatomically normal coronary arteries than in those with fixed coronary stenosis
Heart failure and Cor pulmonale
Ok
Heart failure and Cor pulmonale
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
Underlying cardiac diseases of heart failure and Cor pulmonale
- States that depress systolic ventricular function with reduced ejection fraction (HFrEF eg CAD, dilated cardiomyopathies, valvular disease, congenital heart disase
- States of heart failrue with preserved ejection fraction (HFpEF eg restrictive cardiomyopathies, hypertrophic cardiomyopathy, fibrosis, endomyocardial disorders) also termed diastolic failure
Acute precipitating factors heart failure and Cor pulmonale
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)
Symptoms heart failure Cor pulmonale
Inadequate perfusion of peripheral tissues (fatigue) and elevated intracardiac filling pressures (dyspnea, orthopnea, paroxysmal nocturnal dyspnea ,peripheral edema
PE heart failure and Cor pulmonale
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
Lab heart Paiute and Cor pulmonale
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)
Conditions that mimic CHF
Pulmonary disease
Other causes of peripheral edema
Treat heart failure goal
Symptomatic relied, prevention of adverse cardiac remodeling and prolonging survival.
Mainly with ACE inhibitors and bb for HFrEF once symptoms develop
How control excess fluid retention in CHF
Dietary Na restriction
Diuretics: loop diuretics which you can combine with thiazide or metolazone for augmented effect
Weight goal of diuresis
Loss of 1-1.5 kg/d a day
Ace inhibitors and CHF
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
AE ACE inhibitors
Hypotension so start at lowest dose
What use if ACE inhibitor intolerant(cough or angioedema)
ARB
What is patient develops renal insuffiency and hyperkalemia on ACE inhibitor
Hydralazine plus an oral nitrate
Beta blockers CHF
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)
Aldosterone antagonist CHF
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%.
Why use caution when use aldosterone antagonist with ACE I or ARB
Hyperkalemia
Digoxin CHF: why may is be used in CHF
- Marked systolic dysfunction and (LV dilation low EF, S3)
2. Heart failure with a fib
Does digoxin prolong survival in HF
No but reduces hospitalizations
When is digoxin not indicated in HF
CHF due to pericardial diseas, restrictive cardiomyopathy, or mitral stenosis (unless AF is present).
Contraindication digoxin
Contraindicated in hypertrophic cardiomyopathy and in patient with AV conduction blocks
Dosing digoxin
Depends on age, weight ,and renal function and can be guided by measurement of serum digoxin level (maintain <1 GN/ml)
Digitalis toxicitycause
May be precipitated by hypokalemia, hypoxemia, hypercalcemia, hypomagnesemia, hypothyroidism, or MI
Early signs of digitalis toxicity
Anorexia, nausea, lethargy
Cardiac toxicity digitalis toxicity
Includes ventricular and supraventricular dysrhythmias and all depress of AV bloc. A
What do at first sign of digitalis toxicity
Discontinue the drug: maintain serum K concentration between 4 and 5 molecules/L.
What trat bradyarrhythmias and AV block from digitalis toxicity
Atropine or pacemaker
How trat massive digitalis overdose
Antibodies
Combination or oral vasodilator (hydralazine an disosorbide dinitrate for HF
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
Ivabradine
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
Nitroprusside CHF
Potent vasodilator for patients with markedly elevated systemic vascular resistance.
MOA nitroprusside
Metabolized to thiocyanate, which is excreted via the kidneys.
How avoid thiocyanate toxicity
Follow thiocyanate levels in patients with renal dysfunction or if administered for >2 days.
IV nesiritide
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.
When consider IV nesiritide
Refractory heart failure
IV inotropy agent’s HF
Given to hospital patients for refractory symptoms or acute exacerbation of CHF to augment cardiac output.
Contraindication IV inotropy patients
Hypertrophic cardiomyopathy
Dobutamine
Augments CO without significant peripheral vasoconstriction or tachycardia
Dopamine
Low dose-facilitates diuresis
High dose-positive inotropy effects; peripheral vasoconstriction
Million each
Non sympathetic positive inotropy and vasodilator. The above vasodilator and inotropy agents may be used together for additive effect
Can you use the vasodilator and inotropy agents together
Yup for additive effect
Intima aproach to treat acute decompensated HF can rely on what
Patients hemodynamic profile based on clinical examination and if necessary invasive hemodynamic monitoring
Warm and dry: symptomsdue to conditions other than heart failrue
Treat underlying condition
Warm and wet:
Treat with diuretic and vasodilator
Cold and wet
Treat with IV vasodilators and inotropy agents
Cold and dry
If low filling pressure (PCW<12 mmHg) confirmed, consider trial of volume depletion
When consider implantable cardioverter defibrillator prophylactivally for class II-III heart failure and LVEF120ms
35%
When consider cardiac transplantation
Patients with severe disease and very limited, short term expected survival who meet stringent criteria,
Patients with diastolic HF are treated with salt restriction and diuretics
BB and ACE inhibtiors May be of benefit in blunting neurohormonal activation
Cor pulmonale
RV enlargement and/or altered function resulting from primary lung disease; leads to RV hypertrophy and eventually RV failure
Etiologies Cor pulmonale
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
Symptoms Cor pulmonale
Depend on underlying disorder but include dyspnea, cough, fatigue, and sputum production (in parenchymal disease)
PE Cor pulmonale
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
ECG Cor pulmonale
RV hypertrophy and RA enlargement ; tachyarrhythmias are common
CXR Cor pulmonale
RV and pulmonary artery enlargement
If PAH present, tapering of the pulmonary artery branches
Chest CT Cor pulmonale
Emphysema, interstitial lung disease, and acute pulmonary embolism
V/Q scan
Reliable for diagnosis of thromboemboli.
PLT Cor pulmonale
characterize intrinsic pulmonary disease
Echo Cor pulmonale
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
Right heart cath
Can confirm presence of pulmonary HTN and exclude left heart failure as cause
Goal of treating Cor pulmonale
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
IF RV failure is present in Cor pulmonale treatment
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
Shock
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.
Atrial tachycardia respond to adenosine?
No justventricular tachy
Hypovolemia shock
Hemorrhage
Intravascular volume depletion
Internal sequestration
Cardiogenic shock
Myopathic (acute MI, fulminant myocarditis)
Mechanical (acute MR, VSD..)
Arrhythmic
Extracardiac obstructive shock
Pericardial tamponade
Massive pulmonary embolism
Tension pneumothorax
Distributive shock
Sepsis
Toxic overdoses
Anaphylaxis
Neurogenic
Endocrinologist
Clinical manifestations shock
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
How treat shock
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
PE shock
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
Sepsis
Fever chills, skin lesions may suggest specific pathogens in septic shock
Petechiae or purpura
Neisseria meningitidis of haemophilus influenza
Ecthyma gangrenosum
Pseudomonas aeruginosa
Generalized erythroderma
Toxic shock from staph aureus or strep pyogenes
Acid base shock
Respiratory alkalosis precedes metabolic acidosis
What do if sepsis suspected
Draw blood cultures, perform urinalysis and obtain gram stain and cultures of sputum, urine, and other suspected sites
ECG sepsis
With MI or acute arrhythmia
Chest x ray shock
Heart failure, tension pneumothorax, pneumonia
Echo shock
Cardiac tamponade, left/right ventricular dysfunction, aortic dissection
CVP or pulmonary capillary wedge
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
Bradyarrhythmias arise from what
Failure of impulse initiation (SA node dysfunction)
Impaired electrical conduction (AV blocke
SA node dysfunction etiology
Intrinsic (degenerative, ischemic),or rare. Mutations in Na channel or pacemaker current genes) or extrinsic (drugs, sutomonmic dysfunction)
Symptoms of bradycardia
Fatigue weakness, lightheaded ness, syncope and/or episodes of associated tachycardia in patients with sick sinus syndrome
Diagnose bradyarrhythmias SA node
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
Treat SA node dysfunction
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
AV block
Impaired conduction from atria to ventricles may be structural and permanent or reversible (autonomic, metabolic, drug related)
First degree block
Prolonged, constant PR interval (>.2 s). May be normal or secondary to increased vagal tone or drugs treatment not usually required
Second degree block types
Mobitz I mobit
Mobitz II
Mobitz I
Narrow QRS, progressive increase in PR interval until a ventricular beat is dropped, then sequence is repeated.
When see mobitz I
Drug intoxication (digitalis, bb), increased vagal tone, inferior MI
Treat mobitz I
No therapy required; if symptomatic, use atropine or temporary pacemaker
Mobitz II
Fixed PR interval with occasional dropped beats in 2:1, 3:1, 4:1 pattern; the QRS complex is usually wide.
When see Morbitz II
MI degenerative conduction system disease; more serious than mobitz I-may progress suddenly to complete AV block; permanent pacemaker is indicated
Third degree block
Complete failure of conduction from atria to ventricles; atria and ventricles depolarize independently.
Why get 3rd degree block
MI, digitalis toxicity, or degenerative conduction system disease.
Treat third degree complete AV block
Permanent pacemaker is usually indicated, except when reversible (drug related or appear only transiently in MI without associatioed bundle branch block)
