Cardiovascular



Cardiovascular





2.1 Acute Coronary Syndrome


Events that have sudden onset and could lead to significant morbidity or mortality if not recognized include myocardial infarction, which includes ST-elevation MI (STEMI), myocardial stunning, coronary artery vasospasm, or unstable angina.

Cause: Atherosclerosis (85%), including spasm with superimposed thrombus in 90% of those; emboli (15%) and may also be due to cocaine-induced spasm when cocaine is used as anesthesia or a recreational drug.

Epidem: Increased incidence with h/o the following:


Decreased incidence with:


Pathophys: Platelet aggregations and thrombi on plaque fissures cause thrombosis with or without spasm (Intern Med 2000;39:333); or paradoxical vasoconstriction with stress because plaque prevents normal endothelial cell induction of coronary dilatation.

Sx: Chest pain, substernal, in “distribution of a tree,” worse supine: diaphoresis, dyspnea; associated with heavy exertion 5-40 times more frequently depending on conditioning state; atypical presentations in women; CNS symptoms are the presenting symptoms in 50% of patients > 60 yr and 31% with cardiac syncope have syncope due to ischemia or infarction (Nejm 2002;347:878)

Si: Pericardial rub on day 2+, usually without ST changes; S3 gallop or S4 gallop; fever < 103°F (39.4°C); transient S2 paradoxical split. Chest wall tenderness does not exclude ischemic or infarcting myocardium (Arch IM 1985;145:65). Rectal exam for guaiac.


Crs:



  • 25% are unrecognized and half are asymptomatic—yet prognosis is just as bad (Nejm 1984;311:1144); 15% in-hospital mortality before thrombolytics, now 7-10%; 10% of survivors get severe pump failure, another 10% get persistent angina, 10% “flunk” discharge mini-ETT, another 10% “flunk” maximal ETT at 6 wk follow-up; remaining 50% do fine (J Cardiovasc Risk 1999;6:69); frequent PVCs (> 7/min) post test predictive of increased risk of death (5-yr death rate 11%) (Nejm 2003;348:781).


  • Age-adjusted survival for women may be worse when compared to men, but studies have yet to prove (Am J Cardiol 2000;85:147)—treatment should be gender-blind.


  • Cardiac arrest survival is 3.5% in out-of-hospital CPR, 8.8% if VF/VT; more survivors if bystander CPR initiated (Ann EM 1999;33:44).


  • In the very elderly, aggressive invasive study and treatment do not improve mortality (Jama 2005;293:1329).

Cmplc:



  • Altered binding proteins change meaning of measured levels of quinidine, cholesterol, etc.


  • Aneurysm of left ventricle occurs in 40% of those with anterior MI and 13.5 % overall, develops in first 48 hr, leads to emboli, CHF, PVCs, 75% 5-yr mortality (Eur Hrt J 1990;11:441).


  • Arrhythmias (Physiol Rev 1999;79:917; Eur Hrt J 1999;20:748); Afib is a risk factor for worse outcome (J Am Coll Cardiol 1997;30:406).


  • Dressler syndrome (Cardiol Clin 1990;8:601), which may be on a continuum of pericarditis of AMI; this may lead to pericardial tamponade from inflammation (r/o RV infarct) since both functionally acutely constrict pericardial space by fluid or dilated RV.



  • Heart block occurs in 5% of inferior MIs, 3% of anterior MIs, and in 100% with anterior MI + RBBB causing a 75% mortality (Chest 1976;69:599; Am J Cardiol 1992;69:1135)


  • Mural thrombi without aneurysm in 11% of acute MIs, 2% of others.


  • Papillary muscle rupture causes CHF with a normal-sized left atrium by TEE, occurs most often with inferior MIs, and surgery.


  • Rupture of septal wall to create a VSD or rupture into pericardial sac causing tamponade.


  • Syncope associated with 60% 5-yr survival (Nejm 2002;347:878).


  • Non-hemorrhagic stroke, especially if EF <28% post MI, older age, h/o hypertension or other common stroke risk factors—prevent with warfarin anticoagulation (Circ 1998;97:757).


  • Anxiety neurosis, impotence.

Diff Dx:



  • Of chest pain: pulmonary embolus, aortic dissection, pneumonia, rib fracture, GERD, cholecystitis.


  • Of ST elevation (Nejm 2003;349:2128): pericarditis, myocarditis, hyperkalemia, LBBB, pulmonary embolus, early repolarization (see discussion under “EKG” for Brugada syndrome).

Scoring System:



  • TIMI Risk Score for complications in non-ST Elevation MI or Unstable angina: (1) age > 65 yr; (2) at least 3 risk factors for CAD; (3) prior coronary stenosis of 50% or more; (4) ST segment deviation on EKG; (5) at least 2 anginal events in the prior 24 hr; (6) use of ASA in the prior 7 d; and (7) elevated serum cardiac markers (Jama 2000;284:835). Increased risk of complications with increasing score.



  • Killip classification (Am J Cardiol 1967;20:457; Jama 2003;290:2174) with findings for risk of arrhythmia, cardiac arrest or death (CHF defined as rales, S3 gallop, and venous HT; Pulmonary edema defined as severe CHF; and shock is cardiogenic shock). See Table 2.1.








Table 2.1 Killip Classification




























Condition

Life-threatening
Arrhythmia

Cardiac Arrest

Death


No CHF

36%

5%

6%


CHF

46%

15%

17%


Pulm Edema

73%

46%

38%


Shock

94%

77%

81%


Lab:

Chem Markers: (J Am Coll Cardiol 1999;34:739; Scand J Clin Lab Invest suppl 1999;230:103) These results may alter hospital course, but should not be the determining factors for those who need admission for cardiac evaluation (Heart 1999;82:614). CPK and Troponin may be “erroneously” elevated in those with renal failure (Nephrol Dial Transplant 1999;14:1489). Serial evaluation in ER may increase yield for those having acute MIs (Acad Emerg Med 1997;4:869). Hospital laboratories will determine the parameters that they find useful in determining abnormal marker values based on their specific test and QI testing.

CPK and fractions up in 12 hr, peak at 2 d and last 4 d, CPK-MB subfractions MB2 and MB1 rise in first 6 hr after onset of pain and have 95% sensitivity and specificity; total CPK correlates with MI size; may double in MI, but still be less than upper limit of normal; MB band is increased also by increased death and regeneration of skeletal muscle, and by decreased clearance
in myxedema; MM is increased by hypothyroidism, myopathy; BB band is increased by CNS and/or smooth muscle damage.

Cardiac troponin I and T levels elevate in 4-6 hr and are specific to myocardium (Am Hrt J 1999;137:1137); 95-100% sensitivity, 22-33% specific for infarction but “false positives” really represent ischemia (unstable angina) (Clin Chim Acta 1999;284:161) with suggestive hx—other etiologies are possible such as sepsis, endocrine disorders, rheumatologic disorders, myocarditis, pericarditis, COPD (EM Australas 2004;16:212), pulmonary embolus, cardiomyopathy, renal failure, in those receiving monoclonal antibodies, those receiving cancer therapy, those on anticoagulation and other chronic diseases (Chest 2004;125:1877; Am J Emerg Med 1999;17:225); higher levels correlate with worse outcomes (Am J Cardiol 1999;84:1281); also used perioperatively when surgery may increase CPK; Troponin T levels predictive of ACS even in the setting of abnormal renal function (Nejm 2002;346:2047).

Myoglobin peaks early (2 hr) and is sensitive, but not specific (Ann EM 1987;16:851).

LDH and fractions: isoenzymes 4 and 5 (rapidly migrating) increased, r/o renal and red cell source.

AST (SGOT) up in 24 hr, peaks at 2-4 d, lasts up to 7 d.

Increase in myeloperoxidase level prognostic for MI, and 30-day and 6-mon adverse cardiac events—exact level to be elucidated (Nejm 2003;349:1595).

Acute phase reactants [C-reactive protein (Nejm 2004;350:1387; 2004;351:2599), fibrinogen] and Troponin T may have prognostic value if they are elevated (Nejm 2000;343:1139); Phospholipase A2 predictive for CAD (Nejm 2000;343:1148).

B-type natriuretic peptide, predictive of ongoing cardiac risk (Nejm 2001;345:1014) or other risk for mortality (Nejm 2004;350:655);
useful as ER test, if rapid assay available to help in diagnosis of CHF.

The N-terminal fragment produced by the cleavage of the precursor to BNP is called pro-BNP (the other product is BNP). This is being studied for utility in diagnosis of CHF and long-term mortality in those with CAD (Nejm 2005;352:666).

Pregnancy-associated plasma protein A (PAPP-A): increased level with placque rupture—needs more study (Nejm 2001;345:1022).

Non-invasive lab: ECHO for mitral regurgitation, aneurysm, ejection fraction estimation, and mural thrombi with 77% sensitivity and 93% specificity. Also looking for wall motion abnormalities, although the ECHO exam may not determine the onset of any abnormalities.

Field EKG with telemetry to ER does help (Am Hrt J 1992;123:835). EKG (Nejm 2003;348:933) may show ST elevation (50% sensitivity), duration of elevation correlates with extent of injury, height of at least 1 mm in limb leads and 2 mm in precordial leads; sum of elevation correlates directly with severity of injury (and thus prognosis) (Jama 1998;279:387); T wave inversions (r/o acute cholecystitis). Persistent ST elevation anteriorly has low association with LV aneurysm (Am J Cardiol 1984:84; Eur Hrt J 1994:1500). New LBBB extremely compelling (Ann EM 2000;36:561) and should be treated as acute injury. New RBBB indicates occlusion of anterior descending proximal to first septal branch, new complete RBBB or LBBB denotes higher mortality (J Am Coll Cardiol 1998;31:105). LBBB to be treated as ST elevation even in patient with ASHD, old LBBB, and an H & P consistent with acute infarct—ie, thrombolytic candidate per protocol; may also apply the Sgarbossa criteria for those with old LBBB: (1) ST elevation ≥ 1 mm concordant with QRS complex, (2) ST elevation > 5 mm if discordant with QRS complex, and (3) ST depression
in leads V1 thru V3. The Sgarbossa criteria cannot be used to rule out the possibility of MI (Ann EM 2000;36:561) but rather should be used to identify those who qualify for thrombolytic or invasive therapy (Ann EM 2000;36:566).

Serial EKGs in ER are less helpful than serial serum markers (Ann EM 1992;21:1445), but repeating the EKG in 30-60 min can help determine whether a patient has dynamic changes on the EKG—in other words, not just looking for STEMI. Ideally, look at the ST segment 0.08 sec (2 small boxes) after the J-point to read changes from baseline.

Coronary MRA for screening (Nejm 2001;345:1863)

ETT: May be useful if done from ER in patients who do not have known CAD, an evolving MI, or unstable angina based on EKG and serial markers, yet they are stable and no plausible explanation for their symptoms; heart rate recovery in 1st min is predictive (Nejm 1999;341:1351) and decreased exercise capacity prognostic for mortality (Nejm 2002;346:793).

Radiology: Ventriculogram with technetium scan; ejection fraction, if < 40%, 1-yr mortality climbs steeply from 5%; sestamibi perfusion imaging at rest in those with high suspicion and normal or non-diagnostic EKG (Jama 2002;288:2693)

Other reasons: Abnormal EKG or cardiac injury may be found through the following tests: CBC with diff, metabolic profile, CXR, drug/toxin screens.

Emergency Management for ST Elevation MI: [better patient outcomes with use of clinical pathways (Jama 2002;287:1269)]:

(Nejm 1997;336:847)

Drugs:



  • O2 (Acta Anaesthesiol Scand 1981;25:303)


  • ASA 81 mg, 2-4 tabs po immediately; no difference in regular vs prostacyclin-sparing ASA (Eur Hrt J 1994;15:1196); clopidogrel 300 mg po (a thienopyridine derivative) with ASA
    decreases death or other primary complications of atherosclerotic disease, but increased risk of bleeding, would consider in non-ST elevation MI (Nejm 2001;345:494); the effect of ASA is blocked by COX-2 medications, especially if they are very COX-2 selective (Lancet 2005;365:475).


  • TNG, as sl or iv (Scand J Clin Lab Invest suppl 1984;173:27) if BP OK, especially if continued pain, perhaps even if no pain; especially helpful if any element of CHF or if large anterior MI—Avoid if sildenafil or other drugs for erectile dysfunction, and time of avoidance is specific to the medication—sildenafil needs a 24-hr free window to consider TNG use, and other drugs in this class require longer waiting periods!


  • Narcotic analgesia and/or anxiolysis.


  • Heparin: Unfractionated vs LMWH (J Am Coll Cardiol 2000;35:1699) (Jama 2004;292:55); at least with enoxaparin, no difference for those with early invasive strategy, as well (Jama 2004;292:45)—this was an open label study.


  • Thrombolysis with streptokinase, TPA, Retavase, etc—TPA the standard (Nejm 1993;329:673):



    • Helps all patients including those > 75 yr.


    • If systolic BP ≥ 175 or diastolic ≥ 100, bleeding risk is double.


    • Use if pain is < 6 hr duration, or if 6-12 hr and STs still elevated, or LBBB and good story.


    • More effective re: mortality if used in smokers (Qjm 1999;92:327).


    • Potential complications include bleeding, such as intracranial, cardiac rupture (J Am Coll Cardiol 1999;33:479), or intra-abdominal; intracranial associated with older age and hypertension (Am J Cardiol 1991;68:166).


    • Contraindications may include recent stroke, recent major surgery, recent major dental work, trauma, hemoptysis,
      hematemesis, melena, hematochezia, hematuria, cancer, new headaches, bleeding diathesis, or h/o aneurysms.


    • Not for ST depression, even if markers positive.


    • Prehospital thrombolytics have not been shown to improve outcome and will probably have high skill attrition secondary to paucity of use (Am Hrt J 1991;121:1), unless in areas where transport times are consistently > 1½ hr. With the advent of aeromedical care, transport to a primary catheterization center without thrombolysis may make more sense. In Donegal, Ireland, patients with extended transport times have shown improvement with prehospital thrombolysis, but this is in a setting where a physician responds to the prehospital scene and thrombolysis is given in consult with a cardiologist (Ir Med J 2003;96:70). Thrombolysis vs primary angioplasty showed a favor toward angioplasty for the endpoint of reinfarction but not death or stroke if the procedure could be accomplished within 3 hr (Nejm 2003;349:733) and further analysis shows that a delay of balloon inflation time of > 1 hr compared to the standard time for thrombolysis does not convey a greater benefit when compared to thrombolysis (Am J Cardiol 2003;92:824).


  • G IIb/IIIa agents (Drugs 1999;58:609) helpful around time of catheterization (Am J Cardiol 1999;84:779; 2001;88:A6,62), not proven to be helpful otherwise in combination with thrombolytics at this time, ongoing trials to assess whether lower thrombolytic doses could be used if G IIb/IIIa agents given in conjunction (Lancet 2000;355:337). Pro study of abciximab compared to tirofiban in preventing ischemia (Nejm 2001;344:1888; 2002;346:957)



  • β-blocker within 24 hr of MI (OK to give in ER and continued indefinitely), helps prevent recurrent MIs and fatal ventricular arrhythmias in all (including the elderly) (Prog Cardiovasc Dis 1993;36:261), increase survival for > 6 yr; one example for loading is metoprolol 5 mg iv over 5 min × 3 and then 50-100 mg po.


  • Consider direct thrombin inhibitor such as bivalirudin 0.75 mg/kg iv bolus prior to PCI, followed by 1.75 mg/kg/hr iv infusion per length of procedure for those who are receiving IIb/IIIa agent instead of heparin—preliminary data (Jama 2004;292:696).


  • ACEIs within 24 hr of MI and for 6 wk, but continue indefinitely if EF < 40%; may also help with CHF emergently, as long as no AS with captopril 6.25 mg sl; captopril 50 mg tid increases ETT performance and decreases LV size; especially in anterior MIs; prolong life after MI even if no symptoms but not efficacious in those with preserved left ventricular function (Nejm 2004;351:2058).


  • Angiotensin-receptor blockers (ARBs) such as valsartan may be as effective as ACEIs, but no value in combining these two therapies—head-to-head study of valsartan with captopril (Nejm 2003;349:1893).


  • Eplerenone 25 mg qd for 4 wk and then increased to 50 mg qd to decrease morbidity/mortality after MI in those with EF < 40% (Nejm 2003;348:1309)—this is a selective aldosterone blocker for the mineralcorticoid receptor.


  • PRBC if age > 65 yr and Hct < 30% (Nejm 2001;345:1230); note that transfusion in these patients is associated with higher mortality (Jama 2004;292:1555)


  • MgSO4 perhaps, 8 nm bolus over 5 min, then 65 nm over 24 hr; if Mg low, perhaps for all; improves survival in one study from 89% to 92%; but of no help in ISIS-4.


  • Historical consideration of insulin iv then sc qid for months in all patients. Diabetics with intensive insulin therapy will have
    decreased mortality at 1 yr. Low dose Glucose-Insulin-Potassium (GIK) is not effective (Cardiology 1966;49:239, Cardiovasc Drugs Ther 1999;13:191).

Surgical:



  • Angioplasty (PCI) as primary treatment for STEMI if available (J Invasive Cardiol 1999;11:61; Circ 1999;100:14) and < 12 hr of symptoms gives a better outcome when looking at the triple end-point of death, re-infarction, or CVA but no difference when just looking at death (Jama 2002;287:1943). Discussion of regionalization for primary PCI if available at other facility within 2 hr (this is time to balloon open) of original hospital or from prehospital site (Nejm 2003;349:733), 90 min per Nallamothu (Am J Cardiol 2003;92:824), or facilitated PCI which would be after thrombolysis if symptoms or ischemia persist. Aggressive intervention touted as superior to aggressive medical management is challenged when looking at a 7-yr outcome (Jama 2005;293:1329). PCI is preferred if coincident heart failure or cardiogenic shock (J Am Coll Cardiol 1991;18:1077)—thrombolytics of equivocal efficacy in this setting (Eur Hrt J 1999;20:128). PCI as acute treatment has the findings of 90% successful, 3% require emergency CABG, 5% infarct, and 1% mortality.


  • CABG after angio if low EF (21-49%) and multivessel disease, or if left main disease; can do it 1 mon post-MI, although better 6-mon survival, if done immediately for cardiogenic shock (Nejm 1999;341:625).


  • Atherectomy less good.


2.2 Right Ventricular Infarct

Eur J Cardiol 1976;4:411.

Epidem: Seen with inferior wall MIs (IWMI) and increase the mortality from 6% to 30% (Nejm 1993;328:981); mitral
regurgitation, when severe, is associated with a 50% 1-yr mortality despite all interventions; increased risk also seems to be age related (Circ 1998;98:1714).

Pathophys: Right ventricular infarct syndrome—acute inferior MI, Kussmaul’s sign (paradoxical increases in jugulovenous pulsation with inspiration), high CVP with low PA pressure and low PCWP so all nearly equal (like pericardial tamponade), low cardiac output; occur in 50% of inferior wall MI patients but clinically significant in 30% and nearly 10% of those with CPK levels > 2000 IU; reversible with reperfusion treatment.

Lab/EKG: ST elevation in RV4; get right-sided EKG in all patients with IWMI.

Rx: Consider increasing preload with saline; use dobutamine, nitroprusside, and sequential pacing as needed; avoid nitrates and diuretics; isoproterenol may unload RV but concerns of increasing mortality. Thrombolytics helpful (Am J Cardiol 1984;54:951), but not as good as for other regions of the heart unless heart block or hypotension (larger infarct) (J Am Coll Cardiol 1998;32:876).


2.3 Unstable Angina/non-Q wave MI

Circ 1994;89:81

Complc: See p 13 for TIMI Risk Score.

EKG: ST depressions or even no acute changes

Rx: Unstable angina may be amenable to medical therapy, and acutely should use ASA, nitroglycerin drip, and heparin—unfractionated vs LMWH is an active area of research (Circ 1999;100:1593). If ischemia or pain cannot be remedied, this should be treated in a similar fashion to post-infarction angina and coronary angiography is indicated—a “cooling off” period with antithrombotics is not helpful (Jama 2003;290:1593). Whether treatment with primary coronary catheterization with G IIb/IIIa therapy is a better
treatment is still not fully elucidated (Am J Cardiol 1998;82:731).

Crs: Prognosis is similar for Q-wave and non-Q-wave infarcts, although non-Q-wave MIs are followed by more infarcts and angina but are associated with less CHF; is not affected by 1stdegree heart block, PVCs, Vtach, or RBBB; better prognosis if preinfarction angina preceded.


2.4 Atrial Fibrillation and Flutter

J Cardiovasc Pharmacol Ther 2000;5:11; Nejm 2001;344:1067; 2004;351:2408.

Cause: Associated with: normal variations, idiopathic, CHF, and RHD, atrial dilatation (eg, in mitral stenosis or regurgitation), pericarditis, COPD especially with hypoxia and bronchodilators, ASHD; with hyperthyroidism especially in the elderly as measured by low TSH, which has a 30% 10-yr incidence in contrast to 10% 10-yr incidence with normal TSH and with toxic multinodular goiter; with alcoholic cardiomyopathy or “holiday heart”; marijuana use (Ped Cardiol 2000;21:284); and Wolff-Parkinson-White (WPW) syndrome (Am J Cardiol 2000;85:1256).

Aflut and multifocal atrial tachycardia often (60%) from pulmonary disease including pulmonary emboli and theophylline use.

Wandering atrial pacemaker (WAP), multifocal atrial tachycardia, and sick sinus syndrome (SSS) are also supraventricular arrhythmias.

Epidem: Common; supraventricular prematures are not associated with ASHD or sudden death; 40-65% incidence after cardiac surgery (Ann Thorac Surg 2000;69:300). Afib is more common with increasing BMI (Jama 2004;292:2471). BMI = Weight in lbs/(height in inches)2 × 703.


Pathophys: Unknown, hypotheses of conduction problems vs structural problems as primary insult, probably many variables. Whether dilatation of the atrium(a) is cause or effect is debatable, but is associated with Afib. Many different frequencies and duration of Paroxysmal Afib. (Curr Opin Cardiol 2000;15:54).

Sx: Polyuria, palpitations, and faintness; 51% of cardiac syncope due to arrhythmias (Nejm 2002;347:878)

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Jul 21, 2016 | Posted by in EMERGENCY MEDICINE | Comments Off on Cardiovascular

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