panre and pance review cardiovascular ii
DESCRIPTION
Certification and Recertification Exam Review Physician Assistant Cardiovascular IITRANSCRIPT
Cardiovascular II
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Dr. Donald Sefcik
Donald J. Sefcik is the Associate Dean at the chicago college ofosteopathic Medicine (ccoM), Midwestern university (MWU), inDowners Grove, IL. He is a tenured professor and board certified in bothEmergency Medicine and Family Medicine. From June L997 through May2000, Dr. Sefcik served as Medical Director for the Physician AssistantProgram, College of Health Sciences (CHS), at MWIJ. Dr. Sefcik,s lecturesare based upon his experiences as a clinician and preceptor, tenure as amedical school faculty rnembero and his student assessment research.
Dr. Sefcik has practiced with physician assistants since 1988 and beeninvolved in the clinical training of physician assistants since 1990. Prior tojoining Midwestern University's faculty, Dr. Sefcik was a faculty member inthe Pharmacology Deparfinent at Butler University and in the NursingDepaitment at Marian College, both in Indianapolis, Indiana. Dr. Sefcik hasa Bachelor of Science in Pharmacy (1981), a Master of Science inPharmacology (1994), both from Butler university, illd an MBA (May2004) from Purdue University.
CME ResourcesCertification & Recertification Exam Review
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CertiJication & Recertifi.cation Exam ReviewCME Resources
2004
Cardiovascular Medicine - IIIschemic Heart Disease and Heart Failure
Donald J. Sefcik, D.O., FACOEPLearning Objectives
Upon completion of this portion of the review course, the participant should be able to:
1. Differentiate corrmon causes of chest pain.2. Present an overview of aortic aneurysms and dissection.3. Define ischemic heart disease (II{D) and coronary artery disease (CAD).4. List several risk factors associated with CAD and IHD.5. Compare and contrast stabie angina, unstable angina and Prinzmetal's angina.6. Discuss diagnostic modalities utilized in the evaluation of IHD.7. Describe the events culminating in a myocardial infarction (MI).8. Discuss EKG manifestations of myocardial ischemia/infarction.9. IdentiSr high-risk patients for acute MI.10. Describe how a myocardial infarction is definitively diagnosed.1 1. Discuss indications for acute coronary thrombolysis.12. Describe therapeutic options for an acute MI.13. Describe the rationale for IIID drug therapy.14. Identify potential complications of myocardial infarction.15. Describe pericarditis: etiologies, manifestations & management.16. Cornpare and contrast puhnonary edema and heart failure.17. Differentiate left-sided and right-sided heart failure.18. Conpare and contrast systolic and diastolic heart failure.19. Prescribe appropriate heahnent for acute pulmonary edema.20. Prescribe appropriate therapy for left ventricular dysfunction.
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Certification and Recertification Exam ReviewCardiology - II
2004
Case 1
A 44 year-old male presents for a "checkup". He denies any health problems. Hediscloses to you that he drinks "regularly", smokes 1.5 packs of cigarettes a day anddoesn't exercise ever. His BMI is 33, His blood pressure is 168/102 mrn Hg. Hisfundoscopic examination is unremarkable. You do note that his PMI (point of maximalimpulse) is located in the fifth, left intercostal space, near the midclavicular line.
Case 1.1Which one of the following therapeutic regimens is the optimal choice for this patient?
A. metoprololB, hydrochlorothiazide Sg - bO"fuC, enalapril &l - 5-U,l:D. diltiazemE. lifestylemodification
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proteinuriabradycardiadepressioncephalgiamorbilliform rash
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Case 1.2Eventually, you add propranolol to this patient's therapeutic regimen. Which of thefollowing side effects is most likely?
A.B.c.D.E.
.- V €r .l \,g.,* su\ ,)Ae- - c6'*^ y=ll"t'{u
ovvs
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Certification and Recertification Exam ReviewCardiology - II
2004
Case 2
A 48 year-old hypeftensive female transfers to your practice. She has currentlydiscontinued all medications because she was concerned that her former clinician"prescribed too many medications", although she was happy with his bedside mannerduring the delivery of her five children. She has a history of depression andhypercholesterolem ia.
Case 2.1Which one of the following is the best beta-blocker for this patient?
A.B.c.D.E,
propranololpindololtimolol ..,acebutolol 'f> , Se\ ec'N€-[L.t.r"r \ ,''ol '.,\ n eW.\
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A.B.c.D.E.
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Case 2.2Two weeks after the initiation of therapy for her hypertension, she returns complainingthat when she coughs "she wets her pants". Which of the following medications wasmost likely started two weeks ago?
reserprneclonidinehydrochlorothiazideterazosin
-
d l\uoKpndiltiazem
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Certification and Recertification Exam ReviewCardiology - II
2004
Case 3
A 68 year-old hypertensive female presents complaining that her new antihypertensivemedicaiion causes her to experience "skipping heart beats", swelling of her legs andheadaches. Her blood pressure is 178/96 mm Hg, She has a grade lllA/l diastolic murmur,
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Case 3.1Which one of the following is the most likely cause for her murmur?
A. aortic stenosisB. aortic regurgitationC. mitral stenosisD. tricuspid stenosisE. pulmonic regurgitation
Case 3.2Assuming that this patient was prescribed a calcium channel blocker, which of thefollowing is LEAST likely the agent she was taking?
A. nifedioine;: i;ffiil; \ r:u\o.\ rr,+l"c),\^d^rtC. amlodipine ,/ 'D. isradipine , ,
E. verapamil - n$,r .f,!.y,.r1r.'.J.'p. le'l: putt-{ t'aJorl",l^7}'r,
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Certification and Recertification Exam ReviewCardiology - II
2004
Case 4
A 51 year-old male presents to your office after being discharged for a heart attack. He is
currently taking one aspirin a day. You review his charts and note that he has a history ofhypertension, gout and diabetes type 2. His echocardiogram in the hospital, prior todischarge, revealed an ejection fraction of 52%.
Case 4.1Which one of the following antihypertensive agents is the best choice for this patient?
A. hydrochlorothiazideB. lisinopril Ou-:\ nn T.C. prazosinD. diltiazemE. propranolol
Case 4.2Which one of the following agents would most likely worsen his gout?
A. hydrochlorothiazide '-T\n;r.,,:flC C^ur<: h 1p"*t-,"-"B. clonidineC. methyldopaD. verapamilE. propranolol
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Certification and Recertilication Exam ReviewCardiology _ II
2004
Gase 5
A.B.c.D.E.
rhere are no cotton-woor ipots oin"mo"rr.s;. ;p;,;;i;i;:"'r;.:'j:,:'??ffi:i,B o, crorni.r,,
Case 5,1which one of the following, fundoscopic findings would be most supportive of thediagnosis that you suspeCt?
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= O, $n e--Ch trrnY f.,cl-* ''F
Case 5.2which one of the following diagnostic study combinations would most likely reveal theetiology for this patient,s ophthZtmic piobtem?
A. complete blood count and INR? echocardiogram and carotid doppler studiesc' cr scan of the brain and intraocrt.r pr"rrrre measurementsD' fluoroscein staining and intraocur.i pr"rrrre measure,";;i;E. MRI scan of the briin and
"n ,ortogrm
A 54 year-old male presents with a sudden loss of vision that began 30 minutes prior toarrival' He denies any trauma prior toirre visual ror.. i" oenies pain. Examination ofhis visual acuity reveals that,he r'trr iigl'rt perception oniy. L*"rination of the ipsilateral?il::::::,:"":"3["j::]fifl?y 991eit
a1o ,ignifi.rni ,ia,rowins of the retinar arreriores
macular edema 4,,.-latortuous and dilated retinal veinsretinal at"rilf" r"-grentation of blood lBoxcc.m.\) -:an,increased cup:disc ratio (greaterihan 0.6) J -
isolated hyperemia of the naial naft of tne fundus
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Certification and Recertilication Exam ReviewCardiology - II
2004
Case 6
A 62 year-old male presents complaining of shortness of breath on exerlion for thepast several weeks. He states that his "heart races in his chest" because he getsso short of breath. His chest x-ray is unremarkable.so short of breath. His chest x-ray is unremarkable. ljs-Hemoccult is negative. r
His hemoglobin is 9.4 Gm/dL; McV is Tp fL; RDW is(0.8)\ - ,. r ci. ,-., .,. {L^l!",,, r.x.r$n,. *" "trln cldr"''r'*r'''s {}^tt""t$'
Case 6.1Which one of the following is the most appropriate at this time?
A. order a serum ferritin level, TIBC and reticulocyte countB. order a hemoglobin electrophoresisC. order both serum 812 and folate levelsD. prescribe vitamin 812E. prescribe a multivitamin supplement with vitamins A, B, C, E, and iron
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Case 7\- Ac,"k I .Soo,\
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Ten days after an acute myocardial infarction, a 56 year-old female presentscomplaining of chest pain. The pain is worsened with inspiration. She denies shortnessof breath. Physical examination revels a low-grade fever, bilaterally clear lungs, and anormal sinus rhythm without gallops, murmurs or rubs. An EKG reveals inferiorq-waves, without evidence of ST segment displacement.
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Case 7.1Which one of the following therapies is the most likely to be effective?
A. cephalexin 500 mg orally four times a dayB. doxycycline 100 mg orally twice a dayC. nitroglycerin sublingually
@ibuprofen 600 mg orally four times a dayE. warfarin Smg orally every morning
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Chest PainPrinciples:
1. Any chest or abdominal pain complaint may be a manifestation of heart disease.2. Accurate diagnosis is based upon interpretation of the patient's pain perception.3. The diagnosis, often based solely on history, can be biased and/or misperceived.4. Physicalfindings/ancillary tests may not be helpful, and may be misleading.
Non-Emerqent Etioloqies
Klinkman MS, Stevens D, Gorenflo DW. Episodes of care for Chest PainJ Fam Pract 1994;38:345
A. Musculoskeletal * 36 o/o
. Muscular- Active patients- "Sharp" pain- Exacerbated with movement- Tenderness(reproduciblesymptoms)
. Skeletal (Costochondritis - Tietze's syndrome)- Commonly young women (African-American more commonly)- Pain exacerbated with deep inspiration- No history of repetitious activity/trauma- lf NSAIDs taken - usually have reduced the symptoms \- Tenderness - more commonly left % costosternal margins
J< eain is reproducible in 5 - 10 % of patients with acute cardiac ischemia
B. Gastrointestinal - 19 %. "-itis"
- Relationship to food- Relief with antacids or eating
lk G/ eocktailreso/yes pain in 5 - 10 % of patients with acute cardiac ischemia
. Esophageal spasm- "Squeezing" retrosternal pain/discomfort \ ! - ,,o1.. n-ro{.k_- Associated with GERD {V 'icu
- sr'-rt
- Esophogram fcJroxr.,rf l;wt* Nutcracker of Corkscrew esophagus gsopdi\{],SuS
C. Cardiac - 16 o/o
r Typical angina (next section). MitralValve Prolapse
- "Sharp" or "Dull" pain' Palpitations- Mid-systolic click and murmur
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D.Psychosocial -9%. Anxiety
E. Pulmonary - 5o/o. Bronchitis. Pleurisy/Pleurodynia
F. Atypical - 15 o/o
. No etiology is clear
Ischemic Heart Disease
1. Coronary Syndromes fr*5* f:w'n*y ' S i'rrn';rr!z'-
\J""aG- chest discomfort secondary to myocardiat isJfiemia ..T Stable Demand) Anqina V,3Crt,:u\ pr:'1"1"1 = t'''S\J+
-1*,*+^^t
Occurs with a fixed threshold of increased workload. Manifests as retrosternalchest discomfori, which may include radiation to the arm, back, neck or jaw,
nausea, diaphoresis, shortness of breath, etc., precifitated by:
Exertion (generally) or Emotion (anger) or Eating........
Relieved with Rest (reducing workload) [usually discomfort lasts 5 - 15 minutes]or Nitroglycerin (NTG).
.{r l.Jnstabte (Supplv) Anqina fpreinfarction anqinal C ,.>f n ei,o crricl '. -s a\wr"yS \q
Angina of new onset, angina at rest (or with less exertion), or a pattern of ;1'-1E"ir"5te- J,1g" increasing frequency, severity and duration of anginal episodes, requiring longer
. -.rG{ periods of rest or more NTG to obtain relief of symptoms.\ \t\" L! t'.*1"* Variant (Prinzmetal's) Anqina L ffr qt5 , rf\tJ6tv',ruu )\-
.,c,k .a ffSil:fil5ill?1 L"-'S?:fiy';ffi:,?"JIii["iTI,:J:'T;:, ,io.sl.no& - . - ,-+ ls.i6 rnfirs'\ r{ -p.tt-i"n:'(*/'- . oo"y,1,L fl."Anqina'Equivalent"
-r *'9 nt'J'g(5 ,g-'Y' Ofter6ySplgil dizziness, fatigue, or syncope due to transient myocardial ischemia.
- ''* ' *S,"niuJ*EA
,y1 *r g\. ] +U 'rs ,\c '-lrraA Cl"srr pr'i.ll
Asymptomatic periods of myocardial ischemia.Silent Ml - more common in diabetics and the elderly.
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#bl Myocardial lnfarq-tion h Myocardial Cellular Death
Generally secondary to coronary artery thrombosis, resembling "angina" buttypically greater in severity and duration, often not relieved with rest ornitroglycerin.
\ nequirements for diagnosis (2 of 3):
- A classic history- Evolutionary changes on EKG- Elevation of Cardiac Enzymes/Markers
* Year 2000 ACC/AHA Guidelines: ACS = UA, NSTEMI and STEMI
Clinical Presentation :
Myo c ardi al i schem i a causes.'
A. the "classic discomfort"
B, autonomic nervous system activation- SNS - diaphoresis; vasoconstriction [cool, clammy skin]- PSNS - nausea; weakness [vagal effects]
C. myocardial dysfunction:- ventricular gallops (chamber compliance changes) - Sa gallop (atrial gallop)- dyskinesis (reduced cardiac output)- rales (pulmonary edema)- arrhythmias
P ote nti al com pl i catio n s in cl ude :A. arrhythmias
[electrical - altered transmembrane ion flux]
B. hypotension[mechanical - myocardial cellular dysfunction]
C. embolism[mechanical - ventricular cavity thrombus formation]
D. pericarditis
Iinflammatory]E. pulmonary edema/CHF
[mechanical - myocardial cell dysfunction; valvular dysfunction; tamponade]
The differential diagnosrs of acute chest pain resembling AMI includes:
A. Pericarditis - inflammation of pericardial sac
,r-pleuritic pain; changes with position [reduced leaning forward]; odynophagia( , pericardialfriction rub (may be intermittent)
\. diffuse ST segment elevation-\----- ----==--+
P\eotJr= T Pc^l^€kr$l r Iflc\cJ c la^nb f&{{L'. '
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@irchow's triad - venostasis; hypercoagru*ilry'>-ffiAfrgradient I Al*rrl * n-:."r*l rrCo\ =T.-. CXR - most commonly is normal
- Young males (tall and thin); Smokers; Valsalva Maneuvers \. Secondary ( r"t t$bt nr"\ds )- COPD; Asthma; Pneumonia.,.. * ' tJ \/
. Simple- lntrapleural space pressure is equal to atmospheric pressure- Expiratory fitm rncreases visualization (loss of peripheral lung markings...)
o Tension- Pleural defect acts as "one Way Valve" - prodUces positive pressure
resulting in contralateral shifting of mediastinum; JVD; hypotension......*** po not wait to get a chest x-ray !- Needle thoracostomy, zno ICS/MCL
Pneumonia - lung consolidation. pleuritic painr cough, sputum Produciion, fever. chest x-ray and/or physical signs of consolidation
Thoracic Aorlic dissection. begin as intimal tear - cleavage plane is within media. commonly 50 - 70 year old malesr abrupt on - "tearing" or "ripping"
- typicall(between the shoulder. Classic physical features
- Unequal (absent) Pulses- Focal neurologic deficits- Signs of cardiac tamPonade
**-geck's triad * fiugular venous distention, muffled heaft sounds, hypotension). Gold Standard - Aotlogram. CXR (upright PA) - widened mediastinum - suggestive
Others
B. Pulmonary embolism - pulmonary vascular occlusive evento pleuritic pain; pleural friction rub. SEiItGet with dyspnea
. V/Q scan; Pulmonary angiogram - gold standard
C. Pneumothorax - gas in pleural space. Primary (Spontaneous) - No underlying lung disorder
E.
intimal injVry)
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1. Definition - Myocardial cellular necrosis secondary to coronary artery occlusion, mostcommonly tlie result of thrombus formation upon an atherosclerotic plaque.
Of acute chest painEntergency Department - 30 % patients = coronary ischemic eventPrimary Care ffice - 5 % patients : coronary ischemic event
2. Pathophysiology -
a. HowAVhy does it happen ?
i. Etiology - Coronary artery thrombosis (most common)Ernbolic event , \Coronary aneritis - \-ra,io.w"K,
lrs c\ '!ea'!fCocaine use
ii. Sx/Sx - Anginal type discomfort that is sustained/changedDyspnea common in elderlyAssociated nausea, vomiting, diaplioresis
* Often confirsed with indigestionMay auscultate an 54 gallopMay demonshate signs of acute heart failure
b. Who's at risk ?
i. Maleffemale - Before age70 - Male > FemaleAfter age 70 - Male = Female
( L*/ o hr Pz:opY I e ;;'1V'., ,"..' LltJ
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ii. Age - Increased incidence with age (more common > 40 years old)
iii. Risk Factors - Family history premature coronary artery disease (CAD)HypertensionHypercholesterolemiaCigarette smokingDiabetes mellitusAging/Male sex (< 70 years old)
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3. Differential Diagnosis -
4. LaboratoryIK-Ray -
ott;,," t^*L.*lfi\'n
firt J stung3xJ
see prevlous
EKG -- 50 %o are normaVnondiagnostic at AMI presentation
* ST Elevation - TransmuralMay d
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DIFFEEENTIAL DIAGNOSIS OF *EKG CHANGES'
1. T-Wave Inversion: Myocardial IschemiaAnfarctionSevere LVH or RVH with "Strain"CardiomyopathiesPericarditisIlemorrhagic Stroke
i-
2. ST Segment Elevation: Acute Myocardial Ischemia/InfarctionPericarditisVentricular Aneurysm
3. QRS Changes @evelopment of Q Wave): Myocardial InfarctionSeptal DepolarizationCardiomyopathies
)k' WBC - Often demonstrates leukocytosis,)b Chernistries - Associated risk factors
t EchocardiogramMay demonstrate wall motion abnormalities (hypokinesis)\f CXR - identifies (rules out) other pathology
.t Cardiac En4ymes fMarkers] - May Demonstrate cellular necrosis(CK, AST, LDH; Troponin; Myoglobin)
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Myocardial ischemia results when cellular oxygen demand exceeds oxygen supply. Myocardial oxygendemand is determined by (a) gontractility [inotropic state - a measure otttre toice of contraction],(b) heart rate fdetermines ATP utilization and oxygen consumption], and (c) ventricular wall striss [aproduct of ventricular wall thickness and intraventricular presiure].- Myocardial oxygen supply isdependent upon oxygen,calline capacity of the blood [determined by oxygenatioo anO fremoglobincontentl and coronary blood flow [a result of vascular tone, Iumen pui"ncy *a perfusion pressures].
Myocardial hypoxia causes increased anaerobic metabolism (an innacellular acidosis develops) and animpairment of the ATPase ion pumps (resulting in altered membrane ion movement - the EKG recordsthese changes as T wave ilversion, ST segment displacement, and,/or anhythmias; if cell death occurs,Q waves may eventually develop).
Ischemia of the entire thickness of the ventricular wall is termed transmural; ischemia of the innermostlayer(s) of the ventricular wall is termed subendocardial ischemia. Historically, e wave infarctions werebelieved to represent myocardiai necrosis of a transmural nature, while Non-e-wave infarctions werebelieved to be the result of subendocardial myocardial infarctions. lnterestingiy, ST segment elevationrepresents transmural ischemia (an injury pattern) and will probably result ini Q-wave infarction, while STsegment depression represents subendocardial ischemia and may result in u lion-q-wave infarction.The development of abnormal Q waves (over a 2 - 24 hour period after the onset of clinical symptoms) isindicative of myocardial cellular necrosis.
Finaliy, although the initial mortality is lower in patients suffering Non-Q-wave infarctions than patientshaving Q-wave infarctions, during the subsequent months, the reinfarction rate and risk of death is greaterin the patients suffering the Non-Q-wave infarctions.
Tvpical EI(G Evolution Pattern of Mvocartlial htfsrction
Acutely < 24 hrs 24 - 48 hrs Days later
Q-wave MI sr elevation sr elevation T wave inversion ST normalizationR waves reduced Q wave deepens Twave invertedQ waves appear
Non-Q-wave MI T wave inversionST depression
ST segment Elevation: Elevated if the ST segment is =/> I mm above the baseline,measured at 0.08 seconds (2 mm) after the J point
Note: the shape of the ST segment may be a clue:
a. upward concavity ("smiiing") - benign ???
Weeks later
ST & T normalization
Q wave persists
T waves normalizeNo Q waves
Abnormal ST Sesment Changes
The most definitive changes accompanying acute myocardial ischemia are ST segment alterations.Polarity changes ofthe T waves are less reliable.
.-* b. coved (downward concavity) - acute iniury ???
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f+ronc-,,..1r *,,^^--J:-r :-^L^-:^ r:-r--^.:^-l
;L*--ll**,fvt*-A f";-ro- Causes: [transmural] myocardial ischemia [infarction]
l\ (tt) Prinzmetat'sangina\-,, i acute pericardiris
-1 /^t* ventricular aneurysm
ll twperkalemiaeariy repolarizationventricular hypertrophymyocarditisBundle-branch blocks
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ST segment Depression: Depressed if the ST segmett is =l> I mm below the baseline,measured at 0.08 seconds (2 mm) after the J point
Note: the slope of the ST segment depression may be:
a. downsloping - most indicative (specific)b, horizontal - intermediate specificityc. upsloping - least definitive
Causes: [subendocardial] myocardial ischemiaNon-ST segment elevation AMILVH "strain" patterndigitaiis effectsBundle-branch blockhypokalemia; hypomagnesemia
*** Nonspecific ST-T wave changes
Alterations in the ST-T wave morphology that are not isoelectric and not normal, yet not abnormal enoughto be labeled as ST segment elevation/depression and/or T wave inversion.Causes include: Myocardial Ischemia, ventricular enlargement, drug efflects, electrolyte disorders,
acidosis, hypothermi4 hyperthermi4 hyperventilati on, medical illness
EKG Correlates of Myocardial Ischemia and InfarctionEmergency Medicine Reports - April 23, 2001
A. Focal changes (Inferior, Anterior, Lateral) reflect ischemic area(s).B. Elevation and depression demonstrate 'current of injury' pattern.
AMI location [LVl EKG leads ST sesment chanpe
Anterior wall vl -v4 elevation
Anteriolateral V1 - V6 (+/- I and aVL) elevation
Lateral I, aVL (+l- V5 and V6) elevation
Inferior II.Itr and aVF elevation
Posterior Vl _V3 denression
S e\e./Sft/,-' Joe* nu\ nne,a^ n^f AU<^At\ED EKG Diasnosis and Diagnosis upon tr'inal Hospital DischargeEmergency Medicine Reports - April 23,2001
ED Interpretation AMI Unstable Ansina Noncoronarv Diasnosis
Normal lo/o 4o/o 95%
Nonspecific 3o/o 23o/o 7 5o/o
Abnormal(nreviously documented) 7% 48Vo 45%Abnormal(not oreviouslv documented 25o/o 43o/o 32Vo
Infarction 73% t3% 14o/o
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TEST
CARDIAC MARKERS(Variable values in Literature)
TIME DETECTION TIME PEAK
12 - 24 hours
Myogrobin (i.*,.' caA riwory "rfff"rf O*^tt'
Not speciJic
r-+ --Tlt nL- t^ir)r"-\ {x* ^ t'on'\c
Troponin 3-12hours l0 -2|trours 1f 10 days,1
6 - 8 hoursSmsll Heme proteht
Contrsctile Protein I -SpectJic Myocardial cells ,3,.,ki',* :f rnu:r\ c('-<""l irc Jif-lrc f, (
WA4:y> t'
5. Treatment Plan
a. Lifestyle changes - Stop smokingExercise program (as indicated)Modify coexistent risk factors (Chol, Blood sugar...)
Control hypertensionMinimize stress
b. Nondlug Therapy - Diet - Low Cholesterol./Fat, Low SodiumExercise program, as indicated
c. Treatment -Acutely
1. Patient Position
a. Sitting - lncreases tidal volumeReduces work of breathingHelps in pulmonary edema/CFIF
2. Oxygeriation
a. Patients should receive oxygen (maintain saturation at=/> 95Yo)
b. Nasal prongs at 2-4 liters usually adequate.
c. When oxygen saturation cannot be maintained:/> 950/o, obtain ABG,or when other clinical diagnosis/therapy requires an ABG.Avoid ABG when possible, if patient is thrombolytic candidate.
3. fV Access
a. Two large-bore (16-18 gauge) sites recommended.
10
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lnCruA\+.ll, )4. Monitors
a. Cardiacb. Pulse oximetryc. Blood Pressure
5. Chest Pain Relief
d,
a. Nitroglycerrn \b. Morphi'e
^fta=o .l l^+.^r\ S- .U prrlo^J , \
6. Mortality Reduction u-"rn yor't'/^'\ Oi J t'^'n'A'a. Aspirin(unlesscontraindicated)
* Ticlopidine (TICLID)* Clopidogrel (PLAVIX)
b. Heparin* Unfractionated* Low Molecular Weight Heparin (LMWII)
o Less risk of bleedingr No dosage changes based on coagulation parameters
Thrornboiytic agents (Choice ??)
- Given < 70 minutes post-onset - mortality - L2 %- Given > 70 minutes post-onset- mortality - 9 %
Indications. Typical Chest paino sr t"ry;3'r"Hl'J",ftre,rimb);
> 2 mm (precordial)r Symptoms < 6 - 12 hours (?? beyond in "stuttering" pattern)r LBBB (new onse0
.""EExclusionary Criteria -
. Hemorrhagic CVA within past 6 monthso Recent head trauma or known intracranial masso Uncontrolled hypertension (> 180-2001> 110-120)r Major surgery within past 2 weekso Active or recent Gastrointestinal bleeding. Bleeding disorder or anticoagulationr Aortic dissection or pericarditisr Noncompressable vessel puncturer Prolonged CPRr Previous Streptokinase use (time dependent)
IIb/IIIa Inhibitors
l1
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e. Beta- Blockade- initiated early - may limit or reduce size- later - minimizes reinfarct/arhythmias
f. ACE Inhibitors- Effect on LV remodeling and recurrent ischemia- Post-AMI for reduced EF; clinical CF{F; wall motion abnormalities
Monitor for electrical/rnechanical cornplications
* Electrical
Any dysnhythmias
* Meehanissl
Pulmonary edema/Heart FailureCardiogenic shockPericarditisDressler's syndromeMyocardial wall/Septal ruptureLV Wall Aneurysm formationThrombotic or embolic events
d. Surgery - Percutaneous transluminal angioplasty (PCTA)Coronary angiographyCoronary Artery Bypass Grafting (CABG)
6. Follow Up - Educating the patient about expectations
a. Patient EducationMust treat coexistent conditionsStop smokingCompliance with exercise, diet, medications, etc
b. Future AppointmentsDictated by post-AMI course and complexity of coexistent conditions
c. Emergency VisitsRecurrence of chest discomfortPain not relieved by NitroglycerinAny decompensation/signs of complications
t2
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PERICARDITIS
1. Definition - Inflarnmatory changes of the pericardial sac surrounding the heart
2. Pathophysiology
a. HowAilhy does it happen ?
i. Etiology - IdiopathicViruses - Coxsackie, Echovirus, AdenovirusBacteria - Haemophilus (esp. children)FungalUremiaNeoplasticAutoimmune (SLE, Rheumatoid Arthritis.....)Dru g-induced (procainamide, hydralazine. . . ..)
Post-AMI (Dressler's Syndrome)
ii. Sx/Sx - Acute Pericarditis
Chest painusually sharp and pleuriticoften reduced with sitting up/leaning forwardmay have associated pericardial friction rub
Dyspnea, rales, tachypneaFever, often with myalgiasOdynophagiaCardiac dysrthl'rnias (often supraventricular tachycardias)
Pericardial Tamponade(more pronounced symptoms with acute/larger effusions)
Dyspnea, sometimes with cyanosisDistended neck veinsHypotension - often with thready pulses -lpulsus paradoxus .L, s;s*r,t;<- by ) lc ,n.n rf\glS cn
Quiet pericardium with diminished PMI ,nsp3$d,rrEwart's sign
dullness & bronchial breathing rnedial to tip of left scapula
b. Who's at risk ?
i. MalelFemale - Male > Femaleii. Age - Adolescents & younger adultsiii. Risk factors - Dependent upon etiology (see above)
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3. Differential Diagnosis - Acute MIPneumoniaPleurisyPulmonary EmbolismPneumothoraxAortic dissectionPancreatitisiCho lecystitis
4. LaboratoryD(-Ray - WBC - LeukocytosisESR - Elevated (better to follow treatment and response)Cardiac En4,mes - may be elevated (epicarditis)CXR - may demonstrate pleural effusions/other diagnosis
x large pericardial effusion - "waterbottle heart"EKG
ntay show dffise/global ST segment elevationmay show PR segment depression
Echocardiograrn - identifu pericardial effusion
5. Treatment Plan
a. Lifestyle changes - Activify limited by symptoms
b. Nondrug Therapy -
c. Rx - Aspjrin (in simple uncomplicated cases)
May use otherNSAIDsSome may require corLicosteroids (r/o Tuberculsosis. . ...)
d. Surgery - May require pericardiocentesisMay require pericardiectomy
6. Follow Up
a. Patient EducationUp to i5% may expect recuffencesAdvise on signs of complications (pericardial effi.rsion)Compliance with Rx regimen
b. Future AppointmentsFollow-up in @2 weeks, unless worsensFollow-up CXR & EKG
c. Emergency VisitsS igrrs/Symptoms of decompensationRespiratory/Cardiovascular dysfunction
+ Progressive/Acute dyspnea* Worsening chest pain* Dizzinessllightheadedness (signs of hypotension)
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Left Heart Failure
DyspneaOrthopneaPNDRalesWheezesFrothy Sputum
[oRirc *l
lvarvn iL_--.-__ i
53, (?S4), Tachycardia (?)
Fatigue'Wealness
Manifestations of Hypoxemia (Tachy...)
Rieht Heart Failure
Hepatic CongestionIVDHepatojugular RefluxRUQ Pain
B loating/As cites/AnorexiaLower Extremity Edema
LT]NGS
FatigueWeaknessManifestations of Hypoxemia (Tachy...)
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HEART FAILIIRE
1. Definition
Heart Failure is a nonspecific term.
Inability of the heart to pump adequate biood to meet the metabolic needs of the body.
May be the result of "heart disease" (unable to pump) or the result of "excessive demands".
May be acute or chronic.
May be systolic and/or diastolic in etiology.
2. Pathophysiology
HowMhy does it happen ?
EtiologyNormal ejection fraction @2/3 ventricular volume.Myocardial dysfunction (Heart Failure) reduces ejection fraction.When the result is increased diastolic filling pressures, the organsthat "empty" in the respective ventricular system become congested.
* Congestive Heart Failure (CHF)
a. Primaty Hemt Disorders - usually result in contractile abnonnality- Coronary Heart Disease- Valvular Heart Disease- Cardiomyopathies
b. Excessiye Demands- Increased pressure (afterload)- Increased volume (preload)- Increased tissue oxygen requirements (perfusion)
Heart Failure Glassification
ACC/AHA Staqe Patient Variables NYHA
A High Risk -for LVDI eft ve ntricu I ar dysfu n ction
HTN; CAD; DMFamilv Historv
B Asymptomatic LVD Previous Ml; LVDValvular Heart Disease
I
c Symptomatic LVD Dyspnea and FatigueReduced exercise tolerance
ll- ilt
D Refractory end-stage HF Marked symptoms at restMaximaltherapv
IV
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P t;*c\rr-' Drotk'r-
\ r-+ Fr$'i\t D;rr'$'Jd*
Svstol ic Versus Diastolic Dvsfunction
ra",d,Vtk-
'r s-1 Sli
o ?ffe--t6;k *ne *rLo:L, c" tc-nt e-",,*,ogr6arr1
?rfu: c'.\\&> Vroo.e v'r\bar\g {"'tu (' '( CKu c,^-#''*r en\cgr"--t'r\b.'Who's at risk ?
Systolic (Ejection disorder)[Ejection Fraction < 40%7
Diastolic (Filling disorder)fl mpaired ventricular relaxation
Etiology CADlschemic lnjury (Ml)EIOH history
Chronic HTN crsr cc^-'pl.LVH [LVE] -tnii,\ &Valvular heart Disease h{-tt"AS, AR, MR
Pathology Reduced Ejection Fraction (EF)Dilated Ventricle
Looks large on chest x-ray
Often Normal/Supranormal EFAltered ventricular fillingRestrictive Ventricle
Stiff and noncompliant ,,----."
, ,^!.Y!.{.-^F..^,*l^J \ jClinical Changes Reduced LV EF * \r":o€-
Elevated PCWP ,L.ru.r.{KPulmonary edema
Reduced LV Prbssures "n DD.r
Elevated Atrial Pressures :'l\asPulmonary Edema
SymptomatologySigns
Dyspn ea/Weakness/Fatig u eRalesSsgallopReduced pulse pressure
DyspneaMeakness/FatigueRales/Peripheral EdemaSa gallop
Acute Tx VasodilatorsLoop Diureticslnotropic agenis
VasodilatorsJudicious Diuretic Uselnotropic agents
Chronic Tx Reduced Na intakeACEIA/asodilatorsDiuretics (prn)Di goxin/Beta-B lockers
Reduced Na intakeACEIDiuretics (prn)Beta-Blockers/CCB
Tu*;h,p"o= {rr** ,fi. MalelFemale - Male > Female (ages 40-75) gocr$,q"*$rUr
Male = Female (> 75 years old)
ii. Age - Note above
iii. Risk Factors - Myocardial InfarctionHypertensive Heart Disease
Negative Inotropic drugsAlso note disorders listed under etiology (above)
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3. Differential Diagnosis -
4. LaboratoryIX-RaY'
5. Treatment Plan -
a' Searchfor Reversible Etiologl & Treat if established
b' Lifes tYI e Mo dif cati on.
- Sodium Restiction- Cigarettes- Weight Loss- PhYsical ActivitY
Echocardiogram :{' tast t{orr'-' Prd&JL'{c
E-ipt natiiretic peptide (BNP) [nesiritide]-Jioo ii*l t>'gi% sensitivitlt; > 98% spectftcitvl
CXREKGABGcBcSerum ChemistriesDrue LevelsSear-ch for an underlYing cause
Anv Voiume Overload state, such as:' * Neplrotic SYndrome
-* Cirrirosis
1" ft-;i'lr'nr'ifaZ. t DPh"l3 r+yp<rl)PCe'ni6\
c. Medications.for Acute Pulmonarv Edema
- Oxygen- Diuretics
* LooP- Digitaiis @igoxin ILANOXN])- L"giot"ntin donverting Enzyme (ACE) Inhibitors
- Vasodilators* Nitates
- MorPhine
t gggit DYsfu,nction
o ,Fffi-THF cornerstone of treatmentt'- l--Reduce afterload
- Reduceneurohormonalabnormailities- Slow the Progression
- lf AcE lnhibitors contraindicated or not tolerated, options are:
- Angioteiii" C"t"ptoiBlockers (- AA$'j )- Hyiralazine plus lsosorbide dinitrate
' AmlodiPine
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frtV.c\ {i. E5"^st ot^rr: g'#"h1ar"tnncs
' *-An'Y1n'''1rts
B. Beta-Blockers- Should be used in NYHA Classification ll - lll
- lnitiate at a loew dose- lncrease dose not more often ihan every two weeks- Monitor for signs of decompensation:
Fluid accu mulation (congestion)BradycardiaHeart BlockHypotension
C. Digoxin (LANOXIN) f- Reduces hospitalization rate, but neutral effect on mortality
C\as:'T jI. jtr "Itr
Syshllck\ri-r"t
itF ;Fbnr\hci\L)"rlncreases ejeciion fraciion - 4 - 5 %
Reduce neurohormonal abnormalitiesEffect on baroreceptor abnormalities* Atrial fibrillation (rate unconirolled) and EF < 30 %
D. Diuretics- For symptomatic volume overload
A. Treatment is generally directed toward the underlying problem- Hypedension- Valvular Heart Disease
6. Follow Up
a. Patient EducationEducate @ Underlying problernsEducate on reducing cardiovascular risk factors
Dietary management (sodium restriction)Weight losslnformation regarding drug side effects
b. Fuhrre AppointmentsWeekly (or more frequently) as needed, until stable
c. Emergency VisitsSigns/Slenptons of decompensationRespiratory/Cardiovascular dysfunction
- May redrrcp the cardiac output (may not be the effect you want)- ay cause folate Oepletion *ro**,.*^^kJ- Spiranolactone has been shown to reduce mortality t' r
.._ h.ra.:,K*\{-rn n,1 rsveverrrv,rq,,rJ
nru*_aipn.rls
.- G rrv.\ru'r".;rsxi?*. {" f,rf^f6- "r- /'1 gtt- Jd )
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