medicine management

1. ACUTE
CORONARY
SYNDROME
(ACS)
NUR FARRA NAJWA BINTI ABDUL AZIM
082015100035

4. INTRODUCTION
ISCHEMIC
HEART
DISEASES
CHRONIC
ARTERY
DISEASES
ACUTE
CORONARY
SYNDROME

5. CONT. ACUTE CORONARY
SYNDROME
Acute Myocardial
Infarction With ST-
segment Elevation
Non ST-segment
Elevation Acute
Coronary Syndrome
(NTSE-ACS)
Unstable Angina
Non ST-segment
Elevation Myocardial
Infarction

6. PATHOPHYSIOLOGY
Imbalance oxygen demand and
oxygen supply
(MOD =/ MOS)
Due to partially occluded
thrombus or
Due to disrupted atherosclerotic thrombus
or eroded coronary artery endothelium
Reduction of coronary blood flow and downstream
embolization of platelet aggregate and/or
atherosclerotic debris
Severe ischemic and myocardial
necrosis

7. OTHER CAUSES OF NSTE-ACS
• Dynamic obstruction due to coronary artery spasm ( prinzmetal angina)
• Severe mechanical obstruction due to progress atherosclerosis
• Increase myocardial oxygen demand (fever tachycardia, thyrotoxicosis) in
presence of fixed epicardial coronary artery obstruction
10% has stenosis left main coronary artery
- 35% has 3 vessel CAD
- 20% has 2 vessel CAD
- 15 % has no apparent epicardial coronary artery
stenosis
- Some has obstruction of coronary artery
microcirculation and/or spasm
MAIN CULPRIT FOR ISCHEMIC :
eccentric stenosis with scalloped or
overhanging edge and a narrow neck
on coronary angiograph

8. CLINICAL PRESENTATION
• Chest discomfort
• Severe
• Has at least one of three features
• Diagnosis of NSTEMI is establish if
patient present with clinical feature
and evidence of myocardial necrosis
• Elevated level of biomarker of cardiac
necrosis
- Occur at rest (or on
minimal exertion)
-Last > 10 min
Relatively recent onset (
within prior 2 weeks)
Occur with cresendo
pattern
( more severe, frequemt,
prolonged) than previous
episode

9. HISTORY AND PHYSICAL EXAMINATION
CHEST DISCOMFORMT
• Often severe enough to be
describe as frank pain
• Located substernal or epigastric
• Radiates to left arm, left
shoulder, and neck
• Anginal equivalence may occur
instead chest discomform
• Resemble stable angina
IF LARGE AREA ISCHEMIA AND
LARGE NSTEMI
• Diaphoresis
• Pale
• Cool skin
• Sinus tachycardia
• Third or fourth heart sound
• Rales
• Hyotension

10. ECG
• 20 -25 % patient has ST- segment depression
• Transient in patient without biomarker increase for evidence of myocardial
necrosis
• Persistent for severel day in STEMI
• T wave changes
• Common but less specific sign of ischemia
• Unless deep and new T-wave inversion

11. CARDIAC BIOMARKER
• Patient with STEMI elevated biomarker
• Troponin T troponin I (TnT, TnI)
• Specific and sensitve
• Preferred for myocardial necrosis
• Ck-MB isoform
• Less sensitive alternative
Distinguish patient with
STEMI AND UA
Temporal rise and fall of this plasma
concentration marker and has a directlv
relationship between elevation and
mortality

12. CKMB TIME
RISE 4-6 HR
PEAK 12 HR
DIASSAP]REA 48-72 HR
TROP T AND TROP I TIME
RISE 4-6 HR
REMAIN ELEVATED 2 WEEKS

13. Cont.
• Patient
• without clear clinical history of myocardial ischemia
• Minor elevation of cardiac troponin (cTn)
• Can be caused by
• heart failure
• Myocarditis
• Pulmonary embolism
Thus, in patient in unclear history, without persistent rise of biomarker are
not diagnostic of ACS

14. DIAGOSTIC EVAUTAION
• In addition to clinical examinatiom
• ECG
• Cardiac biomarker
• Stress testing
• CCTA
• Goals
• Recognize or exclude MI
• Detect rest ischemia
• Signify coronary artery obstruction
A 62-year-old man presented for coronary CT
angiography (CCTA) due to chest pain. Free-
breathing prospective CCTA images show the
clearly defined coronary arteries with calcified
plaque (arrows) without motion artifacts. All
images courtesy of Dr. Eun-Ju Kang.

15. Cont .
• Patient with low likelihood of ischemia
• managed in emergency department based clinical pathway (chest pain unit)
• Requires
• Clinial monitoring of recurrent ischemic discomfort.
• Continous monitoring of ECG and cardiac biomarkers
- Obtained at baseline
- After 4-6 hour
- After 12 hour

16. Cont.
• New
• Cardiac biomarker elevation
• ECG changes (ST elevation)
• If
• Pain free
• Negative marker
Proceed stress testing
= determine ischemia present
CCTA
=coronary luminal obstruction
Admitted to
hospital

17. RISK STARTIFICATION
Patient with
documented
NSTE-ACS
1- 10 %,
Early risk of death
(30day)
5-15%,
recurrent risk of ACS

18. Cont.
• Risk assessment by Thrombolysis In Myocardial Infarction Trial (TIMI) , which
include seven independent risk factor.
• The present of abnormally elevated cTn very important
• Extent of myocardial damage
• Other risk include
• Diabetes mellitus
• Renal dysfunction
• Elevated level of Brain Natriutic Peptide
and C-Reactive protein
Patient with ACS without elevation of cTn are
considered to develop unstable angina and have
more favourable prognosis than those with cTn
elevation (STEMI)
Early risk assesmen tuseful in
=predict the risk of recurremt cardiac event
= identify a patient who will derives an
benfit from early invasive strategy

20. TREATMENT
• Patients should
• placed at bed rest
• continuous ECG monitoring (ST-segment deviation and cardiac arrhythmias)
• Ambulation is permitted if the patient shows no recurrence of ischemia
(symptoms or ECG changes) and does not develop an elevation of a bio-marker
of necrosis for 12–24 h.
• Medical therapy involves simultaneous
• anti-ischemic
• antithrombotic treatments
• consideration of coronary revascularization

21. ANTI ISCHEMIC TREATMENT
• Provide relief and prevention of recurrence of chest pain
• Initial treatment should include
• bed rest
• nitrates
• beta adrenergic blockers,
• and inhaled oxygen in the presence of hypoxemia

22. NITRATES
First be given sublingually or by buccal
spray (0.3–0.6 mg)
• IF THE PATIENT IS EXPERIENCING ISCHEMIC PAIN
Intravenous nitroglycerin (5–10 μg/min
-Rate of infusion may be increase by 10ug/min
every 3-5 min until symptom relieved
• IF PAIN PERSISTS AFTER THREE DOSES GIVEN 5
MIN APART
Topical or oral nitrates can be used
• PAIN HAS RESOLVED OR PATIENT WAS PAIN FREE FOR 12-
24 HR
Hypotension
Use of sidlenafil or other PDEi in previous 24-48
hour
• ABSOLUTE CONTRAINDICATION NITRATES USE

23. • Started by the intravenous route
• Targeted to heart rate of 50–60 beats/min
Patients with severe ischemia, but this is
contraindicated in the presence of heart
failure.
• Heart rate–slowing calcium channel blockers
• Verapamil or diltiazem
For patients who have persistent symptoms or ECG
signs of ischemia after treatment with full-dose
nitrates and beta blockers and in patients with
contraindi-cations to either class of these agents
• Angiotensin-converting enzyme (ACE) inhibitors
• Angiotensin receptor blockersAdditional medical therapy
• Early administration of hmg-coa reductase inhibitors
(statins), such as atorvastatin 80 mg/D
• Prior to percutaneous coronary intervention (PCI)
To reduce complications of the procedure
and recurrences of ACS
BETA ADRENERGIC BLOCKERS AND OTHER
AGENTS

24. ANTITHROMBOTIC THERAPY
• This is the second major corner-stone of treatment.
• There are two components of antithrombotic therapy:
• ANTIPLATELET DRUGS AND
• ANTICOAGULANTS

25. ANTIPLATELET DRUGS
ASPIRIN
• . The typical initial dose is 325 mg/d, with lower doses (75–100 mg/d
• Contraindications are active bleeding
PLATELET P2Y12
RECEPTOR BLOCKER
• Clopidogrel added to aspirin, dual antiplatelet therapy, reduction in cardiovascular death, MI, or stroke
• This regimen should continue for at least 1 year in patients with NSTE-ACS, especially those with a
drug-eluting stent, to prevent stent thrombosis
• Prasugrel or ticagrelor used with aspirin, should be considered in patients with NSTE-ACS who develop
a coronary event while receiving clopidogrel and aspirin

26. ANTICOAGULANTS
• Long the mainstay of therapyUNFRAC-TIONATED HEPARIN
(UFH)
• Which has been shown to be superior to UFH in reducing
recurrent cardiac events, especially in patients managed by a
conservative strategy but with some increase in bleeding
THE LOW-MOLECULAR-WEIGHT
HEPARIN (LMWH), ENOXAPARIN
• Causes less bleeding and is used just prior
to and/or during PCI
BIVALIRUDIN, A DIRECT
THROMBIN INHIBITOR
• Have a lower risk of major bleedingINDIRECT FACTOR Xa INHIBITOR,
FONDAPARINUX

27. INVASIVE VERSUS CONSERVATIVE STRATEGY
• Benefit of an early invasive strategy in high-risk patients
• Patients with multiple clinical risk factors,
• ST-segment deviation,
• And/or positive biomarkers
• In this strategy, following treatment with
• Anti-ischemic and antithrombotic agents, coronary arteriography is carried out within
~48 h of presentation
• Followed by coronary revascularization (PCI or coronary artery bypass grafting)
• In low-risk patients, the outcomes from an invasive strategy are similar to
those obtained from a conservative strategy.

28. LONG-TERM MANAGEMENT
• The time of hospital discharge
• “teachable moment” for the patient with NSTE-ACS,
• Review and optimize the medical regimen.
• Risk-factor modification is key, and the caregiver should
• discuss with the patient the importance of smoking cessation
• achieving optimal weight
• daily exercise
• blood-pressure control
• following an appropriate diet,
• control of hyperglycemia (in diabetic patients)
• lipid management as recommended for patients with chronic stable angina

29. Cont.
• There is evidence benefits with long term therapy of 5 clases of
drug that act at different component of the atherothrombotic
process
• Beta blockler
• Statin
• ACEI
• ARB
Anti-platelet now recommended to be the combination of low-dose (75–100
mg/d) aspirin and a P2Y12 inhibitor (clopidogrel, prasugrel, or ticagrelor) for
1 year, with aspirin continued thereafter, prevents or reduces the sever-ity
of any thrombosis that would occur if a plaque were to rupture

32. ACUTE CORONARY SYNDROME
(STEMI)
PREPARED BY :
NUR IZZATUL NAJWA, 036

33. DEFINITION
Any group of clinical symptoms compatible with acute myocardial ischemia and
covers the spectrum of clinical conditions ranging from :
UNSTABLE ANGINA
NON-ST-SEGMENT ELEVATION MYOCARDIAL INFARCTION
ST-SEGMENT ELEVATION MYOCARDIAL INFARCTION

35. STEMI
• Definition of STEMI – New ST elevation at the J point in two contiguous leads of
>1 mm in all leads in absence of left ventricular hypertrophy or left bundle branch
block, other than leads V2-V3 – For leads V2-V3 the following cut points apply: ≥2
mm in men ≥40 years, ≥1.5 mm in women.
• STEMI is a life-threatening, time-sensitive emergency that must be diagnosed and
treated promptly

36. PHYSICAL SIGNS
• Signs of sympathetic activation
• Pallor
• Sweating
• Tachycardia
• Signs of impaired myocardial function
• Hypotension, oliguria, cold peripheries
• Narrow pulse pressure
• Raised jvp
• Third heart sound
• Diffuse apical impulse
• Lung crepitations
• Signs of vagal activation
• Vomiting
• Bradycardia
• Sign of tissue damage
• Fever
• Signs of complication
• Mitral regurgitation
• pericaritis

37. COMPLICATION
• EARLY
• ARRTYHMIA
• CARDIOGENIC SHOCK
• ACUTE HEART FAILURE
• CARDIAC TAMPIONADE
• RUPTURE OF INTERVENTRICULAR
SEPTUM
• PERICARDITIS
• PULMONARY EDEMA
• LATE
• DRESSLERS SYNDROME
• CHRONIC HEART FAILURE

39. ELECTROCARDIOGRAM
• Should be done and interpreted within 10 minutes of arrival
• 12 lead ECG ;
• 3 Standard limb lead (I, II, III)
• 3 Augmented limb lead (aVR, aVL, aVF)
• 6 precordial limb lead (V1 – V6)

40. ELECTROCARDIOGRAM

41. ELECTROCARDIOGRAM
• New ST elevation at the J point in two anatomical contiguous leads of
>1mm in all leads in absence of left ventricular hypertrophy or left
budle branch block, other than leads V2-V3 – For leads V2-V3
(precordial lead) the following cut points apply: ≥2 mm in men ≥40
years, ≥1,5 mm in women.
• In early MI, T waves become tall ( hyperacute myocardial infarction),
transient and last for few hours only.
• Q wave formation

43. ECG AND LOCATION OF MI

45. SHOWS ST ELEVATION BUT NOT STEMI !
Electrolyte abnormalities
Left bundle branch block
Aneurysm of left ventricle
Ventricular hypertrophy
Arrhythmia disease (Brugada syndrome, ventricular
tachycardia)
Takotsubo/Treatment (iatrogenic pericarditis)
Injury (MI or cardiac contusion)
Osborne waves (hypothermia or hypocalcemia)
Non-atherosclerotic (vasospasm or Prinzmetal’s angina

46. ECHOCARDIOGRAM (ECHO)
• To detect the presence or absence of
wall motion abnormalities and value
of ejection fraction

47. OTHERS
• Leukocytosis with a peak on 1st day
• Raised ESR that remain for some days
• Elevated C- reactive protein
• Chest radiography
• Heart size usually normal
• Enlargement cardiac shadow indicate previous myocardial damage or pericardial effusion
• Evidence of pulmonary edema
• Radionuclide scanning
• Shows site of necrosis and extent of impairment of ventricular function (lack of sensitivity and
specificity)

48. Initial management (prehospital care)
Recognition of symptoms by pt and seek for medical attention.
Rapid deployment of emergency medical team capable of performing
resuscitative maneuvers, including defibrillation.
Transport patient to hospital facility accompanied by physicians/paramedics
skilled in providing cardiac life support/manage arrhythmias.
Implementation of reperfusion therapy.

49. Management in emergency department
Control of cardiac discomfort.
Reperfusion therapy. This may involve transfer of pt from non-PCI capable
hospital to PCI capable hospital within 120 minutes.
Aspirin, B-blocker, t-PA. No heparin.
Supplementary O2 therapy (<94%)

50. Control of discomfort
Sublingual nitroglycerine up to 3 doses of 0.4mg at 5 minutes interval.
Morphine in small dose (2-4mg) every 5 minutes.
Beta-blocker if pt do not have:
• - Sign of heart failure, evidence of low-output state, increased risk of cardiogenic shock, and other contraindication
to B-blockade.
If discomfort return with further ischemia (ST-segment/T-wave shift), IV nitroglycerine
should be considered.

53. Limitation of infarct size
1. PRIMARY PERCUTANEOUS
CORONARY INTERVENTION
(PCI)
- Usually angioplasty.
- Applicable to pt with contraindication
to fibrinolytics.
- Preferred when diagnosis is in doubt,
cardiogenic shock is present, bleeding
risk increased, or symptoms has been
present at least 2-3 hours when clot is
more mature and harder to lyse.

54. Limitation of infarct size (cont.)
2. FIBRINOLYSIS
- Should be initiated within 30 min of presentation.
- Tissue plasminogen activator (t-PA), streptokinase, tenecteplase (TNK), reteplase (rPA).
- t-PA – 15mg bolus followed by 50mg IV over 30 min, 35mg next 60 min.
- Streptokinase – 1.5 million units (MU) IV over 1 hr.
- rPA – 10 MU bolus over 2-3 min, followed by 2nd 10 MU bolus after 30 min.
- TNK – IV bolus 0.53mg/kg over 10 seconds.

55. Limitation of infarct size (cont.)
3. Coronary Artery Bypass Graft
(CABG)
• When PCI fails to prevent further ischemia,
CABG is considered.
• Great saphenous vein from the leg is taken
and grafted from aorta or its major branch to
relevant obstructed coronary artery to
immediately restore blood flow.

57. Hospital phase management
1. Monitoring cardiac rhythm and hemodynamic.
2. Limit movement of pt for 1st 3 days.
3. Diet – pt to receive nothing or clear liquid by mouth in 1st 4-
12 hrs. Controlled diet are given.
4. Bowel Management – diet rich in bulk, and stool softener are
given to offset the effect of narcotics used in treatment.
5. Sedation, because pt need to sleep – Diazepam (5mg),
Oxazepam (15-30mg), or Lorazepam (0.5-2mg) 3-4 times a
day. Additional dose may be given at night for better sleep.

58. Complications and their management
1. VENTRICULAR DYSFUNCTION
• Soon after STEMI, LV begins to dilate (Ventricular remodelling) as a result of expansion of infarct.
• Overall chamber enlargement that occurs is related to the size and location of the infarct,
causing more marked hemodynamic impairment, more frequent heart failure, and a poorer
prognosis.
• Progressive dilation and its clinical consequences may be ameliorated by therapy with ACE
inhibitors and other vasodilators (e.g., nitrates)

59. Complications and their management (cont.)
2. HEMODYNAMIC ASSESSMENT
• Pump failure is now the primary cause of in-hospital death from STEMI.
• Positioning of a balloon flotation (Swan-Ganz) catheter in the pulmonary artery permits
monitoring of LV filling pressure; this technique is useful in patients who exhibit hypotension
and/or clinical evidence of CHF.
• Cardiac output can also be determined with a pulmonary artery catheter. With the addition
of intra-arterial pressure monitoring, systemic vascular resistance can be calculated as a
guide to adjusting vasopressor and vasodilator therapy.

60. Complications and their management (cont.)
3. HYPOVOLEMIA
• May be secondary to previous diuretic use, to reduced fluid intake during the
early stages of the illness, and/or to vomiting associated with pain or
medications.
• Hypovolemia should be identified and corrected in patients with STEMI and
hypotension before more vigorous forms of therapy are begun.
• Optimal LV filling or pulmonary artery wedge pressure (generally ~20 mmHg) is
reached by cautious fluid administration during careful monitoring of
oxygenation and cardiac output.

61. SUMMARY