ACS Current Guidelines Review Course Pune 2007Dr. Sheila.ppt

ACS GUIDEINES FOR ICU STAFF

1. Acute Coronary Syndrome
- Current Guidelines
Dr. Sheila Nainan Myatra
Assistant Professor
Department of Anaesthesia ,Critical Care and Pain
Tata Memorial Hospital
Mumbai

2. Objectives
Terminologies
Ischemic Chest Pain
Diagnosis of AMI Clinical, ECG interpretation
and enzymatic rise
Risk stratification
Initial Stabilsation
Definitive therapy including reperfusion
strategies and adjuvant therapy
Complications of AMI
AHA Guidelines for stabilisation of patent with ACS
Circulation December 13,2005

3. Myocardial Ischemia and
Infarction
Myocardial Ischaemia Is inadequate delivery
of oxygen to the heart muscle which may lead
to chest pain.
Myocardial Infarction Irreversible damage or
death of the myocardium as a result of
prolonged inadequate blood flow & oxygen
delivery to the myocardium.

4. Angina Pectoris
An episodic clinical syndrome characterized by
CHEST PAIN or DISCOMFORT of cardiac origin
that usually results from a temporary imbalance
between myocardial O2 supply and demand.”

5. Unstable Angina
Rest Angina
Acute Onset Angina
Angina increasing in severity and/or duration
Variant Angina
Nocturnal Angina
Post MI Angina > 24 hrs

6. Acute Coronary Syndrome

Acute myocardial infarction (AMI) and
Unstable angina (UA)
are part of a spectrum of clinical disease collectively
identified as …Acute Coronary Syndromes (ACS).

7. Risk Factors for CAD
Cigarette Smoking
Diabetes Mellitus
Dyslipidemia
Hypertension
Sedentary Lifestyle
Obesity
 Family History of premature CAD
 Age
 Male Gender
 Postmenopausal state

8. Natural History of CAD:
Evolution of the Major Acute Coronary Syndrome

9. Time is Tissue
Effective Interventions for patients with ACS (particularly
STEMI) are extremely time sensitive
The first healthcare provider can have the biggest impact on
patient outcome if they provide effective risk stratification,
initial stabilisation and timely referral
Delay To Therapy – 3 Intervals
- Onset of symptoms to patient recognition
- During out of hospital transport
- During in- hospital evaluation
4D’s - Door to Data to Decision to Drug (or PCI)

10. Angina Pectoris
Site and Radiation- Typically retro-sternal or left
sided chest pain radiating to the jaw, neck,
arms(inner aspect of the left arm with
parasthesia in hand), back, epigastrium
precipitated by exercise or stress and relieved by
rest BUT NEVER BELOW THE DIAPHRAGM
Severity -varies from ill defined discomfort to
unbearable pain.It is unrelated to degree of
ischaemia , its duration and amount of
myocardium involved.

11. Angina Pectoris
Character- Pressure,choking ,burning ,dull
tightness discomfort, strangling ,hard
constricting, uneasiness,heart burn ,weight
compressing, fullness ,indigestion
Duration and Relief – generally lasts upto 15
mins gets relieved by rest/ relaxation or
sublingual / oral spray of nitrates

12. Atypical Presentation
Elderly
Female
Diabetic

13. Acute MI
The symptoms of AMI are characteristically
more intense than angina
last >15 minutes.
May be present at rest and may not decreased
with nitrates.

14. Potentially lethal Mimics….
Aortic Dissection
Acute pericarditis with effusion and tamponade
Acute myocarditis
Spontaneous Pneumothorax
Pulmonary Embolism
Eosophagial Rupture
Musculoskeletal
Psychogenic and Others

15. Associated Symptoms
Faintness, syncope: Hypotension.
Dyspnoea, Fatigue : Acute heart failure.
Pallor, Anxiety , profuse diaphoresis, nausea,
vomiting, palpitations (arrthymias) :
Increased Sympathetic activity.

16. ECG Presentation
 1.ST Elevation MI (STEMI)
2. ST Depression
3. Non diagnostic ST-segment and T wave abn.
Non ST segment MI (NSTEMI) is diagnosed if
cardiac markers are positive
Sudden cardiac death can occur with any of these
conditions

17. How to Measure
ST- Segment deviation

18. Recognition of AMI
Know where and what to look for
- ST elevation >1 mm (0.1mV)
- IN 2 or more contiguous precordial leads or
2 or more adjacent limb leads

19. Coronary Artery Anatomy

20. Relationship of 12 lead ECG to
coronary artery anatomy

21. Localising Injury in Relation to
Coronary Artery Occlusion

22. Acute Inferior Wall MI

23. Primary Goal of Therapy
Reduce the amount of myocardial necrosis,
preserving left ventricular (LV) function and
preventing heart failure
Prevent major adverse cardiac events
(MACE)
Treat acute, life-threatening complications of
ACS

24. Chest Pain Suggestive of Ischemia
Check vitals ,O2 saturation
IV Access
12 lead ECG
Brief history and examination
Review fibrinolysis checklist
Serum cardiac markers, electrolytes
and coagulation status
Portable xray chest (<30 mins.)


Immediate Assessment
(<10 mins.)
Immediate General treatment

25. Chest Pain Suggestive of Ischeamia
“MONA” greets all patients
 O2 at 4 lits /min
 Aspirin 160 to 325 mg
 NTG SL or spray
 Morphine IV

Immediate Assessment Immediate General treatment

26. Review 12 lead ECG
Classify in < 10 minutes after
arrival

27. STEMI
Admit to
monitored bed
>12 hrs
< 12 hrs
Reperfusion
Strategy

28. UA / NSTEMI
Admit to a monitored Bed
Assess Risk Status

29. Intermediate /Low-Risk UA
Develop High risk or intermediate risk criteria OR troponin
+
No
Admit in monitored bed
Serial cardiac markers,repeat
ECG,consider stress test
Developing High or intermediate
risk criteria OR troponin-positive
Discharge with follow up
Yes
High risk unstable
angina/Non ST
Elevation MI
(UA/NSTEMI)
No
Yes

30. Cardiac Enzymes
Released during myocarial injury and necrosis
Subfractions specific to cardiac muscle are CPK-MB,Troponin I and T,
LDH1 isoenzyme,Myoglobulin
Should be obtained during initial evaluation but therapeutic decisions
should not be delayed in STEMI
Changes in serum concentration over time improve sensitivity for detection
of MI but remain insensitive in first 4-6 hours
Enzyme Rise (hrs.)Peak (hrs.)Return (days)
CPK-MB 4-6 18-24 2-3
Troponin 3-12 24-48 4-14
LDH 8-12 24-72 7-12

31. Troponin T & I
Part of the sarcomere complex.
Cardiac Tp-I has 31 aa which is not present in skeletal
mls. Therefore highly sensitive & specific.
Cardiac Tp-T has 11 aa which is normally not present in
skeletal mls. But can be upgraded in skeletal mls with
injury.
Thus Trop I better than Trop T
The delayed clearance is useful in diagnosing MI in
patents who seek treatment days after chest pain
An elevated level of troponin correlates with an increased
risk of death

32. CPK and Isoforms
Has three isoenzymes MM (muscles), BB (brain), MB (heart)
Highly specific of myocardial injury
If CPK-MB is > 5% of total CPK -- CARDIAC MLS
If CPK-MB is <5% of total CPK -- SKELETAL MLS
In the post-operative setting not useful in diagnosing MI
elevation may be related to skeletal muscle trauma

33. REPERFUSION THERAPY
Most significant advance in the treatment of AMI in
the last decade
For patients who present within 12 hours of onset
of symptoms with no contraindications
Shorter time to reperfusion, greater benefit
FIBRINOLYSIS
Goal - Door to Needle time < 30 mins
PECUTANEOUS CORONARY INTERVENTION
Goal - Door to balloon time < 90 mins

34. FIBRINOLYTICS
In the absence of contraindications and the presence of favourable
risk benefit stratification, it is one option for reperfusion in those
STEMI patients with onset of symptoms < 12 hours (Class I)
Patients treated in the first 70 mins. from symptoms have >50%
reduction in infarct size and 75% reduction in mortality
Tissue Plasminogen Activator (Tpa):Altepase-Provides relative clot
selective fibrinolysis without inducing systemic lytic state, less allergic,
less hemorrhage requiring transfusion and greatest survival benefit so
far
15 mg bolus,0.75 mg /kg over next 30 mins. (not to exceed 50
mg),then 0.5 mg/kg over next 60 mins (not to exceed 35 mg
Others Streptokinase (Dose 1.5 mill U), Anistreplase(APSAC),
Reteplase,TNKase

35. FIBRINOLYTIC THERAPY
Chest pain >15 mins YES
ECG showing STEMI or new LBBB YES
Are There contraindications ?
Systolic BP >180 or diastolic >110
R versus L arm diffeerence in BP > 15 mmhg
Head trauma within 3 months
Recent (within 6 weeks ) major trauma /surgery,GI/GU Bleed
Bleeding or clotting problems or blood thinners
CPR> 10 mins.
Pregnant female
Serious systemic disease (advanced CA ,liver or renal disease)
Is patient at high risk ?
HR > 100 and SBP < 100 mmHg
Pulmonary odema
Signs of shock
Contraindications to fibrinolytic therapy

36. Percutaneous Coronary Intervention
Shown to be superior to fibrinolytics in combined end
points of death, stroke ,reinfaction in many studies
using skilled providers and skilled facilities
Preferred in patients with STEMI and symptoms >3
hours and < 12 hours with door to balloon time < 90
mins. And needle to balloon time < 60 mins.(Class I)
Preferred in patients with contraindications to
fibrinolytics and reasonable in patients with
cardiogenic shock CCF

37. Three Percutaneous Coronary
Interventions (PCI’s)
PTCA:Percutaneo
us Transluminal
Coronary
Angioplasty
PTCA
+ stent
placement
Atherectomy:
“grinds away”
the plaque

38. REPERFUSION THERAPIES-
Fibrinolysis versus PCI
FIBRINOLYSIS
Early presentation (< 3 hours)
Invasive strategy is not an option
Door to balloon is > 90 mins. DB-DN IS > 60 mins.
No contraindication
PCI
Late presentation (> 3 hours)
Skilled PCI facility with surgery backup
Door to Balloon < 90 mins. DB-DN < 60 mins.
Contraindication to fibrinolysis including risk of bleeding and ICH
High risk from STEMI
Diagnosis of STEMI in doubt
If presentation < 3 hrs and no delay for PCI then no preference for either

39. Adjuvant
Therapies for ACS
and AMI

40. Clopidogrel
Irreversibly inhibits the platelet adenosine
diphosphate receptor, resulting in reduction in platelet
aggregation
6 studies have shown decreased incidence of
stroke,MACE in patients with ACS if clopidogrel was
added to aspirin,heparin etc within 4 hours of
presentation
300 mg loading dose in addition to standard care
(aspirin,heparin/LMWH etc) followed by 75 mg OD
improved coronary artery patency and reduced
MACE

41. Beta Adrenergic Receptor
Blockers
Mechanism of action
Blocks catecholamines from binding to
ß-adrenergic receptors
Reduces HR, BP, myocardial contractility
Decreases AV nodal conduction
Decreases incidence of primary VF
Reduces the size of infarct, incidence of cardiac rupture and mortality in
patients who don’t receive fibrinolytic therapy also reduce the incidence of
VF.Significant decrease in death and non fatal infaction in patients treated
with beta blockers soon after infarction
Oral beta blockers should be administered for all types of ACS unless
contraindicated and given irrespective of revascularisation therapy
(Class I)
Contraindications are mod. to severe LV failure, pulmonary edema,
bradycardia, hypotension, poor perfusion, 2
nd
or 3
rd
degree heart block or
reactive airway disease

42. Heparin
Indirect inhibitor of thrombin widely used as
adjunctive therapy for fibrinolysis and with aspirin and
other platelet inhibitors for UA/STEMI
Disadvantages-unpredictable anticoagulation
response, frequent monitoring of aPTT, IV
administration, stimulates platelet activation and can
cause thrombocytopenia
When used in STEMI with fibrin specific lytics give 60
U /kg bolus followed by 12 U /kg per hour
(maximum bolus 4000U and infusion not > 1000U/hr)
An aPTTt of 50 to 70 seconds is considered optimal

43. Heparin Versus LMWH
 UA/NSTEMI
- LMWH (especially enoxiparin ) is beneficial compared with UFH
when given in addition to antiplatelet therapy (Class IIb)
- UFH should be considered if reperfusion is planned in first 24 to
36 hours after onset of symptoms
- Changing from one to other during acute event is not recommended

STEMI
- LMWH (Enoxaparin ) is an acceptable alternative to UFH in patients
< 75 years who are receiving fibrinolytic therapy provided significant
renal dysfunction is not present (Class II b)
- > 75 UFH recommended as ancillary therapy to fibrinolysis (Class
IIa) for any STEMI

44. Glycoprotein IIb/IIIa Inhibitors
The integrin GP IIb/IIIa receptor is considered the
common final pathway to platelet aggregation. GP IIb/IIIa
modulate this receptor activity
Three agents for use :abciximab,eptifibatide and tirofiban
In UA/NSTEMI used in patients with high risk stratification
in conjuction with aspirin ,heparin and clopidogrel and a
strategy of early PCI (Class I)
In STEMI insufficient data to recommend for or against

45. ACE Inhibitors
Mechanism of action
Reduces BP by inhibiting angiotensin-converting enzyme (ACE)
Alters post-AMI LV remodeling by inhibiting tissue ACE
Lowers peripheral vascular resistance by vasodilatation
Reduces mortality and CHF from AMI
Consistent improvement in survival when administered early in patients with AMI with or without reperfusion therapy
Oral ACE recommended in the first 24 hours after onset of symptoms in STEMI patients with pulmonary congestion,
LVEF < 40%in the absence of hypotension (Class I)
Oral therapy for all other AMI with or without reperfusion therapy (Class IIb).IV therapy contraindicated in the first 24
hours due to risk of hypotension (Class III)

46. Calcium Channel Blockers
They have not been shown to reduce mortality after
AMI and in certain patients with CV Disease they are
harmful
There is concern that these agents are still used
frequently in patients with acute MI
Beta blockers are more appropriate choice across a
broad spectrum of patients of MI
Give only when Beta Blockers are contraindicated of
if have given maximum clinical doses without effect
(Class Indeterminate)

47. HMG Coenzyme A Reductase
Inhibitor (Statins)
Several studies show consistent reduction in
indicators of inflammation and complications such as
reinfaction, recurrent angina, and arrythmias when
given within few days of onset of ACS
Little data to suggest administration in ED.
However early initiation (within 24 hours) is safe and
feasible in patients with ACS and AMI (Class I
If already on statin therapy the continue the therapy
(Class II b)

48. Complications Of AMI
Left ventricular dysfuntion manifested by Pulmonary
oedema
Cardiogenic shock.
Acute MR / VSD
Dysrrythmias
Conduction disturbances and blocks.

49. Conclusion
There has been tremendous progress in reducing
death from ACS
Many patients with ACS still die before reaching the
hospital because of failure to recognise signs or
activate emergency system by patient or family in time
Once in health care system provide support of
cardiorespiratory function, early classification based
on ECG
STEMI requires prompt reperfusion, shorter interval
greater the benefit
UA /NSTEMI or normal or non specific ECG require
risk stratification appropriate monitoring and therapy

50. Thank you

51. Cardiogenic Shock
 Cardiogenic shock is decreased cardiac output and
evidence of tissue hypoxia in the presence of adequate
intravascular volume
 Haemodynamic criteria
- sustained hypotension( SBP<90mmHg)
- reduced cardiac index (<2.2 L/min. per m2 )
- elevated PAOP (>15 mm Hg)
 Diagnosis is made after the documentation of myocardial
dysfunction and exclusion or correction of such factors as
hypovolemia,hypoxia and acidosis

52. Causes
 Predominant cause is left ventricular failure in the setting of
an extensive acute infaction
 Other causes
- mechanical complications of infaction
- right ventricular dysfunction
- prolonged CP Bypass
- valvular disease
- myocardial contusion
- sepsis with myocardial depression
- cardiomyopathy

53. Hollenberg, S. M. et. al. Ann Intern Med 1999;131:47-59Hollenberg, S. M. et. al. Ann Intern Med 1999;131:47-59
Pathophysiology
“downward spiral ”in cardiogenic shock

54. Hollenberg, S. M. et. al. Ann Intern Med 1999;131:47-59
Pathophysiology
Potential consequences of myocardial ischemia

55. General Approach
 The clinician must perform a rapid clinical
assesssment to understand the cause while initiating
supportive therapy before shock causes irreversible
damage to the vital organs
 The diagnosis at the bedside is made by the
presence is made by the presence of hypotension
and clinical signs indicative of poor organ perfusion
Cardiogenic shock is diagnosed after
documentation of myocardial dysfunction and
exclusion of alternative causes of hypotension

56. Echocardiography is an excellent initial tool
for confirming the diagnosis and for sorting
through the D/D. Information about overall
and regional systolic and diastolic function,
mechanical causes of shock, RV infaction etc.
 Invasive haemodynamic monitoring can be
critical for confirming the diagnosis and is
extremely useful in allowing optimisation of
pharmacological therapy
General Approach

57. Initial Management
 Maintainance of adequate oxygenation and
ventilation are critical
 Central venous and arterial access, bladder
catheterization and pulse oximetry are routine .
 Invasive haemodynamic monitoring is extremely
useful in optimisation of therapy
 Morphine relieves pain and anxiety reducing
excessive sympathetic activity and decresing oxygen
demand,preload and afterload.

58. Arrhythmias and heart blocks must be corrected
promptly with anti-arrhythmic drugs,cardioversion and
pacing. Correct electrolyte abnomalities
 Measures that improve outcome after MI such as
nitrates,beta blockers and ACE inhibitors should be
withheld till the patient stabilises
 Initial approach to a hypotensive patient should
include fluid administration unless frank pulmonary
edema is present. Fluid infusion is best initiated with
predetermined boluses titrated to clinical endpoints of
heart rate, urine output and blood pressure
Initial Management

59. Initial Management
 Ischemia produces systolic as well as diastolic
dysfunction ,thus elevated filling pressures may be
necessary to maintain the stroke volume in patients
with cardiogenic shock
 When arterial pressure remains inadequate,
therapy with vasopressor agents may be required to
maintain the coronary perfusion pressure
Following initial stabilisation and restoration of
adequate blood pressure,tissue perfusion should be
asseses.If it remains inadequate,inotropic support or
IABP should be initiated

60. If tissue perfusion is adequate but significant
pulmonary congestion remains, diuretics may
be employed. Vasodilators can be considered
as well depending on the blood pressure
 Haemodynamic monitoring with serial
measurements of CO, filling pressures ,mixed
venous oxygen saturation, lactate levels etc.
allows for the titration of vasoactive agents
Initial Management

61. Myocardial `Reperfusion
 Pathophysiological considerations favor interventions to restore flow to
occluded arteries in patients with with cardiogenic shock due to MI
 Although it has been clearly shown that fibrinolytic therapy can reduce
the likelihood of development of shock after initial presentation, it's role in
the management of patients who have already developed shock is less
certain
 Few RCT ,Available trials (GISSI,GUSTO ) have not demonstrated any
reduction in mortality .SHOCK registry showed lower in-hospital mortality
(54% vs 64%)
The reason for decreased thrombolytic efficacy in these patients
probably include haemodynamic,mechanical,metabolic factors that prevent
achievement and maintenance of infarct –related arterial patency
 To date emergency percutaneous revascularization is the only
intervention that has been shown to consistently reduce mortality in these
patients

62. IABP
 IABP reduces systolic afterload and augments diastolic
perfusion pressure,increasing cardiac output and improving
coronary blood flow,these beneficial effects occur without an
increase in oxygen demand in contrast to inotropes and
vasopressors
 IABP however does not produce a a significant
improvement in blood flow distal to a critical coronary
stenosis,and has not been shown to improve mortality when
used alone without reperfusion therapy or revascularisation
 In patients with cardiogenic shock and compromised tissue
perfusion it can be an essential support mechanism to
stabilise the patient and allow time for for definitive therapeutic
measures

63. Case 1
73 year old male patient presented with retrosternal
chest pain
His findings were
Pulse 96/min
BP 140/80
Systemic exam normal
ECG ST elevation V1 – V4, lead I, aVF
What is your management?

64. Initial management of AMI
 Immediate assesment (<10 mins)
 Immediate general treatment “ MONA ’’ greets all patients
(Morphine ,Oxygen, Nitroglycerin, Aspirin)
 Start adjuvant therapy –
IV Beta blockers,Nitrogycerin,Heparin,ACE inhibitors

65. After initial management, 3 hour later patient
continued to have chest pain & findings were
Pulse 120/min regular
BP 70 systolic
RS B/L crepts
UOP last 4 hours 50 ml
ECG ST elevation V1 – V6
What will your management now be?

66. Management of Cardiogenic Shock
 Invasive haemodynamic monitoring
 Haemodynamic support
- Fluids ?
- Vasopressors for hypotension
- Diuretic ?
 Tissue perfusion remains inadequate
- inotropic agent ?
- IABP
 Reperfusion strategy
??


67. Hollenberg, S. M. et. al. Ann Intern Med 1999;131:47-59
Diagnosis and treatment of cardiogenic shock caused by
myocardial infarction

68. Conclusion
 The pathophysiology of shock involves a downward spiral ,ischemia
causes myocardial dysfunction, which worsens ischemia
 Areas of nonfunctional but viable myocardium can also cause or
contribute to the development of cardiogenic shock
The key to a good outcome is an organised approach with rapid
diagnosis and prompt initiation of therapy to maintain BP and CO in order
to reverse and prevent organ hypoperfusion
Early revascularization for cardiogenic in the setting of acute MI
represents one of the most significant new advances in the treatment of
CAD
 In centers without direct angioplasty capability,stabilisation with IABP
and thrombolysis followed by transfer to a tertiary care facility may be the
best option

69. 12 lead ECG
ST-segment elevation or presumed new LBBB is
characterized by ST-segment elevation 1 mm (0.1 mV)
in 2 or more contiguous precordial leads or 2 or more
adjacent limb leads (STEMI)
Ischemic ST-segment depression > 0.5 mm (0.05 mV)
or dynamic T-wave inversion with pain or discomfort
(UA/NSTEMI)
Normal or nondiagnostic changes in ST segment or T
waves are inconclusive and require further risk
stratification. This classification includes patients with
normal ECGs and those with ST-segment deviation of <
0.5 mm (0.05 mV) or T-wave inversion of <0.2 mV.
Serial cardiac studies (and functional testing) are
appropriate.

70. 12 lead ECG
ST-segment elevation or presumed new LBBB is
characterized by ST-segment elevation 1 mm (0.1 mV)
in 2 or more contiguous precordial leads or 2 or more
adjacent limb leads (STEMI)
Ischemic ST-segment depression > 0.5 mm (0.05 mV)
or dynamic T-wave inversion with pain or discomfort
(UA/NSTEMI)
Normal or nondiagnostic changes in ST segment or T
waves are inconclusive and require further risk
stratification. This classification includes patients with
normal ECGs and those with ST-segment deviation of <
0.5 mm (0.05 mV) or T-wave inversion of <0.2 mV.
Serial cardiac studies (and functional testing) are
appropriate.

71. Angina Pectoris
Strangling in the chest
“An episodic clinical syndrome characterised
by CHEST PAIN or DISCOMFORT of cardiac
origin that usually results from a temporary
imbalance between myocardial O2 supply
and demand.”
Often the first symptom of IHD