Download AMI, cerebral stroke, pulmonary oedema

Rules of treatment in selected
emergency states:
AMI,
cerebral stroke,
pulmonary oedema
acute myocardial infarction
AMI
acute coronary syndromes (ACS)
• acute myocardial
infarction (AMI)
• Unstable angina
necrosis
acute coronary syndrome
test
 Cardiac biomarkers
• Ecg
• hFABP – heart fatty acid
binding proteins
• Mioglobin
• Creatine kinase
• Troponins
• Enolase
• Echocardiography
• Lipids
• CBC -complete blood count
ECG
• ST-segment elevation or presumed new LBBB is characterized by
ST-segment elevation >1 mm (0.1 mV) in 2 or more contignous
precordial leads or 2 or more adjacent limb leads and is classified as
ST-elevation MI (STEMI).
• Ischemic ST-segment depression ≥0.5 mm (0.05 mV) or dynamic Twave inversion with pain or discomfort is classified as high-risk
UA/non–ST-elevation MI (NSTEMI). Nonpersistent or transient STsegment elevation ≥0.5 mm for <20 minutes is also included in this
category.
• 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.
Cardiac biomarkers
- creatine kinase (CK)
• Elevation of the serum total CK is a sensitive enzymatic
detector of AMI
• False positive resalts in patients with:
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Muscle disease
Alcohol intoxication
DM
Skeletal muscle trauma
Vigorous exercise
Convulsion
Intramuscular injections
Pulmonary embolism
• Three isoenzymes of CK: CK-BB (brain and kidney), CKMM (skeletal muscle) and CK-MB (heart)
• A ratio (relative index) of CK-MB/total CK > 6% is
indicative of a myocardial rather then other source of the
CK-MB elevation
Cardiac biomarkers
- troponin
• Best diagnostic and prognostic marker of AMI
• The troponin complex consist of three subunits that
regulate the calcium mediated contractil process of
strited muscle. – troponin I, T and C
• Whereas CK-MB usually increases 10 to 20 fold above
the upper limit of the reference range, troponin T and I
typically increase more then 20 times above the
reference range. Troponin T and I are more sensitive in
diagnosis of minor myocardial damage
• Troponin I and T –gold standard in diagnosis of AMI
• < 4-6 h- small sensivity (10- 45%)
• > 8 h- sensivity 95%
• Measurment 2-time: 6- 12 h, 12- 24 h
Cardiac biomarkers
- the level of troponin increase in
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HF
Aortic aneurysm
Pulmonary embolism
Toxic injure of heart muscle (chemiotherapy)
miocarditis
Injury of heart muscle
Chronic renal failure
Acute abdominal problem
burns
other: kardioversion, arrhythmias
Cardiac biomarkers
- mioglobin
• Early marker of necrosis
• Hight negative prognostic value .
Reference range of mioglobin over 8 h
after chest pain exclude MI.
• reference range <70- 110 ng/ml,
• AMI: 600- 1000 ng/ml
Cardiac biomarkers
- the level of mioglobin increase in
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Injury of heart muscle
heatstroke, frostbite, burns
hypothyreosis
hypokaliemia,
Convulsion, febrilis
Sepsis
Alcohol intoxication
Medication - statines, fibrates (rabdomiolizis)
Cardiac biomarkers
• hFABP –heart fatty acid binding proteins
• AST, ALT, LDH (lactic dehydrogenase)
GGTP
• CRP (C-reactive protein), fibrynogen,
BNP, IL-6 (prognostic value)
• GPBB (izoenzym glicogen fosforylaze –
hight sensivity marker of cardiac ischemic in
cardiosurgery)
Cardiac biomarkers
Marker
Range of times
to initial
elevation (h)
Mean time to
peak elevation
(h)
Time to return
to normal range
hFABP
Mioglobin
Troponin T
Troponin I
CK-MB
1.5
1-4
3-12
3-12
3-12
5-10
6-7
24h-2d
24h
24
24h
24h
5-14d
5-10d
48-72h
Initial diagnosis of AMI
• History of cheat pain/discomfort
• ST-elevations or (presumed) new LBBB
on admissin ECG. –reapeated ECG
recordings often needed
• Elevated markers of myocardial necrosis
(troponin, CK-MB)
• 2D echocardiography and perfusion
csintigraphy helpful to rule out AMI
ACS – algorithm (1)
ACS – algorithm (2)
Relef of pain, breathlessness and
anxiety
• Opioids iv (4-8mg morphine) with
additonal doses of 2mg at 5 min intervals
• O2 (2-4l/min) if breathlessness or HF
• Consider iv beta-blockers or nitrates if
opioids fail to relieve pain
• Transquilliser may helpful
Out of hospital menagement
• Recognition
• Monitor, support ABCs. Be prepared to provide
ALS
• pharmacotherapy
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M
O
N
A
• ECG
• Establish iv access
Administer MONA
– M – morphine iv if
pain not relieved by
nitroglycerine
– O – oxygen at 4l/min
– N – nitroglycerine
sublingual, spray or
iv
– A – aspirine 300mg
out-of-hospital fibrinolysis
In summary, out-of-hospital administration of fibrinolytics to
patients with STEMI with no contraindications is safe,
feasible, and reasonable (Class IIa).
• The ECC Guidelines 2005 recommended consideration
of out-of-hospital fibrinolysis for patients with a transport
time >1 hour.
• But in a recent Swiss study, prehospital administration of
fibrinolytics significantly decreased the time to drug
administration even in an urban setting with relatively
short transport intervals (<15 minutes).
Fibrinolytic Therapy:
Contraindications and Cautions for Fibrinolytic Use in
STEMI From ACC/AHA 2004 Guideline Update
Absolute Contraindications
• Any prior intracranial hemorrhage
• Known structural cerebral vascular lesion
(eg, AVM)
• Known malignant intracranial neoplasm
(primary or metastatic)
• Ischemic stroke within 3 months EXCEPT
acute ischemic stroke within 3 hours
• Suspected aortic dissection
• Active bleeding or bleeding diathesis
(excluding menses)
• Significant closed head trauma or facial
trauma within 3 months
Relative Contraindications
• History of chronic, severe, poorly
controlled hypertension
• Severe uncontrolled hypertension on
presentation (SBP >180 mm Hg or
DBP>110 mm Hg)
• History of prior ischemic stroke _3
months, dementia, or known intracranial
pathology not covered in contraindications
• Traumatic or prolonged (>10 minutes)
CPR or major surgery (<3 weeks)
• Recent (within 2 to 4 weeks) internal
bleeding
• Noncompressible vascular punctures
• For streptokinase/anistreplase: prior
exposure (>5 days ago) or prior allergic
reaction to these agents
• Pregnancy
• Active peptic ulcer
• Current use of anticoagulants: the higher
the INR, the higher the risk of bleeding
In hospital treatment
STEMI
• Reperfusion
– pharmacologic – fibrinolytic therapy
– mechanical – primary PCI (percutaneous coronary intervention)
NSTEMI
• fibrinolysis may be harmful
• Pharmaclologic therapy:
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β-Adrenergic Receptor Blockers
Calcium Channel Blockers
Low-Molecular-Weight Heparin
Clopidogrel and ASA
PCI (percutaneous coronary
intervention)
• primary PCI
• PCI combined with fibrinolysis
• Rescue PCI
cerebral stroke
Stroke -Definition
Stroke is defined as a sudden neurologic
deficit due to central nervous ischaemia or
haemorrhage.
• We concentrate here on ischaemic stroke, which
accounts for about 75% of all strokes.
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Ischaemic stroke is caused by focal vessel occlusion
leading to cessation of oxygen and glucose supply to the
brain with subsequent breakdown of the metabolic
processes in the affected territory.
Signs and Symptoms
Symptoms and signs vary with the brain territory
involved. However, certain symptoms are
frequently found. They include:
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contralateral weakness and/or sensory loss
aphasia, apraxia, dysarthria
partial or complete hemianopsia
disturbances of consciousness and confusion
diplopia, vertigo, nystagmus, ataxia
Facial Droop (have patient show teeth or smile):
Normal—both sides of face move equally
Abnormal—one side of face does not move as well as the other side
One-sided motor weakness (right arm).
Main goal in treatment
• Stroke is a medical and occasionally also
a surgical emergency.
• Successful care of the acute stroke victim
begins with the recognition both by the
public and the health professional that
stroke is an emergency, like acute
myocardial infarction (MI) and trauma.
Goals for Management of Patients With
Suspected Stroke Algorithm (1).
Goals for Management of Patients With Suspected Stroke Algorithm (2).
Successful care of the acute stroke victim as an
emergency depends on a 4-step chain:
• (1) rapid recognition of and reaction to
stroke warning signs,
• (2) immediate use of emergency medical
system (EMS) services,
• (3) priority transport with notification of the
receiving hospital (Patients with onset of stroke
symptoms within less than 3 h should be given priority in
evaluation/transportation by the EMS) and
• (4) rapid and accurate diagnosis and
treatment at the hospital.
Emergent diagnostic tests in acute stroke
1 CT
2 ECG and chest X-ray
3 Clinical chemistry
Complete blood count and platelet count,
prothrombin time, INR, PTT
Serum electrolytes, blood glucose
CRP, sedimentation rate
Arterial blood gas analysis, if hypoxia is suspected
Hepatic and renal chemical analyses
4 Pulse oxymetry
5 Lumbar puncture (only if CT is negative, CT and subarachnoidal
haemorrhage is clinically suspected)
6 Duplex and transcranial ultrasound
7 EEG1
8 MRI (magnetic resonance imaging) 1 and MRA1/CTA1(CT
angiography)
9 Diffusion MR1 and perfusion MR1
10 ECG (transthoracic and transoesophageal)*
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PTT = Partial thrombin time; CRP = C-reactive protein. 1 In selected cases.
Emergent diagnostic tests in acute stroke
1 A head CT is the most important diagnostic tool in patients with
suspected stroke to differentiate between ischaemia and
haemorrhage.
2 Vascular imaging (ultrasound, CTA and MRA) in the acute condition
gives additional information about the vessel patency in the brain
and neck vessels and should supplement all imaging procedures
already in the acute phase.
3 MRI/MRA can replace CT if performed appropriately and in particular
T2-weighted imaging is necessary to identify even small
haemorrhages.
4 Diffusion and perfusion MR may be of additional help for assessing
the risk/benefit ratio for early revascularization therapy.
5 Early evaluation of physiological parameters, blood chemistry and
haematology, and cardiac function (ECG, pulse oxymetry, chest Xray) is recommended in the management of acute stroke patients.
Treatment
1. Continuous cardiac monitoring is recommended in the first 48 h of stroke onset
particularly in patients with:
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previous known cardiac disease,
history of arrhythmias,
unstable blood pressure,
clinical signs/symptoms of heart failure,
abnormal baseline ECG and
infarct involving the insular cortex.
2. Oxygenation monitoring with pulse oxymetry is recommended.
3. O2 administration is recommended in case of hypoxaemia (blood gas analysis or
O2sat <92% at pulse oxymetry).
4. Intubation is recommended in case of potentially reversible respiratory insufficiency.
5. Routine blood pressure lowering is not recommended, except for extremely elevated
values (>200–220 mm Hg systolic blood pressure or 120 mm Hg diastolic blood
pressure for ischaemic stroke, >180/105 for haemorrhagic stroke) confirmed by
repeated measurements.
6. Immediate antihypertensive therapy for more moderate hypertension is
recommended in case of stroke and heart failure, aortic dissection, acute myocardial
infarction, acute renal failure, thrombolysis or intravenous heparin, but should be
applied cautiously.
7. Recommended target blood pressure in patients
1. with prior hypertension: 180/100–105 mm Hg,
2. without prior hypertension: 160–180/90–100 mm Hg and
3. under thrombolysis avoid systolic blood pressure above 180 mm Hg.
Treatment
8. Recommended drugs for blood pressure treatment:
 intravenous labetalol or urapidil and
 intravenous sodium nitroprusside, nitroglycerin or oral captopril.
 Avoid nifedipine and any drastic blood pressure decrease.
9. Avoid and treat hypotension particularly in unstable patients by
administering adequate amounts of fluids and, when required,
volume expanders and/or catecholamines (epinephrine 0.1–2 mg/h
plus dobutamine 5–50 mg/h).
10. Monitoring of serum glucose levels is recommended, particularly in
known diabetic patients. - Treatment of serum glucose levels >110
mmol/l with insulin titration is recommended.
11. Glucose solutions are not recommended due to the detrimental
effects of hyperglycaemia.
Treatment
14. Immediate correction of hypoglycaemia is
recommended by intravenous dextrose bolus or
infusion of 10–20% glucose.
15. Treatment of body temperature >37.5° C
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In case of fever, the search of a possible infection (site and
aetiology) is recommended, in order to start tailored antibiotic
treatment.
16. Antibiotic, antimycotic or antiviral prophylaxis is not
recommended in immunocompetent patients.
17. Monitoring and correction of electrolyte and fluid
disturbances are recommended.
Characteristics of selected antihypertensive drugs that may be used in
acute stroke
(modified from Kaplan [1990] and Ringleb et al.1998)
Suggested antihypertensive treatment in
acute ischaemic stroke
(modified from Brott et al. [1994] and Ringleb et al. [1998]; availability of substances
may vary between countries)
Specific Treatment
Thrombolytic Therapy
1. Intravenous rtPA (0.9 mg/kg, maximum 90 mg), with 10% of the dose
given as a bolus followed by an infusion lasting 60 min, is the
recommended treatment within 3 h of onset of ischaemic stroke.
2. The benefit from the use of intravenous rtPA for acute ischaemic stroke
beyond 3 h after onset of the symptoms is smaller, but present up to
4.5 h.
3. Intravenous rtPA is not recommended when the time of onset of stroke
cannot be ascertained reliably; this includes persons whose strokes are
recognised upon awakening.
4. Intravenous administration of streptokinase is dangerous and not
indicated for the management of persons with ischaemic stroke.
5. Data on the efficacy and safety of any other intravenously administered
thrombolytic drugs are not available to provide a recommendation.
6. Intra-arterial treatment of acute MCA occlusion in a 6-hour time window
using pro-urokinase results in a significantly improved outcome.
7. Acute basilar occlusion may be treated with intra-arterial therapy in
selected centres in an institutional protocol as experimental therapy or
within a multicentre clinical trial.
8. Ancrod cannot presently be recommended for use in acute ischaemic
stroke outside the setting of clinical trials.
Specific Treatment
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Aspirin (100–300 mg per day) may be given within 48 h after ischaemic stroke
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There is no recommendation for general use of heparin, lowmolecular weight heparin
or heparinoids after ischaemic stroke
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given within 48 h after stroke reduces mortality and rate of recurrent stroke minimally, but
statistically significantly
If thrombolytic therapy is planned, no aspirin should be given.
Aspirin is not allowed for 24 h after thrombolytic therapy.
Full-dose heparin may be used when there are selected indications such as cardiac sources
with high risk of re-embolism, arterial dissection, or high-grade arterial stenosis prior to
surgery
Low-dose subcutaneous heparin or low-molecular-weight heparins should only be
considered for patients at high risk of DVT or pulmonary embolism.
Infections after stroke should be treated with appropriate antibiotics.
Aspiration pneumonia may not be prevented by nasogastric feeding
Early mobilisation is helpful to prevent numerous complications after stroke including
aspiration pneumonia, DVT and decubital ulcers.
Administration of anticonvulsants to prevent recurrent seizures is strongly
recommended.
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Prophylactic administration of anticonvulsants to patients with recent stroke who have not
had seizures is not recommended
pulmonary oedema
ACUTE HEART FAILURE
Definition
Acute heart failure is defined as
rapid onset of symptoms and signs secondary
to abnormal cardiac function.
• It is often life threatening and requires urgent
treatment. It may occur with or without previous
cardiac disease. The cardiac dysfunction can be
related to systolic or diastolic dysfunction, to
abnormalities of cardiac rhythm or to preload
and afterload mismatch
heart failure
- common causes of HF
• Heart feilure is a
result of acute pump
dysfunction
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IHD
Valvular disfunctin
Cardiomyopathy
Acquired cardiomyopathy
(toxic-alcohol, cocain; or
metabolic –
thyreotoxicosis)
Myocarditis
Constrictive pericarditis
Cardiac tamponade
Systemic hypertension
Other – anemia, cardiac
dysrhythmias
ACUTE HEART FAILURE PRESENT WITH SEVERAL DISTINCT
CLINICAL
1. Acute decompensated heart failure, de novo or
decompensation of chronic heart failure
2. Hypertensive acute heart failure:
3. Pulmonary odema, as an acute heart failure accompanied by
severe respiratory distress and usually O2 saturation < 90% on
room air prior to treatment .
4. Cardiogenic shock: Cardiogenic shock is a continuum from low
cardiac output syndrome to cardiogenic shock
5. High output failure
6. Right heart failure is characterised by low output syndrome with
increased jugular venous pressure, increased liver size and
hypotension
heart failure
- diagnosis
• Echocardiography – gold standard
• Chest X-ray
• Natriuretic peptide (BNP)
Brain natriuretic peptyde
(BNP)
• In normal state atrium is the main cardiac production site of
BNP
• Main stimuli for proBNP synthesis and secretion from cardiac
myocytes are: myocyte stretch caused by volume overload,
neurohormonal activation and hypoxia
• Ventricular proBNP production is strongly upregulated in cardiac
failure and locally in the area surrounding a myocardial
infarction
• biological effects of BNP: diuresis, vasodilatation, inhibition of
renin and aldosterone production and of cardiac and vascular
myocyte growth
Synthesis of NTpBNP and BNP
prepro- BNP (134 amino acids)
Myocyte
cardiac fibroblast
signal peptyde (26 amino acids)
pro- BNP (108 amino acids)
blood
NT-proBNP (76 amino acids)
BNP (32 amino acids)
biologically active
Clinical significance of NTpBNP and
BNP
As a diagnostic tool:
• marker of congestive heart failure, helpfull in assessment of acute
dyspnea
• Predictor of sudden cardiac death and cardiac events in heart
failure
• Predictor of development of heart failure and mortality after acute
coronary syndrome
• For monitoring of cardiotoxicity of antracyclins and of effects of
therapy of heart failure
• NTpBNP vs BNP: more stabile in serum in vivo and in vitro
(storage), 3-6 times longer half-time of persistence in serum, more
stabile concentration with lower sensivity to changes in the amount
of systemic fluids
• Both peptides have an excellent ability to distinguish heart failure
from non-heart failure subject but NTpBNP is more sensitive and
specific (Fonseca)
Medical Treatment of AHF
1.Morphine
2. Anticoagulation
3. Vasodilators
4.ACE inhibitors
5. Diuretics
6.Beta-blocking agents
7. Inotropic agents
Morphine
• Indication
– Early stages of AHF treatment, especially
when
associated with restlessness and dyspnea
• Effects
– Venodilation & mild arterial vasodilation
– ↓ heart rate
• Dosing
– 3 mg boluses, which can be repeaded
Anticoagulation
 • Indication
 Well established in ACS or AFib, with or without AHF
 Less evidence in AHF
 • Effects: few studies!
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Enoxaparine s.c. vs placebo in acutely ill pts*
No clinical improvement
Less DVT (deep vein thrombosis)
No studies of LMWH vs unfractionated heparin
 • Administration
 Careful monitoring of coagulation system
 If Creatinine Clearance < 30 mL/min - Contraindicated or used
with extreme care with anti-Factor Xa level monitoring
IDN – isosorbide dinitrate
Diuretics
• Indication
– Patients with AHF & ADHF with symptoms secondary to fluid retention
• Effects
 Diuresis by  water, NaCl & other ions excretion
 ↓ total body water & Na
 ↓ plasma & EC volume
 ↓ RV & LV filling pressures
 ↓ peripheral congestion & pulmonary edema
 Early vasodilation after i.v. administration
– ↓ RV & LV filling pressures & PVR
– Risk of reflex vasoconstriction after high doses
 May ↓ neurohumoral activation in the short-term (but not in the long-term)
in severe ADHF
 Especially in ACS, administer low doses & give preference to nitrates
Diuretics: Practical Use
• Prefer i.v. loop diuretics (furosemide)
– Therapy can be safely initiated before hospital admission
• Start with individualized doses according to clinical conditions
– Furosemide, 20-40 to 40-100 mg bolus with infusion at 5-40
mg/h
– Prefer a bolus
• Titrate according to clinical response
– Diuresis / Relief of congestive symptoms
• Thiazides & spironolactone can be used in combination
• Dobutamine, dopamine and/or nitrates can be used in combination
– Combinations are more effective and with fewer side effects
than increasing diuretic dose
New Diuretic Agents
• Vasopressin V2 receptor antagonists
• BNP
• Adenosine
Beta-blocking Agents: Indications
• AHF considered a contraindication for beta-blockade
– No study of beta-blocking therapy targeted at improving AHF
– Patients with > basal pulmonary rales or hypotension excluded
from BB trials in AMI
• In AMI, beta-blockers ↓ infarct size, arrhythmias and
pain ....Greater ↓ mortality & morbidity in pts with pulmonary
congestion
• Intravenous BBLs should be considered in pts with:
– Ischemic chest pain resistant to opiates
– Recurrent ischemia
– Hypertension
– Tachycardia
– Tachyarrhythmias
Beta-blocking Agents: Practical
Use
• Use cautiously in patients with overt AHF and >
basal pulmonary rales
– Consider i.v. metoprolol if
• Ongoing ischemia
• Tachycardia
• Patients with AMI who stabilize after AHF
– Start early beta-blocker
• Patients with chronic HF
– Start after AHF stabilization (usually > 4 days)
Inotropic Agents: Indications
• Peripheral hypoperfusion
– Hypotension, ↓ renal function
• With or without congestion or pulmonary
oedema
• Refractory to diuretics & vasodilators at
optimal doses
PDE – phosphodiesteraze inhibitors
Practical Use of Dobutamine
• Indication
– Peripheral hypoperfusion (hypotension,  renal
function) with or without congestion or pulmonary
eodema refractory to diuretics & vasodilators at optimal
doses
• Mode of administration
– Initiated at 2-3 ug/kg/min without a loading dose
– Progressive increase up to 20 ug/kg/min
– Need of higher doses in patients on beta-blocker
therapy
– Possible combination with PDEi (amrinon, milrinon)
PDE – phosphodiesteraze inhibitors
Circulation 2005; 112:
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