CARDIAC EMERGENCIES

MANAGEMENT
PROTOCOL
Acute Heart Failure
Acute Heart Failure is the sudden worsening of the signs and symptoms of heart failure, which
typically includes difficulty breathing (dyspnea), leg or feet swelling, and fatigue and is mostly
due to acute decompensation of Chronic Heart Failure (CHF), but can occur as a first
occurrence. The clinical manifestation may vary from mild decompensation to Acute
Cardiogenic Pulmonary Oedema and Cardiogenic Shock.

Chronic Rheumatic heart disease with valvular heart disease is the most important cause in
Ethiopia but other important causes are congenital heart disease, hypertensive disorders,
Ischemic heart disease, pericardial disease, cardiomyopathy and arrhythmia.

Diagnose Heart Failure Exacerbation

History & Physical exam -Dyspnea on exertion, Paroxysmal Nocturnal Dyspnea, orthopnea, pink
frothy sputum, JVP raised > 4cm and Neck vein distention, Leg edema, S3 gallop, displaced
Point of Maximal Impulse, Basal Crackle . Initial Management

• Evaluate for ABC, put on cardiac monitor , place in semi sitting position,and open IV

• Identify if patient is stable or not using the following important clues:

- BP <90/60(Hypotension) - RR > 35 and other signs of respiratory distress, O2 sat < 90% -
Severe increasing work of breathing /sweating)

Acute heart failure could be stable or unstable (cardiogenic shock or cardiogenic pulmonary
edema

Management of Acute heart failure in different scenarios :

Cardiogenic Pulmonary edema - Normal BP>90/60 but in severe respiratory distress,

fatigued, then endotracheal intubation and mechanical ventilation is necessary.

• Oxygen administration with appropriate system (Support Breathing) -5 to 6 liters / minute by

mask, to achieve oxygen saturation of more than 93%.

Other option to support breathing when saturation is not achieved:

- If noninvasive positive pressure ventilation system is available consider Continuous Positive

Airway Pressure [CPAP] or Bi-level Positive Airway Pressure [BiPAP])

- Should the oxygen saturation be inadequate or the patient develops respiratory muscle
fatigue invasive ventilation might be necessary
• Furosemide(Lasix )40 mg IV or <0.5mg/kg and

• Escalate the dose of furosemide every hr. with 40 mg increment or doubling the dose
depending on response to achieve urine output ≥0.5ml/kg/ hr. The maximum recommended
dose of Furosemide as a single IV bolus is 160-200. (chest auscultation, Sao2 )

Note: there is no standing dose of furosemide that is universal for every patient and decision on
frequency and dosage must be individualized depending on renal status, BP and response.
When there is no response a perfuser can be used to administer continuous Lasix infusion at
10-40mg/hr. If the urine output remains below 1ml/kg/hr., the infusion rate can be increased
each hour as necessary till a maximum dose of 80-160 mg/hr.

• Nitroglycerine 0.4 mg sublingual 3 doses every 5 minutes or isosorbide dinitrate 10mg,

repeat every based on response. If pulmonary edema persists and no evidence of shock IV
Nitroglycerin 5-10 microgram/min infusion

• Morphine 2-4mg IV boluses can be used in anxious pts(for reduction of preload and anxiety)
• If available and increased work of breath, trial of CPAP 12/6

• If after 1 hr. CPAP SaO2 is low and work of breathing is significant then intubate if
mechanical ventilator is available [use high PEEP 10-15]

• Monitoring: includes Resolution of symptoms (dyspnea, orthopnea),V/S and SaO2,urin output

and fluid balance ,Serum electrolytes, upper border of crepitation to see for resolution of lung
congestion, BUN, Creatinine,

• If improved admit to wards, if not ICU

Cardiogenic Shock (BP<90/60 and features of hypo perfusion)

• Put the patient on cardiac monitor stabilize the ABC

• Fluid challenge with N/S 200- 500 cc IV fluid bolus (5 - 10 ml/kg) for restoring vascular volume
and preload, depending on the level of crepitation on the chest

• When invasive monitoring is possible: if CVP is < 15 mmHG fluid is given and if it is >15 mm
HG inotropes/pressers are used.

•Consider vasopressors/inotropes- if SBP is around 90mmHG consider dobutamine, if SBP is

70-90mmHG consider dopamine (3-10 mg/kg/min – 50 mg/kg/min) or if SBP<70mmHG consider
adrenaline 2-10 microgram/ min or escalate the dose of dopamine gradually. If other pressor
are not available adrenaline 2-10 microgram/min with escalation can be used.
• Diuresis with furosemide 20-40mg IV bolus after inotropic support if there are signs and
symptoms of pulmonary edema when BP is elevated to low normal.

• Reduce work of breathing or desaturation through Facemask O2 or undertake ventilator

support like using CPAP/BiPAP.

• Look for treatable causes: If tachyarrhythmia is contributing to cardiogenic shock in heart

failure- Amiodarone or digoxin, pain management in AMI.

•Admit to ICU

Stable Heart Failure

• Lasix 40mg -120 mg based on previous close and renal function status.

• Start ACEI like enalapril or Lisinopril 2.5 mg Po stat if not started.

• Consider digoxin.

• Consider Spironolactone in severe disease with inadequate response to Lasix.

• Discharge with follow up visit and advise patient on lack of salty diet, serial weight
measurement, exercise, smoking cessation and need for outpatient Bblocker therapy.

NB: In all cases identify and treat precipitating factor and underlying cause for the failure.
Precipitating factors are summarized with the Pneumonic – HEART FAILES H- Hypertension, E-
Endocarditis, A- Arrhythmia- Rheumatic fever /Myocarditis, T- Thyrotoxicosis and pregnancy, F-
Fever (infection), A-Anemia, I-Infarction, L-Lack of compliance, E-Embolism (Pulmonary), S-
Stress (emotional, dietary, fluid excess, physical)

4.2. Acute coronary syndrome

Acute coronary syndrome defines a spectrum of clinical presentations that is related to acute
coronary diseases. This involves unstable angina, ST elevation myocardial infarction and non ST
elevation myocardial infarction. The symptoms of acute coronary syndrome can range from no
chest pain to severe chest pain that is significantly distressing to the patient. The Chest
pain/Discomfort Pain lasting for more than 20 minutes, Radiating to the arms, neck or jaw. It
can also be Epigastric pain and Associated Nausea, sweating or diaphoresis, Shortness of
breath, fatigue. Atypical symptoms are common in diabetic patients, elderly and women.

Patients with risk factors are those with Age> 55 for female,>45 for male, male sex, smoking,
family history, Diabetes, Hypertension, Hypercholestromia. Diagnosis: It is made based on
typical clinical features, ECG findings and cardiac markers (CKMB and troponin I)
Diagnosis:

Eg.ST elevation on ECG

Diagnostic tests: 1. ECG: done at presentation; repeat to see changes

*UA/NSTEMI= ST depression/transient elevation or deep T inversion (>=0.3mV) * STEMI=New

ST elevation in 2 contiguous leads >= 2 mm/2 small squares in men or 1.5 mm in women in
leads V2-3 and/or 1mm in other leads OR new LBBB . ECG must also be analyzed for
arrhythmias.

2. Cardiac biomarkers: testing at presentation & 6–12 h after sx onset *Cardiac troponins
( T&I)-rise 20 -50 Xs Upper normal limit in acute MI; rise 4-8 hr after injury; may remain
elevated for 7-10 days; more Specific& Sensitive than CK-MB .Creatine kinase (CK )-rises in 4–8
hr; normalize by 48–72 h.

3. Echocardiography: may show new regional wall motion abnormality, RBS, lipid profiles

4. CXR: to look for pulmonary edema; R/o other DDx like PTE, pericarditis. Management of ACS:
should focus on stabilizing the patient’s condition, relieving ischemic pain, and providing
antithrombotic therapy to reduce myocardial damage and prevent further ischemia. The goal is
early revascularization.

1) General measures: Continuous ECG monitoring for arrhythmia & ST changes

• V/S: frequent until stable, then Q 2- 4hr & as needed

• O2 (2-4 lit/min) keep SaO2>93%

• Bed rest, Sedation with diazepam 5mg po BID,

 VTE(venous thromboembolism) prophylaxis

• NPO except for fluid diet until stable; IV fluid – eg. for inferior MI

• Glycemic control-goal is RBS of 140-180mg/dl(if > 180mg/dl, give regular insulin-1-2IU

for each 50mg/dl increase above 180mg/dl, by measuring RBS Q 6hrs)
2) Medications:
• Nitroglycerin (NTG) : sublingual 0.4 mg Q 5 min for three doses as needed or chest pain
(C/I= low BP, sildenafil use)

• Morphine sulphate: 2–5 mg IV , may be repeated Q 5–30 min as needed to relieve chest
pain (can also use pethidine 25-50mg IM/IV or tramadol 100mg IM)

• Aspirin (ASA): loading: 162–325 mg chewed immediately, then 75–162 mg/d plus

Clopidogrel-loading: 300mg Po, then 75 mg/d for at least 1 yr (but ASA lifelong)

• Metoprolol: 25–50 mg PO q 6 h ,target HR=60-80/min (If HTN, ongoing pain,

tachycardia: give IV over 1–2 min by 5mg increments) or Atenolol 2550mg PO. C/I-
CHF,bradycardia

• Un Fractionated Heparin: Bolus 60–70 U/kg (max 5000 U) IV then infusion of 12–15
U/kg/ h (initial maximum 1000 U/h) titrated to aPTT 50–70 s * If no perfuser,12,500U SC BID is
possible; OR LMWH (Enoxaparin):1 mg/kg SC Q 12 h(if GFR< 30,1mg/kg once daily)

• Warfarin: initially 2.5mg titrated to INR goal of 2-3(eg. for extensive anterior STEMI with
severe left ventricular dysfunction,CHF,atrial fibrillation or LV thrombus)

• Statins: atorvastatin 80mg po/d is preferred. Others options are pravastatin/

simvastatin/lovastatin 40mg Po/day

• ACEIs: start low dose eg. Enalapril/lisinopril 2.5 to 5mg po/d OR captopril 6.25-12.5mg
TID; then escalate gradually to clinically effective dose.

Invasive therapy in ACS: for high risk patients who present early, referral to a better set up
is recommended (If the patient can afford)

• STEMI : fibrinolysis Vs PCI/CABG: Recommended door to PCI time is 90 minutes while

door to thrombolytic in 30minutes.

•In Unstable angina/NSTEMI: PCI/ CABG; but fibrinolysis is not indicated.

Monitoring: Patient should be on monitor to look for electrical complications like

Vtac,Vfib , AV nodal blocks and atrial fibrillation(manage using ACLS algorithm)

o ECG should be repeated every 15-30 minutes. First ECG is diagnostic only in 50%.

o Vital signs: Every 15 minutes until stabilization

 o Cardiac markers: every 6 hours, CK MB and troponin will rise in 4-6 hours .

o Manage chest pain: and follow for clinical improvement.

o Watch for mechanical complications like heart failure, myocardial wall rapture, papillary
wall rapture, septum rupture, ventricular aneurysm, post myocardial infarction pericarditis and
Dressler’s syndrome, and manage accordingly.

o Blood sugar should be determined and preferably maintained at less than 180mg/dl.

o All suspected patients with acute coronary syndrome should be admitted to

resuscitation

o Patients with STEMI should be assessed for eligibility and transferred to a facility where
reperfusion therapy can be provided as soon as possible.

o Patients with unstable angina or NSTEMI with persistent symptoms and complications
should be considered for PCI in coronary care unit.

o All patients with diagnosed acute coronary syndrome should be admitted to intensive
care units at least for the first 48 to 72 hours.

Cardiac Tamponade
The accumulation of fluid in the pericardial space in a quantity sufficient to cause serious
obstruction to the inflow of blood to the ventricles results in cardiac tamponade which causes
results in obstructive cardiogenic shock.

Etiology •
Trauma; gunshot or stab wounds, blunt trauma to the chest
• Inatrogenic accidents: perforationduring cardiac catheterization, central line,
etc • Pericarditis (TBC, Pyogenic, SLE etc)
•Malignant pericardial effusion
• A ruptured aortic aneurysm
• Radiation to the chest
•Other causes: hypothyroidism, uremia,
AMI, etc

Diagnosis Clinical: Beck’s triad is clinical clue for diagnoses, it includes:

•Low blood pressure and weak pulse, and pulsus paradoxus because of low
cardiac output.
 • Raised JVP and distended neck veins because of elevated R atrial pressure.
• Faint/muffled heart sounds and tachycardia

ECG characteristics: reduction in amplitude of the QRS complexes, and electrical alternans of
the P, QRS, or T waves. Echocardiographic diagnostic criteria One or more of the following in
the setting of moderate to large effusion and symptoms or a paradoxical pulse:
• Right atrial systolic collapse and Right ventricular diastolic collapse
• Reciprocal respiratory ventricular inflow (25% reduction mitral inflow
velocity in inspiration)
• Inferior vena cava plethora

Treatment Cardiac tamponade is a medical emergency and patients should be closely

monitored and obtain urgent management:
• Oxygen via nasal prong or face mask
• Volume expansion with isotonic saline ,blood, plasma, as necessary, to
maintain adequate intravascular volume in order increase in cardiac
output after volume expansion

•Bed rest with leg elevation in order to facilitate venous return

• Inotropic drugs (e.g, dobutamine) -These can be useful because they

increase cardiac output without increasing systemic vascular resistance

• Pericardiocentesis: use subxiphoid or anterior approach depending on the pool

of fluid and drain as much as possible fluid in tamponade for therapeutic and diagnostic
purpose.

•After pericardiocentesis, leave the intrapericardial catheter in place after securing it to

the skin using sterile procedure and attaching it to a closed drainage system, periodically check
for reaccumulation of fluid, and drain as needed.

Indication of Emergency pericardiocentesis Emergency pericardiocentesis is indicated

in cardiac tamponade which is diagnoses using clinical features of instability and
echocardiography signs.

Contraindications Relative contraindications are Pericardial effusion of less than 2 cm width

and presence of Bleeding disorder (including platelet count <50 × 109/L, INR >1.5), in that case
consultation is necessary with cardiology expertise.
Complications of Pericardiocentesis: Puncture of the heart, laceration of liver/stomach or
colon in the subxiphoid approach, pneumothorax, and puncture of internal mammary artery.