Circulation assessment + Acute coronary syndrome

Dr.Ahmados
Rapidly assess  blood pressure & pulse. Also  capillary pressure , organ perfusion , ECG
pulse blood pressure Organ perfusion
A narrowed pulse pressure suggests Hypotension is suggestive of severe 1- Kidney : via urine output.
hypovolemic shock intravascular depletion. 2- Brain: via consciousness
level
3- Heart: via chest pain.

Internal bleeding
If narrowed pulse & hypotension with no external bleeding  Rapidly evaluate the abdomen because it is
frequently a source of significant hemorrhage in the multiply injured patient.
- Severe pelvic fracture can be associated with massive intrapelvic hemorrhage.
- TTT: Give the patient crystalloid initially & then blood, if needed, to improve perfusion.
External Hemorrhage
Diagnosis
1) Blood 2) source 3) Amount
Arterial Venous capillary 500 cc 1500 cc 2000 cc
Wow.. red fluid, is it blood ?!  Red jets Blue flow oozing of
Sudden loss of
blood No effect Shock 2 liter of
Pressure
Any simple Any pressure blood (50%) ,
must be
pressure which is fatal
more than
SB
Treatment
Stopping the external hemorrage :
1) By direct pressure with sterile dressings.
2) Proximal control by blood pressure cuff or tourniquet :
Rarely will compression be insufficient to control an arterial hemorrhage from an extremity. A blood pressure cuff inflated
proximal to the wound ( more than systolic pressure ) can serve as an effective tourniquet temporarily until surgical control
of the bleeding can be achieved.
If a tourniquet or a cuff is required, monitor the application time  no application of tourniquet/cuff more than an hour
for fear of ischemia. If prolonged application is required, open the tourniquet/cuff for 2 min. allowing the flow of blood
then apply the tourniquet/cuff again.
3) Clamping by artery forceps.

- Scalp wounds, even small ones, can produce significant blood loss if not controlled
TTT,
1- Sometimes direct pressure and dressings are not sufficient.
2- For uncontrolled scalp wound hemorrhage, the wound should be closed with sutures, staples.
Traumatic Arrest
- If spontaneous cardiac activity is not detected by palpation of the carotid artery , begin
cardiopulmonary resuscitation immediately.
- If the patient has blunt trauma & has been pulseless for less than 5 minutes,
Or
if there is penetrating chest trauma & has been pulseless for less than 15 minutes,
consider emergency thoracotomy.
- If the patient has been pulseless longer than the abovementioned time limits, thoracotomy is not indicated
and has not been shown to improve survival.
Shock
- Definition: Shock is defined as inadequate tissue perfusion
- Classification: classified as mild, moderate, or severe, based primarily on clinical criteria.
- Clinical criteria :
- 2  ------------- 1- tachycardia 2- tachypnea
- 2 ------------- 1- blood pressure & delayed capillary refill (>2 s) 2- level of consciousness
- 2 (coldness)---- 1- Cold extremities 2- cold sweating (diaphoresis)
- With or without pallor.
 N.B. Dr.Ahmados
 Hypotension and oliguria are presumed to be due to shock until proved otherwise.
 Shock in the traumatized patient is due to hypovolemia from hemorrhage in the majority of the cases.
 Do not assume that perfusion is adequate on the basis of supine pulse and blood pressure alone, because
these signs may not change until late in shock. This is particularly true in young healthy adults—who are the
most common victims of multiple trauma.
 Patients taking B-blockers (or other medications that blunt the normal response to adrenergic stimulation)
may not exhibit tachycardia despite profound shock.
- Cardiac tamponade & tension pneumothorax are conditions that can cause shock, which must be
excluded rapidly in the assessment of hypotensive trauma patients.
- Spinal cord or brain injury may contribute or (rarely) may cause shock without concurrent volume loss.
- In a trauma patient, shock should be treated as hypovolemic shock with volume infusions until other causes
of shock are found .

Acute coronary syndrome

- Acute coronary syndrome refers to a spectrum of conditions that develop from blood flow
that is insufficient to meet the metabolic needs of the myocardium.

- Patients with an acute coronary syndrome exist on a clinical continuum from unstable angina
to non\ST-segment elevation myocardial infarction  to ST segment elevation myocardial infarction.

Acute Myocardial Infarction (Coronary Occlusion) :

- Myocardial infarction results when arterial blood flow to the myocardium is suddenly
decreased or interrupted.

- Causes :
1- Atherosclerotic coronary artery disease with plaque rupture and sudden occlusion by thrombus;
2- Vasculitis or emboli are less common causes.
3- Rarely, myocardial infarction with normal coronary arteries, is due to spasm of a coronary artery
Cocaine use has been associated with acute myocardial infarction, probably as a result of coronary spasm with or
without intravascular thrombus formation.

- Pathological consequences :
 During the myocardial infarction,
1) severely ischemic & infarcted muscle contracts and relaxes poorly or not at
all;  decreased cardiac output with cardiogenic shock & acute heart failure.
2) The myocardium is electrically unstable, resulting in ventricular
arrhythmias .

 After myocardial infarction,

1) Ventricular aneurism occurs or may even rupture.
2) The infarcted endocardium attracts platelets and fibrin that may form mural
clots, which can subsequently embolize.
3) If conducting tissue is ischemic or infarcted, conduction abnormalities may
occur.

Upon occlusion of a coronary artery, necrosis occurs in a time-dependent course, proceeding from endocardium to
epicardium, generally over 4–6 hours.

- Clinical features & investigations : read them from internal medicine

book
Treatment
Dr.Ahmados
Aim of TTT :
Receiving aggressive treatment with the goal of rapidly reperfusing ischemic myocardium.
Methods of TTT :
The two methods currently available are:
1- Thrombolytic therapy &
2- Percutaneous coronary intervention (PCI).

A) Immediate Measures : (BE MON)

B: B-blocker E: Enoxaparin M: Morphine O: Oxygen N: Nitroglycerine
1) Begin Oxygen by nasal cannula or mask.
2) Begin intravenous infusion of 0.9% normal saline through a secure intravenous
catheter.

3) Start ECG monitoring, and obtain a a12-lead ECG.

4) Nitroglycerin, 0.4 mg sublingually Repeat if no effect occurs in 5 min.

If chest pain returns and systolic blood pressure is above 100 mm Hg, starts nitroglycerin IV at 10
mg/min & increase by 5 mg/min every 3–5 minutes until systolic blood pressure falls by 10% or chest
pain is relieved. " The systolic blood pressure should not drop below 90 mm Hg."
5) Morphine, 2–8 mg intravenously .

6) Enoxaparin ( low molecular weight heparin )

7) Give 15 mg of B-blockers metoprolol in three 5-mg intravenous injections at 2-minute

intervals.
Contraindications for B-blockers must be abscent ( heart rate <55/min, systolic blood pressure <90
mm Hg, moist rales above the lower third of the lung fields, advanced atrioventricular block, or
history of asthma ).

8) Give the patient aspirin ( a 160- to 325-mg non-enteric-coated to chew ) .

9) If the patient has pulmonary edema, give furosemide, 40 mg by intravenous bolus
injections .

B) Additional Measures :
- Establish a laboratory test database:
1- Blood for typing (and crossmatching if needed)
2- Complete blood count (CBC)
3- Serum creatinine
4- Electrolyte measurements,
5- Blood urea nitrogen determinations,
6- Enzyme levels (preferably CK isoenzymes, cTni or cTnt, etc.).
7- Platelet count, prothrombin time, partial thromboplastin time,
8- Blood for typing (and crossmatching if needed)
 - Monitor urine output.

The above measures are followed by :

C) Options of treatment :
- Option 1: Thrombolytic Therapy Dr.Ahmados
( pharmacological revascularization )

Myocardial reperfusion salvages myocardium resulting in better ventricular function & improves survival if
reperfusion occurs within 6 hours after the onset of symptoms of myocardial infarction.

- Indication:
1- If the duration of chest discomfort is at least 30 minutes and less than 4–6 hours in the patient with
evidence of an ST segment elevation myocardial infarction and no contraindications are present,
especially if PCI is unavailable for more than 90 minutes.
- ST segment elevation of at least 0.1 mV in two or more leads (II, III, aVF or V1–V6, I, aVL) suggests
acute injury in the absence of left bundle branch block.
- An acute true posterior myocardial infarction (with ST depression in leads V1–V4) is also an indication.

2- Patients with ongoing chest pain and a new (or not known to be old) left bundle branch block
should also be considered for pharmacologic reperfusion.
3- Both chest pain and ST elevation are not relieved by 2 to 3 sublingual nitroglycerin tablets.
4- Pas history is present .
5- No contraindications to thrombolytic therapy or anticoagulation therapy are present (see below).

- Contraindication:

Absolute Contraindications

- History of any hemorrhagic cerebrovascular event (stroke, arteriovenous malformation, or

aneurysm) or any nonhemorrhagic cerebrovascular event or transient ischemic attack (within
the last year)
- Any intracranial neoplasm
- Active, internal bleeding (e.g., serious gastrointestinal bleeding) excluding menses
- Suspected aortic dissection

Relative Contraindications

- Recent (within 10 days) puncture of a noncompressible blood vessel

- Poorly controlled hypertension of several years' duration or severe, uncontrolled arterial
hypertension (diastolic blood pressure greater than 110 mm Hg or systolic blood pressure
greater than 180 mm Hg)
- Diabetic hemorrhagic retinopathy or hemorrhagic ophthalmic condition
- Current treatment with an anticoagulant with international normalized ratio greater than two
to three or other bleeding diathesis
- Pregnancy
- Any other condition associated with a predisposition to bleeding (e.g., ulcerative colitis, active
peptic ulcer disease, polycystic kidneys, gastrointestinal arteriovenous malformation, vascular
tumors) or bleeding within 4 weeks
- Prolonged (>5 minutes) or traumatic external cardiac compression or traumatic endotracheal
intubation
- History of nonhemorrhagic cerebrovascular accident beyond 1 year
- Recent (within 4 weeks) trauma or major surgery at a noncompressible site (e.g., coronary
artery bypass surgery, organ biopsy, intra-abdominal surgery, or obstetric delivery )
  Many thrombolytic agents are available, including:
1- streptokinase,
2- anistreplase (APSAC),
3- alteplase (tissue plasminogen activator: t-PA),
4- reteplase (r-PA),
5- tenecteplase (TNK).

N.B.
- The benefit of pharmacologic thrombolysis decreases with each passing hour after myocardial
infarction.
- Some patients with myocardial infarction may benefit from thrombolytics up to 12 hours after
the onset of chest pain, although 6 hours is generally considered the cutoff.
- Intracranial hemorrhage is the most devastating complication of thrombolytic therapy,
occurring in 0.5–3.3% of patients
For reading:
- Alteplase administration over 90 minutes improved survival when compared to streptokinase or 3-hour
alteplase infusion. Even though intracranial bleeding events increased, alteplase demonstrated a long-term survival
advantage presumably secondary to earlier thrombolysis and reperfusion of thrombosed coronary arteries. Compared
to alteplase, TNK may offer advantages of a single bolus administration and fewer intracranial hemorrhage
complications.

- Dosages :

Streptokinase

1.5 million units in 250 mL of 5% dextrose in water, given intravenously over 1 hour.
Because of the risk of serious allergic reactions, streptokinase is contraindicated in patients who have
ever received streptokinase previously.

Anisoylated Plasminogen Streptokinase Activator Complex (APSAC)

30 mg intravenously infused slowly over 5 minutes. Because of the risk of serious allergic reaction,
patients who have received streptokinase or APSAC previously cannot be given the drug again

Alteplase

15 mg intravenous bolus followed by 0.75 mg/kg (maximum 50 mg) intravenous infusion over 30
minutes and then 0.5 mg/kg (maximum 35 mg) over 60 minutes.

Alteplase has a very short half-life (5 minutes)  heparin must be used to prevent reocclusion.
Heparin should be started as a bolus of 60 units/kg at the start of the alteplase infusion followed by a
maintenance dose of 12 units/kg.

Urokinase

0.5 million units over a 10-minute period followed by infusion doses of 1.6–4.5 million units over
18–24 hours.

Reteplase

10-unit intravenous boluses over 2 minutes, with 30 minutes between each dose.

Tenecteplase

Ranging from 30 to 50 mg rapid bolus.

Dr.Ahmados
 Heparin

- Should be used in conjunction with any thrombin-specific thrombolytic agent such as

alteplase.
- Not indicated in streptokinase or APSAC , because of the systemic fibrinolysis achieved by
both.
- Intravenous heparin, 60 units/kg bolus followed by 12 units/kg/h, should be given in a
separate line while alteplase is infusing because of the short half-life of alteplase and the
danger of recurring thrombosis.
- Heparin should be continued for 48 hours or longer, maintaining activated partial
thromboplastin time at twice normal.

Monitoring
Dr.Ahmados
Transfer patients given thrombolytic therapy to an intensive care unit as soon as
possible after initiation of treatment. Monitor the following:

1- blood pressure every 15 minutes during infusion and every 30–60 minutes thereafter
2- ECG rhythm strip for reperfusion arrhythmias and ST segment changes
3- bleeding complications and changes in neurologic status; avoid venous or arterial punctures and
unnecessary trauma
4- 12-lead ECG 4 hours after the start of therapy and as needed (e.g., for recurrence of chest pain)
5- CK with isoenzymes and cTni or cTnt 4 hours after initiation of treatment and at 4-hour intervals
for 24 h.

- Option 2: Percutaneous Coronary Intervention ( coronary revascularization )

Formerly termed angioplasty, PCI involves cardiac catheterization and various techniques to assess and
restore vessel patency on an emergency basis. Coronary artery stenting has become the procedure of choice.

- Indication:
1- In patients with contraindications to thrombolytics, PCI is the only option available to restore perfusion
and salvage myocardium
2- For patients who have received thrombolytics but whose chest pain or ST segment elevation has failed to
resolve.

N.B. If the time to PCI is expected to exceed 90 minutes for a patient with a ST
segment elevation myocardial infarction, thrombolytics should be strongly considered
in order to salvage as much myocardium as possible

Increased rates of normal flow and decreased rates of reocclusion in the infarct-related artery are much more likely
when PCI is chosen over pharmacologic thrombolysis BUT unfortunately, PCI is not widely available

Disposition
Hospitalize all patients with clinical histories suggesting myocardial infarction, and start ECG monitoring
(in a coronary care unit, if possible).

Complications of Myocardial Infarction :

- About 10–15% of patients reaching the hospital with myocardial infarction die during
hospitalization.
- One or more complications occur in over half of all patients with myocardial infarction.
 Cardiogenic Shock
Shock complicating myocardial infarction be caused by:

1- Extensive myocardial infarction with decreased cardiac output (most common),

2- Ruptured ventricular septum  Free-wall myocardial rupture results in tamponade and shock

3- Inappropriate reflex peripheral vasodilatation,

4- Arrhythmias,

5- Hypovolemia,

6- Right ventricular infarction,

7- Severe mitral regurgitation.

Clinical Findings Dr.Ahmados

- Hypotension accompanied by confusion, restlessness, cool skin, oliguria, and metabolic
acidosis .
- Tachycardia

- Pulmonary edema .

N.B. Mild to moderate hypotension alone is common in myocardial infarction and does not itself indicate shock.

- Treatment :
A) General measures :
Airway
- :
management Give oxygen by mask or nasal cannula.

- Patients in shock with respiratory failure require endotracheal intubation.

Venous pressure
monitoring :
- Monitor central pressure with a Swan-Ganz pulmonary artery catheter (or a central
venous pressure catheter, since in acute myocardial infarction, left ventricular filling pressure can be markedly elevated with normal
right ventricular filling pressure, and vice versa ).

- Use an arterial line to measure blood pressure.

Others :

- Give a fluid challenge (200 mL of saline intravenously over 20 minutes) if the patient is not in
congestive heart failure (i.e. no pulmonary edema on chest X-ray).
- Insert a Foley catheter, and measure urine output hourly.

- Correct arrhythmias .

B) Drug therapy :
- Give dopamine (or dobutamine), 2.5–20 mg/kg/min by continuous intravenous infusion.
 - When shock is caused by inappropriate vasodilatation (rare), B-adrenergic drugs such as
norepinephrine are useful.

C) Percutaneous Coronary Intervention

- PCI is effective in patients who develop cardiogenic shock early (within 3–6 hours) after
onset of myocardial infarction.
- PCI should be seriously considered in such patients because thrombolytics are ineffective
in cardiogenic shock associated with an acute myocardial infarction.

Disposition
- All patients with cardiogenic shock must be hospitalized in an intensive care unit.
- Therapy is directed at the likely causes of shock (e.g., fluid administration to patients with
right ventricular infarction).

- Intra-aortic balloon pump (IABP) counterpulsation can increase cardiac output and
improve both coronary and systemic perfusion.

N.B.  IABP counterpulsation is contraindicated in patients with aortic valve disease or those with aortic dissection.

Sources :
Dr.Ahmados 1-
2-
Current Emergency Diagnosis & Treatment - 6th Ed
Oxford Handbook of Accident and Emergency
Medicine