Module: Cardiovascular System 3.

Nitrates
Causes vasodilation and reduces myocardial workload and therefore
Problem 1.11: Chest Pain
myocardial oxygen demand via the reduced preload and afterload.
Study Guide 7: Principles of Management of a Patient with A Myocardial Could also improve coronary blood flow. (0.5mg GTN [nitro-glycerine]
Infarction sublingually)

Keywords
4. Aspirin/ Clopidogrel
- Thrombolytic Aspirin (300mg) orally, chewed in order to prevent further clot formation
- Antiplatelet Agents Clopidogrel (300mg) orally, chewed in order to prevent further clot
- Beta Blockers formation, given to aspirin sensitive patients.
- Cardiac Rehabilitation
- Risk Factors 5. Thrombolytic (given in special cases in small dosage)
- Sedentary life style a. Streptokinase (1,500,000 units/hr)
- Serum lipids, cholesterol b. Urokinase
- Lipid lowering medications c. TPase (alteplase, neteplase, Tenecteplase)

6. Beta Blockers (atenolol, metoprolol, bisoprolol) = intravenously using

a. Management of Ischemic Heart Disease
 Prepare to administer CPR and use defibrillator in case of cardiac arrest.
 Immediate concerns are safety + comfort.
 ECG is done as possible as to establish STEMI or 'Non STEMI'
1. Oxygenation
Oxygen therapy IS given with the appropriate supplemental oxygen
amount to maintain an oxygen saturation >90%, while monitoring
oxygen saturation using pulse oximetry
2. Analgesia
GTN as spray or sublingual (applied under the tongue) or an intravenous
opioid (morphine sulphate [5-10mg], diamorphine [2.5-5mg] +
antiemetic (metoclopramide [l Omg])).
selective beta-blockers. Specifically Bl receptors (epinephrine), reduce
myocardial oxygen consumption by competitive inhibition of Bl
receptors thus lowering heart rate, BP and myocardial contractility,
resulting In prolonged diastole, increasing time for maximal coronary
blood flow
 Calcium channel blockers — used when a patient is asthmatic or has
respiratory problem so this is given instead of beta blockers.
(dihydropyridines, Benzothiazepine, phenylalkylamines)
 Inhibit calcium movement through slow calcium channels of cell
membranes in the myocardium, cardiac conduction tissues + smooth
muscle.
 depress myocardial contractility + infra cardiac conduction
 depress cardiac conduction causes bradycardia (increase diastole)
 ST elevation myocardial infarction (STEM') — usually total vessel occlusion
with reddish fibrin rich thrombus (responsive to thrombolysis) and Non ST
elevation myocardial infarction (non ST EMI) — usually incomplete occlusion
of vessel with greyish white platelet rich thrombus (relatively unresponsive to
thrombolysis). This distinction is made solely on the ECG and is central to our
management — ST elevation infarctions benefit from urgent thrombolysis,
whereas non-ST elevation infarctions do not.

MONA LISA (Mnemonic for acute management of Ml)

M- Morphine

O- Oxygen

N- Nitrates

A- Aspirin

L — loop diuretic (Loop diuretics are diuretics that act at the ascending loop of
Henle in the kidney. They are primarily used in medicine to treat hypertension
and edema often due to congestive heart failure or renal insufficiency)

I — IV access — for bloods, for IV (nitroglycerin) causes venodilation at low

doses, but at higher doses dilates both arteries and veins.

S — streptokinase (thrombolysis) / PCI - if STEMI

A — Antiplatelet (e.g. clopidogrel)

2. Part Of Question 1
3. Complications
a. Arrhythmia

Cardiac Failure
Clinical assessment
Acute left heart failure
Acute de novo left ventricular failure presents with a sudden onset of dyspnoea
at rest that rapidly progresses to acute respiratory distress, orthopnoea and
prostration.
The patient appears agitated, pale and clammy. The peripheries are cool to the
touch and the pulse is rapid. Inappropriate bradycardia or excessive tachycardia
should be identified promptly, as this may be the precipitant for the acute
episode of heart failure. The BP is usually high because of sympathetic nervous
system activation, but may be normal or low if the patient is in cardiogenic shock.
Auscultation occasionally identifies the murmur of a catastrophic valvular or
septal rupture, or reveals a triple ‘gallop’ rhythm. Crepitations are heard at the
lung bases, consistent with pulmonary oedema.
Management of acute pulmonary oedema
This is urgent:
 Sit the patient up in order to reduce pulmonary congestion.
 Give oxygen (high-flow, high-concentration). Noninvasive positive
pressure ventilation (continuous positive airways pressure (CPAP) of 5–
10 mmHg) by a tight-fitting facemask results in a more rapid
improvement in the patient’s clinical state.
 Administer nitrates, such as i.v. glyceryl trinitrate 200 μg/min or buccal
glyceryl trinitrate 2–5 mg, titrated upwards every 10 minutes, until
clinical improvement occurs or systolic BP falls to < 110 mmHg.
 Administer a loop diuretic such as furosemide50–100 mg
The patient should initially be kept on strict bed rest with continuous monitoring
of cardiac rhythm, BP and pulse oximetry. Intravenous opiates may be cautiously
used when patients are in extremis. They reduce sympathetically mediated
peripheral vasoconstriction but may cause respiratory depression and
exacerbation of hypoxaemia and hypercapni
Chronic Heart Failure
A low cardiac output causes fatigue, listlessness and a poor effort tolerance; the
peripheries are cold and the BP is low. To maintain perfusion of vital organs,
blood flow is diverted away from skeletal muscle and this may contribute to
fatigue and weakness. Poor renal perfusion leads to oliguria and uraemia
In ambulant patients, the oedema affects the ankles, whereas in bed-bound
patients it collects around the thighs and sacrum. Chronic heart failure is
sometimes associated with marked weight loss (cardiac cachexia) caused by
combination of anorexia and impaired absorption due to gastrointestinal
congestion, poor tissue perfusion due to a low cardiac output, and skeletal
muscle atrophy due to immobility.
Management of chronic heart failure system. These drugs also prevent the undesirable activation of the renin–
angiotensin system caused by diuretic therapy.
General measures
Angiotensin receptor blocker (ARB) therapy
Education of patients and their relatives about the causes and treatment of heart
failure can help adherence to a management plan. In patients with coronary These drugs act by blocking the action of angiotensin II on the heart, peripheral
heart disease, secondary preventative measures, such as low-dose aspirin and vasculature and kidney. In heart failure, they produce beneficial haemodynamic
lipid-lowering therapy, are required. However, statins do not appear to be changes that are similar to the effects of ACE inhibitor
effective in patients with severe heart failure.
Beta-adrenoceptor blocker therapy
Drug therapy
Beta-blockade helps to counteract the deleterious effects of enhanced
Drugs that reduce preload are appropriate in patients with high end-diastolic sympathetic stimulation and reduces the risk of arrhythmias and sudden death
filling pressures and evidence of pulmonary or systemic venous congestion. Beta-blockers are more effective at reducing mortality than ACE inhibitors
Those that reduce afterload or increase myocardial contractility are more useful
in patients with signs and symptoms of a low cardiac output
4. Risk Factors
Diuretic therapy
Done Previously
In heart failure, diuretics produce an increase in urinary sodium and water
excretion, leading to a reduction in blood and plasma volume. Although a fall in 5. Management
preload (ventricular filling pressure) tends to reduce cardiac output, the ‘Starling
curve’ in heart failure is flat, so there may be a substantial and beneficial fall in Done Previously
filling pressure with little change in cardiac output. Nevertheless, excessive
diuretic therapy may cause an undesirable fall in cardiac output, with a rising
serum urea, hypotension and increasing lethargy, especially in patients with a
marked diastolic component to their heart failure

Vasodilator therapy

Angiotensin-converting enzyme (ACE) inhibition therapy

This interrupts the vicious circle of neurohumoral activation that is characteristic

of moderate and severe heart failure by preventing the conversion of angiotensin
I to angiotensin II, thereby preventing salt and water retention, peripheral
arterial and venous vasoconstriction, and activation of the sympathetic nervous