Alterations in CV

Function
Integrative Pathophysiology
Tutorial Exercise

While the heart pumps blood to deliver

O2 and nutrients to the tissues, the heart
must also be adequately perfused to
stay alive...
Acute Coronary Syndrome is…
a) An inflammatory disease characterized by abnormal
sub-endothelial lipid deposition in the coronary
arteries
b) A stable condition that results from an imbalance in
myocardial O2 supply and demand, without tissue
necrosis
c) Abnormal heart function with signs & symptoms of
low cardiac output and/or pulmonary/systemic
congestion
d) A spectrum of ischemic diseases including unstable
angina, NSTEMI, & STEMI 2
Case Study
A 65-year-old is admitted to the Cardiac Care Unit (CCI) with a
diagnosis of myocardial infarction. Prior to arrival the patient
described severe substernal chest pain lasting over 4 hours that
was accompanied by a “choking feeling”, severe shortness of
breath (SOB), and diaphoresis.

The patient described the

pain as a deep pressure
that was unrelieved by rest,
antacids, or an oral
nitroglycerin spray.

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Patient History
Obtained on admission to the ED
• Diagnosed with stable angina, high cholesterol and
HTN roughly 7 years ago
• Type 2 DM for approximately two decades
• Cigarette smoker
(2 packs / day for past 45 years)

Why is this data significant?

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Atherosclerosis

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Current Medications
• Aspirin (ASA) 81 mg (taken on route to ED)
• Metoprolol 100 mg
• Ramipril 10 mg
• Atorvastatin 40 mg
• Nitroglycerine spray (prn)

To what drug class do each of these medications

belong?

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Which statement regarding these
medications is CORRECT?
a) Beta blockers increase myocardial O2 supply by dilating
coronary arteries
b) ACE inhibitors block the release of renin from the kidneys,
thereby reducing blood volume and vascular resistance
c) ASA helps to break up established thrombus, thereby
restoring blood flow to the myocardium
d) Nitroglycerine dilates coronary arteries and has
antithrombotic effect, helping to relieve angina
e) Statins increase hepatic cholesterol synthesis and reduce
hepatic excretion of low density lipoproteins (LDL)

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ER Physical Assessment Data
• BP 160/100, HR 122, RR 34, Temp 36
• Individual in obvious distress
• Coherent, able to move all limbs spontaneously and
purposefully
• Skin cool, pale and diaphoretic; no peripheral edema
• Normal heart sounds; lung fields are clear
• Continues to experience SOB and chest pain
• Received O2 and Morphine

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ECG results
• Cardiac monitor reveals sinus tachycardia
• 12-lead ECG reveals an ST-segment elevation
suggesting a transmural MI has occurred

R R

S
T P
P T

Q S Q

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Question
For this client, which of the following ECG abnormalities
would likely persist, years after leaving the CCU?

a) ST-segment elevation
b) ST-segment depression
c) Deep or wide Q-wave
d) T-wave inversion
e) Reduced RR-interval

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Rationale

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Diagnostics
Which of the following is correctly matched?
Test: Allows for assessment/detection of:
Pulmonary vascular congestion and
a) X-ray ventricular dilation

b) Echocardiogram Extent of coronary arterial patency

c) Angiogram Heart valve function and heart wall

kinetics

d) PTT Electrical activity in right ventricle and

sino-atrial node
e) 15-lead ECG Hemostatic function (clotting cascade)
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Case Progression
Admitted to Coronary Care Unit (CCU)
• BP 150/100, HR 112, RR30
• Chest pain now mild, dull ache – no longer in obvious
distress
• Patient receives carvedilol IV
• Nitroglycerin IV is started

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A turn for the worse...
• 1 hour later the patient experiences a sudden onset
of shortness of breath (SOB)
• Auscultation – reveals diffuse crackles throughout
both lung fields
• 10 minutes later – patient reports severe chest pain
• HR 130, BP 140/100
• 12-lead ECG reveals a left bundle branch block
• O2 and nitroglycerin infusion increased

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Left Bundle Branch Block

Common sites for

atherosclerotic
plaque formation

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Which intervention would be most
appropriate at this time?
a) Increase O2 administration to 100% to ensure
myocardial demands are met
b) Administer a beta-agonist to improve cardiac output
by increasing HR and contractility
c) Initiate reperfusion therapy involving fibrinolysis,
PCI and/or CABG
d) Administer an ACE-I or ARB to reduced cardiac
workload

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A slippery slope...
The patient continues to experience chest pain and SOB and
becomes increasingly restless and agitated
• 100% O2 and nitroglycerin increased with no improvement
• BP 40/? - nitroglycerine halted
• BP 80/? – jugular venous distension noted as well as crackles
throughout the lungs

You suspect that the patient has developed Acute Heart

Failure...

Abnormal heart function with signs & symptoms of low cardiac

output and/or pulmonary/systemic congestion
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Left VS Right Hear Failure

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Other types of heart failure
• Systolic vs Diastolic
– Impaired ventricular contraction
– Inadequate ventricular filling
• Acute vs Chronic
– Sudden – no compensatory mechanisms
– Insidious onset – compensatory mechanisms with
remodeling (hypertrophy / dilation)

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Question
What endogenous hormone helps to reduce preload?

a) Anti-diuretic hormone
b) Angiotensin II
c) Aldosterone
d) Atrial natriuretic peptide

Nesiritide, a synthetic form of brain natriuretic peptide, can

be used to treat volume overload in decompensated HF
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Take home messages
• While the heart pumps blood to deliver O2 and
nutrients to the tissues, the heart must also be
adequately perfused to stay alive...
• ACS – a spectrum of ischemic diseases – can cause HF
• Heart Failure is a condition of abnormal pumping
function leading to pulm/systemic signs/symptoms
• Overall goal of therapy is to preserve myocardial
tissue by inc. perfusion and dec. workload
– Directly relates to QoL
Time is tissue!
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