Group 8. Problem based learning. Patient cases with heart failure and mcc.

Coronary artery disease (mcc)

Ethiology
Myocardial damage associated with a lack or cessation of blood supply to the heart, which leads
to ischemia or oxygen starvation of the heart muscle.
The disease can manifest itself in chronic (angina pectoris, post-infarct arteriosclerosis, heart
failure) or acute (cardiac arrest, heart attack) forms.
The causes of mcc are:
-arteriopathy (97-98% of cases are associated with total or partial occlusion of the artery by
lipoproteins) Coronary artery disease starts when fats, cholesterols and other substances collect
on the inner walls of the heart arteries. This condition is called atherosclerosis. The buildup is
called plaque. Plaque can cause the arteries to narrow, blocking blood flow. The plaque can also
burst, leading to a blood clot.
-thromboembolism
-spasm of the coronary arteries
-hyperlipidemia
-high BP
-smoking
-hypodenamia and obesity
Presenting Complains
The coronary arthery disease does not give visual symptoms until the actual result comes. Patient
can live their lives without knowing that something is wrong, when soon we will notice
complains about angina pectories, or even heart attack.
Signs and Symptoms
1) Chest pain ( angina pectories) – you may feel discomfort or feeling that somebody is
stading on your chest. The pain usually occurs on the middle or by lest side of the chest.
Stable angina is the one that comes with coronary artery disease, so you will experince
the pain durign physical activities.
2) Shortness of breath
3) Fatigue
4) Heart attack
Pathophysiology
The development of coronary heart disease is based on an imbalance between the need of the
heart muscle for blood supply and the actual coronary blood flow. This imbalance can develop
due to a sharply increased need of the myocardium for blood supply, but its insufficient
implementation, or with normal need, but a sharp decrease in coronary circulation. The
deficiency of myocardial blood supply is especially pronounced in cases where coronary blood
flow is reduced, and the need of the heart muscle for blood flow increases sharply. Insufficient
blood supply to the tissues of the heart, their oxygen starvation is manifested in various forms of
coronary heart disease.
Atherosclerosis is caused by an inflammatory process. The initial stage in atherosclerosis
developmentoccurs when the normal functioning of endothelial cells which allow smooth flow
of blood along the vesselis disrupted. The trigger is an inflammatory response, with release of
cytokines and cell surface adhesionmolecules such as VCAM-1, causing monocytes and T
lymphocytes to adhere to the endothelium. A changing shape of the endothelial cells increases
the permeability of the arterial wall, allowing lymphocytes and lipoprotein particles, especially
low-density lipoprotein (LDL), to enter the intima. Once under the endothelial surface,
monocytes differentiate into macrophages, take up oxidized LDL, and become lipid-laden ‘foam
cells’ which eventually die, but the lipid accumulates forming fatty streaks which evolve
overtime into atherosclerotic plaques. These plaques, composed of a lipid core surrounded by
smooth musclecells and connective tissue fibres, may undergo calcification. In the initial stages
of the development ofcoronary atherosclerosis, the diameter of the arterial lumen remains
unaffected as there is expansion of themedia and the external elastic membrane during atheroma
development (known as positive remodelling).
Investigations
 EKG – in order to diagnose how the heart is functioning; if the situation is critical you
may see ST elevation (heart attack) or NSTEMI. Usually, when we are talking about
EKG, we are trying to explain the nature of stable angina. NSTEMI is differentiated from
STEMI using an electrocardiogram (ECG). NSTEMI rarely progresses to STEMI because it tends
to affect minor blood vessels servicing the heart.
 Echocardiogram – shows how blood moves to the heart and what are the heart beats
 Exercise stress test – this one is done with ECG or echocardiogram. If you cannot
exercise, you will be given medication, that will imitate the physical activity to your
heart.
 Nuclear stress test – similar to the the exercise stress test, but also adds images to ECG of
how heart functions and blood flows during stress and at rest
 CT scan – can show Calcium deposits. Sometimes the dye is used, and if so, the test is
called – CT coronary angiogram
 Cardiac catheterasation or angiogram – the tube inserts to the groin or to the wrist and
gently guided to the hear using the X-ray. Dye flows through the catheter and makes the
picture more visible. If you have an artery blockage that needs treatment the baloon on
the tip of the catheter can be inflated to open the artery. A mesh tube is used to keep
artery opened.
 LDL, HDL
 Triglycerids levels
 BP
 Blood sugars
 Lipoprotein apo
Diagnosing
To diagnose coronary artery disease, a health care provider will examine you. You'll likely be
asked questions about your medical history and any symptoms. Blood tests are usually done to
check your overall health.
Treatment
Treatment for coronary artery disease usually involves lifestyle changes such as not
smoking, eating healthy and exercising more. Sometimes, medications and procedures
are needed.

Medications

There are many drugs available to treat coronary artery disease, including:

 Cholesterol drugs. Medications can help lower bad cholesterol and reduce
plaque buildup in the arteries. Such drugs include statins, niacin, fibrates
and bile acid sequestrants.
 Aspirin. Aspirin helps thin the blood and prevent blood clots. Daily low-dose
aspirin therapy may be recommended for the primary prevention of heart
attack or stroke in some people.

Daily use of aspirin can have serious side effects, including bleeding in the
stomach and intestines. Don't start taking a daily aspirin without talking to
your health care provider.

 Beta blockers. These drugs slow the heart rate. They also lower blood
pressure. If you've had a heart attack, beta blockers may reduce the risk of
future attacks.
 Calcium channel blockers. One of these drugs may be recommended if
you can't take beta blockers or beta blockers don't work. Calcium channel
blockers can help improve symptoms of chest pain.
 Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II
receptor blockers (ARBs). These medicines lower blood pressure. They
may help keep coronary artery disease from getting worse.
 Nitroglycerin. This medicine widens the heart arteries. It can help control
or relieve chest pain. Nitroglycerin is available as a pill, spray or patch.
 Ranolazine. This medication may help people with chest pain (angina). It
may be prescribed with or instead of a beta blocker.
Patient’s case

A 67-year-old woman sought emergency medical care due to prolonged chest pain. In
April 2009 the patient had prolonged chest pain and at that time she sought medical care.
She was admitted at the hospital and diagnosed with myocardial infarction.

The patient had hypertension, diabetes mellitus, dyslipidemia and was a smoker.

During the patient's evolution, after the myocardial infarction, she was submitted to a
coronary angiography in, which disclosed the presence of lesions with 70% obstruction in
the right coronary, anterior descending and circumflex arteries.
Heart failure
Ethiology
Heart failure occurs when the heart muscle doesn't pump blood as well as it should. When this happens,
blood often backs up and fluid can build up in the lungs, causing shortness of breath.
Certain heart conditions gradually leave the heart too weak or stiff to fill and pump blood properly. These
conditions include narrowed arteries in the heart and high blood pressure.

There are different types of heart failure:

1)Left-sided heart failure
2)Right-sided heart failure
3)High-output heart failure (This is the rare type of conjestive hear failure)
We will look through the causes based on this 3 types of the heart failure:
Left-sided heart failure
This condition occurs when the lest side of the heart does not functioning properly and cannot
sufficiently pump blood to the orgars causing the blood build-up to the lungs and organ damage.
We can divide this type in 2:
-Systolic heart failure (which happens when the ventricle cannot pump the blood to organs,
because of its weakness. This condition is also known as reduced ejection fracture.
- Diastolic heart failure (which is explaned by stiffening of the heart muscle, so it cannot relax
properly). The common name that can be used is preserved ejection fracture.
The causes can be:
 Coronary artery disease
 Heart attack
 High blood pressure
 Valvular heart disease
 Abnormal heart rhythms
 Infiltrating diseases such as amyloid or sarcoid
Right-sided heart failure
Right-sided heart failure is also called right ventricular heart failure.
The causes:

 Blood builds up in your veins, vessels that carry blood from the body back to the
heart.
 This buildup increases pressure in your veins.
 The pressure pushes fluid out of your veins and into other tissue.
 Fluid builds up in your legs, abdomen or other areas of your body, causing
swelling.
The signs and symptoms:

1. Shortness of breath (dyspnea), especially during physical activity or when lying

flat.
2. Persistent coughing or wheezing, often accompanied by white or pink blood-
tinged phlegm.
3. Fatigue and weakness, especially during physical exertion.
4. Swelling (edema) in the legs, ankles, feet, or abdomen due to fluid retention.
5. Rapid or irregular heartbeat (palpitations).
6. Reduced ability to exercise.
7. Sudden weight gain due to fluid retention.
8. Loss of appetite and nausea.
9. Difficulty concentrating or decreased alertness.
10. Increased need to urinate at night (nocturia).
11. Swelling or enlargement of the liver and abdomen.
12. Decreased ability to concentrate or decreased alertness.
13. Dizziness or lightheadedness.

Pathphysiology
The pathophysiology of heart failure involves a complex interplay of various mechanisms that
ultimately result in the heart's inability to pump blood efficiently to meet the body's demands.
Here's a simplified overview:

1. Impaired Cardiac Function: Heart failure often begins with an underlying condition
that damages the heart muscle, such as coronary artery disease, hypertension, myocardial
infarction (heart attack), or cardiomyopathy. These conditions can lead to structural
changes in the heart, including chamber enlargement, thickening of the heart muscle
(hypertrophy), or scarring, all of which impair the heart's ability to pump effectively.
2. Reduced Cardiac Output: As the heart's pumping ability diminishes, it fails to eject an
adequate amount of blood with each contraction, leading to a reduction in cardiac output
—the amount of blood pumped by the heart per minute. This reduction in cardiac output
results in decreased oxygen delivery to tissues and organs throughout the body, leading to
symptoms such as fatigue and shortness of breath.
3. Activation of Neurohormonal Pathways: To compensate for reduced cardiac output,
the body activates various neurohormonal pathways, including the sympathetic nervous
system and the renin-angiotensin-aldosterone system (RAAS). These pathways aim to
increase heart rate, constrict blood vessels, and retain sodium and water to maintain blood
pressure and perfusion to vital organs. However, chronic activation of these pathways can
contribute to further cardiac remodeling and dysfunction over time.
4. Fluid Retention and Congestion: The activation of neurohormonal pathways leads to
fluid retention, primarily through the kidneys' retention of sodium and water. This fluid
accumulates in the body's tissues, leading to symptoms such as peripheral edema
(swelling of the legs, ankles, and feet), pulmonary congestion (fluid accumulation in the
lungs), and abdominal distension. Fluid overload exacerbates symptoms of heart failure
and can lead to complications such as pulmonary edema and pleural effusion.
5. Myocardial Remodeling and Fibrosis: Chronic stress on the heart muscle leads to
myocardial remodeling, characterized by changes in the heart's size, shape, and function.
This remodeling process involves cardiac hypertrophy, dilation of the heart chambers,
and the deposition of collagen (fibrosis) in the myocardium. While initially adaptive,
 these changes ultimately contribute to further impairment of cardiac function and
exacerbate heart failure progression.

Overall, heart failure is a multifactorial condition resulting from a combination of underlying

cardiac dysfunction, compensatory neurohormonal activation, and maladaptive remodeling
processes. Effective management strategies aim to alleviate symptoms, slow disease progression,
and improve patients' quality of life by targeting these underlying pathophysiological
mechanisms.

Diagnosing
Diagnosing heart failure typically involves a combination of medical history, physical
examination, and various diagnostic tests. Here are some common investigations used
in the evaluation of heart failure:

1. Medical History and Physical Examination: The healthcare provider will start by
taking a detailed medical history, including symptoms, risk factors, past medical
conditions, and medications. A thorough physical examination will be conducted
to assess for signs of heart failure, such as abnormal heart sounds (e.g., murmurs,
gallops), fluid retention (edema), and abnormal lung sounds (e.g., crackles).
2. Blood Tests: Blood tests may be ordered to assess for markers of heart failure,
such as brain natriuretic peptide (BNP) and N-terminal pro-B-type natriuretic
peptide (NT-proBNP). Elevated levels of these peptides are indicative of
myocardial stress and can aid in the diagnosis and prognosis of heart failure.
3. Imaging Studies:
 Echocardiography: This non-invasive imaging test uses sound waves to
create detailed images of the heart's structure and function.
Echocardiography can assess for abnormalities in cardiac chambers, valves,
wall motion, ejection fraction, and the presence of pericardial effusion.
 Chest X-ray: A chest X-ray may be performed to evaluate for signs of
pulmonary congestion, such as pulmonary edema, cardiomegaly (enlarged
heart), and pleural effusions.
 Cardiac MRI: Cardiac magnetic resonance imaging (MRI) provides
detailed images of the heart's structure and function and may be used to
assess myocardial viability, myocardial fibrosis, and cardiac chamber
dimensions.
4. Electrocardiogram (ECG): An ECG records the heart's electrical activity and can
help identify rhythm disturbances, conduction abnormalities, and signs of
myocardial ischemia or infarction.
5. Exercise Stress Test: In some cases, an exercise stress test may be performed to
evaluate the heart's response to physical activity and assess exercise capacity.
This test can help identify exercise-induced symptoms and abnormalities in heart
rate, blood pressure, and ECG.
6. Cardiac Catheterization and Coronary Angiography: Invasive procedures such
as cardiac catheterization and coronary angiography may be performed to
evaluate coronary artery disease and assess for blockages or abnormalities in the
coronary arteries.
 7. Other Tests: Depending on the clinical presentation and suspected underlying
causes, additional tests such as pulmonary function tests, thyroid function tests,
and sleep studies may be ordered to assess for comorbid conditions contributing
to heart failure symptoms.

Treatment
The treatment of heart failure aims to improve symptoms, reduce the risk of disease progression,
prevent complications, and improve quality of life. It typically involves a combination of
lifestyle modifications, medications, and, in some cases, surgical interventions. Here's an
overview of the treatment options for heart failure:

1. Lifestyle Modifications:
 Dietary Changes: Following a heart-healthy diet low in sodium, saturated fats,
and cholesterol can help manage fluid retention and reduce the risk of
complications.
 Fluid Restriction: Limiting fluid intake may be recommended to prevent fluid
overload in individuals with advanced heart failure or severe symptoms.
 Regular Exercise: Engaging in regular physical activity, as tolerated, can
improve cardiovascular fitness, muscle strength, and overall well-being.
However, exercise should be tailored to each individual's capabilities and guided
by healthcare providers.
2. Medications:
 Angiotensin-Converting Enzyme (ACE) Inhibitors or Angiotensin II
Receptor Blockers (ARBs): These medications help dilate blood vessels, reduce
blood pressure, and improve cardiac function by blocking the effects of
angiotensin II, a hormone that causes vasoconstriction and sodium retention.
 Beta-Blockers: Beta-blockers slow the heart rate, reduce blood pressure, and
improve cardiac function by blocking the effects of adrenaline on the heart.
 Diuretics: Diuretics help eliminate excess fluid and sodium from the body,
reducing fluid retention and relieving symptoms such as edema and shortness of
breath.
 Aldosterone Antagonists: Medications such as spironolactone and eplerenone
block the effects of aldosterone, a hormone that promotes sodium and water
retention, to reduce fluid overload and improve outcomes in heart failure patients.
 Sacubitril/Valsartan (ARNI): This medication combines an angiotensin
receptor-neprilysin inhibitor (ARNI) with an angiotensin II receptor blocker
(ARB) to improve outcomes in certain patients with heart failure with reduced
ejection fraction (HFrEF).
 Digoxin: Digoxin may be used to improve symptoms and reduce hospitalizations
in patients with heart failure, particularly those with atrial fibrillation or persistent
symptoms despite optimal medical therapy.
3. Device Therapy:
 Implantable Cardioverter-Defibrillator (ICD): ICDs are implanted devices that
monitor heart rhythm and deliver electric shocks to restore normal heart rhythm in
the event of life-threatening arrhythmias.
 Cardiac Resynchronization Therapy (CRT): CRT involves implanting a
special pacemaker that coordinates the contractions of the heart's chambers to
improve cardiac function in patients with heart failure and conduction delays.
 Left Ventricular Assist Devices (LVADs): LVADs are mechanical pumps
implanted in the chest to help the heart pump blood in patients with severe heart
 failure who are awaiting heart transplantation or as destination therapy for those
who are not candidates for transplantation.
4. Surgical Interventions:
 Coronary Artery Bypass Grafting (CABG): CABG surgery may be
recommended to bypass blocked coronary arteries and improve blood flow to the
heart muscle in patients with coronary artery disease and heart failure.
 Heart Transplantation: Heart transplantation may be considered for patients
with end-stage heart failure who have failed medical therapy and are otherwise
healthy enough to undergo the procedure.
5. Education and Support:
 Patient education about heart failure, its management, medication adherence,
dietary restrictions, and symptom monitoring is crucial for optimizing treatment
outcomes.
 Cardiac rehabilitation programs provide structured exercise, education, and
support for patients with heart failure to improve cardiovascular health and
quality of life.

Treatment plans for heart failure are individualized based on the patient's symptoms, underlying
causes, disease severity, comorbidities, and response to therapy. Regular follow-up with
healthcare providers is essential for monitoring symptoms, adjusting medications, and
optimizing treatment outcomes.
Patient’s case

Patient Profile:

 Name: Mr. John Smith

 Age: 65
 Gender: Male
 Occupation: Retired
 Medical History: Hypertension, Type 2 Diabetes Mellitus, Hyperlipidemia

Chief Complaint: Mr. John Smith presents to the cardiology clinic with complaints of
increasing shortness of breath, especially with minimal exertion, and swelling in his
ankles over the past few weeks. He reports feeling fatigued and has noticed a decrease
in his ability to perform daily activities, such as climbing stairs or walking short
distances.

History of Present Illness: Mr. Smith reports that his symptoms started gradually and
have been worsening over the past month. He has also experienced episodes of
nocturnal coughing and orthopnea, where he feels short of breath when lying flat and
finds relief when sitting upright. He denies any chest pain or palpitations but mentions
occasional dizziness upon standing.

Past Medical History:

 Hypertension: Diagnosed 10 years ago, currently managed with amlodipine and

lisinopril.
  Type 2 Diabetes Mellitus: Diagnosed 15 years ago, managed with metformin and
glipizide.
 Hyperlipidemia: Diagnosed 5 years ago, managed with atorvastatin.
 No history of coronary artery disease or myocardial infarction.

Social History: Mr. Smith is a retired school teacher and lives with his wife. He reports a
sedentary lifestyle since retirement but denies smoking or alcohol use. He follows a
balanced diet but admits to occasional indulgence in salty snacks.

Family History: His father passed away from a stroke, and his mother had hypertension
and died of heart failure.

Physical Examination:

 Vital Signs: Blood pressure 150/90 mmHg, heart rate 90 bpm, respiratory rate 20
breaths/min, temperature 98.6°F (37°C)
 General: Appears fatigued, no acute distress
 Cardiovascular: Regular rhythm, no murmurs or gallops, jugular venous
distension, bilateral ankle edema
 Respiratory: Bilateral crackles heard in lung bases
 Abdomen: Soft and non-tender, no hepatomegaly or ascites
 Neurological: Alert and oriented, no focal deficits

Diagnostic Workup:

1. Electrocardiogram (ECG): Sinus rhythm, no significant ST-T wave changes.

2. Chest X-ray: Cardiomegaly, pulmonary congestion consistent with heart failure.
3. Echocardiography: Left ventricular ejection fraction (LVEF) of 35%, global
hypokinesis, mild mitral regurgitation, no significant valvular abnormalities.
4. Blood Tests: Elevated BNP levels (700 pg/mL), indicative of myocardial stress and
heart failure.

Diagnosis: Mr. John Smith is diagnosed with heart failure with reduced ejection fraction
(HFrEF), likely secondary to underlying hypertension and diabetes mellitus.

Treatment Plan:

1. Initiation of heart failure medications, including an ACE inhibitor (lisinopril) and a

beta-blocker (metoprolol succinate), titrated to target doses.
2. Diuretic therapy with furosemide to relieve fluid overload and symptoms of
congestion.
3. Dietary counseling to limit sodium intake and fluid restriction to manage fluid
retention.
4. Patient education on heart failure management, symptom monitoring,
medication adherence, and lifestyle modifications.
5. Close follow-up with cardiology for symptom assessment, medication
adjustments, and optimization of treatment.