An overview of important cardiac conditions

1. Coronary Heart Disease,
Myocardial Infarction,
and Heart Failure
Provided Courtesy of Nutrition.com
Review Date 12/13
G-0967
A Review of the Basics

2. Defining Heart Disease
Heart disease is a broad term used to describe a
range of diseases that affect your heart, such as:
• Coronary heart disease (CHD)
• Atherosclerosis
• Myocardial infarction (MI)
• Heart failure (formerly called congestive heart
failure)

3. Risk Factors for CHD
and MI
• Smoking
• High intake of alcohol
• Obesity
• Sedentary lifestyle
• Diabetes
• Hypertension

4. Risk Factors for CHD
and MI (cont’d)
• More than 34 years of age for males and
55 years of age for females (risk increases after
menopause)
• Family history—genetics
• Hypertension
• Stress
• Chronic kidney disease

5. Risk Factors for CHD
and MI (cont’d)
• High low-density lipoprotein (LDL) cholesterol
• Low high-density lipoprotein (HDL) cholesterol
• Left ventricular hypertrophy

6. Risk Factors
for Heart Failure
• Obesity
• Hypertension
• Overweight or obesity
• Ischemic heart disease
• Changes in cardiovascular structure, such as
diseases to the heart valves or muscle

7. Coronary Heart
Disease: An Overview
• Blood flow to the vessels surrounding the
heart is blocked
• The major underlying cause of CHD is
atherosclerosis or a buildup of plaque in
the arteries

8. Plaque Development
• Many factors speed up plaque development:
̶ Elevated cholesterol and triglyceride levels
̶ Hypertension
̶ Infection that initiates the inflammatory response
̶ Elevated iron levels—carry free radicals that damage lining
̶ Elevated homocysteine level
̶ Cigarette smoking
̶ Diabetes
̶ Obesity
̶ Oxidized (LDL) levels

9. The Atherosclerotic
Process
• Buildup of smooth muscle cells, macrophages,
and lymphocytes
• Smooth muscle cells form a matrix of
connective tissue
• Lipid and cholesterol accumulates in the matrix

10. The Atherosclerotic
Process (cont’d)
• Lipid deposits and other materials (including
cellular waste, fibrin, and calcium) build up and
form a plaque
• After injury, platelets adhere to the arterial wall
and release growth factors, which promote
lesion development

11. Coronary Heart Disease
Development
• Steps to development of CHD:
̶ Fatty streaks form, often in people younger than
30 years of age
̶ People are asymptomatic during this first stage of CHD
̶ Plasma LDL enters the injured endothelial wall and
forms a plaque that sometimes is prone to rupture
̶ Acute, complicated lesions with rupture and either
nonocclusive or occlusive thrombus form (occlusive
form often results in MI and sudden death)
̶ Hemorrhage into plaque produces thrombi—thrombus
formation with arterial lumen initiated

12. Coronary Heart Disease
Development (cont’d)
• Steps to development of CHD (cont’d):
̶ Progressive narrowing of lumen
̶ Insufficient blood flow to myocardium (ischemia) results
̶ Chest pain or angina pectoris occurs

13. Signs and Symptoms of
Coronary Heart Disease
• Chest pain
• Hypertension
• Increased pulse
• Increased respiration
• Dyspnea on exertion
• Pallor of skin
• Light-headedness with exertion
• Diminished peripheral pulses
• Intermittent claudication—cramping of the lower
extremities

14. Treatment of Coronary
Heart Disease
• Antihyperlipidemic agents
• Medications that lower triglycerides
• Antiplatelets (aspirin)
• Antihypertensives
• Antianginals (nitroglycerin)
• Antimicrobials

15. Angina Pectoris:
An Overview
• Chest pain caused by myocardial ischemia from
reduced blood flow and/or reduced oxygen supply
to the myocardium
• Angina is a warning sign that a heart attack (MI)
may occur

16. Angina Pectoris:
An Overview (cont’d)
• Aerobic metabolism switches to anaerobic
metabolism:
̶ Lactic acid buildup
̶ Release of histamine, bradykinins, and enzymes, which
stimulate nerve fibers in the myocardium, sending pain
impulses to the central nervous system

17. Angina Pectoris:
An Overview (cont’d)
• Other causes of decreased oxygen supply to the
myocardium:
̶ Congestive heart failure
̶ Congenital heart defects
̶ Pulmonary hypertension
̶ Left ventricular hypertrophy
̶ Cardiomyopathy
̶ Severe hypertension
̶ Narrowing of the aortic valve

18. Angina Pectoris:
An Overview (cont’d)
• Other causes of decreased oxygen supply to the
myocardium (cont’d):
̶ Leakage of the aortic valve
̶ Ventricle wall thickening
̶ Atheroma leading to arterial narrowing
• Silent ischemia—decreased oxygen supply with no
pain

19. Causes of Increased
Oxygen Demand
• Causes of increased oxygen demand on the
myocardium:
̶ Anemia
̶ Exercise
̶ Thyrotoxicosis
̶ Substance abuse, particularly cocaine
̶ Hyperthyroidism
̶ Emotional stress

20. Four Types of Angina
• Stable:
̶ Caused by specific amount of activity
̶ Predictable
̶ Relieved with rest and nitrates
• Unstable:
̶ Pain occurs with increasing frequency, severity, and
duration over time
̶ Unpredictable
̶ May occur at rest
̶ High risk for MI

21. Four Types of Angina
(cont’d)
• Prinzmetal’s (variant):
̶ Has no identified cause
̶ May occur at same time of day
̶ May intensify or worsen over time
̶ Is usually caused by coronary artery spasm
• Angina decubitus:
̶ Occurs when a person is lying down with no cause
̶ Occurs because gravity redistributes body fluids

22. Signs and Symptoms
of Angina
• Pressure or heaviness in chest beneath
breastbone—women are likely to have unusual
types of chest discomfort
• Pain may occur down shoulder or inside of arms,
or in the throat, jaw, or teeth
• Stomach pain, especially after eating
• Sweating

23. Signs and Symptoms
of Angina (cont’d)
• Light-headedness
• Hypotension
• Pulse changes
• Indigestion

24. Treatment of Angina
• Antianginals (nitroglycerin)
• Antiplatelets (aspirin)
• ACE inhibitors
• Beta-blockers
• Calcium channel blockers
• Thrombolytic therapy (if thrombi are the cause)
• Oxygen administration
• Percutaneous transluminal coronary angioplasty or
coronary artery bypass graft to prevent MI

25. Myocardial Infarction:
An Overview
• Death of cells in the myocardium, usually related
to prolonged or severe ischemia
• Necrosis, tissue damage, and sometimes death
results
• Cause of MI include:
̶ Sudden onset of ventricular fibrillation
̶ Embolus (most common cause)
̶ Thrombosis
̶ Atherosclerotic occlusion
̶ Prolonged vasospasm

26. Myocardial Infarction
Progression
• Cellular injury occurs from lack of oxygen:
̶ If prolonged, will lead to cell death
• Scar replaces muscle, but cannot contract or
conduct impulses:
̶ Location of damage is determined by which artery is
blocked
• Damage begins at subendocardial level:
̶ Will progress to the epicardium within 1 to 6 hours

27. Myocardial Infarction
Progression (cont’d)
• Damaged cells lead to decreased contractility:
̶ Less blood ejected by left ventricle with each beat
̶ Decreased blood pressure
̶ Decreased tissue perfusion

28. • Pain, typically in middle of chest, radiating to
jaws, arms (usually the left), abdomen, and/or
shoulders, and lasting 20 minutes:
̶ Possible to have no pain or atypical pan (particularly
in females)
̶ Sudden onset of pain, not associated with activity
Myocardial Infarction:
Signs and Symptoms

29. Myocardial Infarction:
Signs and Symptoms
(cont’d)
• Tachycardia
• Excessive perspiration
• Painful breathing and/or difficulty breathing
• Anxiety/panic
• Nausea/vomiting
• Fever
• Stomach pain, often confused with indigestion

30. Laboratory Evaluation
• Creatinine kinase
• Trophin
• Myoglobin

31. Myocardial Infarction
Complications
• If more than 50% of heart tissue is damaged,
severe disability or death will result

32. Myocardial Infarction
Complications (cont’d)
• Pericarditis may develop up to 2 months later:
̶ Fever
̶ Pericardial effusion
̶ Pleurisy
̶ Pleural effusion
̶ Joint pain
̶ Rupture of heart muscle
̶ Ventricular aneurysm
̶ Blood clots
̶ Hypotension

33. Treatment Following
Myocardial Infarction
• Antianginals (nitroglycerin)
• Analgesics
• Electrolyte replacement
• Calcium channel blockers
• Beta-blockers
• Antihypertensives
• Anticoagulants

34. Treatment Following
Myocardial Infarction
(cont’d)
• Antiarrhythmics
• Thrombolytics
• Oxygen
• Mild antianxiety agents

35. Heart Failure:
An Overview
• Inability of the heart to pump sufficiently to meet
metabolic needs, leading to decreased tissue
perfusion as a result of decreased cardiac output
• Acute or chronic
• Left sided or right sided
• Systolic or diastolic

36. Causes of Heart Failure
• Hypertension
• MI
• Cardiomyopathies
• Congenital heart disease
• Valve disorders
• Side effect of medication or alcohol

37. Types of Heart Failure
• Systolic dysfunction:
̶ Heart contracts with less force and cannot pump out as
much blood to the rest of the body as normal
̶ Blood accumulates in the ventricles and veins
• Diastolic dysfunction:
̶ Heart is stiff and does not relax after contracting
̶ Heart does not allow as much blood to enter its
chambers from the veins, and the blood accumulates in
the veins

38. Types of Heart Failure
(cont’d)
• Left sided:
̶ More common
̶ Fluid backs into lungs
̶ Signs and symptoms include:
•Fatigue
•Activity intolerance
•Dizziness
•Syncope
•Dyspnea
•Coughing
•Pulmonary crackles
•Tacycardia
• urine output
•Shortness of breath
when lying down

39. Types of Heart Failure
(cont’d)
• Right sided:
̶ Caused by pulmonary hypertension or right ventricular
infarction
̶ Fluid backs into rest of body, with abdominal organ
congestion and peripheral edema
̶ Signs and symptoms include:
•Lower extremity edema
in the ambulatory
•Sacral edema in the
bedridden
•Liver engorgement and right
upper quadrant pain
•Anorexia and nausea
•Jugular venous distension

40. Types of Heart Failure
(cont’d)
• Biventricular (signs and symptoms of both left and
right heart failure):
̶ Signs and symptoms include:
•All symptoms of right and
left heart failure
•Dyspnea at rest
•Hepatomegaly and
splenomegaly
•Abdominal pressure
•Ascites
•Anorexia
•Nausea and vomiting
• digestion and absorption of
nutrients
•Dysrhythmias
•Cardiogenic shock or acute
pulmonary edema

41. Cardiac Cachexia
• 10% to 15% of patients with heart failure
develop cardiac cachexia
• Loss of 6% of nonedematous body weight
over 6 months
• Concurrent loss of cardiac muscle mass as a
result

42. Cardiac Cachexia
(cont’d)
• Many other metabolic changes:
̶ Increased catabolic catecholamines
̶ Tumor necrosis factor is increased, contributing to
a lower body mass index and catabolic state

43. Treatment of Coronary
Heart Disease
• Diuretics
• Dopamine
• Analgesics
• Antihypertensives
• ACE inhibitors
• Direct vasodilators
• Antidysrhythmics
• Cardiac glycosides (digitalis)
• Aldosterone agonists

44. Treatment of Coronary
Heart Disease (cont’d)
• Antibiotics, if necessary
• Iron supplementation, if necessary
• Supplemental oxygen
• Nitrates
• Beta-blockers
• Anticoagulants

45. References
Academy of Nutrition and Dietetics. Nutrition Care Manual ®
[by subscription]. Nutrition Care Manual Web site.
www.nutritioncaremanual.org. Accessed December 1, 2013.
Cleveland Clinic. Acute myocardial infarction. Cleveland Clinic Center of
Continuing Education Web site.
http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/
cardiology/acute-myocardial-infarction/. Accessed
December 1, 2013.
Cleveland Clinic. Heart failure. Cleveland Clinic Center for Continuing
Education Web site.
http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/
cardiology/heart-failure. Accessed December 1, 2013.

46. References (cont’d)
Raymond JL, Couch SC. Medical nutrition therapy for cardiovascular
disease. In: Mahan, LK, Escott-Stump S, Raymond JL. Krause’s Food and
the Nutrition Care Process. 13th ed. St Louis, MO: Elsevier Saunders;
2012:742-781.
The Merck Manual for Health Care Professionals. Cardiovascular
disorders. Merck Manuals Web site.
http://www.merckmanuals.com/professional/cardiovascular_disorders.ht
ml. Accessed December 1, 2013.
What is angina? National Heart, Lung, and Blood Institute Web site.
http://www.nhlbi.nih.gov/health/health-topics/topics/angina/. Accessed
December 1, 2013.