Exam 3 [Diseases Of Heart] Flashcards
Cause of Ischemic Heart Disease
Usually atherosclerosis
Cause of Hypertension Heart Disease
Obesity -> Hypertension -> Atherosclerosis
Cause of Valvular Disease
May be Congenital or a Complication of other Heart Diseases
Heart diseases that cause Valvular disease
- Rheumatic fever
- Infective Endocarditis
- Ischemic heart Disease
- Cardiomyopathies
Major Manifestations of Heart Disease
- Pain
- Change in Size (usually enlargement)
- Failure
- Arrythmias
Hypertrophy Definition
Increased muscle mass of a ventricle (decreasing size of chamber)
Heart Dilation definition
- Heart muscles becomes flabby/hypotonic
- Ventricle stretches (enlarging the chamber)
Cause of Arrythmias
- Ischemia
- Myocarditis
- Drugs
- Electrolyte abnormalities
Effect of an Arrythmia
Decreased Cardiac Output
Cause of “Low Output Failure” & What is “Low Output Failure”?
Caused by heart disease, failure of the pump
Cause of “High Output Failure” & What is “High Output Failure”?
Caused by diseases not of the myocardium, Heart can’t pump fast enough to meet tissues needs
Example of Low Output Failure
- Acute MI
- Cardiac Tamponade
- tension Pneumothorax
- Pulmonary Embolism
- Acute Valve failure
Example of High Output Failure
- Anemia
- Hyperthyroidism
- Pregnancy
What is “Forward Failure”?
Failure of delivery of the correct amount of blood to the tissues
What is “Backward Failure”?
Congestion of blood in the venous system due to failure of heart to keep blood circulating
Examples of Left Ventricular Failure:
1) Ischemic heart Disease
2) Hypertensive Heart Disease
3) Aortic OR Mitral Valve disease
4) Myocarditis
5) Cardiomyopathy
6) Cardiac Amyloidosis
7) High Out-Put States
Examples of Right Ventricular Failure:
1) MC: Left Ventricular Failure
2) Chronic Pulmonary Disease (cor pulmonale)
3) Pulmonary OR Tricuspid Valve Stenosis
4) Congenital Heart Disease
What is the most common cause of isolated Right Ventricular Failure?
Chronic Pulmonary Disease (cor pulmonale)
Systemic Effects of Acute LVF (forward failure)
1) Hypotension
2) Syncope
3) Cardiogenic Shock
4) Sudden Death
Systemic Effects of Acute LVF (backward failure)
Pulmonary Edema
Systemic Effects of Chronic LVF (forward failure)
1) Ischemia of all organs
2) Hypoxia of Kidneys (Sodium/Fluid retention)
Systemic Effects of Chronic LVF (backward failure)
Pulmonary Congestion
Systemic Effects of Acute RVF (forward failure)
Sudden Death
Systemic Effects of Acute RVF (backward failure)
Sudden, Painful Swelling of the Liver & Increased Jugular Venous Pressure
Systemic Effects of Chronic RVF (forward failure)
No Clinical Consequences
Systemic Effects of Chronic RVF (backward failure)
- Swelling of ankles
- Venous Congestion of Liver “Nutmeg Liver”
- Increased Jugular Venous Pressure
- Hypoxia of Kidneys (Sodium/Fluid retention)
4 Types of Ischemic heart Disease
1) Angina Pectoris
2) Chronic Ischemic heart Disease
3) Myocardial infarction
4) Sudden Cardiac Death
When does “Typical (Stable)” Angina Pectoris become a problem?
When Vessel is narrowed 75% or more of the area of the Lumen
Cause of “Typical (Stable)” Angina Pectoris
Atherosclerosis
Symptoms of “Typical (Stable)” Angina Pectoris
- Recurrent chest pain w/ activity or stress
- Pain is limited in duration & relieved by rest
- Pain usually Substernal OR radiates to left arm, jaw & upper abdomen
What medication can decrease “Typical (Stable)” Angina Pectoris Pain?
Sublingual Nitroglycerin (Vasodilator)
“Unstable” Angina Pectoris is associated with
Atherosclerosis
Cause of “Unstable” Angina Pectoris
Worsening symptoms of angina due to Thrombus formation over plaque of atherosclerosis
What brings on the symptoms of “Unstable” Angina Pectoris?
Exercise
- less exercise needed to bring symptoms as time passes, eventually rest can bring symptoms
“Unstable” Angina Pectoris is also known as:
Crescendo Angina because it usually ends in a Myocardial Infarction
Cause of “Variant (Prinzmetal)” Angina Pectoris
- Unknown
- But it is due to Vasospasm NOT ATHEROSCLEROSIS
When does pain occur in “Variant (Prinzmetal)” Angina Pectoris?
Often at rest
Heart Attack = ???
MI = ???
Heart Attack = Clinical Syndrome
MI = Autopsy Finding
“A heart attack may not be produced by an AMI”
Myocardial Infarction Risk Factors:
1) Atherosclerosis
2) Systemic Hypertetion
3) Diabetes Mellitus
4) Smoking
5) Emotional Stress/ Physical Activity
6) Hypoxia (anemia or respiratory diseases)
What heart layers are damaged by Myocardial Infarction?
Endocardium or Pericardium
+ necrosis of muscle
Most Myocardial Infarction’s affect what chamber of the heart?
Left Ventricle
Arteries MCly causing a Myocardial Infarction & their Percentages
Right Coronary Artery (30%)
Left Anterior Descending Artery (50%)
Left Circumflex Artery (20%)
Enzymatic Proteins in Myocardial Infarction & When they rise
Troponins
CPK-MB (rise in 3-6 hours, peak at 18-24 hours)
SGOT & LDH also rise
ECG Features in a Myocardial Infarction
Elevation of ST Segment + Q Waves
- T wave Inversion
Risk Factors of Chronic Ischemic Heart Disease (Ischemic Cardiomyopathy)
1) Patchy loss of muscle w/ fibrosis and inflammatory cells
2) Chronic LVF or an arrhythmia (such as a heart block)
What is Chronic Ischemic Heart Disease (Ischemic Cardiomyopathy)?
- Multiple atherosclerotic narrowing in the blood vessels
- Irregular chronic MI
Definition of Sudden Cardiac Death:
Unexpected death due to a lethal arrythmia such as asystole or sustained ventricular fibrilation
Risk Factors of Sudden Cardiac Death:
1) Patients w/ atherosclerosis
2) People who smoke cigarettes
What decreases most rapidly following cessation of smoking?
Risk of Sudden Cardiac Death
Risk factors of the development of Ischemic Heart Disease:
Are basically the same as for Atherosclerosis
(Incidence for CIHD is used from the measurement of incidence of atherosclerosis in a population)
Pathology of Hypertensive Heart Disease:
- Left ventricular hypertrophy
- Left ventricular failure (40% of deaths in hypertensive patients)
- Ischemic heart disease
Cause of Acute Cor Pulmonale
- Pulmonary Hypertension leading to increased pressure in R. Side of the heart
- Massive Pulmonary Embolism
Cause of Chronic Cor pulmonale
- COPD
- Autoimmune Diseases
- Blood clots in lungs
- Cystic Fibrosis
- Scarring of Lung tissue
- Severe Kyphoscoliosis
Pathophysiology of Acute Cor Pulmonale
- Increased pressure in R. Side of heart
- R. Ventricular dilatation & failure
Pathophysiology of Chronic Cor Pulmonale
- Increased R. Ventricular afterload
- Preserve’s stroke volume until Myocardium fails due to Ischemia or other pathological condition
Etiology of Mitral Stenosis
- Chronic Rheumatic heart Disease
- Female 9:1
Pathophysiology of Mitral Stenosis
- Increased resistance to transmittal flow
- Thickening of valve leaflets (narrowing the valve)
Etiology of Mitral Regurgitation
- 50% due to chronic rheumatic heart disease combined with aortic stenosis
- “Fen-Phen” induced valvular fibrosis
Mitral Valve prolapse is seen in what population?
1% of young adults (mostly females)
Mitral Valve prolapse is due to:
Degeneration of the valve
(A.k.a. “Floppy Valve Syndrome”)
Rupture of what can lead to Mitral Regurgitation?
- Chordate Tendinae (due to endocarditis)
- Papillary muscles (due to MI)
Pathophysiology of Mitral Regurgitation
- Volume & pressure is transmitted backward from left atrium to the pulmonary vasculature
- disruption of the papillary muscles, chordate tendinae or valve leaflets (chronic = L. Ventricle)
Etiology of Aortic Stenosis
- Rheumatic Aortis Stenosis
- Congenital bicuspid valves (50% of cases)
- Hypertrophic cardiomyopathy
Pathophysiology of Aortic Stenosis
- Ventricle can no longer compensate -> L. Ventricle enlargement
- Reduced ejection fraction & CO
- Lipid accumulation
- Inflammation
- Calcification & Fibrosis of the valve
Etiology of Aortic Regurgitation
- Rheumatic heart disease (50%) usually associated with aortic stenosis & mitral valve disease
- Syphilitic Aneurysm
- Valve rupture due to endocarditis
Pathophysiology of Aortic Regurgitation
- Increase in regurgitation volume in L. Ventricle
- Poor forward flow
- Diastolic pressure increases -> acute pulmonary edema & cardiogenic shock
Examples of Pulmonary Valve Stenosis
1) Congenital
2) Tetralogy of Fallot
3) Carcinoid Syndrome
Populations affected by Rheumatic Fever
- children 5-15 years old
- lower social economic groups
Etiology of Rheumatic fever
- Occurs 2-6 weeks following streptococcal pharyngitis
- Group A streptococcus (streptococcus pyogenes)
Antigen/Antibodies in Rheumatic Fever
- Associated w/ HLA-B5 antigen
- Cross reacting antibodies (hypersensitivity Type II)
Rheumatic Fever affects what layers of the heart?
All of Them
Acute vs. Chronic presentation of Rheumatic Fever
Acute = “acute rheumatic carditis”
Chronic = “chronic valvular deformities”
Affect of Rheumatic Fever on the Endocardium
Vegetations on the heart valves
Affect of Rheumatic Fever on the Myocardium
(Myocarditis)
- Becomes pale, flabby & hypotonic
- Aschoff Body = Characteristic Lesion***
Affect of Rheumatic Fever on the Pericardium
(Pericarditis) Only in the most severe cases
Clinical Features of Rheumatic Fever
- Fever
- Arthritis
- congestive heart failure, chest pain, shortness of breath
- fatigue
- chorea ( uncontrollable body movements)
What is Chronic Rheumatic Heart Disease?
Severe valvular scarring occurring weeks to years after acute rheumatic fever
Most common valvular lesions
1) Mitral Stenosis & Mitral Incompetence
2) Aortic Valve Lesions
3) Tricuspid Valve Lesions (10%)
Complications of Chronic Rheumatic Heart Disease
1) Bacterial Endocarditis
2) Mural thrombi in the Atria or Ventricles
3) Cor pulmonale
4) Congestive Heart failure
5) Adhesive Pericarditis
Nonbacterial Thrombotic Endocarditis Pathophysiology
- has vegetations
- nondestuctive
Libman-Sacks Endocarditis Pathophysiology
Immune complex sterile vegetations on heart valves
Acute Infective Endocarditis Organisms
Staph Aureus OR Streptococcus Pyogenes
Acute Infective Endocarditis Presentation
- Lasts less than 6 weeks
- May have completely normal heart
- may produce perforation of a valve
Subacute Infective Endocarditis Presentation
- Present longer than 6 weeks
- Patient has pre-existing cardiac abnormality
- Rarely perforates the valve
Subacute Infective Endocarditis Organisms
Staphlococcus Epidermis OR Streptococcus Viridans
Infective Endocarditis: Populations affected
1) Patients w/ Cardiac Abnormalities
2) Valve replacement surgery
3) Intravenous Drug abusers
Pathology of Infective Endocarditis
1) vegetations on endocardium of valves that contain organisms
2) often large, hemorrhagic & friable producing septic emboli
Complications of Infectious Endocarditis
1) Valve dysfunction w/ changing murmurs
2) Septic Emboli producing mycotic aneurysyms/abscesses
3) Immune complex diseases
4) Microinfarctions from Emboli
Causes of Infectious Myocarditis
1) Viral infections
2) bacterial
3) Protozoa
4) Fungi
5) helminths
Causes of Noninfectious Myocarditis
1) rheumatic fever
2) systemic lupus erthematosus
3) Allergic drug reactions
4) cardiac transplantation rejection
5) sarcoidosis
Causes of Dilated Cardiomyopathy
1) Post-Myocarditis
2) Alcohol Toxicity
3) Pregnancy
4) Chemical Toxicity
5) Idiopathic dilated cardiomyopathy
Pathology of Dilated Cardiomyopathy
- general enlargement/dilation
- poor contracting -> stagnant blood leading to mural thrombi & thromboemboli
- may produce Arrythmias
Populations affected in Dilated Cardiomyopathy
- MC 20-60 years old
- Men > Women
- May be familial distribution
Clinical aspects of Dilated Cardiomyopathy
- Progressive congestive cardiac failure
- Death
Management of Dilated Cardiomyopathy
Cardiac Transplant
Peripartum Cardiomyopathy
Exception (50% of patients recover spontaneously after pregnancy)
Causes of Hypertrophic Cardiomyopathy
- 50% Autosomal Dominant (chromosome 14)
- All else = Idiopathic
Pathology of Hypertrophic Cardiomyopathy
- Assymetric myocardial hypertrophy in the Interventricular Septum
- Heart weighs > 800 mg’s
- Ventricular outflow obstruction
- Dilated Left Atrium
Clinical Effects of Hypertrophic Cardiomyopathy
- Sudden death
- Dyspnea, syncope & dizziness
- systolic ejection murmur
- angina pain
Risks following Hypertrophic Cardiomyopathy
- Bacterial Endocarditis
- Progressive myocardial Fibrosis produces congestive cardiac failure
Causes of Restrictive Cardiomyopathy
1) Cardiac amyloidosis
2) Sarcoidosis
3) Radiation injury
4) Hemochromatosis
Pathology of Restrictive Cardiomyopathy
- ventricular muscle becomes rigid & loses compliance
- ventricle difficult to fill, but ejection is not forceful
Clinical Effects of Restrictive Cardiomyopathy
- Fatigue, Exertional Dyspnea, Anginal pain
- May have arrythmias (including heart blocks)
In later stages of Restrictive Cardiomyopathy…
Development of Congestive Cardiac Failure
Causes of Obliterative Cardiomyopathy
1) tropical endocardial fibrosis
2) eosinophilic endomyocardial fibrosis (Loffler’s Syndrome)
Pathology of Obliterative Cardiomyopathy
- Atria are normal sized
- Thick & Opaque Endocardium
- Thick Valves
-Endocardium Fibrosis extends to Myocardium - Eosinophil Infiltration
Clinical Features of Obliterative Cardiomyopathy
- Tropical form in equatorial Africa
- Major Fibrosis & eosinophilia of Cardiac Muscle
- Restrictive Disease
Obliterative Cardiomyopathy accounts for what percent of childhood Heart disease?
10%
Most common congenital defect diagnosed vs. most common that is prevalent:
Diagnosed: VSD
Most Prevalent: ASD (not diagnosed until adulthood)
Risk Factors of Congenital heart disease
1) In-Utero Infectinos
2) Chromosomal Defects
3) In-Utero Chemical Exposure (FAS)
4) In-Utero Radiation Exposure
5) Premature Delivery
Effects of Congenital heart disease
1) abnormal blood flow -> murmurs
2) Shunts of blood from one side of the heart to the other
3) Short circuits of blood through circulation
4) Infective Endocarditis
5) Failure to thrive
Presence or absence of a shunt percentages in Congenital heart disease
W/O: 20%
W/: 80%
Acyanotic Congenital Heart Diseases
With a Shunt there is no cyanosis because direction of blood flow is Left to Right
Cyanotic Congenital Heart Diseases
Right to Left shunt so it bypasses the lungs
Small VSD (maladie de Roger) Produces:
1) Produces low volume shunt in systole
2) Produces pansystolic murmur
Small VSD (maladie de Roger) Symptoms
-Few symptoms
- Defect decreases in size as child grows & may close spontaneously
What is a Large VSD
- Volume overload & hypertrophy of both ventricles
- Pansystolic murmur
What happens due to a Large VSD?
- Pulmonary Hypertension from increased pulmonary blood flow
- Thick & Narrow pulmonary vessels
- Eventually pressure in R. atrium increases so much that shunt flow decreases in volume & reverses itself
Patient with a LArge VSD are at risk for:
Infective Endocarditis
ASD Symptoms
(Usually none)
Patent Foramen Ovale doesnt produce symptoms, but functionally there is no movement of blood.
ASD Clinical features
- R. Ventricular Hypertrophy
- Delayed pulmonary valve closing (Split S2)
- Can produce a pulmonary ejection murmur
ASD Main Complication
- Pulmonary Hypertension
- Increased Righ side pressure
- Eventually reversal of the shunt
What is Patent Ductus Arteriosus
-Ductus Arteriosus fails to close after birth
- Premature Infants
What medication can potentially close ductus arteriosus?
Indomethacin
Patent Ductus Arteriosus Pathology
- Continual blood flow from aorta to pulmonary circulation -> Pulmonary Hypertension
- “Machinery murmur” during entire cardiac cycle
Left to Right Shunt Defects
1) VSD
2) ASD
3) Patent Ductus Arteriosus
Right to Left Shunt Defects
[THESE PRODUCE CYANOSIS]
1) Tetrlogy of Fallot
2) Transportation of the Great Vessels
3) Eisenmenger’s Syndrome
Tetralogy of Fallot Components
1) Over-riding Aorta
2) Pulmonary Stenosis
3) Right Ventricular Hypertrophy
4) Ventricular Septal Defect
Tetralogy of Fallot Pathology & Treatment
- Pulmonary. Stenosis increases R. Ventricle pressure
- Surgery
Tetralogy of Fallot Characteristic Behavior
Children running distance would have to squat down on their heels to equilibrate pressures
Transposition of the Great Vessels Pathology
-Truncus Arteriosus forms abnormally
- Pulmonary trunk arises from L. Ventricle
- Aorta arises from R. Ventricle
(2 separate circulations)
Transposition of the Great Vessels Fatality
Immediately unless Foramen Ovale & Ductus Arteriosus do not close
What is Eisenmenger’s Syndrome
- A reversal of a previously acyanotic shunt that now produces cyanosis
- Once shunt reverses -> fatal and no longer eligible for surgery
reversal of a shunt in Eisenmenger’s Syndrome makes the individual prone to:
Paradoxical Emboli
Chronic Adhesive Pericarditis
May occur following bacterial infection of the pericardium where there was pus formation and exudate in the pericardium
Chronic Restrictive Pericarditis
- Associated with Tuberculosis
- Tuberculosis Pericarditis encased the heart in fibrous tissue
Glycogen Storage Diseases that affect the heart
Pompe’s Disease
Myxoma
[Benign tumor of the heart]
- MC Primary Heart Tumor
- MC in Left Atrium
Pompe’s Disease “Glycogenosis Type II”: What is it?
- Autosomal Recessive
- Lysosomal storage disorder
- Alpha-Glucosidase (DAA) Deficiency
- cant metabolize glycogen
Pompe’s Disease “Glycogenosis Type II”: Accumulation of Glucose Causes what?
- Mental retardation
- enlarged heart, liver & spleen
- cardiac muscle failure
