Cardiovascular Flashcards
What valve has only 2 leaflets?
Mitral valve
3 layers of the heart wall
Epicardium: outer layer next to pericardial fluid
Myocardium: muscular part
Endocardium: next to blood
3 layers of blood vessels
Adventitia: connection between blood vessels and connective tissue (outer layer)
Media: contractile and smooth muscle
Endothelium: inner layer
Arteries versus veins for pressure, flow and walls
Veins have lower pressure, non-pulsatile flow, and thinner walls
Also have valves and bigger lumen
What is a congenital heart disease
Defects involving heart or large arteries and veins that are present at birth
3 general causes of congenital heart disease
- Heart developed and functional by 10th week of gestation (primitive tube that septates, twists, and segments)
- Endogenous causes (chromosomal)
- Exogenous causes (infections or toxins)
Atrial septal defect
and clinical presentations
Atrial septum is improperly closed
Various types
Clinical presentations: murmur, paradoxical emboli, infection, arrhythmia
Usually of minor consequence
Ventricular septal defect
and clinical presentations
Ventricular septum improperly closed
Various types
Clinical presentation: murmur, pulmonary hypertension, infection, cyanosis (late)
Spontaneous or surgical closure
Complex defects
Multiple anatomical abnormalities
Several types
Which disease has early versus late cyanosis
Late: ventricular septal defect
Early: Tetralogy of Fallot
Tetralogy of Fallot
10% of CHD
Clinical presentations: cyanosis (early), murmur, failure to thrive, infection
Requires surgical repair
4 problems in tetralogy of Fallot
- Overriding aorta
- Pulmonary stenosis
- Ventricular septal defect
- Right ventricle hypertrophy
Is atherosclerosis systemic or localized?
Systemic arterial disease
Usually involves multiple vascular territories so it is generalized
What hormone is protective against atherosclerosis?
Estrogen
What initiated atherosclerosis? (and 2 examples)
Initiated by endothelial injury
Ex: Physical (hypertension) or metabolic (diabetes, obesity)
Athero versus Sclero
Sclero is hard: collagen and calcified material
Athero is soft: lipids and necrotic debris
4 Modifiable risk factors
Dyslipidemia
Hypertension
Diabetes mellitus
Smoking
3 Not modifiable factors
Age
Sex
Family history
2 Protective factors
Exercise
Estrogen
Aortic dissection
Blood tunnels between aortic layers
Can appear as aneurysm
Unrelated to atherosclerosis
3 Aneurysm complications
Rupture
Thrombosis
Mass effect (impinges on other structures, like a tumor)
Claudication
Cramping in the legs when exercising, caused by obstruction of the arteries
Can only walk a very little bit before they get tired and have pain in their legs/feet/butt
4 presentations of ischemic heart disease
Angina pectoris
Acute myocardial infarction
Congestive heart failure
Sudden death
At what percentage of stenosis do you start to get major problems?
Over 50%
Then can get ischemic heart disease
Under 50% and the arteries can dilate enough that the lumen stays the same diameter
How can you date a myocardial infarction?
Its irreversible injury from ischemia too long, so can date ischemic myocyte death 1-4 days: cell death, neutrophils 4-5 days: macrophages 1-2 weeks: granulation tissue >2 weeks: scar formation
5 outcomes after ischemic heart disease
Thrombus Rupture of heart wall Aneurysm Congestive heart failure Death
2 things you can look for as serologic evidence of myocyte death
Troponin I/T
Creatinine kinase-MB
(levels of both increase)
What is infective endocarditis?
Infection of endocardial surfaces
Most often valvular
4 predisposing factors to infective endocarditis
Structural diseases
Skin or mucosal breaks (portals of entry)
Immunosuppression
Intracardiac devices and prostheses
What are the 3 main bacteria that cause infective endocarditis?
Staph
Strep
Enterococcus
What are the 2 main fungi that cause infective endocarditis
Candida
Aspergillus
Acute bacterial endocarditis
Febrile illness of sudden onset
Subacute bacterial endocarditis
A lingering weakness accompanied by mild temperature elevations that wax and wane over a prolonged period
Normal arterial blood pressure
120 (systolic) over 80 (distolic)
Measuring the left ventricle pressure
2 vasoactive substances
Epinephrine
Norepinephrine
What factor does contractility increase?
Stroke volume
What pressure is considered hypertension
140 over 90 or higher
Only need to have one
Essential disease
Same as primary
Dont know what the cause it
Aortic coarctation
Narrowing of the lower descending aorta
Correctabe with surgery
BP in legs will be much lower than in the arms
Cardiomegaly
Increase in heart weight
Reflects LV myocyte hypertrophy (increase in size)
Accompanied by interstitial fibrosis (stiff LV)
Takes many years to develop
Causes increased metabolic demands of the heart and leads to heart failure
Pressure hypertrophy versus volume hypertrophy
Pressure: increase in the ventricular thickness, narrowing of the lumen, new sarcomeres assemble in parallel
Volume: thickness stays the same but there is a lot of dilation going on, new sarcomeres assemble in series
Benign hypertension
Causes hyalinization of the arterioles and fibrosis of the wall of small arteries
Malignant hypertension
Sudden onset
Systolic pressure over 200, and diastolic over 100
May cause fibrinoid necrosis of these vessels and concentric proliferation of smooth muscles in arterioles (proliferative endarteriolitis)
Proliferative endarteriolitis
In malignant hypertension
May cause fibrinoid necrosis of these vessels and concentric proliferation of smooth muscles in arterioles
Hypertensive encephalopathy
Refers to the vascular changes in the brain that usually cause acute or chronic cerebral ischemia
Hypertensive retinopathy
Retinal changes that can impair vision and can eventually cause blindness
Cardiomyopathy
A heterogenous group of diseases of the myocardium
Mechanical and/or electrical dysfunction
Inappropriate ventricular hypertrophy or dilatation
Due to a variety of causes that frequently are genetic
Exclude ischemic, hypertensive, valvular and congenital forms of heart disease
Incurable - need heart transplant
Dilated cardiomyopathy
and complications
Ventricles are markedly dilated and the heart appears to have a myocardium that is either flabby or thinned and has been partially replaced by fibrous tissue
Systolic dysfunction and arrhythmia
No obvious causes
Complications: congestive heart failure, mural thrombus, sudden death
Hypertrophic cardiomyopathy
Extensive thickening of the left ventricular myocardium
Runs in families - autosomal dominant (66% familial, 33% sporadic)
#1 cause of sudden death in young athletes
Diastolic dysfunction and arrhythmis
Mostly effects sarcomeric proteins
Restrictive cardiomyopathy
Inability of the heart to expand adequately during diastole nor contract forcefully enough during systole
Often occurs because the myocardium is infiltrated with some abnormal material like amyloid
Diastolic dysfunction
Arrhythmogenic cardiomyopathy
Common cause of sudden death in young athletes
Arrhythmia and systolic dysfunction
100% genetic (familial and sporadic are 50% each)
Mostly cell adhesion proteins
Fibrofatty myocardial replacement, frequently only RV involved
