Cardiovascular System Flashcards
Describe the anatomy of the heart
What are the mechanisms of heart failure?
Six pathophysiological mechanisms of heart failure:
- Failure of the pump
- Obstruction to flow
- Regurgitant flow
- Shunted flow
- Disorders of cardiac conduction
- Rupture of the heart or major vessel
Describe cardiovascular disease (CVD)
- Collective term for diseases of the heart and blood vessels
- Leading contributor of mortality worldwide (Accounts for 50% greater mortality than for all forms of cancer combined!)
- Affects ~1:6 Australians or 4.2 million (18.3%)
- Heart Failure = common endpoint for many forms of cardiac disease
Vascular Disease:
- Obstruction of the lumen
- Weakening of the vessel walls
Types of CVD:
Diseases of arteries
:
a) Atherosclerosis
b) Hypertension
c) Aneurysm
Diseases of veins
:
a) Varicose vein
b) Thrombophlebiti
c) Phlebothrombosis
What is atherosclerosis and how is it caused?
- Blood vessels (specifically arteries) become thick, less elastic and stiff — sometimes restricting blood flow to organs and tissues
- Atherosclerosisis one pattern/specific type of arteriosclerosis
- Caused by the buildup of fatty plaques, cholesterol, cellular waste products, calcium, and fibrin etc. in artery walls
- Chronic inflammatory disorder of intima of large arteries
- Characterised by formation of fibrofatty plaques = atheroma
- Major cause of death & morbidity in developed countries
- Can lead Myocardial Infarction, Ischemic Heart Disease, stroke, aortic aneurysms, leg gangrene etc.)
- Begins early in life but presents when there is end organ damage
- Fatty Streaks
What are fatty streaks in atherosclerosis?
- Fatty streaks are the first signs of atherosclerosis -> visible without magnification
- Consist of lipid-containing foam cells in the arterial wall
Describe the pathogenesis of atherosclerosis
- Earliest event inatherogenesisis chronic injury to theendothelium
and resultant endothelial dysfunction— leading to increased permeability, leukocyte adhesion, and thrombosis. Caused by:
- Trauma
- Hypertension
- Turbulent blood flow
- Free radicals
- Hyperlipidemia
- Toxins
- Viruses
- Immune reactions
- Chronically elevated blood glucose levels - Accumulation of lipoproteins (mainly oxidized LDL and cholesterol crystals) in the vessel wall
- Fatty Streaks
3.
- Platelet adhesion
- Monocyte adhesion to the endothelium, migration into the intima, and differentiation into macrophages and foam cells
- Lipid accumulation within macrophages
- In response to lipid accumulation, macrophages (monocytes) release inflammatory cytokines and growth factors which induce:
- Smooth muscle migration into intima
- Smooth muscle cell proliferation and extra cellular matrix production above plaque
What is the composition of atheromatous plaque?
What are the risk factors of atherosclerosis?
What is hypertension (high blood pressure)?
- Average adult blood pressure is around 120/80 mmHg
- Considerable variation in blood pressure between persons possible
- Systolic pressure: Contraction of left ventricle -> forcing blood into the aorta and out
- Diastolic pressure: Relaxation of the left ventricle of the heart
- Hypertension is common and is a silent disease
- Increased blood pressure: Sustained diastolic pressure >90 mmHg and or a sustained systolic pressure >140 mmHg
- ~ 2.6 million Australians reported having hypertension in 2015
- Detection: regularly check blood pressure
- If not treated, organ damage to kidneys, heart and brain
Describe the vascular histology of hypertension
Accelerates atherogenesis
Degenerative changes in walls of large & medium arteries -> potentiates aortic dissection and cerebrovascular hemorrhage
- Causes damage to the media of arterioles
- End organ damage
- Blood Vessels (atherosclerosis, arteriolosclerosis)
- Heart (LVH, IHD, MI)
- Kidney (nephrosclerosis)
- Eyes (retinopathy)
- Brain (stroke)
Name and describe two cardiovascular changes to due hypertension
Systemic Hypertension
- Left ventricular hypertrophy
- Heart failure in time
- Arrhythmias
- Severe atherosclerosis
- Renal disease
- Stroke
- Aortic wall dissection
Cor Pulmonale (Pulmonary Hypertension):
Right-sided failure secondary to intrinsic pulmonary disease
A) Right ventricle dilation (acute)
B) Right ventricle hypertrophy (chronic)
- Emphysema
- Scaring conditions of the lung
- Chronic embolisation
What is the difference between primary (essential) and secondary hypertension?
Essential = primary hypertension (majority):
No single cause determinable
Secondary hypertension:
A clearly identifiable cause of the high blood pressure is determined
- Primary renal disease
- Endocrine tumors
- Cardiovascular
- Neurologic
What is an aneurysm and what are the types?
- Abnormal dilation in the wall of a blood vessel or the wall of the heart
- Especially in the heart (aorta) and Circle of Willis
Clinical course:
- Rupture into peritoneal cavity -> hemorrhage
- Obstruction of a branch vessel -> ischemia
- Embolism from atheroma
- Local pressure -> e.g. compression of ureter
Three types:
- True
- False
- Dissecting
What are the differences between true, false and dissecting aneurysms?
True aneurysms:
- Expansion of the arterial wall (e.g. atherosclerotic aneurysms)
False aneurysm:
- Breach in the vascular wall leading to an extravascular hematoma that freely communicates with the intravascular space
Dissecting aneurysms
- Occur when blood enters the wall of the artery dissecting between its layers
What is valvular heart disease and the different types?
Valvular heart disease: when any valve in the heart has damage or is diseased
Types:
- Stenosis
- Insufficiency (regurgitation or incompetence)
What is stenosis?
- Failure of valve to open completely
- Obstructed forward flow
Causes:
- Rheumatic Fever
- Calcification
What is insufficiency (regurgitation/incompetence)?
- Incompetent valves
- Failure of valve to close completely -> regurgitation
Causes
a. Infective Endocarditis
b. Pericardial Disease
- Pericarditis
c. Myocarditis
d. Cardiomyopathy
What is rheumatic fever and how does it lead to stenosis?
- Cause: Streptococcal infection
- Antibodies are produced against Streptococcal protein
- Antibodies can cross react with self (connective tissue)
- Type II hypersensitivity (80% in children 5-15)
- Many systems become involved (Joint symptoms, Skin, Heart, CNS)
- Main cause of mitral stenosis
- Aschoff bodies = inflammatory foci, found in heart layers
- Eventually replaced by scarring in chronic RF , this infection can scar the mitral valve, causing it to thicken with scar tissue and narrow leading to mitral stenosis
What is calcification and how can it lead to stenosis?
- Buildup of calcium deposits around the aortic valve
- Most common cause of aortic stenosis
- Calcium deposits can cause the valve opening to become narrow. Severe narrowing can reduce blood flow through the aortic valve leading to aortic stenosis.
What is infective endocarditis and how can it lead to valve insufficiency?
- Microbial infection of heart valves or mural endocardium
- Streptococcus
- Previously damaged valves are at greater risk
- Destroys valve
- Formation of necrotic debris, thrombus and organisms and destruction of the underlying cardiac tissues (=vegetations)
- Regurgitation -> symptoms of pulmonary congestion & fatigue
- Fever, nonspecific fatigue, loss of weight, and flulike syndromes
What is pericarditis and pericardial disease and how can they lead to valve insufficiency?
- Pericarditis = inflammation of the pericardium (sac-like structure made of two tissue layers that surrounds and protects the heart)
“Bread and butter” pericarditis (fibrinous/ serofibrinous)
- Viral, Lyme disease, Renal Failure, Cancer
- Effusions
- CHF, Cancer
- Fibrosis leading to restriction of heart motion
Pericardial diseases can present clinically as
- acute pericarditis: pericardial effusion (fluid in thepericardialcavity)
- can result in cardiac tamponade (when enough fluid accumulates in the pericardial sac compressing the heart and leading to a decrease in cardiac output and shock)
- constrictive pericarditis (chronic, inflammation of thepericardium) -> TB can lead to a granulomatous pericarditis that may calcify and produce a “constrictive” pericarditis
What is myocarditis and how can it lead to valve insufficiency?
- Viruses mostly in US
- Rarely bacteria of TB
- Parasites (e.g. Toxoplasmosis)
Complications
:
- Heart failure
- Rhythm disturbances
- Scarring of muscle
- Mural thrombus and embolization
In histology, look around the smaller vessels of the myocardium for the inflammation
What is cardiomyopathy and how can it lead to valve insufficiency?
- Disease of the heart muscle
- Weakened and, paradoxically, hyperplastic myocardium
Primary: Of unknown cause
Secondary to something else
- Alcohol
- Heavy metals
- Viral?
Name and describe the different types of cardiomyopathy
Dilated Cardiomyopathy:
- progressive cardiac dilation
- contractile (systolic) dysfunction
- ischemic cardiomyopathy
Hypertrophic Cardiomyopathy:
- myocardial hypertrophy
- defective diastolic filling
- in one third of cases—ventricular outflow obstruction
Restrictive Cardiomyopathy:
- primary decrease in ventricular compliance, resulting in impaired ventricular filling during diastole (simply put, the wall is stiffer
Causes shown in image
What is a myocardial infarction?
- Myocardial infarction = “heart attack”
- Death of cardiac muscle from ischemia
- 90% caused by thrombosed artery (disruption of atherosclerotic plaque à thrombus) -> total occlusion
- Severe crushing chest pain often accompanied by sweating, nausea, vomiting & dyspnea
Generally lasts for several hours
Complications:
- Cardiogenic shock
- Cardiac failure
- Arrhythmias
- Mural thrombosis
- Rupture or death
Name and describe the morphological types of myocardial infarction?
Transmural infarction (common)
- Ischemic necrosis involving full or nearly full ventricular wall thickness in the distribution of a single coronary artery.
- Cause: Coronary atherosclerosis, acute plaque change, superimposed thrombosis
Subendocardial infarct
- Necrosis usually limited to the inner one third or at most one half of the ventricular wall (localised or sometimes circumferential)
- Subendocardium not well perfused so susceptible to ischemic infarct from hypotension in presence of non-critical stenosis
- Cause: Acute coronary thrombosis, hypotension etc.
What are the gross morphological changes over time after myocardial infarction?
What are the microscopic morphological changes over time after myocardial infarction?
Early Acute MI (1-3hrs):
- 1-3hrs: Wavy myocardial fibres but no inflammatory cells
- 2-3hrs: Staining defect in myocardial fibre cytoplasm with tetrazolium or basic fuchsin dye
Early Acute MI (4-12hrs)
:
- Coagulation necrosis with loss of cross striations, contraction bands, edema, hemorrhage, and early neutrophilic infiltrate
Acute MI (18-24hrs)
:
- Continuing coagulation necrosis, pyknosis of nuclei, and marginal contraction bands
- nuclei often not present
- extensive hemorrhage at the border of the infarction -> grossly apparent hyperemic border
3-7 Days:
- Macrophage and mononuclear infiltration begins, fibrovascular response begins
- still some neutrophilic infiltrate but increasingly more macrophages and monocytes
- prominent necrosis and hemorrhage
- beginning of fibrosis
7-21 Days:
- Fibrovascular response with prominent granulation tissue containing capillaries and fibroblasts
- healing of a myocardial infarction (mainly repair)
- ingrowth of capillaries along with fibroblasts and macrophages filled with hemosiderin
- granulation tissue peaks around 1-2 weeks
- Cardiac troponin markers may still be present in the blood up to weeks following the initial ischemic event
> 21 Days/3 Weeks:
- healing (repair) is well under way
- more extensivecollagen depositionin the region of myocardium that was infarcted
> 2months:
- remote myocardial infarction is evidenced by acollagenous scar(partially re-organized)
- some residual surviving myocardial fibers (red)
- Note: This scar tissue is non-functional
- reduction in ejection fraction is related to the extent of scarring
Describe pulmonary and peripheral edema and explain how they can occur in Congestive Heart Failure
Pulmonary Edema:
- A condition caused by excess fluid in the lungs
- When the heart is not able to pump efficiently, blood can back up into the veins that take blood through the lungs.
- As the pressure in these blood vessels increases, fluid is pushed into the air spaces (alveoli) in the lungs.
Peripheral Edema:
- Edema in tissues perfused by the peripheral vascular system, usually in the lower limbs.
- The heart’s lower chambers stop pumping blood well. As a result, small blood vessels leak fluid into nearby tissues
What are the four major congenital shunts and where do they occur?
Left-to-Right Shunts:
- Atrial Septal Defect (ASD): left atrium -> right atrium
- Ventricular Septal Defect (VSD): left ventricle -> right ventricle
- Patent Ductus Arteriosus (PDA): a persistent opening between the aorta and the pulmonary artery
Right-to-Left Shunts:
Tetralogy of Fallot
- Transposition of the great arteries = aorta arises from the right ventricle and the pulmonary artery arises from the left ventricle
- Often presents with cyanosis early in life
