CV disorders Flashcards
1
Q
What is ischemia?
A
Reduction in blood flow that doesn’t meet needs for oxygen
2
Q
What is infarction?
A
Necrotic tissue resulting from prolonged ischemia
3
Q
What is the leading cause of death in the US?
A
Atherosclerosis
4
Q
Why do men have a higher risk for atherosclerosis?
A
Estrogen has protective factors against cardiac disease
5
Q
How does cholesterol get where it needs to go in the body?
A
Lipoproteins; they carry a core of cholesterol
6
Q
What do LDLs do?
A
Deposit cholesterol in distal tissues -> atherosclerosis
7
Q
What do HDLs do?
A
They are cardioprotective - they take cholesterol from distal portions and bring it to the liver to metabolize
8
Q
How is HTN a risk factor for atherosclerosis?
A
HTN can cause microtears in the blood vessels
9
Q
How is DM a risk factor for atherosclerosis?
A
Glycation end products (products of glucose metabolism) can rise too much and cause microtears in blood vessels
Can allow entry of lipids into blood vessels
10
Q
What are the 3 types of lesions in atherosclerosis?
A
Fatty streak
Fibrous atheromatous plaque
Complicated lesion
11
Q
What is a fatty streak?
A
Early discoloration of the intima due to infiltration by macrophages and lipids
12
Q
What is a fibrous atheromatous plaque?
A
Further invasion of the intima, triggering the inflammatory process
13
Q
What is a complicated lesion?
A
Hemorrhage within the lesion or ulceration of the lesion, leading to thrombosis
14
Q
What happens in a fatty streak?
A
Development begins under the blood vessel -> influx of monocytes -> monocytes become macrophages -> macrophages eat all the lipids -> development of fatty streak
15
Q
How does a fatty streak turn into a fibrous atheromatous plaque?
A
The inflammatory process is initiated
16
Q
What happens in a fibrous atheromatous plaque?
A
The vessel becomes less elastic
Subendothelial is exposed to material in the blood stream -> clotting
17
Q
What is the process of atherosclerosis?
A
Endothelial injury -> fatty streak -> smooth muscle tries to repair damage -> fibrous atheromatous plaque -> complicated lesion
18
Q
What is the process of atherosclerosis? (with details of each step)
A
Endothelial injury occurs and allows the entry of lipids into intima
Fatty streak develops
- Monocytes migrate into vessel wall
- Monocytes differentiate into macrophages
- Release toxic oxygen to oxidize LDL
- Toxic oxygen further damages endothelium
- Platelets adhere to damages endothelium
- Monocytes engulf lipids and become “foam cells”
Smooth muscle tries to repair damage
- Foam cells recruit smooth muscle cells
- Smooth muscle proliferates and produces ECM (collagen)
Fibrous atheromatous plaque forms
- Superficial smooth muscle cap is created
- Macrophages, lymphocytes, foam cells, smooth muscle cells, fatty debris are under fibrous cap
- Core can be necrotic and unstable
- Can extend into lumen, slowing blood flow
Complicated lesion
- Unstable cap can rupture (or keep growing and occlude vessel
- Coagulation cascade initiated
19
Q
What is stable angina?
A
Chest pain occurring from the demand of oxygen outweighing the supply of oxygen
20
Q
How does pain in stable angina occur?
A
Prolonged ischemia -> anaerobic metabolism (instead of aerobic) -> build up of lactic acid
21
Q
What is coronary blood flow regulated by?
A
Cardiac oxygen
22
Q
What are oxygen requirements dependent on?
A
Metabolic activity of the heart
23
Q
What are the two types of plaques in ACS?
A
Stable plaque and unstable plaque
24
Q
What is a stable plaque?
A
A plaque that obstructs blood flow over time
25
What is an unstable plaque?
Plaque (with a rigid cap) that can rupture due to hemodynamic stress -> expose lipid core to blood -> stimulate platelet aggregation/thrombus formation -> smooth muscle/foam cells stimulate extrinsic pathway -> result in acute vascular occlusion
26
In ACS, what is the extent of damage dependent on?
Location of occlusion
Extent and duration of occlusion
Amount of tissue supplied by the vessel
Metabolic needs of the heart
27
How can ischemia affect the 3 layers of the heart?
All layers can be affected (transmural) or only some
28
Which area of the heart is affected first in ischemia?
The area below the endocardium
29
What areas of the heart will a right coronary artery obstruction affect?
Right atrium/right ventricle
30
What areas of the heart will a left main coronary artery obstruction affect?
Septum, anterior wall of left ventricle, lateral wall of left ventricle, posterior wall
31
What is a left main coronary artery obstruction called and why?
Widow maker because it obstructs blood flow to the circumflex and left anterior descending arteries
32
Why is the area below the endocardium affected first during an MI?
Coronary arteries run outside epicardium and send in feeding blood vessels that penetrate
Arteries have highest % of blood oxygen -> when it penetrates down, the tissue around will extract O2 -> decrease in O2 as you go deeper from epicardium to endocardium
33
How long do you have to reverse damage from ACS?
About 40 minutes
34
What happens in ACS?
Damage from anaerobic metabolism
- No energy
- Decrease in contractile force
- Glycogen depletion and mitochondrial swelling
- Failure of LV to pump possible
Ventricular remodeling to compensate for infarcted areas (which become thin and dilated)
35
How is stable angina presented?
Pain associated with exertion and relieved by rest
Constricting, squeezing, stabbing
Consistent with same intensity and character
36
How is stable angina pain relieved?
Rest or nitroglycerin
37
How can you get acute coronary syndrome?
May result from stable angina or without warning
38
What is unstable angina/NSTEMI and what are characteristics?
Pain at rest
Pain may vary in intensity, frequency, character
Differentiate based on biomarkers
39
What is STEMI and what are characteristics?
Myocardial infarction
Could be acute onset or progression from NSTEMI
Crushing, suffocating, constricting substernal pain
Prolonged pain
Radiates to jaw, neck, left arm
Nausea and vomiting
Fatigue and weakness
40
What are biomarkers of USA?
Creatine kinase myocardial band
Troponin (elevation is more specific to cardiac tissue -> damage has been done to cardiac tissue -> more helpful in diagnosis)
41
How do you interpret EKG in the context of MI?
ST depression -> ischemia (recoverable - can restore blood flow)
ST elevation -> sign of myocardial injury (cannot recover after this)
42
What is heart failure?
Disorder where the heart is unable to pump a sufficient amount of blood to meet the body's demands
43
What is preload?
Volume of blood that stretches the ventricle at the end of diastole
44
What is afterload?
Force the ventricle has to overcome to get the blood out
45
What is contractility?
The contractile force of the ventricle - how well does the heart contract?
46
Why is having too much preload bad?
Having too much blood stretches the heart muscle and can cause the actin and myosin fibers to no longer be touching, so the ventricle can't contract well (dilated cardiomyopathy)
47
What is systolic dysfunction in HF?
Decrease in cardiac contractility
| EF <50%
48
What happens in systolic dysfunction in HF?
Preload increases -> ventricle dilates -> increased left ventricular end diastolic pressure -> pulmonary HTN -> pulmonary edema
49
What is the etiology of systolic dysfunction?
Impaired contractility
Volume overload
Pressure overload
50
What can cause systolic dysfunction?
LV dilation to accommodate pressure increase in right side of the heart -> increased preload -> volume increase
Ischemic heart disease -> can't get blood out -> EF drops
Cardiomyopathy (heart becomes rigid) -> weak contraction
Volume overload - floppy valve somewhere
Pressure overload - high pressure in aorta -> afterload increase -> ventricle squeezes and meets resistance to get blood out
51
What is diastolic dysfunction in HF?
Abnormal relaxation of ventricles
52
In what populations is diastolic dysfunction higher?
Women, obesity, HTN, DM
53
What is the etiology of diastolic dysfunction?
Impaired ability of ventricle to expand
Increased wall thickness and reduced LV chamber size
Delayed diastolic relaxation - ventricle begins to fill while still stiff
54
What is a good metaphor to remember diastolic dysfunction by?
Filling up a stiff balloon with air - have to overcome the initial stiffness to get air in
55
How does diastolic dysfunction affect the heart pumping blood?
Normal ejection fraction, but start with a low volume
56
What can cause diastolic dysfunction in HF?
Pericardium issues (ex: fluid accumulation, leading to restriction)
57
What is delayed diastolic relaxation?
Phase in diastole where it actively relaxes and pulls blood down from the atrium
58
What are symptoms of right ventricular dysfunction in HF?
Systemic symptoms
| Peripheral edema, liver congestion, anorexia, elevated JFC
59
What are symptoms of left ventricular dysfunction in HF?
Initially pulmonary and progress to systemic
| Activity intolerance, cyanosis, hypoxia, orthopnea, paroxysmal nocturnal dypsnea
60
What happens in left ventricular dysfunction?
Blood won't make it to the rest of the body
No O2 to peripheral tissues/brain
Fatigue/lightheadedness
Pressure build up to capillaries in lungs -> fluid in lungs
61
What happens in right ventricular dysfunction?
Less volume to the lungs
Built up pressure into the system - RA -> vena cava -> jugular veins -> liver -> fluid leaking out of capillaries -> liver congestion/edema
62
What is an aneurysm?
An abnormal localized dilation of blood vessel
63
What is the etiology of aneurysms
Weakness in blood vessel caused by congenital defect, trauma, infection, atherosclerosis
Aneurysm growth can put pressure on surrounding structures or rupture
64
How do aneurysms manifest?
Depends on location
Some possibilities:
- Asymptomatic
- Substernal, back, neck pain
- Dyspnea and cough if tracheal impingement
- Hoarseness if pressure on laryngeal nerve
- Difficulty swallowing if pressure on esophagus
65
What is an aortic dissection?
Hemorrhage into vessel wall that tears along the length of the vessel
- Can coagulate and obstruct other vessels
66
What vessel is more affected in aortic dissections?
Ascending aorta
67
What is the etiology of an aortic dissection?
Weakness of vessel, HTN, connective tissue diseases, surgery increasing risk
68
What is the epidemiology of aortic dissections?
Most common in men between 40 and 60
69
How do aortic dissections manifest?
Abrupt, excruciating tearing or ripping pain
BP and pulse unobtainable in area
Syncope, paralysis, hemiplegia could occur
70
What can happen in an aortic dissection of the common carotid?
Obstruction of brain - complaints of lightheadedness
71
What can happen in an aortic dissection of the left subclavian?
Issues with left arm
72
What can happen in an aortic dissection of the ascending aorta?
Can obstruct vessels that branch off
73
What is hypertrophic cardiomyopathy?
Unexplained LV hypertrophy
74
With what is hypertrophic cardiomyopathy associated?
Thickened ventricular septum, abnormal filling during diastole, LV outflow obstruction
- Most common cause of sudden death in athletes
75
What is the etiology of hypertrophic cardiomyopathy?
Autosomal dominant genetic predisposition
| Abnormal coding for cardiac muscle proteins
76
What is pericarditis?
Inflammation of pericardium
| Stiff pericardium makes it difficult for the heart to expand
77
What is the etiology of pericarditis?
Infection, trauma, medications
78
What does pericarditis often lead to?
Pericardial effusion -> increased fluid volume in pericardial sac -> increased pressure on heart
79
How does pericarditis affect pressure around the heart?
Pressure on right side are lower and more vulnerable to being compressed, so manifestations typically appear as right sided heart failure
Decreased venous return -> decreased preload -> tachycardia to compensate
80
How does pericarditis affect the right side of the heart?
Right chambers are squeezed -> symptoms of right sided heart failure
Pressure built in RV -> RV won't take blood from RA -> high afterload in RA -> low volume of blood making it to the body -> BP goes down -> stretch receptors in aorta sense low volume -> sensors compensate by increased HR
81
What is endocarditis?
Infection of the heart lining
82
What is the etiology of endocarditis?
Invasion of heart valves and endocardium by bacteria -> bacteria into blood stream -> endothelial damage, altered hemodynamics, bacteremia lead to thrombus -> thrombus seeded by bacteria -> development/growth of friable vegetations -> destruction of cardiac tissue
83
What are vegetations?
Calcium based deposits that develop on valves as a result of bacteria initiating damage
84
Which valves are most commonly affect in endocarditis?
Aortic and mitral
85
How does endocarditis manifest?
Fever, murmur, splinter hemorrhages
86
What are splinter hemorrhages?
Tiny vegetations crack off and travel and obstruct tiny vessels
87
How is mitral valve prolapse related to endocarditis?
The mitral valve balloons back up into the atrium and increases the risk of development
88
What is rheumatic heart disease?
When a deformity of heart valves occurs
89
How does one get rheumatic heart disease?
The body creates an autoimmune response against the M protein on group A beta-hemolytic strep
Antibodies are created and react with antigens in the body
Antibodies bind to receptors on heart valve -> vegetations -> Aschoff bodies develop -> valves become stenotic
90
What are aschoff bodies?
Necrotic tissue surrounded by immune cells
91
How does rheumatic heart disease manifest?
Arthralgia to severe arthritis
Vegetations and scarring causing deformities
Subcutaneous nodules over extensor muscles of wrist, elbow, ankle, knee
92
Which valves are most commonly affected in rheumatic heart disease?
Mitral/aortic
93
What is the difference between rheumatic heart disease and endocarditis?
RHD is abnormal response to M protein
| Endocarditis is bacterial introduction to the body
94
What are the 5 types of valvular heart disease?
```
Mitral valve stenosis
Mitral valve regurgitation
Mitral valve prolapse
Aortic stenosis
Aortic regurgitation
```
95
What happens in mitral valve stenosis?
Narrow mitral valve from rheumatic fever or congenital abnormality
Fibrous replacement of valve resulting in stiff valves
Increased resistance -> pulmonary vascular congestion
96
What happens in mitral valve regurgitation?
Valve doesn't close properly from rheumatic heart disease, rupture chordae tendinae, ruptured papillary muscles, LV dilation
Bidirectional flow -> increased pressure in RA -> chamber dilation -> pulmonary congestion
97
What happens in MVP?
"Floppy" valve from genetic disorder -> fibrotic changes develop on valves - can cause mitral regurgitation
Valve "balloons" up into LA -> some regurgitation -> bidirectional flow -> dilation in LA -> pulmonary congestion
98
What happens in aortic stenosis?
Narrow aortic valve lumen - congenital or calcification
| Impaired LV outflow -> LV hypertrophy to accommodate -> increase cardiac workload -> angina, syncope, heart failure
99
What happens in aortic regurgitation?
Incompetent atrial valve allows backflow from aorta to LV - rheumatic fever, congenital abnormalities, aortic dilation
Ventricle squeezes -> bidirectional flow -> residual blood in LV -> pressure increases -> chamber size decreases
100
What is congenital heart disease?
Birth defect occurring in the heart between 4th and 7th week of gestation - genetic and environmental influences
101
What happens in congenital heart disease?
Shunting of blood to path of least resistance
Cyanosis
Disruption of pulmonary blood flow
102
What is the difference between left to right shunt and right to left shunt in congenital heart disease?
LTR are usually acyanotic
- Patent ductus arteriosus, septal defects
RTL shunts are usually cyanotic
- Tetralogy of Fallot, transposition of great vessels
103
What happens during the disruption of pulmonary blood flow?
Reduced pulmonary blood flow causes fatigue, dyspnea
- Pulmonary stenosis
Increase in pulmonary blood flow stimulates vasoconstriction of pulmonary artery
Pulmonary HTN can occur in LTR shunts
Pulmonary stenosis + hole will force blood to the left side of the heart
104
What is patent ductus arteriosus?
Channel that goes from pulmonary artery to aorta in utero
105
What happens in congenital patent ductus arteriosus?
Hole stays open, so blood with go from aorta -> pulmonary artery -> lungs -> LA -> LV -> some oxygenated blood to aorta and some oxygenated blood out of pulmonary artery (cyanotic)
106
What is patent foramen ovale?
Congenital heart disease
| Persistent opening in atrial or ventricular septum
107
What happens in patent foramen ovale (atrial septum)?
Can develop L to R shunt
Dilation of R heart
Fixed split S2 due to delayed closure of pulmonic valve
Oxygenated blood -> LV -> L to R because of pressure difference
108
What are the types of patent foramen ovale?
Congenital abnormalities in atrial/ventricular septum
109
What happens in patent foramen ovale (ventricular septum)?
Can be asymptomatic or can develop heart failure
Can develop L to R shunt
Tachypnea, diaphoresis, failure to thrive
Pulmonary HTN due to increased volume
Can develop increase in pulmonary vascular resistance
Cyanosis from no O2 making it to the body
110
What are the 4 defects of Tetralogy of Fallot?
Ventricular septal defect
Shifting of aorta to the right
Pulmonary outflow obstruction
Right ventricular hypertrophy
111
What happens in Tetralogy of Fallot?
Deoxygenated blood sent through systemic circulation
Blood comes in RA -> RV (deoxygenated blood) -> tries to push out through pulmonary artery, but it’s stenotic -> goes through hole in septum -> blood leaves through to aorta and the rest of the body -> deoxygenated blood to the rest of the body -> cyanosis
112
What is transposition of great vessels?
When the aorta rises from right ventricle, pulmonary artery arises from left ventricle
113
What happens in transposition of great vessels?
Aorta and pulmonary artery are reversed
- RA -> RV -> aorta -> body (no oxygenation)
- LA -> LV -> pulmonary -> lungs (oxygenated blood never gets anywhere)
Ventricular septal defect present in 50%, allowing blood mixing
Cyanosis
