Mod 5 CV Disorders Flashcards
1
Q
What are 3 types of Hypertension?
A
Primary, secondary, or malignant
2
Q
Etiology of Primary Hypertension?
A
Occurs w/o evidence of other diseases
- largely idiopathic but has many contributing factors ranging from family history to lifestyle factors
3
Q
Etiology of Secondary Hypertension?
- What are the most common causes?
A
Caused by other diseases/complication’s in the body. The main are:
- Renal disease
- Excess Adrenocorticosteroids
- Coarctation of the Aorta
- Pregnancy
4
Q
Why are the majority of cases of Secondary Hypertension caused by Renal Disease?
A
Usually atherosclerotic in origin (decreased blood flow to the kidneys)
- Results in retention of salt and water (due to stimulation of the RAA system) leading to hypertension
- (sum) The system vasoconstricts bc of low blood flow. Renin releases ACE II —> vasoconstriction. Long term RAA state is bad.
5
Q
What is Cushing’s syndrome?
A
Body makes too much cortisol (hormone related to stress response)
- Rare pituitary disorder that is progressive
- Seen w/excess adrenocorticosteroids
- Increased cortisol = increased BP
- Suppresses immune system by reducing production of WBC
6
Q
What is Excess Adrenocorticosteroids associated with?
A
Seen in primary hyperaldosteronism.
- leads to secondary hypetension
- Cushing’s syndrome
7
Q
Why does excess adrenocorticosteroids cause secondary hypertension?
A
Excess mineralocorticoids, like aldosterone, can lead to increased sodium and water retention, resulting in elevated blood pressure.
8
Q
Why does Coarctation of the Aorta cause secondary hypertension
A
Causes reduced blood flow to the kidneys —> triggers the RAA system
- Water retention and hypertension result
- Viscous cycle?
9
Q
What stage of hypertension is associated as a hypertensive crisis?
A
Malignant Hypertension (most severe)
10
Q
What is the origin of Malignant Hypertension?
- expected course?
A
Occurs when someone w/secondary hypertension develops an accelerated and potentially fatal form of the disease.
- Can result in Stroke and end organ damage
11
Q
What is Malignant hypertension defined as (categorically)?
A
Elevations in blood pressure with diastolic pressures > 120mmHg
12
Q
What is the cascading effect of malignant hypertension?
- Whats the worst outcomes at its end stage?
A
Can end with Stroke and end organ damage.
- Causes severe damage to the vascular system
- Can result in encephalopathy and cerebral edema
- Convulsions and coma in severe cases
13
Q
How does Malignant Hypertension manifest?
A
- Headaches and confusion
- Motor and sensory deficits
- Visual disturbances
14
Q
What is encephalopathy?
A
Dysfunction or disease of the brain that results in altered brain function, which can manifest as a wide range of neurological symptoms.
- Brain function and structures are affected basically
15
Q
Pathophysiology of Hypertension in the body?
- what are the 2 mechanisms of failure?
- what are the long term consequences?
A
- Decreased blood flow to target organs leads to a cascade of varying consequences.
- Compensation leading to increasing blood volume and blood pressure (vasoconstriction) via kidneys (one example)
- Damage to vascular endothelium that causes the lumen to narrow as a result of plaque forming (healing response). Leads to decreased blood flow distally.
16
Q
What is the expected Pathophysiology of target organ damage in the Heart because of hypertension?
A
Causes hypertrophy of the LV, increasing the risk of ischemia/MI
- LV has to work harder
17
Q
What is the anticipated Pathophysiology of Cerebrovascular target organ damage due to hypertension?
- Cerebrovascular = blood flow in the brain
A
Leads to increased risk of stroke
- secondary degree bleed or clot
18
Q
What is the expected Pathophysiology of target organ damage in the Peripheral Vasculature because of hypertension?
A
Leads to the development of atherosclerosis
- Atherosclerosis is the build up of fat (and other substances) on the arterial walls aka plaque
- Leads to blood clots and increased resistance
19
Q
What is the expected Pathophysiology of target organ damage in the Renal system because of hypertension?
A
Stimulation of RAA system
- worsens hypertension because it stims the retention of water and salt (fluids) causing a increase in blood volume and blood pressure
20
Q
Clinical manifestations of Hypertension?
A
Increased BP
- usually asymptomatic (if early)
- headaches
- Often the first symptoms are due to complications of hypertension can expect things like chest pain, stroke symptoms, or CHF symptoms
21
Q
Management of Primary Hypertension?
A
Lifestyle changes
- Weight loss
- Reduced sodium intake
- Regular physical activity
- Mod in alcohol intake
- Smoking cessation
- Healthy diet
22
Q
What is the clinical definition of Coronary Artery Disease (CAD)
A
Narrowing of 1 or more coronary arteries due to a build up of fatty deposits within the arterial wall.
- Results in reduced blood flow, causing less O2 and nutrients to be delivered to the heart muscles by the affected arteries
23
Q
What is a lack of blood flow referred to as?
A
Ischemia
- When in the heart in the case of coronary artery disease, it is referred to as ischemic heart disease
24
Q
What are risk factors of Coronary Artery Disease (CAD)
A
- Increased cholesterol
- Diabetes
- Hypertension
- Smoking
- Age (Men > 45 y___Women > 55 y)
- Family history
- Physical inactivity
- Obesity
- Stress
25
How can you prevent Coronary Artery Disease (CAD)?
- Lifestyle changes (healthy diet, regular exercise, limit smoking and alcohol intake)
- Control blood pressure
- Control blood sugar
26
Pathophysiology of Coronary Artery Disease (CAD)?
An atherosclerotic process.
- Cholesterol and calcium deposited beneath endothelium
- Fatty streaks develop
- Scar tissue formation at sites result in plaques
27
What is the make up of plaque?
- Is Plaque hard or soft?
- is it natural?
Cholesterol and calcium deposits that settle and harden
- Firm outer layer w/soft inner core of cholesterol
- Cholesterol is a natural part of aging, but risk factors accelerate it
28
What are the 2 main causes of Coronary Artery Disease?
1. Lumen narrows
2. Plaque Ruptures (etiology of most MIs)
29
What is the most common cause of origin for MI’s?
Plaque Rupture
30
Why is Lumen Narrowing a problem?
- why does it lead to Coronary Artery Disease (CAD) ?
Results in decreased blood flow to the myocardium
- Chronic ischemia can lead to myocardial fibrosis and decreased ventricular wall compliance
- causes a decreased ejection fraction, cause heart can’t pump well
31
how does Coronary Artery Disease (CAD) present when the lumen narrows?
Chest pain because of resulting ischemia
32
why are Plaque Ruptures a problem?
- snow ball effect?
Plaque rupture exposes the lipid core, which results in platelet adherence (lead to thrombosis/blood clots)
- Clot development further narrows the lumen and may result in complete occlusion (and MI)
33
What are clinical manifestations of Coronary Artery Disease (CAD)
These are “non-specific” and can appear gradually as the coronary arteries slowly narrow.
- Heartburn
- Palpitations
- Dizziness or fainting
- Nausea or vomiting
- Diaphoresis
- Exertional Angina (chest pain)
- SOBOE
- Jaw/back/arm pain (mostly in men), especially left-sided
34
What lab tests help diagnose/identify Coronary Artery Disease (CAD), but are not definitive?
- aka non-diagnostic (2)
- High Cholesterol levels
- High levels of C-reactive protein (CRP)
35
What are C-Reactive Proteins (CRP)?
Marker of inflammation, produced by liver
36
what exam findings help diagnose Coronary Artery Disease (CAD)?
- Lab tests (CRP & cholesterol levels)
- ECG
- Cardiac Stress Test
- Thallium Stress Test
- **Coronary Angiography**
37
How does a ECG help diagnose Coronary Artery Disease (CAD)?
May reveal ischemia, MI, or rhythm disorders
38
How does a Cardiac Stress Test help diagnose Coronary Artery Disease (CAD)?
ECG may show exertional myocardial ischemia
39
How does a Thallium Stress Test help diagnose Coronary Artery Disease (CAD)?
Combines nuclear imagining of blood flow to the myocardium at rest and under exertion
40
What is the gold standard for diagnosing Coronary Artery Disease (CAD)?
Coronary Angiography
- best evaluates the extent and locations of blockages
- Indicates whether Tx should include angioplasty or CABGs
41
How is a Coronary Angiography performed?
- **Catheter is inserted into a artery** (usually femoral) and threaded up the aorta to the openings of the coronary arteries
- **Dye is injected** and fluoroscopy captures the image of blood flow
42
What is non invasive management of Coronary Artery Disease?
- Lifestyle change (healthy diet, exercise, limit smoking/alcohol)
- Medical Management
43
What drug classes are used to treat Coronary Artery Disease? (6)
- Daily low-dose aspirin
- Statins
- Nitroglycerin
- β - blockers (lols)
- Calcium Channel blockers (pines and 1 zem)
- ACE inhibitors (prils)
44
What are invasive treatments (management) of Coronary Artery Disease
- Angioplasty = Percutaneous Transluminal Coronary Angioplasty (PTCA)
- Stenting
- CABG
45
How does Angioplasty or Percutaneous Transluminal Coronary Angioplasty (PTCA) manage Coronary Artery disease
Results in widening of the artery and plaque being flattened against the wall of the artery
46
What is the process of Angioplasty or Percutaneous Transluminal Coronary Angioplasty (PTCA)?
Often done at the time of angiography
- A balloon tipped catheter is threaded into coronary artery
- When balloon is in position, it is inflated. Flattening the walls of the artery
47
How does Stenting manage Coronary Artery disease?
Helps prevent restenosis or at least lengthen the time before it occur so.
- Prevents renarrowing basically
48
How is Stenting performed?
Often done during angiography.
- Stents are inserted, often done w/PTCA
- very similar to PTCA its basically another step
49
How does Coronary Artery Bypass Graft (CABG) help w/Coronary Artery Disease?
**Blocked parts of the arteries are bypassed by grafting a vessel above and below the blockage**
- vessel used for grafting is usually the Saphenous vein, internal mammaary artery, or radial artery
50
When is Coronary Artery Bypass Graft (CABG) performed?
Treats Severe Coronary Artery Disease (CAD) that has not responded to meds or PTCA.
51
What vessels are used for Coronary Artery Bypass Grafting?
Vessel used for grafting are usually the Saphenous vein, internal mammaary artery, or radial artery
52
How are the numbers of Coronary Artery Bypass Grafts (CABG) listed/recorded?
CABGx1 = one operation
Refers to how many grafts they’ve done
53
What are different Coronary Artery Bypass Graft (CABG) methods?
- Traditional approach
- Off pump or Beating heart
- MICAB/MICS
54
What is the traditional method for a Coronary Artery Bypass Graft (CABG)?
- pros and cons?
Full sternotomy **heart is stopped** and heart-lung bypass is used.
- Pros = still heart
- Cons = pump time, cutting through breast bone
55
What is the Off pump or Beating heart method for a Coronary Artery Bypass Graft (CABG)?
Full Sternotomy but **heart is not stopped**
- no bypass machine is required
56
What is the MICABS/MICS method for Coronary Artery Bypass Grafts (CABG)?
No sternotomy; **Access via intercostal region**
- Typically for from of the heart vessels; 1 or 2
57
What are the risk factors of Myocardial Infarction (MI)?
Most MI’s are caused by a ruptured atherosclerotic plaque, so the risk factors for the development of CAD are also risk factors for an MI!
- Smoking/drugs/alcohol
- Hyperlipidemia
- Diabetes melkite’s
- Poorly controlled HTN
- Type A personality
- Family history/sedentary lifestyle
58
Etiology of Myocardial Infarctions?
AN area of the myocardium is deprived of O2 because of:
- Decreased supply of O2
- Increased O2 demand
59
CAD causes that would lead to decreased O2 demand?
- snowball affect?
A decrease in O2 supply for CAD or arterial faults can result from insufficient blood flow or absence. Most commonly, they lead to Myocardial Infarction. The following are reasons why that could happen:
- **Plaque rupture and thrombus formation**
- Vasospasm of coronary artery
- Hypoxia
- Profound Hypotension
- Embolus to coronary arteries
- Aneurysm of coronary artery
- Arteritis
60
What are reasons that would cause increased O2 demand from a cardio stand point?
- Inotropic drugs
- Cocaine
- Ampetamines
- Ephedrine
61
where are the most severe sites for infarctions?
RCA and LCA because they supply blood for the whole body
62
What are the stages of a myocardial Infarction (MI)
Myocardium deprived of O2 -> Ischemia -> Injury and than infarction
63
What is Reperfusion injury?
When blood supply is restored to an area of the body that has experienced a period of reduced or interrupted blood flow, typically as a result of ischemia (lack of blood flow).
- sudden reintroduction of oxygen can cause a burst of oxidative stress, resulting in the production of harmful molecules called reactive oxygen species (ROS). These molecules can damage cells and tissues.
64
What can the area of infarction be described as?
Transmural or Subendocardial
65
What is a transmural infarction?
when the area affected by a infarction reaches full thickness of myocardium
66
What is a subendocardial infarction?
When an area of infarction only affects partial thickness of myocardium
67
what is the time frame of a Myocardial infarction and injury?
- 0-30 mins = reversible injury
- 1-2 hrs = onset of irreversible injury
- 4-12 hrs = beginning of necrosis
68
How long does necrosis and development of scar tissue occur?
Continued necrosis and development of scar tissue occurs up until 8th week post-infarct
69
When is the risk of myocardial rupture greatest?
At 4-7 days post-infarct
- tougher fibrotic scar tissue starts to form a 7-10 days post-infarct
70
cClinical manifestations of Myocardial Infarctions (MI)
**1/3 MI’s are silent**
- Pain/discomfort (tightness/radiating pain)
- Dyspnea
- Atypical presentation is common in women, elderly, or long standing diabetics = higher mortality
71
What is our first indicator of a myocardial infarction (MI)?
- what do we look at next?
- Hint: lab data
If you’re having a heart attack, it may take longer to have spikes in blood, which is why we look at myoglobin first
- High myoglobin
- High Troponin is next, the wave form is more important to look at than the number itself
72
What are common presentations of a Myocardial Infarction on a ECG?
- ST segment depression or elevation
- T wave peaking, flattening, or inversion
- Q wave is deepening or widening, potential loss of R wave resulting in a deep QS wave
73
How many people have diagnostic changes on their initial ECGs with Myocardial Infarctions (MI)
50%
74
What are the two classifications of a Myocardial Infarction (MI) based on ECGs?
- Don’t mix this up with area of affect
STEMi and Non-Stemi
75
How many continues leads are necessary to confirm changes in a myocardial infarction (MI)?
2 or more leads, and they need to be next to each other
76
What is a STEMI classified Myocardial Infarction?
- How do they Dx?
Pts presentation and St elevation on 2 or more contiguous leads provides immediate Dx (w/o need of cardiac enzymes)
- Means Pt. can be considered for re-perfusion therapy
77
What is Non-Stemi classified Myocardial Infarction?
- How do they Dx?
Relies on serum markers (ECG alone doesn’t confirm)
- the pattern is important
78
What tool helps locate areas of ischemia, infarct, or injury?
12 Lead ECG
79
How does a 12 lead ECG give us information on the location of blockage in a artery?
When a specific coronary artery is blocked, it can result in predictable changes of specific leads.
80
When is ST segment elevation considered pathological?
If it occurs in 2 or more anatomically contiguous leads
81
What leads would indicate a lateral injury in the heart?
Leads 1, AVL, V5, and V6
82
What leads would indicate a Inferior injury in the heart?
Leads II, III, and aVf
83
What leads would indicate a Septal injury in the heart?
V1 and V2
84
What leads would indicate a Anterior injury in the heart?
V3 and V4
85
Management of Myocardial Infarction?
- Medical support (supportive and pharmaceutical) -> think the mnemonic MONA
- **Repercussion therapy**
86
What are medical interventions/support active care to manage Myocardial Infarctions?
“MONA”
- Morphine (Pain relief and vasodilator = reduced afterload)
- Oxygen (increase O2 content = increase myocardial blood supply)
- Nitrates (Vasodilating effects)
- Aspirin (Reduce platelet aggregation)
- B-blockers (Reduce SNS stim, post MI and reduce afterload)
87
What category of Pts should have reperfusion therapy?
- how is reperfusion therapy initiated?
Patients with STEMI, treat with:
- Thrombolytics
- Angioplasty
88
Which patients should not be given Nitrates?
Those w/a inferior STEMI
- Nitrates refer to nitroglycerin
89
What is reperfusion therapy?
- Methods?
The goal is to reduce mortality and limit the infarct size via
- Thrombolytics (clot buster)
- Percutaneous Coronary Intervention(PCI)
- CABG
90
How do Thrombolytics initiate reperfusion therapy?
- Dissolve the blood and platelet clots
- Best if used within 60-90 mins of onset
- Risk of bleeding must be considered
91
What is Heart Failure defined as?
The inability of the heart to pump enough blood to meet the bodies metabolic needs
- may affect left or right ventricles (or both)
92
Should Cor pulmonale and right heart failure be referenced as interchangeably?
Cor Pulmonale involves PVR not necessarily due to the right heart
- usually Right Heart Failure (RHF)
- Right side heart failure is usually secondary to something else
93
How can heart failure be classified under?
High output or Low output (which can be systolic/diastolic in origin)
94
What is Left sided Heart Failure caused by and what is the resulting snowball affect?
Caused by failure of the left ventricle to move blood from the lungs out of the body
- Results in blood backing up into the pulmonary system
95
What is Right sided Heart Failure caused by and what is the resulting snowball affect?
Caused by failure of right ventricle to pump the returning venous blood out to the lungs.
- Results in blood backing up into systemic circulation
96
What does it mean when a heart is Supranormal, but still inadequate
The heart has high output due to the heart working fast, but w/o the heart being filled in time.
- aka high need, but unable to meet requirements
97
What is High output Heart Failure?
When there is excessive need for cardiac output.
- uncommon
98
What is Low output Heart Failure?
Impaired pumping ability of the heart **caused by disorders** -> secondary?
- Can be **systolic/diastolic in origin (and both)
99
What is Low output Systolic Heart Failure?
- Etiology?
Impaired ejection of blood from the heart during systole.
- Results from conditions that either **impair the contractility of the heart** or **Produce a volume or pressure overload on the heart**
- Results in decrease stroke volume and thus a decreased ejection fraction
100
What disorders could lead to low output systolic heart failure?
Anything that decreases stroke volume and ejection fraction:
- CAD
- Prior MI
- A-fib
- Valve disease/dysfunction
- alcohol
- infection
- cardio myopathy
101
What is low output diastolic heart failure?
Impaired relaxation of the heart during diastole
- results in decreased stroke volume
- Anything that restricts diastolic filling
- Increased ventricular thickness (and thus decreases chamber size)
- Delay diastolic relaxation **(fibrosis)**
102
What disorders could lead to low output diastolic heart failure?
Anything that restrict diastolic fill properly:
- Ventricular hypertrophy from long term hypertension
- aortic stenosis
- diabetes
- Constrictive pericarditis
103
Add stuff on this
104
What are indirect causes of Heart Failure?
- Fluid overload
- Renal failure
- Sepsis
105
What are the most common direct causes of heart failure?
- Myocardial ischemia
- Myocardial infarction
106
What are direct causes of heart failure?
- Myocardial ischemia
- Myocardial infarction
- Arrhythmias
- Heart valve lesions
- Congenital malformations
- Pericarditis
- Cardiomyopathies
107
What factors cause right heart failure (cor pulmonale)?
- COPD
- Pulmonary Embolism
- Pulmonary Hypertension
108
What are indirect causes of Heart Failure?
- Fluid overload
- Renal failure
- Sepsis
- factors that cause RHF (cor pulmonale) bc all right sided failure is secondary
109
What symptoms are associated w/left sided heart failure?
- Exertional dyspnea
- Orthopnea
- PND
- Cough
- Frothy, blood-tinged sputum
- Cyanosis
- O/A: Fine/coarse crackles,
“cardiac” wheezes
- Increased PAWP
110
What is Paroxysmal nocturnal dyspnea?
SOB that awakens Pt 1-2 hrs after falling asleep.
- Usually relieved by moving into upright position
- Exertional dyspnea or orthopnea can be expected
111
What is Orthopnea?
Discomfort/SOB when laying down
112
What symptoms are associated w/Right sided heart failure?
- Peripheral/dependent edema
- Fatigue
- JVD
- Hepatomegaly
- Ascites
- Cyanosis
- Increased CVP
113
What 2 factors are expected in the event of Heart failure?
1. Inadequate Cardiac Output (CO)
2. Compensatory mechanisms
Inadequate CO from whatever origin can trigger compensatory mechanisms
114
What compensatory mechanisms get triggered by heart failure?
To be specific, inadequate cardiac output triggers the following:
- Frank starling mechanism (stretch)
- Increased SNS activity
- RAA mechanism
- Myocardial hypertrophy
115
Briefly describe the frank starling mechanism
Increased preload = increased stretch = increased force of contraction = increased stroke volume.
- **Frank starling mech is normally responsible for maintaining normal CO**
- Heart can overstretch though
116
How does the frank starling mechanism compensate for heart failure?
When end diastolic volumes increase (reflected by increased PAWP and CVP)
- **the mech becomes ineffective when the myocardial fibers overstretch**
- CO can't increase w/increased physical activity
117
How and why does the SNS mechanism trigger as a result of Heart failure?
Increased SNS activity is triggered by a decrease in SV and CO.
- Leads to systemic vasoconstriction in order to maintain perfusion to vital organs despite lower SV
- Also increases HR and contractility
118
Why is a increase in SNS activity problematic in heart failure?
Increased SVR leads to increased afterload and further myocardial demand
119
Why/how does heart failure trigger the RAA system?
- What does the trigger cascade look like?
- end results?
1. Decreased SV and CO results in decreased perfusion in the kidneys.
2. kidneys respond by releasing renin which activates the RAA system
3. Aldosterone causes sodium and water retention = **increases blood volume**
4. Angiotensin II causes **vasoconstriction**
5. Culmination of the above increases end diastolic volumes and increased CO via frank starling mech
120
What is the main problem with compensatory mechanisms?
inefficiencies and failure lead to volume problems
- Snowballs into frank starling mech (overstretch)
- leads to decompensated heart failure
121
What does increased SVR lead to in decompensated heart failure?
Increase in myocardial demand
122
What does increased HR lead to in decompensated heart failure?
Increase in myocardial demand, shortens diastole
123
What does stimulation of the RAA system lead to in decompensated heart failure?
Increases in filling pressure, further contributes to fluid overload worsening clinical manifestations
124
What does stimulation of the Frank Starling Mechanism lead to in decompensated heart failure?
Overstretch in myocardial fibers
125
How does Myocardial Hypertrophy lead to in decompensated heart failure?
Increase in myocardial oxygen requirements, may reduce chambers size causing diastolic failure (ventricle gets more muscular and large = less space in chaber)
126
How does heart failure present on a CxR?
- Cardiomegaly
- Left heart failure = diffuse bilateral infiltrates (butterfly pattern), pleural effusions, kerley B lines
127
What exams can be used to help diagnose heart failure?
- Echocardiography
- ECG (see MI or abnormal arrhythmias)
128
What are *acute* treatments for heart failure? (3)
- acute = active but short term
- list the primary's in this card
1. Preload reduction via **diuretics** (and others)
2. Afterload reduction via B-blockers
3. Inotropic support (use w/caution) via milrinone, digoxin, dobutamine, dopamine, NE etc.
- O2 and NIPPV during this if pulmonary edema is present
129
What drugs can be given to reduce preload?
- Diuretics
- Nitroglcerin
- morphine
130
What are acute treatments for pulmonary edema?
1. Oxygen and NIPPV
2. Diuretics
131
What drugs can be given to reduce afterload?
- B-blockers
- Nitroglyercin, nitroprusside
- ACE inhibitors
132
Why does CPAP work well for CHF?
CPAP pushes back fluid and surfactant back to where it should be
133
What does a 1:1 ratio on a intra aortic balloon pump mean?
It inflates/deflates for every beat of the heart
134
If a patient is on BiPAP for heart failure, what back up rate should you ensure is used?
4
- Ensure they're getting ventilated
- Ensure they're hitting their rates and Vts
135
When using NIPPV for heart failure (acute treatment) when would you use BiPAP vs CPAP?
- BiPAP = SOB and has WOB
- CPAP = no WOB
136
Aside from a back up rate, what should you monitor and ensure is set appropriately on the patient?
Titrate IPAP to appropriate Vt
137
What are general/long term treatments for heart failure?
- Restriction of dietary sodium
- Diuretics
- Nitroglycerin or long acting nitrates
- ACE inhibitors/B-blockers
- Cardiac rehab
138
What are 2 types of Valvular Disorders?
Stenosis and Incompetence
139
What are Valvular Disorders defined as?
A disorder that can affect any one of the 4 heart valves
140
What are Incompetence mechanical disruptions in Valvular Disorders?
Valve does not close properly; resulting in **regurgitant flow**
141
What is reflected by poor valvular function?
- Obstruction in the flow of blood (stenotic valve disorder)
- Allowing backward flow of blood (regurg)
142
Why would stenosis occur?
Narrowing can be caused by thickening of stenotic valve leaflets
143
Why would a Transesophageal echocardiography (TEE) be used for patients in prolonged a.fib?
Need to make sure there isn't a big clot before we cause their valve to shut and push further into further if there is one
