Exam 2 Flashcards
(329 cards)
1
Q
4 non-modifiable major risk factors for atherosclerosis
A
increasing age
male gender
family history
genetic abnormalities
2
Q
5 modifiable major risk factors for atherosclerosis
A
**cigarette smoking** hyperlipidemia hypertension diabetes C reactive protein
3
Q
3 minor modifiable risk factors for atherosclerosis
A
inactivity
stress
obesity
4
Q
Atherosclerotic risk factors are synergistic and therefore impose more than an additive effect - describe how much the risk increases with two and three risk factors, respectively
A
two risk factors = 4 fold risk
three risk factors = 7 fold risk
5
Q
What is the most important component of the total cholesterol in increasing coronary risk?
A
LDL
6
Q
The ratio of LDL to HDL should be no more than what?
A
4 to 1
7
Q
As total serum cholesterol rises above what level does coronary risk increase linearly?
A
160 mg/dl
8
Q
Name one significant risk factor (lipoprotein) related to atherosclerosis that is independent of LDL levels
A
lipoprotein A
9
Q
List the 6 dyslipoproteinemias as well as what major changes they’re associated with in terms of lipid levels
A
I - familial lipoprotein lipase deficiency (increased chylomicrons, no premature AS)
IIa - familial hypercholesterolemia (increased LDL, premature AS)
IIb - familial combined hypercholesterolemia (increased LDL and VLDL, premature AS)
III - familial type III lipoproteinemia (increased IDL, premature AS)
IV - familial hypertriglyceridemia (increased VLDL, premature AS)
V - only familial AI/CII deficiency - no HDL, severe AS
10
Q
Name 4 secondary genetic disorders associated with dyslipoproteinemias and atherosclerosis
A
nephrotic syndrome
hypothyroidism
alcoholism
diabetes mellitus
11
Q
After what age does hypertension become a stronger risk factor (5 fold) for atherosclerosis than hypercholesteroemia?
A
age 45
12
Q
Tell me about the impact of smoking vs. not smoking in the development of athersclerosis
A
risk of disease increases 200% for smokers
leading preventable COD in US is smoking
cessation of smoking halves the increased risk - 50% reduction in year 1
by year 5 after smoking cessation, risk of CAD or MI approximates that of non-smokers
13
Q
Describe the relation of diabetes mellitus to atherosclerosis in terms of how it relates to accelerated disease progression
A
MI = two fold increase
stroke = significantly increased incidence
gangrene = 100 fold increase in incidence
14
Q
What does the CRP test indicate to us about atherosclerosis ?
A
as CRP levels go up, it indicates over time that atherosclerosis goes up because it is an inflammatory process
CRP = C reactive protein, an acute phase protein
15
Q
Describe two unusual associations with atherosclerosis in terms of illnesses/disease states
A
- elevated plasma homocysteine - folate and vitamin B treatment reduces cardiovascular disease in women
- Clamydia pneumonia presence in plaques - antibiotic tx DOES NOT reduce recurrent ischemic clinical events in patients
16
Q
List the 5 features of atherosclerotic lesions that make them histologically similar to a chronic inflammation reaction
A
- inflammation by macrophages and lymphocytes
- mesenchymal cell proliferation
- fibrosis
- cell necrosis
- neovascularization
17
Q
Many of the recognized mediators of inflammation appear in atherosclerotic lesions; name a few
A
oxygen-derived free radicals, proteolytic enzymes, immune complexes, cytokines and growth factors, components of complement, prostaglandins and leukotrienes
18
Q
Describe the 3 primary components of the current hypothesis for atherogenesis
A
- starts with endothelial cell injury (non-denuding) induced by hypercholesterolemia, disturbed flow, etc
- vascular response to injury
- macrophages release agents locally which sustain a chronic inflammatory reaction
19
Q
Describe the process of endothelial injury as it occurs and kicks off the process of atherogenesis
A
- triggering event
- endothelial cells overexpress VCAM1 which increases cellular adhesion, recruits inflammatory cells and releases cytokines
- primarily tissue macrophage will accumulate modified lipids to form foam cells and fatty streaks
20
Q
Macrophages are a key player in inflammation - describe 4 major influences they have on the development of atherosclerosis
A
- plasma LDL, on entry into the intima, undergoes MODIFICATION OR OXIDATION by free radicals and taken up by macrophages via scavenger receptors and others to become foam cells
- oxidized LDL is CYTOTOXIC to endothelial cells, and acts to attract, proliferate, immobilize and activate the macrophage
- macrophages, SMCs, and endothelial cells release MCP1, which recruits more monocytes in the media, and causes recruitment and proliferation of smooth muscle cells
- activated macrophages release ADDITIONAL CYTOKINES
21
Q
Atherosclerotic lesions also contain lipid accumulations, which can be seen histologically by what type of cells?
A
foam cells
22
Q
What are foam cells?
A
macrophages (and smooth muscle cells) whose cytoplasm is packed with droplets of cholesterol esters
23
Q
Foam cell action leads to the release of what 3 kinds of cells/proteins in the cell in the development of atherosclerosis?
A
growth factors
hydrolytic enzymes
active oxygen metabolites
24
Q
Describe the process of atherogenesis as it progresses from endothelial cell dysfunction to plaque formation (7)
A
- endothelial cell dysfunction due to triggering events
- recruitment of monocytes - adhesion and emigration into intima
- release of inflammatory mediators like cytokine MCP1 and oxidation of LDLs
- activation of macrophages
- foam cell formation with lipid uptake in macrophages
- release of cytokines, MMPs, ROS, tissue factor and recruitment of smooth muscle cell precursors then proliferation
- atherosclerotic plaque formation and death of macrophage
25
Name the 3 key features of atherosclerosis
smooth muscle cell proliferation
accumulation of CT elements (collagen, elastin, proteoglycans)
lipid deposition (intra and extracellular)
26
PDGF is important in the development of atherosclerosis - what does it do?
important in causing proliferation of smooth muscle cells in atherosclerotic lesions
27
List the 5 primary cell types associated with atherosclerosis development and a couple important proteins/cell factors
```
endothelial cell
smooth muscle cell
platelets
macrophages
T lymphocytes
```
LDL, PDGF, MCP1
28
Name 3 characteristic lesions of atherosclerosis
fatty streaks
proliferative lesions
firbofatty plaques (Atheroma)
29
Hemodynamics play a role in atherogenesis - describe 3 ways how
- pressure (hypertension is a risk factor in development)
- regions of low shear and/or disturbed flow
- flow recirculation zones (eddies) - associated with arterial branches and bifurcations
30
Why does it matter if there are regions of low shear and/or disturbed flow in the vasculature?
atherosclerotic plaques form in regions of low and/or unstable shear stress
lesions often form in the branch points of vessels where there are changes in flow
leads to development of eddies
31
Active MMPs play what role in the development of atherosclerosis?
lead to basement membrane degradation and endothelial cell death
32
Name 4 complications that can result from atherosclerotic lesions
1. calcification
2. hemorrhage
3. thrombosis
4. ulceration or rupture (majority of MI's due to this)
33
Describe the composition of a "vulnerable" plaque, as well as the risks associated with them and some major consequences of them
- soft plaques with lipid-filled cores, most often eccentric, most often only 40-60% stenotic
- prone to rupture (shoulder region) due to plaque hemorrhage or to fibrous cap disruption
- thrombotic occlusion of coronary artery and acute MI or ischemia
- moderately stenotic, vulnerable complex plaques are hard to detect/treat prophylactically
34
Name 4 plaque changes that are all risk factors in developing acute coronary syndrome
superficial erosion
ulceration
fissuring
deep hemorrhage
35
Vulnerable plaques undergo inflammatory changes and what else as they progress to causing an MI?
rupture, release WBC, form thrombus
36
What is the earliest sign of endothelial dysfunction?
formation of foam cells (made of macrophages and oxidized LDL)
37
What is an atheroma?
accumulated lipid, cells and other components of a plaque disrupt the artery wall
38
2 stages of atherosclerosis development in the first decade
foam cells
| fatty streak
39
2 stages of atherosclerosis development in the third decade
intermediate lesion
| atheroma
40
2 stages of atherosclerosis development in the fourth decade
fibrous plaque
| complicated lesion rupture
41
Differentiate between pre-clinical phase and clinical phase of atherosclerosis
PRE-CLINICAL (young) =
normal artery >> fatty streak >> fibrofatty plaque >> advanced/vulnerable plaque
CLINICAL (middle age and elderly) =
aneurysm and rupture, occlusion by thrombus, critical stenosis
42
List the primary therapies in clinical atherosclerosis used in asymptomatic or anginal stages with atherosclerotic plaques
statins, control BP and DM, control clotting, diet and lifestyle change
43
List the secondary therapies used in clinical atherosclerosis when ACS or stroke may occur due to plaque rupture and/or thrombus formation
tissue plasminogen activator, angioplasty with stent placement (coronary or carotid), carotid endarterectomy, CABG
44
Atherosclerotic lesions tend to be localized how?
atherosclerosis is a focal, segmental disease
adjacent regions may be totally uninvolved
affects major arteries
occur around heart, at branch points, at non-branch points, superficial leg, etc.
45
What is the ankle brachial pressure index (ABPI) and why is it important?
ABPI value greater than 1.3 is considered abnormal, and suggests calcification of the walls of the arteries and incompressible vessels, reflecting severe peripheral vascular disease
ABPI may be an independent predictor of mortality, as it reflects the burden of atherosclerosis
Simple, inexpensive, non-invasive
High sensitivity and specificity
Patient needs to have been supine for 10 minutes
Normally, BP in legs is similar to arms
Perform in every smoker over 50, every diabetic over 50, all patients over 70
>/= 1.0 to 1.4 ratio of ankle to brachial = normal
46
Atherosclerosis results in ISCHEMIC INJURY to the organs and tissues nourished by affected arteries; list 5 important clinical manifestations of this
```
MI
ischemic stroke
peripheral arterial disease (can lead to gangrene)
visceral infarction
atherosclerotic aneurysms
```
47
How can the identification of an atherosclerotic plaque in one place be a warning sign?
plaques found in one area of the vascular tree are usually accompanied by lesions in other areas as well
48
Describe the symptoms of atherosclerosis
the silent killer!
does not produce symptoms until it severely narrows the artery or until it causes a sudden obstruction
symptoms depend on where disease occurs
critical stenosis begins when a diseased artery has a 50% reduction in internal diameter (75% reduction in luminal area)
Most commonly - intermittent claudication
Severe disease - hair loss, thickened nails, smooth/shiny skin, reduced skin temp, pallor/cyanosis, pain while at rest, ulcers or gangrene
49
Describe Glagov's coronary remodeling hypothesis for atherosclerosis
lumen size is the same regardless of CAD until you overstretch the serosa enough that the buildup of the plaque actually reduces lumen size because the artery can no longer compensate by expanding outward
50
What is the importance of coronary remodeling in atherosclerosis?
remodeling preserves lumen size
51
Describe the differences found on coronary angiogram 4 hrs after an MI and 12-24 hrs after an MI
4 hrs after = thrombosed coronary artery in 90% of patients
12-24 hrs after = occlusion seen only in 60% of patients, suggesting some occlusions resolve due to fibrinolysis, relaxation of spasm, or both
52
Blood flow is restricted only in highly stenosed vessels - explain the relevance of this
when the lumen is reduced by 70-80% of its normal area, the vessel can no longer dilate enough to meet demands for increased blood flow (i.e. during exercise)
53
Most common cause of a heart attack
atherosclerosis
54
Which family of lipoproteins are all atherogenic?
apoB
55
Which lipoprotein is present in HDL?
apoA1
56
chylomicrons
made in intestines
delivery dietary triglycerides to tissues via hydrolysis by LPL
57
VLDLs
made in the liver
deliver triglycerides from the liver to extra-hepatic tissues (mainly by LPL)
58
LDLs
deliver cholesterol/cholesterol esters to tissues, including teh liver
59
HDLs
made primarily in the liver
reverse cholesterol transport from extra-hepatic tissues to the liver
60
Lp(a)
LDL with an additional apo(a) chain attached to its apoB 100
structurally similar to plasminogen
increased CV risk from atherogenicity, reduced plasmin generation, inflammatory state
genetic predisposition, resistant to diet or most meds
61
small dense LDL
development produced by insulin resistance, high TG, low HDL environment
increased atherogenicity
may result in underestimation of LDL particle number and total LDL burden
62
ACC/AHA's 4 major statin benefit groups
1. secondary prevention - clinical ASCVD: high intensity tx unless can't tolerance or >75 yoa; then start with mod intensity tx
2. primary prevention - individuals with primary elevations of LDL-C greater than or equal to 190 mg/dl: high intensity tx
3. primary prevention - diabetics age 40-75 and LDL-C 70 to 189 mg/dl: moderate to high intensity tx
4. primary prevention - without diabetes, but an estimated 10 year CVD risk 7.5% or higher, age 40 to 75 and LDL-c 70 to 189: moderate to high intensity therapy
63
Common adverse effects associated with statin use
```
myopathy
hepatotoxicity
diabetes
CNS - memory loss
GI complaints
```
64
Role of PCSK9 molecule in lipid metabolism
proprotein convertase subtilisin kexin type 9
regulates expression of LDL receptors - handcuffs LDL particle to receptor, so receptor is broken down, too
65
Inhibiting PCSK9 affects the lipid profile how?
decreases LDL via increased clearance and increased LDL receptor levels
reduces LDL-C 60-70%
66
Hepatic lipase
hydrolyzes TAGs in IDL to facilitate conversion to LDL
67
CETP
transfers cholesteryl esters from HDL to other lipoproteins in exchange for TG, phospholipids and cholesterol
present on HDL
68
LCAT
transfers fatty acids from lecithin to C to form CE in HDL
keeps cholesterol concentration low in the phospholipid monolayer
present on HDL
69
What do pacemakers do? What are they composed of?
identify intrinsic cardiac electrical activity and provide electrical stimuli to cause cardiac contraction when cardiac activity is inappropriately slow or absent
composed of pulse generator and lead system
70
Pulse generator of pacemaker
placed Subcutaneously or submuscularly
power source: lithium-iodine battery, lifespan 5-10 years, output voltage decreases gradually
predictable end of life behavior with low risk of sudden failure
71
Pacemaker lead system
endocardial leads placed via central access - placed in right ventricle and/or atria
conductor surrounded by insulation
fixed to endocardium via screws or tines
72
AAIR vs. VVIR
atrial lead = AAIR
ventricular lead = VVIR
73
Capture
the depolarization and resultant contraction of the atria or ventricles in response to a pacemaker stimulus
74
Capture Threshold
the minimum amount of electrical energy that consistently produces a cardiac depolarization
75
Strength-Duration Relationship (pacemaker)
Voltage over time (time that is required for a depolarization)
Rheobase - the minimum energy that given over an infinite time will result in stimulation
Chronaxie - the minimum duration for an impulse that is 2X rheobase to result in stimulation
76
Fusion beat
when pacemaker output occurs at the same time as an intrinsic beat and BOTH CONTRIBUTE to the depolarization
the beat is a fusion of paced beat and intrinsic beat (produces a moderately sized spike)
77
Pseudofusion
when an intrinsic impulse occurs before the pacemaker output is delivered
the pacemaker output DOES NOT contribute to the depolarization and the beat looks like an intrinsic beat on the ECG (usually a narrow QRS with a spike in it)
78
Atrial sensing/inhibition
AAI
79
Ventricular sensing/inhibition
VVI
80
List 3 possible pacemaker complications
- failure to output (should send out beat but doesn't)
- failure to capture (sends something out but it isn't sensed)
- sensing abnormalities
81
Pacemaker failure to output, definition and etiologies
No pacing spike present despite indication to pace
battery failure, lead fracture, break in lead insulation, oversensing, cross-talk
82
Pacemaker failure to capture, definition and etiologies
pacing spike is not followed by either an atrial or ventricular complex
lead fracture or dislodgement, break in lead insulation, elevated pacing threshold, MI at lead tip, drugs, metabolic issues, cardiac perforation
83
Sensing abnormalities of pacemaker
pacemaker does not recognize normal beats and generates an unnecessary pacemaker site
84
5 indications for a pacemaker
- patients with symptomatic bradycardias
- sinus node disease
- AV node blocks
- certain pts requiring meds that slow the heart
- resynchronization therapy for pts with heart failure
85
Definition of heart failure
clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood
86
Cardiac dyssynchrony in CHF
dyssynchronous contraction btwn septum and side wall of left ventricle
results in ineffective pumping with reduced stroke volume and cardiac output
pts with ejection fraction <35% and QRS >120 ms
87
Cardiac resynchronization therapy (CRT)
biventricular pacing
resynchronizes contraction of left ventricle to improve stroke volume and reduce oxygen demand
improves symptoms of CHF and reduces mortality
88
Magnet inhibition**
closes an internal reed switch: causes sensing to be inhibited, temporarily turns pacemaker into "asynchronous" mode (Set rate) >> VOO
DOES NOT TURN PACEMAKER OFF
rate provides info about battery life - distinct rates for BOL (beginning of life), ERI (elective replacement indicator), and EOL (end of life)
89
ICD
implantable cardioverter defibrillator
90
Therapies provided by today's dual-chamber ICDs (atrium, vent, and both)
Atrium = AT/AF tachyarrhythmia detection
Vent= VT/VF detection, antitachycardia pacing, defibrillation
Both = bradycardia sensing and pacing, biventricular pacing
91
Indications for an ICD**
patients with dilated cardiomyopathy are at increased risk of fatal ventricular tachyarrhythmias
ICD indicated for PRIMARY PREVENTION of sudden cardiac death in pts with NYHA class II to III heart failure, LVEF 35% or less
92
List 4 possible ICD complications
- sensing and pacing failures
- inappropriate cardioversion
- ineffective cardioversion/defibrillation
- device deactivation
93
ICD failure to deliver therapies - etiologies and appropriate failure to treat
Etiologies: failure to sense, lead fracture, electromagnetic interference, inadvertent ICD deactivation
appropriate failure to treat: if programmed cut off at 180 bpm and Vtach occurs at 160 bpm, no therapies will be delivered
94
ICD inappropriate shocks - definition and etiologies
provokes pain and anxiety
etiologies - rapid sinus tachycardia, SVT, a fib, T wave oversensing, lead fracture, insulation breakage, electromagnetic interference
95
Describe the management of ICD inappropriate shocks
treat underlying arrhythmia
magnet over ICD will inhibit further shocks: does NOT inhibit bradycardic pacing, may hear a "beep" when magnet applied, pt needs to be monitored and external defibrillator immediately available until device reprogrammed
96
4 examples of electromagnetic interference
metal detectors, cell phones, arc welding, medical cautery devices
97
Dry lungs vs. wet lungs and intrathoracic impedance monitoring
dry lungs - high impedance
wet lungs - low impedance
98
Hoff's definition of atherosclerosis
fatty infiltration of the tunica intima (endothelial layer) of a coronary artery, with or without significant luminal narrowing
99
Describe the pathogenesis of atherosclerosis according to Dr. Hoff
response to injury model:
endothelial injury (CO, LDL, mechanical)
monocytes attach to endothelial cell
growth factors released
platelets may participate
complex lesions evolve over years
100
Dr Hoff mentions four major cellular players in atherosclerosis development - name each
endothelial cells
smooth muscle cells
macrophages
platelets
101
Describe the role of the endothelium in the development of atherosclerosis
- first site of lesions
- monolayer with receptors for many molecules
- produces vasoactive substances
102
Describe the role of smooth muscle cells in the development of atherosclerosis
- more advanced lesions
- foam cells (lipid-laden)
- may participate in growth of lesions
103
Describe the role of macrophages in the development of atherosclerosis
- scavenge foreign substances
- secrete chemotactic factors
- principal cells of early lesions
- foam cells
104
Describe the role of platelets in the development of atherosclerosis
- may be important in initiating lesions
- secrete potent molecules (i.e. growth factors)
- stimulate vasoconstriction and thrombosis
105
Fatty streak lesion
- earliest evidence of atherosclerosis - even seen in children and young adults
- intimal collection of macrophages and lipid-laden smooth muscle (Foam cells) by age 10
- probably convert to complex lesions
106
Intimal thickening and atherosclerosis
may be simple thickening or a response to stress
107
Fibrous plaque
- advanced lesion - cholesteryl esters, debris, etc.
- white, raised, impinges on lumen, can limit perfusion
- may become complicated by: calcification, ulceration, hemorrhage into plaque, thrombosis
108
List the 3 major modifiable risk factors for atherosclerosis according to Dr. Hoff
cigarette smoking
diabetes
hypertension (140/90 or on meds)
109
Describe the role of family history of premaure CAD as a risk factor for atherosclerosis
CAD in male first degree relative <55
CAD in female first degree relative < 65
110
Most common cause of death in diabetic patients
atherosclerosis and its consequences
111
How does diabetes play into the risk of developing atherosclerosis?
diabetes is a "risk equivalent" for CAD with 10 yr risk of a hard CVD event >20%
112
What is diabetic dyslipidemia?
abnormal lipoproteins
smaller, denser LDL particles; LDL near normal
low HDL
elevated triglycerides
113
What is metabolic syndrome? (requires any 3)
- diabetic dyslipidemia
- primary arterial hypertension
- central abdominal obesity
- insulin resistance - may be the central factor
114
What is the prevalence of metabolic syndrome in CAD patients?
50%
115
Describe the mechanisms by which cigarette smoking enhances atherosclerosis (6)
- hemodynamic stress (increase HR & BP)
- endothelial injury and dysfunction (inhibit NO production)
- atherogenic lipid profile (increase LDL and decrease HDL)
- enhanced coagulability
- arrhythmogenesis
- relative hypoxia (carbon monoxide)
116
List 4 associated outcomes with coronary atherosclerosis
1. acute coronary syndromes (ACS): unstable angina pectoris (MI), myocardial infarction (STEMI and non-STEMI)
2. sudden death (primary VT/VF)
3. dilated (ischemic) cardiomyopathy
4. atrial fibrillation/flutter
117
4 methods of primary prevention of atherosclerosis
appropriate diet, regular exercise, optimum weight, stop smoking
118
Secondary prevention methods for coronary atherosclerosis (pt has ASCVD or risk equivalent)
- treat dyslipidemias with statin
- treat diabetes (HbA1C <7)
- control BP
- stop smoking
- regular, mod. exercise
- optimize weight
- dietary changes
119
What 3 things have the most influence on oxygen demand in the heart?
heart rate
contractility
systolic wall tension
120
What factors influence supply to the myocardial tissue?
extravascular compressive forces, neural control, humoral factors, autoregulation, metabolic control all affecting vascular resistance
diastolic phase affecting coronary blood flow
oxygen carrying capacity affecting supply
121
In ischemia, demand exceeds fixed supply, name 3 etiologies
coronary occlusive disease
coronary spasm
combinations (mixed angina)
122
Describe the hemodynamic effect of coronary spasm in obstructive coronary atherosclerosis (4 steps)
atherosclerotic lesions (40% obstruction)
superimposed vasoconstriction (80% obstruction)
reduced distal flow
myocardial ischemia
123
Angina pectoris
heavy, pressure, band-like, crushing
often silent (i.e. asymptomatic)
124
Stable vs. unstable angina
stable = same pattern each time
unstable = new onset, subjectively worse discomfort onset with less activity, angina at rest (decubitus)
125
Angina pectoris
heavy, pressure, band-like, crushing
often silent (i.e. asymptomatic)
men 5.7%, women 6.7%
126
Tell me what we use stress testing to diagnosis, what the prognosis indicates
Diagnosis of atypical chest discomfort
Prognosis: stable angina, post-MI, post-revascularization
127
Exercise stress testing
- treadmill (usual) provides graded level of exertion
- bicycle ergometer
- exercise to 85% predicted max HR for age
128
Pharmacologic stress testing
- used when exercise is impractical/impossible
adenosine, dipyridamole: vasodilate, therefore increase HR and work
dobutamine: increased contractility aka increased oxygen demand
129
Describe what a positive stress test presents as (3 ways)
1. segment shift: ST depression (subendocardial) vs. elevation (transmural)
2. development of symptoms (angina), esp. at low stress
3. development of ventricular dysrhythmia - VPDs or VT
130
Stress testing is highly predictive if one of two things is present - what are they?
typical symptoms of angina develop
OR
ECG shows horizontal or downsloping ST depression of 1 mm or more at 80 ms (0.08 sec) after J point
131
How do we know that a dx is certain with a stress test?
ST depression > 2mm
132
What is the value of adding imaging (echo or nuclear) to stress testing? (4)
- Increases predictive power
- Superior to plain stress testing for dx of myocardial ischemia
- aids in dx of multivessel disease, localizing the culprit vessel
- info on extent of myocardial impairment or injury
133
Describe the 3 possible outcomes of myocardial ischemia
myocardial infarction >> no return of contractile function
chronic ischemia without infarction >> persistent ischemic dysfunction: hibernating myocardium >> relief or stunned paths
relief of ischemia >> salvage of previously ischemic myocardium >> transient dysfunction = stunned >> return of contractile function
134
Describe the development of irreversible injury/infarction from myocardial ischemia
Depletion of high-energy phosphate bonds:
- ATP not replaced (lost oxidative metabolism)
- sarcolemmal gradients of Na, K reduced
- Ca2+ overload: phospholipases, proteases activated, mitochondrial death, activation of ATPases
Catabolite accumulation: enzyme denaturaion, membrane damage, cell swelling, cell death
135
Describe the methodolgy behind reducing myocardial injury (6)
1. Increase oxygen supply: reperfusion (thrombolysis, PCI, CABGs), coronary vasodilation (nitrates, dihydropyridines)
2. Decrease oxygen demand: beta blockers (decrease HR & contractility), decrease BP, reduce preload (diuretics, nitrates), reduce circulating catecholamines
136
Nitrates and myocardial ischemia therapy
- decrease preload (Venodilators): decreased LV filling means decreased LV size and less wall tension
- coronary dilation, possibly even in stenotic segments
- enhance endothelial function
- decrease O2 demand by reducing demand and increasing supply
137
Beta blockers and myocardial ischemia therapy
- decrease HR and contractility (decrease oxygen demand)
| - NO EFFECT ON OXYGEN SUPPLY
138
Calcium antagonists and myocardial ischemia therapy
- variable properties depending on molecule
- prevention of spasm (relaxed vasomotor tone?)
- reduction of afterload via vasodilatory effects
- some (i.e. verapamil, diltiazem) reduce contractility and/or heart rate
- REDUCE OXYGEN DEMAND AND INCREASE SUPPLY
- used infrequently
139
Describe the favorable effects of calcium antagonists in chronic stable angina
- afterload reduction
- verapamil and diltiazem reduce heart rate slightly
- reduction in contractility but some make HR increase
- may dilate coronary arteries
140
Name the 2 reperfusion strategies/procedures for myocardial ischemia
Percutaneous Coronary Intervention (PCI) = angioplasty/stent
Coronary Artery Bypass Graft Surgery (CABGS)
141
What is the most common reason for visits to the doctor AND for the use of prescription drugs in the US?
Systemic arterial HTN
142
Which sex is more likely to have hypertension?
males
143
Which race is most likely to have hypertension?
non-hispanic blacks
144
What's the lifetime risk of normotensive people at age 55 for developing hypertension?
90%
145
What's one word you would use to describe the risk factors for hypertension as a group?
synergistic
146
What's the significance/outcomes of the JNC 8 guidelines for systemic hypertension?
- does not change the definition of hypertension
- makes recommendations for BP levels to begin drug therapy depending on: age, coexisting conditions (i.e. diabetes, renal disease), and race
- based on best evidence available
147
How will using a blood pressure cuff that is not the correct size affect your reading?
Narrow cuff or too-loose cuff will overestimate BP
148
You're supposed to take the BP in both arms. Which reading do you use if one is higher for one arm than the other?
use the arm with the higher reading
149
Describe the indirect (Korotkoff) vs direct methods of taking BP
Indirect:
- inflate cuff 20 mmHg above anticipated SBP
- deflate no faster than 2-3 mm Hg per sec
- record 1st and 5th sounds (except in kids)
Direct: intra-arterial catheter
150
Tell me what the 5 Korotkoff sounds are
1. tapping sounds appear
2. soft murmurs
3. louder murmurs
4. muffling of sounds
5. disappearance
151
Borderline hypertension
BP only occasionally exceeds normal
152
Primary hypertension
elevated systemic BP without known cause
153
Secondary hypertension
elevated systemic BP for which a cause can be identified
154
Hypertensive emergency
Life-threatening
Focal or generalized symptoms of acute, ongoing, target organ damage (retinal/CNS, cardiac, etc) requiring a rapid reduction of BP
(dBP generally 120 or more)
155
Malignant hypertension
now called hypertensive retinopathy grades III & IV and severe BP elevation
indicative of target organ damage
156
Hypertensive encephalopathy
signs and/or symptoms of cerebral edema caused by severe and/or sudden rises in BP
(BP high and patient often in stupor)
157
Describe the 4 grades of hypertensive retinopathy according to the Keith-Wagener Barker indications
Grade 1 - arteriolar narrowing
Grade 2 - AV nicking
Grade 3 - hemorrhages/exudates
Grade 4 - papilledema
Grades 3 and 4 are indicative of target organ damage
158
List a few severe possible CNS consequences of hypertension
- decreasing cognitive function with age
- transient ischemic attack (extracranial atherosclerosis)
- stroke, either thromboembolic or hemorrhagic
159
Describe the ways in which renal function is disturbed with systemic hypertension
- subtle renal dysfunction may be a root cause of primary systemic arterial hypertension
- intraglomerular hypertension results in albuminuria (glomerular leak) in most SAH patients
- nephrosclerosis results in loss of renal concentrating ability - end result is renal failure and eventually uremia
160
What is the leading cause of end-stage renal disease?
systemic arterial hypertension
161
Describe what happens with the cardiac and vascular tissue as a result of hypertension
Cardiac:
Early = increased LV mass results in loss of LV diastolic function (poor filling)
Chronic = LVH with eventual LV dilation and failure with eventual death
Vascular:
SAH is one of the major risk factors for ASCVD, MI, heart failure and sudden cardiac death
162
List 5 vascular complications of hypertension related to being hypertensive
accelerated malignant phase, hemorrhagic stroke, congestive heart failure, nephrosclerosis, aortic dissection
163
List 5 atherosclerotic consequences of hypertension
coronary heart disease, sudden death, other arrhythmias, atherothrombotic stroke, peripheral vascular disease
164
What are the 3 goals of evaluating systemic hypertension in a patient?
- assess cardiovascular risk factors and/or disorders that will affect tx
- look for identifiable reasons for SAH
- determine target organ damage if any (renal, CNS, cardiac)
165
List some identifiable causes of secondary hypertension
Chronic renal parenchymal disease, primary aldosteronism, renovascular disease, chronic steroid therapy, pheochromocytoma, coarctation of aorta, sleep apnea, thyroid or parathyroid disease, drug induced
166
Most often, SAH is asymptomatic. However, list some symptoms related to the CNS that a patient may present with
headache, dizziness, blurred vision, confusion, stupor, stroke/TIA
167
Most often, SAH is asymptomatic. However, list some symptoms related to the cardiovascular system that a patient may present with
chest pain, dyspnea on exertion, palpitations, impotence, epistaxis
168
Most often, SAH is asymptomatic. However, list some symptoms related to the renal system that a patient may present with
hematuria
169
What are some key things to ask in a history if your patient has/may have SAH?
age, race, ethnicity, symptoms of target organ damage, family history, other illness/previous BP issues, risk/symptoms suggesting secondary HTN, lifestyle, meds
170
List some cardiovascular risk factors associated with hypertension
smoking, obesity, dyslipidemia, diabetes, age for men >55 and women >65, sedentary lifestyle, family history of premature cardiovascular disease in men <55 and women <65
171
List 5 diseases that are especially significant in a patient with hypertension
ischemic heart disease (IHD) = most common form of target organ damage
heart failure = often a result of systemic hypertension and IHD
diabetes
chronic kidney disease (microalbuminemia or estimated GFR <60 ml/min)
cerebrovascular disease
172
List some important parts to include on physical exam in a patient with hypertension (7)
general appearance and vitals, serial/bilateral BP measure while sitting, HEENT with fundoscopic exam**, pulmonary, cardiovascular including carotid pulses, abdominal especially aortic bruits, neurologic
173
How to determine the correct cuff size for BP
2/3 length of upper arm
bladder should encircle the arm at least 80%
mercury manometer best
174
Patient guidelines for food/drink prior to BP measurement
```
at least 5 min of quiet
no caffeine 1 hour
no smoking 15 min
no adrenergic stimulants
quiet, warm setting
```
175
List the parts of a minimum lab evaluation in new cases of SAH (7)
```
dispstick urinalysis
fasting blood glucose
hematocrit
serum creatinine
serum K+ and Ca2+
lipid panel
ECG
```
176
ECG for SAH patient (when is it indicated)
- indicated if diastolic 90-94 and no other CV risk factors or target organ damage
- indicated if severe or refractory SAH - absence of LVH in this setting suggests HTN of recent onset or white coat HTN
- also when concomitant heart disease needs evaluation or if the type of heart disease suggests a specific antiHTN therapy
- pts who have bundle branch block on ECG
- if LVH seen on echo, medical tx needed >>> non-pharmacological tx if LV mass is normal
177
Describe the pathology of atherosclerosis as well as which arteries are most commonly involved
Segmental lesions causing stenosis or occlusion usually localized in large and medium-sized vessels
Involve:
abdominal aorta & iliac arteries 30%, femoral and popliteal 80-90%, more distal vessels 40-50%
178
List some non-invasive testing that can be performed for atherosclerosis
H & P, digital pulse volume recordings, duplex US, doppler, transcutaneous oximetry, stress testing, MRA, segmental pressure measurements
179
Definition of shock
that state wherein the cardiovascular system cannot maintain adequate cellular perfusion
tissue oxygenation & nutrient flow deficient - result is cell dysfunction, then tissue dysfunction
may quickly become irreversible, leading to immediate death
180
4 components of tissue perfusion
cardiac function - preload, afterload, contractility, HR, venous return
arterial pressure
vascular function - distribution of cardiac output, microvascular functions
cell function - oxygen delivery (cell energy generation, substrate utilization)
181
Name the 3 classes of shock
cardiogenic, hypovolemic, distributive
182
Cardiogenic shock
severe myocardial dysfunction with markedly reduced CO (i.e. AMI)
large amounts of contractile myocardium lost function severely depressed resulting in reduced CO (decreased LVEF)
etiologies: acute MI, dilated cardiomyopathy, valvular (acute MR, endocarditis), arrhythmia (v tach)
**LV function is the most important indicator of overall prognosis**
183
Hypovolemic shock
loss of circulating blood volume, hemorrhage, sever burns
184
Distributive shock
abnormal shunting of blood flow
many etiologies: SEPSIS, drug overdose, anaphylaxis, neurogenic, etc.
185
5 Clinical characterizations of shock
very low systolic arterial BP (60 or less), tachycardia, oliguria, mental obtundation, cool/mottled extremities
186
Hypovolemic shock
reduced/loss of circulating blood volume resulting in reduced cardiac filling and decreased CO
etiologies: blood loss (hemorrhage, severe burns), fluid depletion
187
Distributive shock
abnormal shunting of blood flow
profound peripheral vasodilation: CO can be high or normal, tissue perfusion is severely reduced
many etiologies: SEPSIS, drug overdose, anaphylaxis, neurogenic, etc.
188
5 clinical characterizations of shock
very low systolic arterial BP (60 or less), tachycardia, oliguria, mental obtundation, cool/mottled extremities
189
List some of the multiorgan consequences of shock
Acidemia, myocardial dysfunction, pulmonary (ARDS), renal (ATN), GI (hepatic injury, intestinal ischemia/injury), CNS (post-anoxic encephaloaphy; death)
190
List some general principles of therapy for shock (6)
1. intensive care: cardiac rhythm monitoring, IV meds/fluids (increase volume), ventilatory support
2. oxygen supplement if needed (pulse ox.)
3. ABGs (to manage acid/base status)
4. vasopressors as needed (dopamine)
5. inotropics as needed (dobutamine)
6. antibiotics as needed
191
Define the prognosis of shock (cardiogenic vs hypovolemic vs septic)
Cardiogenic = mortality rates >70%
Hypovolemic = mortality is directly proportional to rapidity of fluid/blood replacement, duration of hypotension, and degree of tissue injury
Septic = mortality depends on organism, duration of shock, about 40-55% die within 30 days
192
Etiologies of aortic regurgitation
Valvular: congenital bicupsid valve***, degeneration of aging, rheumatic fever, endocarditis, degeneration of bioprosthesis
Aortic root dilation or injury (50% of pure AR cases): trauma, Marfan's, annuloaortic ectasia
193
Describe the hemodynamic pathophysiology of aortic regurgitation (5)
- Blood ejected by LV regurgitates, resulting in:
- increased LVEDV & increased LVEDP = LV hypertrophy and eventual LV dilation
- LV ejection fraction becomes normal to high (includes normal EF plus regurgitant volume) and SV is normal to high
- results in marked LVH (cor bovinum)
- eventually, LV dilation and failure occur
Falling pressure in aorta during diastole
194
Name some clinical manifestations of aortic regurgitation during the history
- hx of underlying disease (RF, endocarditis)
- long illness up to 6 decades
- can by asymptomatic until LV issues start (usu. 4-5 decades in)
- DYSPNEA: classic late symptom secondary to CHF, PND, orthopnea, RV failure (portal and systemic edema)
- non-specific chest pain
- palpitations (often VPDS)
- angina pectoris (late)
195
Clinical manifestations of aortic regurgitation on physical exam
- wide pulse pressure, up to 100 mmHg
- VL apex diffuse, hyperdynamic, displaced left and downward
- S1 and S2 normal to soft (S2 may be absent, single, narrowly or paradoxically split)
- S3 common with LV dysfunction
- Aortic ejection sounds frequent
- Korotkoff sounds often persist to zero
196
Clinical manifestations of aortic regurgitation on physical exam
- wide pulse pressure, up to 100 mmHg
- VL apex diffuse, hyperdynamic, displaced left and downward
- S1 and S2 normal to soft (S2 may be absent, single, narrowly or paradoxically split)
- S3 common with LV dysfunction
- Aortic ejection sounds frequent
- Korotkoff sounds often persist to zero
- MURMURS
- MANY EPONYMOUS SIGNS
197
Describe the murmurs often heard with aortic regurgitation
Most common: diastolic, decrescendo, blowing or musical at 2nd RICS, best heard sitting forward, full expiration
the longer the murmur, the worse the regurgitation**
Austin Flint murmur: mid to late diastolic rumble of functional MS (mitral valve may be normal), anterior mitral leaflet prevented from full excursion by regurgitant jet in LV outflow
198
List some of the eponymous signs of aortic regurgitation on physical exam
Austin Flint murmur, corrigan pulse, de Musset's sign, Hill's sign, Muller's sign, Quicke's pulse, Traube's sign
199
Clinical manifestations of aortic regurgitation on ECG
not specific or sensitive
can have: LVH, left axis deviation, ST-T changes, LA enlargement, AV conduction abnormalities (late)
200
Clinical manifestations of aortic regurgitation on chest x-ray and nuclear imaging
Chest X-ray:
- may show calcification of aortic root/cusps, esp. when AR coexists with AS
- dilation/calcification of aortic root and arch
- marked cardiomegaly
- pulmonary congestion
Nuclear Imaging:
- useful in estimating LV function and severity of AR
201
Why would we use echocardiogarphy on patients with aortic regurg?
- Discover etiology: bicuspid valve, flail leaflet, thickened/calcified cusps, aortic root dilation, vegetations
- shows wall motion & thickness to assess LV function
- fluttering of anterior MV leaflet seen in diastole, even with mild AR
- can help find/estimate severity of associated AS
202
Describe the general tx plan for aortic regurgitation
- commonly long clinical course
- often associated with good prognosis for many years, even when severe (75% survive 5 yrs after dx and 50% after 10)
- findings associated with poor outcome = advanced age, progressive symptoms, atrial fibrillation, end systolic diameter of LV >25 mm/cm
- if mild to moderate AR, follow clinically/echo every 12-24 mo. and if severe, every 6 months
- if LV dysfunction, avoid vigorous sports/heavy exertion
203
Describe the pharmacologic tx used in aortic regurgitation
- Reduce high systemic diastolic blood pressure (increases AR)
- Avoid Beta Blockers
- Vasodilators (ACEI's, DHPs) to reduce afterload and improve LV ejection indicated as short term tx for HF while awaiting AVR, as chronic tx for those unable to have AVr, as chronic tx after AVR if LV dysfunction is present, in asymptomatic patients
204
Talk about the use of valvular replacement in cases of aortic regurgitation
- Contraindicated in chornic, severe asymptomatic AR, patients with good exercise tolerance, EF >50%, severe LV dilation
- Deferred when still mild or moderate AR and without symptoms
- IN THE ABSENCE OF CONTRAINDICATIONS OR SERIOUS COMORBIDITY, AVR IS ADVISABLE FOR SYMPTOMATIC PATIENTS
- patients should be followed carefully for symptoms & relative changes in LV function
205
Natural history of aortic stenosis
- Long latent period without symptoms: systolic peak gradient may be 150 mmHg or more, max LV systolic pressure can approach 300
- When symptoms develop, prognosis is poor: angina or syncope (survive 1 -3 yrs), heart failure (50% refusing surgery died in 18 months)
- With medical tx, about half survive for 5 yrs
- Valve area decreases about 0.12 cm2/year
206
List the etiologies of aortic stenosis in patients <75 yo
Congenital bicuspid about 50% of cases: congenitally stenotic valve may be unicuspid, bicuspid or tricuspid
Post-inflammatory about 25%
About 18% degenerative
207
List the etiologies of aortic stenosis in patients >75 yo
50% degenerative
27% bicuspid
25% post-inflammatory
208
Describe the hemodynamic pathophysiology of aortic stenosis
- obstruction to outflow = pressure gradient across the valve
- increased LVEDP increases wall stress
- reduced subendocardial perfusion
- LV hypertrophy
- when valve area <1 cm, most patients become symptomatic
- considered severe when area <0.5-0.7 or pressure gradient >50 mmHg
- peak of aortic pressure is after peak of LV pressure
209
Clinical manifestations of aortic stenosis on history (6)
- may give hx of rheumatic fever
- often asymp. for decades
- ANGINA PECTORIS: 2/3 of patients with critical AS, increased O2 demand plus decreased delivery owing to compression of coronaries, about half also have obstructive CAD
- SYNCOPE: commonly secondary to exertion, fixed cardiac output and systemic vasodilation result in decreased cerebral perfusion
- GI BLEEDING: angiodysplasia or idiopathic
- Heart failure: late and ominous
210
Describe clinical manifestations of aortic stenosis on physical exam (2)
Pulsus parvus et tardus =
arterial pulses are small and late, carotids display a systolic THRILL, carotids peak after LV apical impulse
Apical impulse =
sustained lift, moves left and downward in HF, systolic thrill may be found (parasternal second LICS most commonly, occasionally in suprasternal notch)
211
Describe what might be heard on auscultation with aortic stenosis
S1 may be normal to soft
S2 varies: often single, A2 may be softened, P2 can be buried in prolonged murmur, both components fuse with prolonged systole, may be paradoxically split if LV failing
212
Describe the murmur heard with aortic stenosis
commonly heart best at base of heart, crescendo/decresendo usually loud, peaks late, commonly radiates to carotids, occasionally to apex
may have diastolic murmur of AR
213
Describe what might be seen on chest x-ray and echocardiography of aortic stenosis
Chest X-ray: not specific, may show calcification of aortic root/cusps, post-stenotic dilation of aorta, cardiomegaly, pulmonary congestion late
Echocardiography - allows visualization & measurement of AoV orifice, shows wall motion & thickness to assess LV function, allows calculation of valvular pressure gradient, helps find and estimate severity of AR
214
Describe the ECG of aortic stenosis
not specific
can demonstrate: LVH, left axis deviation, ST-T changes, LA enlargement
stress ECG may be dangerous
215
Describe the general tx for aortic stenosis
- asymptomatic: watch/report
- if stenosis critical, avoid exercise
- prophylaxis against endocarditis
- clinically re-evaluate often (if mild, echo every 2 yrs, if severe by asymp. echo every 6-12 mo.)
- exercise stress test CONTRAINDICATED in symptomatic patients
216
Medical tx of aortic stenosis
- ONLY asymptomatic patients
- pharm therapy generally not used: diuretics reduce fluid burden but may cause orthostasis, digitalis to improve LV funciton, AVOID beta blockers
- atrial fibrillations should be cardioverted promptly if possible due to loss of LV filling
217
Describe the role of valve replacement in aortic stenosis (mainstay)
- requires cardiac cath and coronary angios
- usually performed when AS is severe
- aysmp. pts without LV issues are not candidates
- pts with severe stenosis undergoing other procedures may need valve replacement
- results in better LV function and improved hemodynamics
- operative mortality (2-5% without LV failure, 1% pts <70 yo, 4.3% in isolated replacement, 8% in replacement + CABGS)
218
What are the 2 transcatheter therapies for aortic stenosis?
balloon valvuloplasty
| valve replacement
219
List some common etiologies of mitral regurgitation
rheumatic disease, infective endocarditis, collagen vascular disease, cardiomyopathy, ischemic heart disease, mitral valve prolapse
220
List the 4 valve structures that may be involved in mitral regurgitation
leaflets, mitral annulus, chordae tenidnae, papillary muscles
221
Describe some of the changes in the leaflets that lead to MR
- Chronic rheumatic heart disease: shortening, thickening, deformity or retraction of MV cusps
- Infective endocarditis: may perforate a cusp or cause cusp retraction, vegetations may prevent coaptation
222
Describe some of the changes in the mitral annulus that lead to MR
- Dilation: any disease that dilates the LV
| - Calcification: idiopathic in most cases, can cause severe MR & more common in women
223
Describe some of the changes in the chordae tendinae that lead to MR
- In mitral valve prolapse they lengthen and rupture
| - Infective endocarditis, trauma, others may also cause rupture of chordae with secondary MR
224
Describe some of the changes in the papillary muscles that lead to MR
- Usually from ischemia or rupture
- Posterior papillary muscle most commonly involved
- Rupture of papillary muscle during MI is usually fatal owing to acuteness of MR
225
Describe the pathophysiology of MR
- Impedance to LV ejection (afterload) is lowered
- Volume of regurg affected by many variables like LV/LA gradient, flexibility of annulus, cusp integrity, etc.
- In most pts, LV function is preserved up to 20 yrs but eventually fails
226
Describe the hemodynamic pathophysiology of MR
Early MR ejection fraction is high
If severe, symptomatic: ejection fraction normal to low, excess volume maintained in LA & pulmonary circulation, LV goes into diastolic overload and fails
227
Aspects of the history of patient with MR
- look for etiology
- principle symptom is DYSPNEA (usually exertional then later PND or orthopnea)
- palpitations, hemoptysis, systemic emboli, angina pectoris, signs/symptoms of RV failure
228
Clinical manifestations of MR on physical exam
- Carotid artery pulses: sharp in severe MR, owing to higher stroke volumes
- Apical impulse: brisk & hyperdynamic, displaced left and downward (LV dilation)
- Occasional late-systolic LA thrust palpabel at left parasternal area
229
Manifestations on auscultation in patient with MR
S1 soft in MV leaflets still flexible
S2 widely split owing to earlier A2
A2 commonly softer than P2 when pulmonary HTN present
S3 common due to volume excess
Triscupsid murmur if RV dilated
S4 in RV
230
Describe the MR murmur
Holosystolic, blowing, loudest at apex, radiates to axilla, commences with S1, occasionally lasts through S2, constant loudness
Occasionally, diastolic murmur commencing with S3
231
Cornerstone of diagnosis for valvular disease
echocardiography
232
Manifestations on chest x-ray and echocardiography for MR
X ray: LA enlarged, cardiomegaly, mitral annulus calcification sometimes
Echocardiograph: increased LA&LV size with increased wall motion, underlying cause can often be seen (ruptured chordae, flail LV leaflet, vegetations, calcified annulus)
Doppler techniques for severity
233
ECG manifestations for MR patient
not specific
can demonstrate LA conduction abnormality, RVH, atrial fibrillation
234
General tx for MR
- Treat LV failure as needed: 1) afterload reduction (ACEIs) 2) in acute MR, nitroprusside IV, if hypotensive dobutamine
- A fib present: anticoagulable
- Digitalis to slow a fib, improve inotropism
- Prophylaxis against infective endocarditis
- Prognosis is poor without surgery
235
Surgical Tx for MR
Repair is more common than replacement now
Repair: prolapsing or redundant valve cusps resected
Replacement: LV function can deteriorate owing to loss of integrity of annulus, chordae, papiallary muscle; prosthetic valves present problems
236
Valve repair in MR is best in... (5)
child with pliable valve
adults with MR from mitral prolapse
annulus dilation is the cause
ischemic papillary muscle
chordal rupture or cusp perforation from enodcarditis
237
Main etiology of mitral stenosis
Rhuematic fever - 99% of pathologic specimens obtained during MV replacement
2/3 with rheumatic MS are female, 25% with rheumatic heart have MS only, 40% have mixed MS/MR
238
List 4 conditions that mimic MS
left atrial myxoma
left atrial ball-valve thrombus
infective endocarditis with large vegetations
cor triatriatum (congenital)
239
Describe the pathophysiology of MV stenosis, including the hemodynamics
obstruction to LV inflow = pressure gradient across the valve
Normal MV orifice = 4-6
Mild = area ~2
Critical = area ~1 or less
Critical MS: transvalvular pressure gradient about 20 mmHg therefore needed to maintain resting CO, increased LA pressure means increased pulmonary pressures
240
Describe some common aspects of the history in a patient with MS
- rheumatic fever
- SYSTEMIC EMBOLIZATION: may be first symptom of MS, even when valvular stenosis is mild, go to cerebral circulation in about 50%, related to size of LA appendage, level of cardiac output, presence of a fib
- endocarditis
- chest pain
- hemoptysis
241
Manifestations on physical exam in patients with MS
- mitral facies: purple/pink cheeks in severe MS, owing to low ouptut and vasoconstriction
- arterial pulses normal to reduced
- apical impulse is inconspicuous to absent: occasionally, apical thrill
242
Manifestations on auscultation of MS
S1 is LOUD
P2 accentuated as pulmonary artery pressure rises (as compliance decreases, P2 occurs later and later until S2 becomes single)
OPENING SNAP due to sudden deceleration and tensing of cusps at max MV excursion: occurs afte rP2 but only where leaflets are flexible, disappears late in course of MS
S4 in RV
243
Describe the murmurs of MS
Diastolic murmur: low pitched, rumbling, mid-diastolic, best heard at apex, duration correlates with degree of stenosis, commences with opening snap
Graham-Steel murmur: sign of severe pulmonary HTN, pulmonic insufficiency
Tricuspid murmur (if RV dilated)
244
Manifestations on x-ray and echocardiography in MS patient
X-ray: LA enlarged, when severe: RV and RA also large, maybe calcifications
Echocardiograph: thickened, sometimes calcified leaflets separate poorly in diastole, valve area measurable, increased LA size, thrombus in appendage
Hockey stick** appearance
Doppler for MR, AR, other valve lesions
245
ECG of MS
not specific
can demonstrate: LA conduction abnormality (90%), RVH, atrial fibrillation
246
Natural hx of MS
15-20 yr latency after RF before symptoms develop in temperate climates
eventually, as LA dilates, patients can develop atrial fibrillation, embolization, etc.
247
General tx of MS
- prophylaxis against endocarditis
- avoid strenuous activity
- anticoagulants for prophylaxis against emboli, esp. stroke
- maintain sinus rhythm
- reduce salt/water intake
248
Medical tx for a fib and MS
- anticoagulable with heparin then DC cardioversion
| - if cardioversion not posible, slow vent rate to improve CO (beta blockers, NDHP CCBs, digitalis)
249
Valve surgery tx for MS
Coronary angiogram if discrepancy between clincal findings and echo, pts with COPD, angina, men >40, women >50 with risk factors for CAD
250
List the 4 valve surgeries for MS tx
balloon valvotomy
closed valvotomy
open valvotomy & repair
MV replacement
251
List 3 benefits for SAH tx
avoid/reduce target organ damage
persistent/uniform reduction in stroke
likely reduces CAD risk
252
How does weight loss influence SAH?
decrease of 1 kg found to decrease BP 1.6/1.3 mmHg
253
General tx goals of drug therapy for SAH
- intent to reduce systemic BP below initial tx thresholds
```
Drug classes:
diuretics
CCBs
ACEIs
ARBs
Beta blockers/alpha blockers
vasodilators
```
254
Drug tx of choice for SAH
thiazide diuretics
255
Drug tx of choice fof SAH in people >18 yo with chronic kidney disease
ACEI or ARB
256
Main goal of BP therapy?
attain and maintain goal BP
if goal not reached in a month, increase dose of initial drug or add second drug from one of the recommended classes and continue to assess BP
if goal not reached with two drugs, add a third
257
MI tends to result from what?
rupture or erosion of a vulnerable plaque in the milieu of inflammation and procoagulation
258
What typically happens right after a plaque ruptures?
blood is exposed to inner plaque material resulting in activation of platelets, thrombin generation and thrombus formation
259
One significant thing to note about plaque rupture as far as clinical manifestation goes
This is a dynamic process that can be clinically silent with eventual lysis of the thrombus or incorporation into the plaque (atherothrombosis) or it can result in an acute coronary syndrome
260
True or false: most plaque ruptures do not result in a clinical cardiac event
True
261
ACS can manifest in what ways? Name the 2 major ways and how they are characterized
Unstable angina, non-ST elevation MI (NSTEMI) - caused by non-occlusive platelet rich "white" thrombus
ST elevation MI (STEMI) - from an occlusive fibrin rich "red" thrombus
262
Vulnerable plaques - characteristics, outcomes
Often non-obstructive 40-60% stenoses that would not produce an abnormal stress test or justify elective stenting if identified prior to the event
Thin fibrous cap atheroma, large atherosclerotic burden (>70%), minimal luminal diameter <4 mm, protruding calcium
263
Killip Classification system for risk stratification of AMI
class 1 = no rales, no S3, 30-40% of cases in CCU, mortality 8
class 2 = rales over <50% or S3, 40-50% of cases in CCU, mortality 30
class 3 = rales over >50% (pulmonary edema), 5-10% in CCU, mortality 44
class 4 = shock, 10% of CCU, mortality 80-100
264
Leads with ST ELEVATION correlate with the anatomic area of injury: list 3 locations/indications
II, III, AVF = inferior MI with RCA damage (or left circumflex)
I, AVL - high lateral MI, LCA
V1-V4 = anterior MI, LAD
265
Cardiac Troponin changes associated with MI (4)
Rises within ~3 hrs of AMI
Released continually after myocycte injury
Peaks 24-48 hrs
Remain elevated 5-10 days after myocardial injury
266
Creatine Kinase MB (CKMB) changes associated with MI (3)
Rises within 4 hrs of AMI
Peaks in ~24 hrs
Returns to normal 2-3 days after myocardial injury
267
Initial ED tx of ACS (9)
- O2
- Aspirin
- Sublingual Nitro
- Anticoagulant
- Beta blocker
- IV nitro drip if symptoms persist
- Second antiplatelet agent
- Morphine
- Cardiac cath
268
Initial ED tx of ACS (9)
- O2
- Aspirin
- Sublingual Nitro
- Anticoagulant
- Beta blocker
- IV nitro drip if symptoms persist
- Second antiplatelet agent
- Morphine
- Cardiac cath
AFTER YOU GET AN ECG
269
4 major characteristics of vulnerable plaque
Thin fibrous cap, large atherosclerotic burden (>70%), minimal luminal diameter < 4mm, protruding calcium
270
Definition of MI
evidence of myocardial necrosis in a clinical setting consistent with acute myocardial ischemia
rise and/or fall of cardiac biomarker with at least one above the 99th percentile
symtpoms
ST segment-T wave changes
271
STEMI (5)
- results from complete occlusion of coronary blood flow and transmural myocardial damage
- myocardium is continually lost until perfusion is restored
- ST elevation localizes the area of injury and the culprit artery
- typically involves a fibrin rich "red clot"
- requires immediate reperfusion with either thrombolytic therapy or primary PCI
272
What happens if perfusion is not restored in STEMI? (esp. if from a proximal LAD occlusion)
- major myocardial damage can occur with outright shock or if less severe, reduced EF, early infarct expansion, late LV remodeling leading to ischemic cardiomyopathy
- this can result in chronic heart failure as well as increased risk for venricular arrhythmias and sudden cardiac death, esp. when EF <35%
273
Normal ejection fraction value
55-70%
274
Inferior STEMI from a proximal RCA occlusion can result in associated RV infarction - list the clinical manifestations/indications (4)
- constellation of hypotension with elevated neck veins and clear lung fields
- check lead V4R (placed in V4 position on RIGHT side of chest)
- avoid preload reducers, caution with beta blockers
- if hypotensive, may initially try modest IV fluid boluses
275
NSTEMI (4)
- results from a ruptured/eroded plaque with acute thrombus formation and INCOMPLETE obstruction of blood flow
- typically involves a platelet rich white clot
- thrombolytics are CONTRAINDICATED
- ECG may be normal, show ST depression or T wave inversion (do not localize to area of ischemia or culprit vessel)
276
NSTEMI tx plan
initial management involves medical stabilization with ASA, P2Y12 inhibitors, anticoags, beta blockers, nitrates, statins, +/- GP2b3a inhibitors followed by cardiac cath electively in the next 24-48 hrs (Earlier with refractory ischemia/symptoms, hemodynamic or electrical instability)
277
Post MI medical therapy includes what 9 things?
- ASA for life
- P2Y12 inhibitor for 1 year
- Beta blockers
- ACEI if EF <40% class I (or <50%)
- Aldosterone antagonist for HF and EF <40%
- high intensity statins
- PRN nitroglycerine
- outpatient cardiac rehab
- early office follow up
NOT CCB routinely
278
anterior wall MI vs inferior wall MI
1. Anterior: LAD occlusion = widow maker, high catecholamine state
2. Inferior: RCA occlusion, high vagal tone state
279
Who should undergo cardiac catheterization?
elevated troponins, dynamic ST changes, recurrent symptoms, low ejection fraction
280
List some common post MI complications
arrhythmia, heart failure, embolus, pericarditis, papillary muscle rupture, VSD, free wall rupture, LV aneurysm, cardiogenic shock
281
List 4 possible ventricular arrhythmias
ventricular premature beats
accelerated intraventricular rhythm
ventricular tachycardia
ventricular formation
282
Name 2 kinds of bradyarrhythmias
sinus bradycardia
AV block
283
PVCs (define, tx)
common, along with short runs of NSVT
don't require specific treatment: correct electrolytes, beta blockers
284
Accelerated Idioventricular Rhythm
slow V tach, implies reperfusion, vent rate 60-110
results from enhanced automaticity of Purkinje fibers
often observed shortly after successful reperfusion
paroxysmal episodes during first 2 days
285
V tach (description and tx)
VT induced by ischemia is typically polymorphic
VT resulting from scar is typically monomorphic
higher risk with greater myocardial damage and/or ongoing ischemia
immediate cardioversion if hemodynamically unstable
amiodarone for sustained episodes
286
V fib
Late VT/VF: 48 hrs after MI associated with increased risk of sudden cardiac death following discharge
treatment: immediate defibrillation, amiodarone, BB, correct lytes, R/O recurrent ischemia, reinfarct
287
V fib
Late VT/VF: 48 hrs after MI associated with increased risk of sudden cardiac death following discharge***
treatment: immediate defibrillation, amiodarone, BB, correct lytes, R/O recurrent ischemia, reinfarct
288
Sinus bradycardia
may be seen during acute phase of MI from sinus node ischemia (RCA >LCX > dual) or high parasympathetic tone
289
AV block inferior MI
block AT AV node level, usually transient
290
AV block anterior MI
rare, usually BELOW AV node level, implies extensive infarct with bundle branch involvement, usually permanent
needs pacemaker
291
AV block anterior MI
rare, usually BELOW AV node level, implies extensive infarct with bundle branch involvement, usually permanent
needs pacemaker***
292
Heart Failure: acute MI phase
may be secondary to diastolic dysfunciton or a combo of systolic & diastolic dysfunction
can vary from mild pulmonary congestion (K2) to fulminant pulmonary edema (K3)
manage with vasodilators, +/- diuretic, cautious morphine, biPap possible intubation
293
Heart failure: post acute phase
usually secondary to systolic dysfunction
manage with diuretic, ACEI, aldosterone antagonists, beta blocker once compensated
294
Describe the cycle of LV remodeling
1. LV dysfunction
2. decreased CO, BP
3. compensation (frank starling, neurohormonal and inflammation)
4. Increased CO, BP, oxidative stress
5. remodeling
6. back to start
295
Cardioembolism
most commonly associated with large AWMI
risk increased with reduced EF, apical wall motion abnormality, LV aneurysm development
echo can help diagnose
tx = anticoagulation with warfarin
296
Early Pericarditis (within 1st week)
- in transmural infarcts
- from local inflammation of pericardium overlying infarcted myocardium
- pleuritic type chest pain (radiates to trap)
- friction rub
- ECG changes may be masked by AMI
- treat with high dose aspirin, colchicine
NO NSAIDS OR STEROIDS
297
Late pericarditis (1-8 weeks)
Dressler's syndrome
autoimmune mechanism
systemic symptoms too
treat with aspirin, colchicine
298
Name the 5 populations with increased risk of ventricular septal defect***
older patients, females, history of HTN, first MI, delayed or absent reperfusion
299
Clinical presentation of VSD
chest pain, dyspnea, hypotension, biventricular failure, harsh, holosystolic murmur on left sternal border, thrill in 1/2 of pts, S3, loud P2, TR
300
Ventricular septal rupture management (3 aspects)
1. hemodynamic support: intra-aortic balloon pump, advanced mechanical circulatory support, vasodilators if BP allows or pressors
2. surgical closure: tx of choice, earlier is best
3. Percutaneous device closure: for pts too high risk for surgery
301
Acute mitral regurgitation - which part of the heart is involved?**
Papillary muscle dysfunction, rupture of chordae or papillary muscle
**Primarily in setting of inferior MI involving the posteromedial papillary muscle (Due to single blood supply)**
302
Clinical presentation of acute mitral regurg
heart failure, may be sudden onset, new systolic murmur
303
Acute MR management
ventilator if needed
IABP esp in hypotension
afterload reduction
surgery = tx of choice
304
VSD vs papillary muscle rupture ***
VSD murmur loud, MR faint
Thrill in VSD patients, rare in MR
VSD associated with AWMI, IWMI equally
Acute MR predominantly seen with IWMI
305
Clinical presentation of free wall rupture and diagnosis/tx
acute: sudden hemodynamic collapse, cardiac tamponade, PEA arrest, transient bradycardia, restless, nauseated, anxious prior to event
subacute: contained rupture, pericardial pain, hypotension
dx: echo, PA catheter
tx: surgery
306
True aneursym vs pseudoaneurysm (3**)
True:
1. wide base
2. walls made of myocardium
3. low risk of rupture
Pseudo:
1. narrow base
2. walls made of pericardium and thrombus
3. high risk of rupture
307
Intra-aortic balloon pump
augments coronary blood flow during diastole
decreases afterload during systole by deflating at the onset of systole
reduces myocardial ischemia
308
List the major etiologies of peripheral arterial disease
*atherosclerosis*, thrombosis, embolism, vasculitis, fibromuscular dysplasia, cystic adventitial disease, trauma
309
List some symptoms of peripheral arterial disease
intermittent claudication (most common), when severe: hair loss, nail thickening, shiny skin, pallor, pain while at rest
half of people asymptomatic
310
Compare a normal ABI to one seen in patients with occlusive disease/PAD and patients with severe ischemia/PAD
normal is 1 - 1.4 ratio of ankle to brachial
<0.9 in pts with occlusive disease/PAD
<0.5 in pts with severe ischemia/PAD
311
Pharmacological and other tx of PAD
tx of HLP, HTN, DM
PDE inhibitor, platelet inhibitors
exercise, lifestyle changes, supportive measures, non-operative interventions, surgery (revascularization)
312
In which 3 situations do we refer a PAD patient to interventional radiologist vs vascular surgeon
pain at rest, non-healing lower extremity ulcers associated with low ABIs, severe/debilitating claudication
313
Acuter arterial occlusion - what happens and what causes it (2)
resulting in sudden cessation of blood flow to an extremity
emoblism, thrombus in situ
314
Acute arterial occlusion of embolic source
most common sources are heart, aorta and large arteries
cardiac: a fib, ACS, prosthetic valves, endocarditis, atrial myxoma
aortic aneurysms
large arterial bifurcations
315
Acute Arterial Occlusion due to thrombus in situ
occurs most frequently in atherosclerotic vessels at site of stenosis
in bypass grafts, PV, hypercoagulable states
316
**Fibromuscular Dysplasia**
hyperplastic disorder affecting medium sized and small renal arteries
usually in young, healthy females
often diagnosed during workup for secondary HTN
usually involve carotid and renal arteries
Tx: PTA and surgery
317
**Thromboangiitis Obliterans**
inflammatory disease of small and medium sized arteries and veins of the extremities
young men who are smokers
Raynaud's phenomenon in ends of digits, ulcers and pain are typical
Tx: immediate stop of smoking
318
Atheroembolism
subset of acute arterial occlusion
multiple small deposits of fibrin, platelets, cholesterol debris embolizing downstream
acute pain and tenderness at site of emboli
319
Raynaud's (phenomenon vs disease)
syndrome manifested by attacks of pallor and cyanosis of the digits in response to cold or emotion
Primary = disease
Secondary = phenomenon
females > males, onset age 20-40
320
Livido Reticularis
localized areas on extremities develop a reddish/blue rete or net-like appearance
primary/idiopathic disorder vs secondary
321
**Venous thrombosis**
presence of thrombus within a superficial or deep vein and the accompanying inflammatory response in the vessel wall
Virchow's triad for predisposing factors (stasis, vascular damage, hypercoagulability)
other risks: pregnancy, ACS, CHF, estrogen, neoplasms, during orthopedic surgical procedures
322
What is virchow's triad??**
stasis, vascular damage, hypercoagulability
323
Deep Venous Thrombosis
clot present in deep veins of lower extremities
risk factors = Virchow's triad
predisposing factors = immobilization, surgery, trauma, estrogen, etc.
symptoms: pain, swelling, redness, fever, edema, increased girth
dx: d dimer, doppler, ascending contrast venography (gold)
324
Pulmonary emoblism ** (esp. risk and clinical presentation)
an occlusion of a pulmonary artery by a detached fragment
risks: surgery, injury, immobility, tobacco use, estrogen, infection, prolonged anesthesia, cancer, HTN
clinical: tachypnea, course/diminished lung sounds, chest pain/pleurisy, hemoptysis
dx: pulmonary angiography beset
tx: heparin, coumadin, thrombolytics, surgery
325
Chronic venous insufficiency
may result from DVT and/or valvular incompetence
signs: dull ache worsening with prolonged standing, resolves with leg elevation
increased leg circumference, edema, superficial varicose veins, erythema, dermatitis, hyperpigmentation
tx: rare surgical intervention
326
Etiology/description of MI in general
Reduced tissue perfusion; oxygen demand exceeds supply
Supply and demand problem:
Supply is reduced – coronary atherosclerosis, coronary spasm, etc. and/or
Demand is increased – exercise, anxiety, pain, etc.
327
General symptoms of MI
Chest discomfort – pressure, tightness, band-like, squeezing, oppressive (angina pectoris)
Most often exertional
DOE, nausea, other GI
Refers to left jaw, shoulder, ulnar left arm
Physical exam may be normal or there could be cardiac findings: cardiomegaly, murmurs (S4), look for evidence of other disease like HTN, diabetes, etc.
328
Testing, Dx, Tx of MI in general
```
Testing:
Resting ECG
Basic labs: lipid panel, H/H or CBC, blood chemistry panel, urinalysis
Exercise stress testing
Echocardiography
```
Diagnosis:
Determined via stress testing
Drug Therapy:
Nitrates
Beta Blockers
Calcium Channel Blockers
329
Symptoms/description of angina pectoris
Pressure, tightness, band-like, squeezing, oppressive
Generally lasts <30 min
Onset usually gradual
Relieved by stopping activity, taking meds
Worsened by increased work and lying down
