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Cardiology > Exam 2 > Flashcards

Exam 2 Flashcards

1
Q

4 non-modifiable major risk factors for atherosclerosis

A

increasing age
male gender
family history
genetic abnormalities

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2
Q

5 modifiable major risk factors for atherosclerosis

A 
**cigarette smoking**
hyperlipidemia
hypertension 
diabetes
C reactive protein
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3
Q

3 minor modifiable risk factors for atherosclerosis

A

inactivity
stress
obesity

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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

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5
Q

What is the most important component of the total cholesterol in increasing coronary risk?

A

LDL

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6
Q

The ratio of LDL to HDL should be no more than what?

A

4 to 1

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7
Q

As total serum cholesterol rises above what level does coronary risk increase linearly?

A

160 mg/dl

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8
Q

Name one significant risk factor (lipoprotein) related to atherosclerosis that is independent of LDL levels

A

lipoprotein A

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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

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10
Q

Name 4 secondary genetic disorders associated with dyslipoproteinemias and atherosclerosis

A

nephrotic syndrome
hypothyroidism
alcoholism
diabetes mellitus

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11
Q

After what age does hypertension become a stronger risk factor (5 fold) for atherosclerosis than hypercholesteroemia?

A

age 45

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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

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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

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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

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15
Q

Describe two unusual associations with atherosclerosis in terms of illnesses/disease states

A
  1. elevated plasma homocysteine - folate and vitamin B treatment reduces cardiovascular disease in women
  2. Clamydia pneumonia presence in plaques - antibiotic tx DOES NOT reduce recurrent ischemic clinical events in patients
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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
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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

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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
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19
Q

Describe the process of endothelial injury as it occurs and kicks off the process of atherogenesis

A
  1. triggering event
  2. endothelial cells overexpress VCAM1 which increases cellular adhesion, recruits inflammatory cells and releases cytokines
  3. primarily tissue macrophage will accumulate modified lipids to form foam cells and fatty streaks
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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
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21
Q

Atherosclerotic lesions also contain lipid accumulations, which can be seen histologically by what type of cells?

A

foam cells

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22
Q

What are foam cells?

A

macrophages (and smooth muscle cells) whose cytoplasm is packed with droplets of cholesterol esters

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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

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24
Q

Describe the process of atherogenesis as it progresses from endothelial cell dysfunction to plaque formation (7)

A
  1. endothelial cell dysfunction due to triggering events
  2. recruitment of monocytes - adhesion and emigration into intima
  3. release of inflammatory mediators like cytokine MCP1 and oxidation of LDLs
  4. activation of macrophages
  5. foam cell formation with lipid uptake in macrophages
  6. release of cytokines, MMPs, ROS, tissue factor and recruitment of smooth muscle cell precursors then proliferation
  7. atherosclerotic plaque formation and death of macrophage
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25
Q

Name the 3 key features of atherosclerosis

A

smooth muscle cell proliferation

accumulation of CT elements (collagen, elastin, proteoglycans)

lipid deposition (intra and extracellular)

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26
Q

PDGF is important in the development of atherosclerosis - what does it do?

A

important in causing proliferation of smooth muscle cells in atherosclerotic lesions

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27
Q

List the 5 primary cell types associated with atherosclerosis development and a couple important proteins/cell factors

A 
endothelial cell
smooth muscle cell
platelets
macrophages 
T lymphocytes

LDL, PDGF, MCP1

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28
Q

Name 3 characteristic lesions of atherosclerosis

A

fatty streaks

proliferative lesions

firbofatty plaques (Atheroma)

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29
Q

Hemodynamics play a role in atherogenesis - describe 3 ways how

A
  • 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
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30
Q

Why does it matter if there are regions of low shear and/or disturbed flow in the vasculature?

A

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

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31
Q

Active MMPs play what role in the development of atherosclerosis?

A

lead to basement membrane degradation and endothelial cell death

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32
Q

Name 4 complications that can result from atherosclerotic lesions

A
  1. calcification
  2. hemorrhage
  3. thrombosis
  4. ulceration or rupture (majority of MI’s due to this)
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33
Q

Describe the composition of a “vulnerable” plaque, as well as the risks associated with them and some major consequences of them

A
  • 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
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34
Q

Name 4 plaque changes that are all risk factors in developing acute coronary syndrome

A

superficial erosion
ulceration
fissuring
deep hemorrhage

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35
Q

Vulnerable plaques undergo inflammatory changes and what else as they progress to causing an MI?

A

rupture, release WBC, form thrombus

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36
Q

What is the earliest sign of endothelial dysfunction?

A

formation of foam cells (made of macrophages and oxidized LDL)

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37
Q

What is an atheroma?

A

accumulated lipid, cells and other components of a plaque disrupt the artery wall

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38
Q

2 stages of atherosclerosis development in the first decade

A

foam cells

fatty streak

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39
Q

2 stages of atherosclerosis development in the third decade

A

intermediate lesion

atheroma

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40
Q

2 stages of atherosclerosis development in the fourth decade

A

fibrous plaque

complicated lesion rupture

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41
Q

Differentiate between pre-clinical phase and clinical phase of atherosclerosis

A

PRE-CLINICAL (young) =
normal artery&raquo_space; fatty streak&raquo_space; fibrofatty plaque&raquo_space; advanced/vulnerable plaque

CLINICAL (middle age and elderly) =
aneurysm and rupture, occlusion by thrombus, critical stenosis

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42
Q

List the primary therapies in clinical atherosclerosis used in asymptomatic or anginal stages with atherosclerotic plaques

A

statins, control BP and DM, control clotting, diet and lifestyle change

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43
Q

List the secondary therapies used in clinical atherosclerosis when ACS or stroke may occur due to plaque rupture and/or thrombus formation

A

tissue plasminogen activator, angioplasty with stent placement (coronary or carotid), carotid endarterectomy, CABG

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44
Q

Atherosclerotic lesions tend to be localized how?

A

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.

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45
Q

What is the ankle brachial pressure index (ABPI) and why is it important?

A

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

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46
Q

Atherosclerosis results in ISCHEMIC INJURY to the organs and tissues nourished by affected arteries; list 5 important clinical manifestations of this

A 
MI
ischemic stroke
peripheral arterial disease (can lead to gangrene) 
visceral infarction
atherosclerotic aneurysms
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47
Q

How can the identification of an atherosclerotic plaque in one place be a warning sign?

A

plaques found in one area of the vascular tree are usually accompanied by lesions in other areas as well

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48
Q

Describe the symptoms of atherosclerosis

A

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

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49
Q

Describe Glagov’s coronary remodeling hypothesis for atherosclerosis

A

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

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50
Q

What is the importance of coronary remodeling in atherosclerosis?

A

remodeling preserves lumen size

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51
Q

Describe the differences found on coronary angiogram 4 hrs after an MI and 12-24 hrs after an MI

A

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

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52
Q

Blood flow is restricted only in highly stenosed vessels - explain the relevance of this

A

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)

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53
Q

Most common cause of a heart attack

A

atherosclerosis

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54
Q

Which family of lipoproteins are all atherogenic?

A

apoB

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55
Q

Which lipoprotein is present in HDL?

A

apoA1

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56
Q

chylomicrons

A

made in intestines

delivery dietary triglycerides to tissues via hydrolysis by LPL

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57
Q

VLDLs

A

made in the liver

deliver triglycerides from the liver to extra-hepatic tissues (mainly by LPL)

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58
Q

LDLs

A

deliver cholesterol/cholesterol esters to tissues, including teh liver

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59
Q

HDLs

A

made primarily in the liver

reverse cholesterol transport from extra-hepatic tissues to the liver

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60
Q

Lp(a)

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

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61
Q

small dense LDL

A

development produced by insulin resistance, high TG, low HDL environment

increased atherogenicity

may result in underestimation of LDL particle number and total LDL burden

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62
Q

ACC/AHA’s 4 major statin benefit groups

A
  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
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63
Q

Common adverse effects associated with statin use

A 
myopathy 
hepatotoxicity 
diabetes
CNS - memory loss
GI complaints
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64
Q

Role of PCSK9 molecule in lipid metabolism

A

proprotein convertase subtilisin kexin type 9

regulates expression of LDL receptors - handcuffs LDL particle to receptor, so receptor is broken down, too

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65
Q

Inhibiting PCSK9 affects the lipid profile how?

A

decreases LDL via increased clearance and increased LDL receptor levels

reduces LDL-C 60-70%

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66
Q

Hepatic lipase

A

hydrolyzes TAGs in IDL to facilitate conversion to LDL

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67
Q

CETP

A

transfers cholesteryl esters from HDL to other lipoproteins in exchange for TG, phospholipids and cholesterol

present on HDL

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68
Q

LCAT

A

transfers fatty acids from lecithin to C to form CE in HDL

keeps cholesterol concentration low in the phospholipid monolayer

present on HDL

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69
Q

What do pacemakers do? What are they composed of?

A

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

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70
Q

Pulse generator of pacemaker

A

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

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71
Q

Pacemaker lead system

A

endocardial leads placed via central access - placed in right ventricle and/or atria

conductor surrounded by insulation

fixed to endocardium via screws or tines

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72
Q

AAIR vs. VVIR

A

atrial lead = AAIR

ventricular lead = VVIR

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73
Q

Capture

A

the depolarization and resultant contraction of the atria or ventricles in response to a pacemaker stimulus

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74
Q

Capture Threshold

A

the minimum amount of electrical energy that consistently produces a cardiac depolarization

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75
Q

Strength-Duration Relationship (pacemaker)

A

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

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76
Q

Fusion beat

A

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)

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77
Q

Pseudofusion

A

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)

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78
Q

Atrial sensing/inhibition

A

AAI

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79
Q

Ventricular sensing/inhibition

A

VVI

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80
Q

List 3 possible pacemaker complications

A
  • failure to output (should send out beat but doesn’t)
  • failure to capture (sends something out but it isn’t sensed)
  • sensing abnormalities
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81
Q

Pacemaker failure to output, definition and etiologies

A

No pacing spike present despite indication to pace

battery failure, lead fracture, break in lead insulation, oversensing, cross-talk

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82
Q

Pacemaker failure to capture, definition and etiologies

A

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

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83
Q

Sensing abnormalities of pacemaker

A

pacemaker does not recognize normal beats and generates an unnecessary pacemaker site

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84
Q

5 indications for a pacemaker

A
  • 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
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85
Q

Definition of heart failure

A

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

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86
Q

Cardiac dyssynchrony in CHF

A

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

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87
Q

Cardiac resynchronization therapy (CRT)

A

biventricular pacing

resynchronizes contraction of left ventricle to improve stroke volume and reduce oxygen demand

improves symptoms of CHF and reduces mortality

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88
Q

Magnet inhibition**

A

closes an internal reed switch: causes sensing to be inhibited, temporarily turns pacemaker into “asynchronous” mode (Set rate)&raquo_space; 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)

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89
Q

ICD

A

implantable cardioverter defibrillator

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90
Q

Therapies provided by today’s dual-chamber ICDs (atrium, vent, and both)

A

Atrium = AT/AF tachyarrhythmia detection

Vent= VT/VF detection, antitachycardia pacing, defibrillation

Both = bradycardia sensing and pacing, biventricular pacing

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91
Q

Indications for an ICD**

A

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

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92
Q

List 4 possible ICD complications

A
  • sensing and pacing failures
  • inappropriate cardioversion
  • ineffective cardioversion/defibrillation
  • device deactivation
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93
Q

ICD failure to deliver therapies - etiologies and appropriate failure to treat

A

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

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94
Q

ICD inappropriate shocks - definition and etiologies

A

provokes pain and anxiety

etiologies - rapid sinus tachycardia, SVT, a fib, T wave oversensing, lead fracture, insulation breakage, electromagnetic interference

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95
Q

Describe the management of ICD inappropriate shocks

A

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

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96
Q

4 examples of electromagnetic interference

A

metal detectors, cell phones, arc welding, medical cautery devices

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97
Q

Dry lungs vs. wet lungs and intrathoracic impedance monitoring

A

dry lungs - high impedance

wet lungs - low impedance

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98
Q

Hoff’s definition of atherosclerosis

A

fatty infiltration of the tunica intima (endothelial layer) of a coronary artery, with or without significant luminal narrowing

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99
Q

Describe the pathogenesis of atherosclerosis according to Dr. Hoff

A

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

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100
Q

Dr Hoff mentions four major cellular players in atherosclerosis development - name each

A

endothelial cells
smooth muscle cells
macrophages
platelets

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101
Q

Describe the role of the endothelium in the development of atherosclerosis

A
  • first site of lesions
  • monolayer with receptors for many molecules
  • produces vasoactive substances
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102
Q

Describe the role of smooth muscle cells in the development of atherosclerosis

A
  • more advanced lesions
  • foam cells (lipid-laden)
  • may participate in growth of lesions
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103
Q

Describe the role of macrophages in the development of atherosclerosis

A
  • scavenge foreign substances
  • secrete chemotactic factors
  • principal cells of early lesions
  • foam cells
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104
Q

Describe the role of platelets in the development of atherosclerosis

A
  • may be important in initiating lesions
  • secrete potent molecules (i.e. growth factors)
  • stimulate vasoconstriction and thrombosis
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105
Q

Fatty streak lesion

A
  • 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
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106
Q

Intimal thickening and atherosclerosis

A

may be simple thickening or a response to stress

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107
Q

Fibrous plaque

A
  • advanced lesion - cholesteryl esters, debris, etc.
  • white, raised, impinges on lumen, can limit perfusion
  • may become complicated by: calcification, ulceration, hemorrhage into plaque, thrombosis
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108
Q

List the 3 major modifiable risk factors for atherosclerosis according to Dr. Hoff

A

cigarette smoking
diabetes
hypertension (140/90 or on meds)

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109
Q

Describe the role of family history of premaure CAD as a risk factor for atherosclerosis

A

CAD in male first degree relative <55

CAD in female first degree relative < 65

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110
Q

Most common cause of death in diabetic patients

A

atherosclerosis and its consequences

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111
Q

How does diabetes play into the risk of developing atherosclerosis?

A

diabetes is a “risk equivalent” for CAD with 10 yr risk of a hard CVD event >20%

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112
Q

What is diabetic dyslipidemia?

A

abnormal lipoproteins

smaller, denser LDL particles; LDL near normal

low HDL

elevated triglycerides

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113
Q

What is metabolic syndrome? (requires any 3)

A
  • diabetic dyslipidemia
  • primary arterial hypertension
  • central abdominal obesity
  • insulin resistance - may be the central factor
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114
Q

What is the prevalence of metabolic syndrome in CAD patients?

A

50%

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115
Q

Describe the mechanisms by which cigarette smoking enhances atherosclerosis (6)

A
  • 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)
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116
Q

List 4 associated outcomes with coronary atherosclerosis

A
  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
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117
Q

4 methods of primary prevention of atherosclerosis

A

appropriate diet, regular exercise, optimum weight, stop smoking

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118
Q

Secondary prevention methods for coronary atherosclerosis (pt has ASCVD or risk equivalent)

A
  • treat dyslipidemias with statin
  • treat diabetes (HbA1C <7)
  • control BP
  • stop smoking
  • regular, mod. exercise
  • optimize weight
  • dietary changes
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119
Q

What 3 things have the most influence on oxygen demand in the heart?

A

heart rate
contractility
systolic wall tension

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120
Q

What factors influence supply to the myocardial tissue?

A

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

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121
Q

In ischemia, demand exceeds fixed supply, name 3 etiologies

A

coronary occlusive disease
coronary spasm
combinations (mixed angina)

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122
Q

Describe the hemodynamic effect of coronary spasm in obstructive coronary atherosclerosis (4 steps)

A

atherosclerotic lesions (40% obstruction)

superimposed vasoconstriction (80% obstruction)

reduced distal flow

myocardial ischemia

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123
Q

Angina pectoris

A

heavy, pressure, band-like, crushing

often silent (i.e. asymptomatic)

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124
Q

Stable vs. unstable angina

A

stable = same pattern each time

unstable = new onset, subjectively worse discomfort onset with less activity, angina at rest (decubitus)

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125
Q

Angina pectoris

A

heavy, pressure, band-like, crushing

often silent (i.e. asymptomatic)

men 5.7%, women 6.7%

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126
Q

Tell me what we use stress testing to diagnosis, what the prognosis indicates

A

Diagnosis of atypical chest discomfort

Prognosis: stable angina, post-MI, post-revascularization

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127
Q

Exercise stress testing

A
  • treadmill (usual) provides graded level of exertion
  • bicycle ergometer
  • exercise to 85% predicted max HR for age
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128
Q

Pharmacologic stress testing

A
  • used when exercise is impractical/impossible

adenosine, dipyridamole: vasodilate, therefore increase HR and work

dobutamine: increased contractility aka increased oxygen demand

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129
Q

Describe what a positive stress test presents as (3 ways)

A
  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
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130
Q

Stress testing is highly predictive if one of two things is present - what are they?

A

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

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131
Q

How do we know that a dx is certain with a stress test?

A

ST depression > 2mm

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132
Q

What is the value of adding imaging (echo or nuclear) to stress testing? (4)

A
  • 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
Q

Describe the 3 possible outcomes of myocardial ischemia

A

myocardial infarction&raquo_space; no return of contractile function

chronic ischemia without infarction&raquo_space; persistent ischemic dysfunction: hibernating myocardium&raquo_space; relief or stunned paths

relief of ischemia&raquo_space; salvage of previously ischemic myocardium&raquo_space; transient dysfunction = stunned&raquo_space; return of contractile function

134
Q

Describe the development of irreversible injury/infarction from myocardial ischemia

A

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
Q

Describe the methodolgy behind reducing myocardial injury (6)

A
  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
Q

Nitrates and myocardial ischemia therapy

A
  • 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
Q

Beta blockers and myocardial ischemia therapy

A
  • decrease HR and contractility (decrease oxygen demand)

- NO EFFECT ON OXYGEN SUPPLY

138
Q

Calcium antagonists and myocardial ischemia therapy

A
  • 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
Q

Describe the favorable effects of calcium antagonists in chronic stable angina

A
  • afterload reduction
  • verapamil and diltiazem reduce heart rate slightly
  • reduction in contractility but some make HR increase
  • may dilate coronary arteries
140
Q

Name the 2 reperfusion strategies/procedures for myocardial ischemia

A

Percutaneous Coronary Intervention (PCI) = angioplasty/stent

Coronary Artery Bypass Graft Surgery (CABGS)

141
Q

What is the most common reason for visits to the doctor AND for the use of prescription drugs in the US?

A

Systemic arterial HTN

142
Q

Which sex is more likely to have hypertension?

A

males

143
Q

Which race is most likely to have hypertension?

A

non-hispanic blacks

144
Q

What’s the lifetime risk of normotensive people at age 55 for developing hypertension?

A

90%

145
Q

What’s one word you would use to describe the risk factors for hypertension as a group?

A

synergistic

146
Q

What’s the significance/outcomes of the JNC 8 guidelines for systemic hypertension?

A
  • 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
Q

How will using a blood pressure cuff that is not the correct size affect your reading?

A

Narrow cuff or too-loose cuff will overestimate BP

148
Q

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?

A

use the arm with the higher reading

149
Q

Describe the indirect (Korotkoff) vs direct methods of taking BP

A

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
Q

Tell me what the 5 Korotkoff sounds are

A
  1. tapping sounds appear
  2. soft murmurs
  3. louder murmurs
  4. muffling of sounds
  5. disappearance
151
Q

Borderline hypertension

A

BP only occasionally exceeds normal

152
Q

Primary hypertension

A

elevated systemic BP without known cause

153
Q

Secondary hypertension

A

elevated systemic BP for which a cause can be identified

154
Q

Hypertensive emergency

A

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
Q

Malignant hypertension

A

now called hypertensive retinopathy grades III & IV and severe BP elevation

indicative of target organ damage

156
Q

Hypertensive encephalopathy

A

signs and/or symptoms of cerebral edema caused by severe and/or sudden rises in BP

(BP high and patient often in stupor)

157
Q

Describe the 4 grades of hypertensive retinopathy according to the Keith-Wagener Barker indications

A

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
Q

List a few severe possible CNS consequences of hypertension

A
  • decreasing cognitive function with age
  • transient ischemic attack (extracranial atherosclerosis)
  • stroke, either thromboembolic or hemorrhagic
159
Q

Describe the ways in which renal function is disturbed with systemic hypertension

A
  • 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
Q

What is the leading cause of end-stage renal disease?

A

systemic arterial hypertension

161
Q

Describe what happens with the cardiac and vascular tissue as a result of hypertension

A

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
Q

List 5 vascular complications of hypertension related to being hypertensive

A

accelerated malignant phase, hemorrhagic stroke, congestive heart failure, nephrosclerosis, aortic dissection

163
Q

List 5 atherosclerotic consequences of hypertension

A

coronary heart disease, sudden death, other arrhythmias, atherothrombotic stroke, peripheral vascular disease

164
Q

What are the 3 goals of evaluating systemic hypertension in a patient?

A
  • 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
Q

List some identifiable causes of secondary hypertension

A

Chronic renal parenchymal disease, primary aldosteronism, renovascular disease, chronic steroid therapy, pheochromocytoma, coarctation of aorta, sleep apnea, thyroid or parathyroid disease, drug induced

166
Q

Most often, SAH is asymptomatic. However, list some symptoms related to the CNS that a patient may present with

A

headache, dizziness, blurred vision, confusion, stupor, stroke/TIA

167
Q

Most often, SAH is asymptomatic. However, list some symptoms related to the cardiovascular system that a patient may present with

A

chest pain, dyspnea on exertion, palpitations, impotence, epistaxis

168
Q

Most often, SAH is asymptomatic. However, list some symptoms related to the renal system that a patient may present with

A

hematuria

169
Q

What are some key things to ask in a history if your patient has/may have SAH?

A

age, race, ethnicity, symptoms of target organ damage, family history, other illness/previous BP issues, risk/symptoms suggesting secondary HTN, lifestyle, meds

170
Q

List some cardiovascular risk factors associated with hypertension

A

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
Q

List 5 diseases that are especially significant in a patient with hypertension

A

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
Q

List some important parts to include on physical exam in a patient with hypertension (7)

A

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
Q

How to determine the correct cuff size for BP

A

2/3 length of upper arm

bladder should encircle the arm at least 80%

mercury manometer best

174
Q

Patient guidelines for food/drink prior to BP measurement

A 
at least 5 min of quiet 
no caffeine 1 hour
no smoking 15 min 
no adrenergic stimulants
quiet, warm setting
175
Q

List the parts of a minimum lab evaluation in new cases of SAH (7)

A 
dispstick urinalysis
fasting blood glucose 
hematocrit
serum creatinine
serum K+ and Ca2+
lipid panel 
ECG
176
Q

ECG for SAH patient (when is it indicated)

A
  • 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&raquo_space;> non-pharmacological tx if LV mass is normal
177
Q

Describe the pathology of atherosclerosis as well as which arteries are most commonly involved

A

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
Q

List some non-invasive testing that can be performed for atherosclerosis

A

H & P, digital pulse volume recordings, duplex US, doppler, transcutaneous oximetry, stress testing, MRA, segmental pressure measurements

179
Q

Definition of shock

A

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
Q

4 components of tissue perfusion

A

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
Q

Name the 3 classes of shock

A

cardiogenic, hypovolemic, distributive

182
Q

Cardiogenic shock

A

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
Q

Hypovolemic shock

A

loss of circulating blood volume, hemorrhage, sever burns

184
Q

Distributive shock

A

abnormal shunting of blood flow

many etiologies: SEPSIS, drug overdose, anaphylaxis, neurogenic, etc.

185
Q

5 Clinical characterizations of shock

A

very low systolic arterial BP (60 or less), tachycardia, oliguria, mental obtundation, cool/mottled extremities

186
Q

Hypovolemic shock

A

reduced/loss of circulating blood volume resulting in reduced cardiac filling and decreased CO

etiologies: blood loss (hemorrhage, severe burns), fluid depletion

187
Q

Distributive shock

A

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
Q

5 clinical characterizations of shock

A

very low systolic arterial BP (60 or less), tachycardia, oliguria, mental obtundation, cool/mottled extremities

189
Q

List some of the multiorgan consequences of shock

A

Acidemia, myocardial dysfunction, pulmonary (ARDS), renal (ATN), GI (hepatic injury, intestinal ischemia/injury), CNS (post-anoxic encephaloaphy; death)

190
Q

List some general principles of therapy for shock (6)

A
  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
Q

Define the prognosis of shock (cardiogenic vs hypovolemic vs septic)

A

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
Q

Etiologies of aortic regurgitation

A

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
Q

Describe the hemodynamic pathophysiology of aortic regurgitation (5)

A
  • 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
Q

Name some clinical manifestations of aortic regurgitation during the history

A
  • 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
Q

Clinical manifestations of aortic regurgitation on physical exam

A
  • 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
Q

Clinical manifestations of aortic regurgitation on physical exam

A
  • 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
Q

Describe the murmurs often heard with aortic regurgitation

A

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
Q

List some of the eponymous signs of aortic regurgitation on physical exam

A

Austin Flint murmur, corrigan pulse, de Musset’s sign, Hill’s sign, Muller’s sign, Quicke’s pulse, Traube’s sign

199
Q

Clinical manifestations of aortic regurgitation on ECG

A

not specific or sensitive

can have: LVH, left axis deviation, ST-T changes, LA enlargement, AV conduction abnormalities (late)

200
Q

Clinical manifestations of aortic regurgitation on chest x-ray and nuclear imaging

A

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
Q

Why would we use echocardiogarphy on patients with aortic regurg?

A
  • 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
Q

Describe the general tx plan for aortic regurgitation

A
  • 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
Q

Describe the pharmacologic tx used in aortic regurgitation

A
  • 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
Q

Talk about the use of valvular replacement in cases of aortic regurgitation

A
  • 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
Q

Natural history of aortic stenosis

A
  • 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
Q

List the etiologies of aortic stenosis in patients <75 yo

A

Congenital bicuspid about 50% of cases: congenitally stenotic valve may be unicuspid, bicuspid or tricuspid

Post-inflammatory about 25%

About 18% degenerative

207
Q

List the etiologies of aortic stenosis in patients >75 yo

A

50% degenerative
27% bicuspid
25% post-inflammatory

208
Q

Describe the hemodynamic pathophysiology of aortic stenosis

A
  • 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
Q

Clinical manifestations of aortic stenosis on history (6)

A
  • 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
Q

Describe clinical manifestations of aortic stenosis on physical exam (2)

A

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
Q

Describe what might be heard on auscultation with aortic stenosis

A

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
Q

Describe the murmur heard with aortic stenosis

A

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
Q

Describe what might be seen on chest x-ray and echocardiography of aortic stenosis

A

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
Q

Describe the ECG of aortic stenosis

A

not specific

can demonstrate: LVH, left axis deviation, ST-T changes, LA enlargement

stress ECG may be dangerous

215
Q

Describe the general tx for aortic stenosis

A
  • 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
Q

Medical tx of aortic stenosis

A
  • 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
Q

Describe the role of valve replacement in aortic stenosis (mainstay)

A
  • 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
Q

What are the 2 transcatheter therapies for aortic stenosis?

A

balloon valvuloplasty

valve replacement

219
Q

List some common etiologies of mitral regurgitation

A

rheumatic disease, infective endocarditis, collagen vascular disease, cardiomyopathy, ischemic heart disease, mitral valve prolapse

220
Q

List the 4 valve structures that may be involved in mitral regurgitation

A

leaflets, mitral annulus, chordae tenidnae, papillary muscles

221
Q

Describe some of the changes in the leaflets that lead to MR

A
  • 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
Q

Describe some of the changes in the mitral annulus that lead to MR

A
  • Dilation: any disease that dilates the LV

- Calcification: idiopathic in most cases, can cause severe MR & more common in women

223
Q

Describe some of the changes in the chordae tendinae that lead to MR

A
  • In mitral valve prolapse they lengthen and rupture

- Infective endocarditis, trauma, others may also cause rupture of chordae with secondary MR

224
Q

Describe some of the changes in the papillary muscles that lead to MR

A
  • 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
Q

Describe the pathophysiology of MR

A
  • 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
Q

Describe the hemodynamic pathophysiology of MR

A

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
Q

Aspects of the history of patient with MR

A
  • 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
Q

Clinical manifestations of MR on physical exam

A
  • 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
Q

Manifestations on auscultation in patient with MR

A

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
Q

Describe the MR murmur

A

Holosystolic, blowing, loudest at apex, radiates to axilla, commences with S1, occasionally lasts through S2, constant loudness

Occasionally, diastolic murmur commencing with S3

231
Q

Cornerstone of diagnosis for valvular disease

A

echocardiography

232
Q

Manifestations on chest x-ray and echocardiography for MR

A

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
Q

ECG manifestations for MR patient

A

not specific

can demonstrate LA conduction abnormality, RVH, atrial fibrillation

234
Q

General tx for MR

A
  • 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
Q

Surgical Tx for MR

A

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
Q

Valve repair in MR is best in… (5)

A

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
Q

Main etiology of mitral stenosis

A

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
Q

List 4 conditions that mimic MS

A

left atrial myxoma

left atrial ball-valve thrombus

infective endocarditis with large vegetations

cor triatriatum (congenital)

239
Q

Describe the pathophysiology of MV stenosis, including the hemodynamics

A

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
Q

Describe some common aspects of the history in a patient with MS

A
  • 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
Q

Manifestations on physical exam in patients with MS

A
  • 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
Q

Manifestations on auscultation of MS

A

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
Q

Describe the murmurs of MS

A

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
Q

Manifestations on x-ray and echocardiography in MS patient

A

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
Q

ECG of MS

A

not specific

can demonstrate: LA conduction abnormality (90%), RVH, atrial fibrillation

246
Q

Natural hx of MS

A

15-20 yr latency after RF before symptoms develop in temperate climates

eventually, as LA dilates, patients can develop atrial fibrillation, embolization, etc.

247
Q

General tx of MS

A
  • prophylaxis against endocarditis
  • avoid strenuous activity
  • anticoagulants for prophylaxis against emboli, esp. stroke
  • maintain sinus rhythm
  • reduce salt/water intake
248
Q

Medical tx for a fib and MS

A
  • anticoagulable with heparin then DC cardioversion

- if cardioversion not posible, slow vent rate to improve CO (beta blockers, NDHP CCBs, digitalis)

249
Q

Valve surgery tx for MS

A

Coronary angiogram if discrepancy between clincal findings and echo, pts with COPD, angina, men >40, women >50 with risk factors for CAD

250
Q

List the 4 valve surgeries for MS tx

A

balloon valvotomy
closed valvotomy
open valvotomy & repair
MV replacement

251
Q

List 3 benefits for SAH tx

A

avoid/reduce target organ damage

persistent/uniform reduction in stroke

likely reduces CAD risk

252
Q

How does weight loss influence SAH?

A

decrease of 1 kg found to decrease BP 1.6/1.3 mmHg

253
Q

General tx goals of drug therapy for SAH

A
  • intent to reduce systemic BP below initial tx thresholds
Drug classes: 
diuretics
CCBs
ACEIs
ARBs
Beta blockers/alpha blockers
vasodilators
254
Q

Drug tx of choice for SAH

A

thiazide diuretics

255
Q

Drug tx of choice fof SAH in people >18 yo with chronic kidney disease

A

ACEI or ARB

256
Q

Main goal of BP therapy?

A

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
Q

MI tends to result from what?

A

rupture or erosion of a vulnerable plaque in the milieu of inflammation and procoagulation

258
Q

What typically happens right after a plaque ruptures?

A

blood is exposed to inner plaque material resulting in activation of platelets, thrombin generation and thrombus formation

259
Q

One significant thing to note about plaque rupture as far as clinical manifestation goes

A

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
Q

True or false: most plaque ruptures do not result in a clinical cardiac event

A

True

261
Q

ACS can manifest in what ways? Name the 2 major ways and how they are characterized

A

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
Q

Vulnerable plaques - characteristics, outcomes

A

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
Q

Killip Classification system for risk stratification of AMI

A

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
Q

Leads with ST ELEVATION correlate with the anatomic area of injury: list 3 locations/indications

A

II, III, AVF = inferior MI with RCA damage (or left circumflex)

I, AVL - high lateral MI, LCA

V1-V4 = anterior MI, LAD

265
Q

Cardiac Troponin changes associated with MI (4)

A

Rises within ~3 hrs of AMI

Released continually after myocycte injury

Peaks 24-48 hrs

Remain elevated 5-10 days after myocardial injury

266
Q

Creatine Kinase MB (CKMB) changes associated with MI (3)

A

Rises within 4 hrs of AMI

Peaks in ~24 hrs

Returns to normal 2-3 days after myocardial injury

267
Q

Initial ED tx of ACS (9)

A
  • O2
  • Aspirin
  • Sublingual Nitro
  • Anticoagulant
  • Beta blocker
  • IV nitro drip if symptoms persist
  • Second antiplatelet agent
  • Morphine
  • Cardiac cath
268
Q

Initial ED tx of ACS (9)

A
  • 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
Q

4 major characteristics of vulnerable plaque

A

Thin fibrous cap, large atherosclerotic burden (>70%), minimal luminal diameter < 4mm, protruding calcium

270
Q

Definition of MI

A

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
Q

STEMI (5)

A
  • 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
Q

What happens if perfusion is not restored in STEMI? (esp. if from a proximal LAD occlusion)

A
  • 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
Q

Normal ejection fraction value

A

55-70%

274
Q

Inferior STEMI from a proximal RCA occlusion can result in associated RV infarction - list the clinical manifestations/indications (4)

A
  • 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
Q

NSTEMI (4)

A
  • 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
Q

NSTEMI tx plan

A

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
Q

Post MI medical therapy includes what 9 things?

A
  • 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
Q

anterior wall MI vs inferior wall MI

A
  1. Anterior: LAD occlusion = widow maker, high catecholamine state
  2. Inferior: RCA occlusion, high vagal tone state
279
Q

Who should undergo cardiac catheterization?

A

elevated troponins, dynamic ST changes, recurrent symptoms, low ejection fraction

280
Q

List some common post MI complications

A

arrhythmia, heart failure, embolus, pericarditis, papillary muscle rupture, VSD, free wall rupture, LV aneurysm, cardiogenic shock

281
Q

List 4 possible ventricular arrhythmias

A

ventricular premature beats

accelerated intraventricular rhythm

ventricular tachycardia

ventricular formation

282
Q

Name 2 kinds of bradyarrhythmias

A

sinus bradycardia

AV block

283
Q

PVCs (define, tx)

A

common, along with short runs of NSVT

don’t require specific treatment: correct electrolytes, beta blockers

284
Q

Accelerated Idioventricular Rhythm

A

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
Q

V tach (description and tx)

A

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
Q

V fib

A

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
Q

V fib

A

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
Q

Sinus bradycardia

A

may be seen during acute phase of MI from sinus node ischemia (RCA >LCX > dual) or high parasympathetic tone

289
Q

AV block inferior MI

A

block AT AV node level, usually transient

290
Q

AV block anterior MI

A

rare, usually BELOW AV node level, implies extensive infarct with bundle branch involvement, usually permanent

needs pacemaker

291
Q

AV block anterior MI

A

rare, usually BELOW AV node level, implies extensive infarct with bundle branch involvement, usually permanent

needs pacemaker***

292
Q

Heart Failure: acute MI phase

A

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
Q

Heart failure: post acute phase

A

usually secondary to systolic dysfunction

manage with diuretic, ACEI, aldosterone antagonists, beta blocker once compensated

294
Q

Describe the cycle of LV remodeling

A
  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
Q

Cardioembolism

A

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
Q

Early Pericarditis (within 1st week)

A
  • 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
Q

Late pericarditis (1-8 weeks)

A

Dressler’s syndrome

autoimmune mechanism

systemic symptoms too

treat with aspirin, colchicine

298
Q

Name the 5 populations with increased risk of ventricular septal defect***

A

older patients, females, history of HTN, first MI, delayed or absent reperfusion

299
Q

Clinical presentation of VSD

A

chest pain, dyspnea, hypotension, biventricular failure, harsh, holosystolic murmur on left sternal border, thrill in 1/2 of pts, S3, loud P2, TR

300
Q

Ventricular septal rupture management (3 aspects)

A
  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
Q

Acute mitral regurgitation - which part of the heart is involved?**

A

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
Q

Clinical presentation of acute mitral regurg

A

heart failure, may be sudden onset, new systolic murmur

303
Q

Acute MR management

A

ventilator if needed

IABP esp in hypotension

afterload reduction

surgery = tx of choice

304
Q

VSD vs papillary muscle rupture ***

A

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
Q

Clinical presentation of free wall rupture and diagnosis/tx

A

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
Q

True aneursym vs pseudoaneurysm (3**)

A

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
Q

Intra-aortic balloon pump

A

augments coronary blood flow during diastole

decreases afterload during systole by deflating at the onset of systole

reduces myocardial ischemia

308
Q

List the major etiologies of peripheral arterial disease

A

atherosclerosis, thrombosis, embolism, vasculitis, fibromuscular dysplasia, cystic adventitial disease, trauma

309
Q

List some symptoms of peripheral arterial disease

A

intermittent claudication (most common), when severe: hair loss, nail thickening, shiny skin, pallor, pain while at rest

half of people asymptomatic

310
Q

Compare a normal ABI to one seen in patients with occlusive disease/PAD and patients with severe ischemia/PAD

A

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
Q

Pharmacological and other tx of PAD

A

tx of HLP, HTN, DM

PDE inhibitor, platelet inhibitors

exercise, lifestyle changes, supportive measures, non-operative interventions, surgery (revascularization)

312
Q

In which 3 situations do we refer a PAD patient to interventional radiologist vs vascular surgeon

A

pain at rest, non-healing lower extremity ulcers associated with low ABIs, severe/debilitating claudication

313
Q

Acuter arterial occlusion - what happens and what causes it (2)

A

resulting in sudden cessation of blood flow to an extremity

emoblism, thrombus in situ

314
Q

Acute arterial occlusion of embolic source

A

most common sources are heart, aorta and large arteries

cardiac: a fib, ACS, prosthetic valves, endocarditis, atrial myxoma

aortic aneurysms

large arterial bifurcations

315
Q

Acute Arterial Occlusion due to thrombus in situ

A

occurs most frequently in atherosclerotic vessels at site of stenosis

in bypass grafts, PV, hypercoagulable states

316
Q

Fibromuscular Dysplasia

A

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
Q

Thromboangiitis Obliterans

A

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
Q

Atheroembolism

A

subset of acute arterial occlusion

multiple small deposits of fibrin, platelets, cholesterol debris embolizing downstream

acute pain and tenderness at site of emboli

319
Q

Raynaud’s (phenomenon vs disease)

A

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
Q

Livido Reticularis

A

localized areas on extremities develop a reddish/blue rete or net-like appearance

primary/idiopathic disorder vs secondary

321
Q

Venous thrombosis

A

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
Q

What is virchow’s triad??**

A

stasis, vascular damage, hypercoagulability

323
Q

Deep Venous Thrombosis

A

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
Q

Pulmonary emoblism ** (esp. risk and clinical presentation)

A

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
Q

Chronic venous insufficiency

A

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
Q

Etiology/description of MI in general

A

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
Q

General symptoms of MI

A

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
Q

Testing, Dx, Tx of MI in general

A 
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
Q

Symptoms/description of angina pectoris

A

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

Cardiology (3 decks)

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