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CVPR > Unit 2 > Flashcards

Unit 2 Flashcards

1
Q

Identify risk factors for development of coronary atherosclerosis

A

Treatable:

  • smoking (thrombogenic, platelet activation, inc fibrinogen)
  • hypertension (inc shear stress –> endo cell injury, pathologic cell signaling, circulating hormones, LVH)
  • dyslipidemia (high LDL –> pro-inflamm and atherogenic and low HDL which can be beneficial)

Treatable, but may not reduce risk for CAD:

  • diabetes (inc 1.5-2 fold; assoc w/ inflammation, oxidative stress, dyslipidemia)
  • obesity
  • inflammation (lipid laden macrophages in wall –> pro-inflamm)
  • stress
  • sedentary lifestyle

Not treatable:

  • male
  • old age
  • most genetic factors
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2
Q

Recognize distinguishing features of the coronary circulation

A
  • myocardium cannot do anaerobic metabolism; depends on aerobic metabolism
  • the only way of increasing myocardial O2 supply is to increase blood flow rate
  • due to compression of CAs during systole, LV is perfused in diastole
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3
Q

Describe key elements of pathophysiology of stable coronary heart disease

A
  • obstruction in coronary artery limits flow –> myocardial ischemia
  • tissue blood flow does not meet O2 reqs especially when demand inc
  • imbalance between O2 supply and demand –> ischemia –> angina pectoris
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4
Q

Describe pathophysiology and treatment of unstable coronary heart disease (unstable angina or myocardial infarction)

A
  • inflammation in arterial wall
  • weakened fibromuscular cap
  • plaque fissure
  • lipids and tissue factor exposed to blood –> thrombosis –> severe/complete vessel occlusion –> MI
  • cardinal symptom: severe and unremitting chest discomfort at rest
  • within minutes, impaired SR reuptake –> diastolic dysfunction –> inc LV filling pressure –> pulm congestion/dedema
  • dec high energy phosphates, intracellular acidosis –> systolic dysfunction
  • ECG signs
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5
Q

Briefly describe coronary circulation

A
  • aorta gives rise to left coronary artery –> left circumflex artery and left anterior descending artery
  • aorta gives rise to right coronary artery –> posterior interventricular in the back
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6
Q

What are principle determinants of myocardial oxygen supply and demand?

A

Supply:

1) coronary blood flow rate
- perfusion pressure
- perfusion time (1/HR) aka how much time in diastole
- vascular resistance of coronary bed

2) O2 content of blood

O2 delivery = CVF rate * oxygen content

Demand:

1) Heart rate
2) Wall tension (T=P*r/u)
3) Inotropic state

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7
Q

What is autoregulation?

A
  • An adaptive mechanism to maintain perfusion in the face of altered perfusion pressure
  • changes in arteriole size to adjust to changes in pressure to maintain flow
  • basically, if pressure differential gets bigger, then resistance gets bigger to maintain flow because flow = deltaP/res
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8
Q

Describe treatment for stable coronary heart disease

A

Treatment:

1) Increasing O2 supply
- inc diastolic perfusion pressure by preventing hypotension
- inc diastolic time with rate-slowing drugs
- dec coronary resistance with vasodilators or coronary angioplasty/bypass
- inc O2 content by treating anemia and hypoxemia

2) Decreasing O2 demand
- dec systolic pressure with antihypertensive drugs
- dec wall tension by limiting LV size by limiting excessive preload (with diuretics and nitrates)
- dec inotropic state to attenuate contractile state (with beta or Ca channel blockers)

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9
Q

Describe the progression of atherosclerosis

A

normal –> fatty streak (endo injury, lipid deposition, mac/T-cell recruitment) –> fibrous plaque –> occlusive atherosclerotic plaque (activated mac; smooth muscle proliferation forms fibrous cap; lipid accumulation) –> plaque rupture –> angina, MI, stroke

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10
Q

When there is a stenosis, how does autoregulation help?

A
  • stenosis causes a pressure drop
  • without autoreg, the pressure drop would result in dec flow because:

flow = deltaP/res

  • however, autoreg is able to dilate downstream vessels in response to decreased pressure differential (compared to 0 mmHg at the venous end) so that flow is maintained (dec deltaP/dec res = same flow)
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11
Q

Describe approaches to diagnosis of coronary artery disease

A

Presentation:

  • chest pain
  • dyspnea
  • risk factors

Physical exam:

  • normal
  • CV dysfunction prior to MI (CHF)
  • atherosclerosis

Tests:

  • ECG at rest/changes with exercise (ST segment elev/dep, T wave immersion, Q waves)
  • imaging (echo, CT, angiography)
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12
Q

Describe approaches to treatment with medications of CAD

A

Stable angina:

  • nitrates and beta blockers (to decrease demand on heart)
  • control BP with anti-hypertensives
  • lower cholesterol with statin
  • aspirin to prevent thrombi
  • ACEi or ARBs for LV dysfunction
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13
Q

Describe approaches to coronary angioplasty and stents

A
  • early coronary angioplasty dec risk of recurrent ischemic events in unstable angina
  • balloon dilation of stenosed area –> larger lumen –> dec resistance –> inc flow
  • problems: acute occlusion (solve with stents and antiplatelet) and restenosis (solve with stents)
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14
Q

Describe approaches to coronary bypass surgery

A
  • maybe better than angioplasty when multiple blockages
  • many types of grafts: internal mammary artery, saphenous vein, prosthetic material
  • basically bypassing blockage in LAD (or whatever artery) by connect an artery from left subclavian artery to downstream from the blockage
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15
Q

Describe coronary angiography

A
  • gives an image of the vessel lumen, but does not tell about the vessel wall (underestimates pathologic extent of CAD)
  • can diagnose coronary obstruction
  • guides angioplasty/surgery
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16
Q

What are the general modes of treatment for CAD?

A
  • modify risk factors (diet, exercise, no smoking)
  • drugs to treat angina, BP, lipids, platelets, ACEis/ARBs
  • revascularize (angioplasty/bypass surgery)
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17
Q

How do you acutely treat unstable angina?

A
  • hospitalization
  • IV nitroglycerin (nitrate = vasodilator)
  • beta blocker
  • aspirin/anti-platelet
  • anticoag
  • early catheterization
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18
Q

How do you treat acute MI with ST elevation?

A
  • immediate aspirin, nitroglycerin, maybe beta blocker

- reperfusion therapy ASAP - coronary angioplasty or thrombolytic therapy

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19
Q

Recognize that the normal endothelium is anti-inflammatory, anti-thrombotic, and vasodilatory

A

Normal endo cells:

  • impermeable to large molecules
  • anti-inflam
  • resists leukocyte adhesion
  • promotes vasodilation
  • resists thrombosis

Activated endo cells:

  • inc permeability
  • inc inflam cytokines
  • inc leukocyte adhesion
  • dec vasodilation
  • dec anti-thrombosis

(also activated means activated by inflammation)

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20
Q

Differentiate mechanisms of ischemia depending on the vascular bed, all of which involve endothelial dysfunction

A

1) Narrowing of vessel by fibrous plaque:
- plaque builds up and you get a stenosis
- seen in renal artery stenosis, myocardial ischemia, limb claudication, and limb ischemia

2) Plaque ulceration/rupture:
- plaque breaks through fibrous cap and have thrombosis
- seen in thrombolic stroke, unstable angina, and MI

3) Intraplaque hemorrhage:
- can have bleeding that occurs within the plaque itself
- seen in thrombolic troke, unstable angina, and MI

4) Peripheral emboli:
- pieces of plaque can break off and get stuck somewhere else
- seen in embolic stroke, atheroembolic renal disease, and limb ischemia

5) Weakening of vessel wall:
- integrity of vessel wall is weakened leading to aneurysm
- seen anywhere

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21
Q

What is the endothelium?

A
  • a single layer of cells comprising tissue that lines blood and lymph vessels, heart, and other cavities
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22
Q

Describe the three layers of the blood vessel wall

A
  • Tunica intima: endothelial cells and CT
  • Internal elastic lamina between TI and TM
  • Tunica media: smooth muscle cells and CT
  • External elastic lamina between TM and TA
  • Tunica adventitia: loose CT and provides structure
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23
Q

Describe the contents of the walls of large arteries, smaller arteries, and arterioles

A
  • large arteries: more elastin
  • smaller arteries: more collagen
  • arterioles: more smooth muscle
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24
Q

Describe the difference between normal and activated smooth muscle cells

A

Normal SMC:

  • normal contractile function
  • maintains ECM
  • contained in TM

Activated SMC:

  • inc inflam cytokines
  • inc ECM synth
  • migration into subintima
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25
Q

How is NO produced and how does it work?

A
  • receptor on endo cell activated by ACh, serotonin, thrombin, bradykinin or shear stress
  • activates eNOS which converts L-Arginine to NO with a lot of cofactors
  • NO diffuses to the smooth muscle in TM
  • NO causes cGMP mediated vasodilation
  • in diseased states where NO is dec –> leads to inflammatory state
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26
Q

Describe the steps in the formation of atherosclerotic plaque

A
  • monocyte infiltration (in an inflammatory state)
  • phenotypic change to macrophage
  • macrophages get activated and are called foam cells (early sign of atherosclerosis) and secrete cytokines that lead to degradation of endothelium
  • changes phenotype of SMC (migrating and dividing uncontrollably)
  • increased fibrosis and apoptosis
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27
Q

What are the 3 stages of atherosclerosis?

A

1) fatty streak:
- endo dysfunction
- lipoprotein entry and modification
- leukocyte recruitment
- foam cell formation

2) plaque progression:
- SMC migration into TI
- altered ECM synth and degradation

3) plaque disruption:
- disrupt plaque integrity
- trombus formation

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28
Q

Compare vulnerable and stable plaques

A

Stable:

  • lots of fibrous tissue
  • calcified
  • less lipid content
  • less inflammation
  • less apoptosis

Vulnerable:

  • less fibrous tissue
  • less calcified
  • more lipid content
  • more inflammation
  • more apoptosis
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29
Q

What are the main mechanisms of stroke?

A
  • atheroembolism (from carotid bifurcation lesion)

- lesion does not need to be completely obstructive (

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30
Q

What are the main vascular mechanisms of CAD?

A
  • MI and angina are results of CAD but have different vascular pathology
  • MI: rupture plaque, in-situ thrombosis, doesn’t need to be obstructive prior to rupture
  • stabilize with anticoag and vasodilators (if non-occlusive thrombosis)
  • clinical emergency/recanalize if occlusive thrombus
  • angina: stable, obstructive (>70%) lesion
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31
Q

Describe the potential effects of coronary thrombus

A

1) small thrombus
- no ECG changes
- healing and plaque gets bigger

2) partially occlusive thrombus
- ST seg depression and/or T wave inversion
- if inc troponin I and other markers –> non STEMI
- if no inc troponin I and other markers –> unstable angina

3) occlusive thrombus
- transient ischemia –> same as partially occlusive thrombus
- prolonged ischemia –> ST elev –> inc troponin I –> STEMI

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32
Q

Describe the vascular pathology differences between claudication and acute limb ischemia as forms of PAD

A

Claudication:

  • obstructive, stable plaque
  • analogous to angina

Acute limb ischemia:

  • acute event blocks flow
  • athero/thromboembolus
  • rarely in-situ thrombosis (unstable plaque_
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33
Q

What are the differences generally between stable and unstable plaques?

A

Stable:

  • less bio active
  • causes angine and caludication (exertional ischemia) if obstructive
  • less likely to be thrombotic and embolic

Unstable:

  • more bio active
  • can cause MI and stroke
  • can be thrombotic and embolic
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34
Q

What are the differences between venous and arterial thrombosis?

A

Venous:

  • fibrin rich
  • RBC
  • areas of stasis
  • genetic predis
  • environmental predis
  • treat with anticoag

Arterial:

  • platelet rich
  • plaque rupture
  • high flow
  • atherosclerosis, trauma, APLA (antiphospholipid antibodies)
  • antiplatelet therapy
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35
Q

Describe the spectrum of acute coronary syndrome and its pathophysiology

A

STEMI
- complete coronary vessel occlusion

NSTEMI
- partial coronary vessel occlusion with myocardial necrosis

Unstable angina
- partial coronary vessel occlusion without myocardial necrosis

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36
Q

Distinguish non-ST elevation myocardial infarction (NSTEMI), ST-elevation myocardial infarction (STEMI), and unstable angina (UA)

A

STEMI:

  • prolonged, severe chest pain
  • total occlusion
  • inc biomarkers
  • ST elevation

NSTEMI:

  • prolonged, severe chest pain
  • partial occlusion
  • inc biomarkers
  • ST depression

Unstable angina:

  • angina that is escalating, at rest, or new onset
  • partial occlusion
  • no inc biomarkers
  • ST depression
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37
Q

Clinically diagnose acute coronary syndrome based on symptoms, ECG, and biomarkers

A

ECG:

  • subendocardial ischemia shows a ST depression
  • transmural ischemia shows a ST elevation
  • with a partial occlusion and no infarct, can show ST dep during symptoms and normal when symptom-free (can cause symptoms but not long enough to cause damage)

Biomarkers:

  • Troponin I and T are sensitive and specific for myocardium
  • rise 3-4hrs after onset of pain
  • peak at 18-36hrs
  • CK-MB is not as specific for myocardium
  • rise 3-8hrs after onset of pain
  • peaks at 24hrs

Symptoms:

  • angina: chest pain
  • stable - pain when inc O2 demand and can reproduce
  • unstable - inc in duration, intensity, or frequency; less provocation or at rest; new onset
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38
Q

Explain the basis behind the treatment of ST elevation myocardial infarction

A
  • artery is 100% occluded –> open it with cardiac catheterization if 90min then consider fibrinolytics
  • can also give beta blockers or nitrates if stable
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39
Q

Explain the basis behind the treatment of non-ST elevation myocardial infarction and unstable angina

A
  • artery is partially occluded –> stop thrombosis from completely occluding artery with anticoag and antiplatelet
  • can also give beta blockers or nitrates if stable
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40
Q

What is the definition of ACS?

A

Acute Coronary Syndrome is any array of clinical symptoms resulting from underlying acute myocardial ischemia

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41
Q

What are causes of ACS?

A
  • *atherosclerotic plaque rupture with thrombus –> partial or complete thrombosis
  • coronary embolism
  • congenital anomalies
  • coronary trauma or aneurysm
  • severe coronary artery spasm
  • inc blood viscosity
  • spontaneous coronary dissection
  • inc myocardial O2 demand
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42
Q

If you have prolonged ischemia, what happens?

A
  • myocyte death and tissue necrosis –> STEMI or NSTEMI
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43
Q

What is the time to initial elevation, time to peak elevation, and time to return to normal for CK-MB?

A

Time to initial elevation:
- 4-6hrs

Time to peak elevation:
- 18hrs

Time to return to normal:
- 2-4days

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44
Q

What is the time to initial elevation, time to peak elevation, and time to return to normal for troponin I?

A

Time to initial elevation:
- 4-6hrs

Time to peak elevation:
- 12hrs

Time to return to normal:
- 3-10days

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45
Q

What is the difference between stable and unstable angina?

A

Stable angina:
- occurs with inc myocardial O2 demand in a reproducible fashion

Unstable angina:

  • discomfort which is new in onset OR inc in duration, frequency, or intensity with less exertion or at rest compared to previous episodes of discomfort
  • on spectrum of ACS
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46
Q

What is the general goals for treating ACS?

A

1) relieve ischemia by opening artery and reducing myocardial O2 demand
2) prevent adverse outcomes

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47
Q

What is a differential diagnosis for chest pain?

A
  • ACS/angina
  • aortic stenosis/insuff/dissection
  • HOCM
  • severe HTN
  • pericarditis
  • GERD
  • costochondritis
  • PE
  • lots of others
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48
Q

Describe the difference between transmural and subendocardial myocardial ischemia

A

Transmural:

  • ischemia spans entire wall of myocardium
  • usually due to complete occlusion

Subendocardial:

  • involves innermost layer of myocardium
  • usually due to partial occlusion
  • subendocardial layer has highest pressure from ventricle and smallest collateral flow
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49
Q

Recognize basic concepts and discuss uses of chest x-ray

A
  • on xrays, the higher the density, the whiter the color
  • bone is white, tissue is gray, air is black
  • PA view minimizes magnification of heart
  • also a lateral view
  • uses radiation
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50
Q

Recognize basic concepts and discuss uses of echocardiogram

A
  • doppler; ultrasound waves sent into body and returns to transducer
  • can show 2D motion
  • color doppler of bood flow
  • M mode can look at different axis and as a result different chamber sizes
  • send microbubbles to visualize a sort of static appearance that don’t pass through pulm caps and don’t show in left heart unless connection between right and left heart
  • can look at chamber size, function, structure, valves, etc.
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51
Q

Recognize basic concepts and discuss uses of cardiac stress tests

A
  • cause ischemia by inc O2 demand on heart
  • see inc in sys BP and dec in dias BP
  • ST dep in ECG
  • inc in HR by >85%
  • tiredness, dyspnea
  • can look at blood flow/perfusion imaging
  • can look at wall motion with echo
  • good for detecting left main or 3 vessel CAD
  • fast for 2hrs before
  • monitor ECG, BP, and HR
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52
Q

Recognize basic concepts and discuss uses of cardiac MRI

A
  • 3D imaging
  • non-ionizing radiation
  • contraindications: metallic implants, kidney dysfunction
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53
Q

Recognize basic concepts and discuss uses of cardiac CT/CT angiography

A
  • noninvasive
  • radiation
  • doesn’t use catheter
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54
Q

Recognize basic concepts and discuss uses of catheterization/coronary angiography

A
  • insert catheter into artery or vein and move to heart/coronary arteries to image
  • measure pressure gradients
  • can use contrast for angiography
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55
Q

Differentiate and recognize indications and contraindications for exercise ECG

A

Exercise Treadmill Test:

1) indications:
- screen for CAD
- eval chest pain
- exercise capacity
- eval after revascularization
2) contraindications:
- unstable angina
- untreated arrhythmias
- uncompensated HF
- AV heart block
- acute myo/pericarditis
- aortic stenosis
- HOCM
- uncontrolled HTN
- acute systemic illness
- low cost

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56
Q

Differentiate and recognize indications and contraindications for echocardiography/radionuclide stress test

A

Indications:

  • abnormal baseline ECG, digoxin, WPW
  • inc sensitivity
  • localization
  • preop cardiac risk assessment
  • myocardial viability

Contraindications:

  • unstable angina
  • untreated arrhythmias
  • uncomp HF
  • AV heart block
  • acute myo/pericarditis
  • aortic stenosis
  • HOCM
  • uncontrolled HTN
  • acute systemic illness
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57
Q

Discuss the use of echocardiography in evaluation of patients with shortness of breath, valve disease, chest pain, heart failure, coronary artery disease, and acute coronary syndromes including myocardial infarction

A
  • ultrasound into body and returns to transducer producing a 2D image
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58
Q

Discuss the use of cardiac enzymes in evaluation of patients with shortness of breath, valve disease, chest pain, heart failure, coronary artery disease, and acute coronary syndromes including myocardial infarction

A

Natriuretic peptides:

  • BNP found in ventricles
  • released in response to stretch/inc vol in ventricles
  • inc BNP = inc LVEDP, NYHA class, HF diagnosis >55yo
  • BNP is higher in females and elderly
  • BNP inc in renal insuff
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59
Q

The causes of ischemic heart disease and exacerbating factors in coronary atherosclerosis

A
  • ischemic heart disease = syndromes caused by myocardial ischemia when demand>supply
  • > 90% of cases are due to coronoary atherosclerosis with reduced coronary blood flow
  • symptoms are associated with >70% occlusion
  • > 90% can lead to symptoms at rest
  • acute changes in plaque morphology (hemorrhage or rupture and/or embolus)
  • coronary artery thrombosis
  • coronary artery vasospasm
  • platelet aggregation
  • hypotensive episode
  • inc myocardial O2 demand
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60
Q

The pathogenesis of myocardial infarction and differences between transmural and subendocardial infarcts

A
  • irreversible myocyte necrosis due to prolonged ischemia
  • most cases caused by acute coronary artery thrombosis due to atherosclerotic plaque rupture
  • MIs usually begin in subendocardial region because it is the most poorly perfused then move outwards to become transmural in hours

Transmural infarct:
- full thickness of myocardium; more common and usually due to thrombus in coronary artery

Subendocardial infarct:
- affects inner third/half of myocardium and usually due to hypoperfusion due to hypotension or shock

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61
Q

Factors that may influence the ultimate size of an infarct

A
  • site of occlusion
  • duration of ischemia
  • collateral vessels supply outer layer so more likely to be subendocardial
  • metabolic needs of myocardium
  • reperfusion injury: after restoring blood flow due to mitochondrial dysfunction, myofibril hypercontracture with cytoskeletal damage and cell death due to Ca influx; damage to membrane proteins; leukocyte aggregation; platelet and complement activation
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62
Q

Know the following summary of the chronologic sequence of morphologic light microscopic changes in MIs:

a) contraction bands & myocyte necrosis
b) neutrophilic infiltrates
c) macrophages
d) granulation tissue
e) fibrosis (weeks later)

A
  • 4-12hrs: wavy fibers (noncontractile ischemic fibers stretch with systole)
  • 18-24hrs: coagulation necrosis, contraction bands at periphery of infarct, neutrophilic infiltrate
  • 24-72hrs: max neutrophilic infiltrate
  • 4-7days: macrophages with disintegration of necrotic myocytes (max softening)
  • 10days: granulation tissue
  • 4-8wks: fibrosis
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63
Q

Complication of acute MI and their clinico-pathological correlations

A
  • 25% sudden cardiac death
  • 80-90% complications if make to hospital
  • arrhythmia
  • LV failure and pulm edema
  • cardiogenic shock
  • pericarditis
  • rupture of papillary muscle
  • ventricular aneurysm
  • rupture of wall leading to cardiac tamponade in 3wks
  • mural thrombus/embolism
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64
Q

Main cardiac pathologic finding in hypertensive (systemic) heart disease

A
  • concentric hypertrophy (sarcomeres in parallel to long axis of myocyte –> inc diameter) –> inc in wall thickness and O2 demand –> likely ischemic injury
  • HTN can be caused by primary idiopathic HTN (most common) and also renal artery stenosis, endocrine problems, and vascular problems like coarctation of aorta
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65
Q

Definition of aneurysm and etiologies and main clinicopathologic features of aneurysms

A
  • aneurysms are localized abnormal dilation of a vessel and occur due to weakening of the wall
  • can be caused by atherosclerosis, HTN, vasculitis, developmental defect, infection, congenital disease
  • occlusion of vessel –> ischemia/infarction
  • thromboembolism
  • rupture
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66
Q

Understand vessel dissection and know the predisposing causes of aortic dissection

A
  • blood tears/dissect media of aorta and can go back into lumen, paricardial sac, or branches or even mediastinum
  • sudden onset of severe pain radiating to the back
  • unequal pulses, murmur, hypotension
  • HTN can be a risk factor as well as CT disorders (marfan syndrome)
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67
Q

The clinicopathologic features of temporal arteritis, leukocytoclastic vasculitis, polyarteritis nodosa and Wegener’s granulomatosis

A

Temporal (giant cell) arteritis:

  • most common
  • segmental chronic granulomatous vasculitis of temporal artery
  • elderly women
  • headache, tenderness, visual problems
  • corticosteroids help a lot

Leukocytoclastic vasculitis:

  • arterioles, capillaries, venules affected
  • usually due to drugs or infections

Polyarteritis nodosa:

  • acute segmental necrotizing in small and medium arteries usually in kidneys, GI tract, and heart
  • thrombus –> organ infarcts and aneurysms
  • middle aged men
  • immunosuppressants help

Kawasaki’s disease:
- acute necrotizing vaculitis in children that targets coronary arteries

Wegener’s granulomatosis:
- idiopathic necrotizing granulomatous vasculitis of small/medium arteries and veins especially upper and lower resp tracts and kidneys

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68
Q

Which vascular lesions are benign and malignant

A

Benign:

  • granuloma pyogenicum (polypoid granulation tissue nodule on skin; reactive process; due to trauma or pregnancy)
  • capillary and cavernous hemangioma (vascular neoplasm affecting skin)

Intermediate:

  • Kaposi sarcoma (malignant tumor with skin, mucosal, or organ involvement)
  • hemangioendothelioma

Malignant:
- angiosarcoma (malignant tumor involving skin, soft tissue, breast, or liver)

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69
Q

What are clinical manifestations secondary to insuff blood supply to heart?

A

1) angina pectoris:
- chest pain due to ischemia

2) acute MI:
- irreversible myocyte necrosis due to prolonged ischemia

3) chronic ischemic heart disease:
- progressive cardiac decompensation due to atherosclerosis with acute infarct or small ischemic events
- replace myocardium with fibrous tissue

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70
Q

What is the difference between stable and unstable plaques?

A

Stable:
- dense fibrous caps with minimal inflammation and small lipid cores

Unstable:

  • prone to rupture
  • thin fibrous cap
  • large lipid core
  • increased inflammation
  • neovascularization
  • hemorrhage
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71
Q

What determines the location of an infarct?

A
  • where the occlusion occurs and right vs. left dominance
  • usually infarct of left ventricle and septum
  • some extend into right ventricle
  • occlusion of LAD –> anterior, apical and septal LV infarct
  • occlusion of RCA –> posterior LV and septum
  • occlusion of LCA –> lateral left ventricle wall
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72
Q

Describe the morphology of MIs

A

0-30min: reversible ultrastructural and biochemical changes (mitochondria welling, sarcoplasmic edema, dec glycogen)

1-2hrs: irreversible changes (very swollen mitochondria, nuclear clumping, sarcolemma disruption –> release of intracellular proteins and disruption of ion gradients)

4-12hrs: wavy fibers (noncontractile ischemic fibers stretch with systole)

18-24hrs: coagulation necrosis, contraction bands at periphery of infarct, neutrophilic infiltrate

24-72hrs: max neutrophilic infiltrate

4-7days: macrophages with disintegration of necrotic myocytes (max softening)

10days: granulation tissue

4-8wks: fibrosis

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73
Q

What can cause cor pulmonale?

A
  • primary lung disease due to chronic obstructive airways disease
  • pulm vessel disease (PE)
  • chest movement disorder
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74
Q

What are berry aneurysms?

A
  • congenital defects in media of arteries at bifurcation of cerebral vessels (circle of willis)
  • most frequent cause of spontaneous subarachnoid hemorrhage
  • multiple at once
  • onset presents as severe headache
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75
Q

Describe atherosclerotic aneurysms

A
  • plaque compresses underlying media –> thinning of wall along with inflammation degrading ECM
  • usually occur >50yo
  • most common site is lower abdominal aorta below renal arteries
  • half of patients are hypertensive
  • many are asymptomatic and present with just a pulsating mass
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76
Q

What is vasculitis?

A
  • inflammatory process involving vessels with inflammation and damage to vessel wall
  • narrowing of lumen, fibrosis, thrombosis with ischemia/infarction, aneurysm formation
  • immune complex deposition
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77
Q

Describe the general mechanisms of platelet function, coagulation, and fibrinolysis, with special emphasis on the sites and targets for pharmacotherapeutic interventions in disorders of hemostasis

A

Common targets:

  • warfarin inhibits synthesis of vitamin K dependent factors 2, 7, 9, 10 as well as protein C and S (which inhibit factor 5 and 8)
  • heparin combines with antithrombin III to inactivate 2a and 10a
  • LMWHs combine with antithrombin III to inactivate 10a only
  • dabigatran inactivates 2a
  • rivaroxaban inactivates 10a
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78
Q

Review the process of primary hemostasis

A

1) damage to vessel exposes collagen of subendothelial layer
2) transient vasoconstriction
3) platelets adhere to damaged endothelium with vWF and get activated
4) platelets get activated and release ADP and TXA2 causing platelet aggregation with GP2b3a receptors
5) fibrin binds to GP2b3a receptors and holds platelets together
6) endo cells release PGI2 that is antiaggregatory and vasodilatory as well as plasmin to start fibrinolysis

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79
Q

Review the process of secondary hemostasis

A
  • tissue damage exposes TF –> activates factor 7 –> activates factor 10
  • 10a activates thrombin from prothrombin
  • thrombin activates fibrin from fibrinogen
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80
Q

What are common lab test for blood coagulation?

A

aPTT

  • intrinsic pathway
  • monitors heparin therapy

PT

  • extrinsic pathway
  • monitors warfarin therapy

ECT (ecarin clotting time)
- monitor anticoag therapy with direct thrombin/2a inhibitors (dibgatran)

TT (thrombin time)

  • prolonged if fibrinogen levels low
  • monitors dabigatran toxicity
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81
Q

What are regulators of coagulation and fibrinolysis?

A

1) prostacyclin and NO cause vasodilation and inhibit aggregation
2) ATIII inhibits 2a, 10a (9a, 12a) and is accelerated with heparin
3) protein C/S inactivates factor 5a and 8a –> dec rate of prothrombin and factor 10 formation
4) fibrinolysis by activation of plasminogen to plasmin by tPA

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82
Q

Describe the mechanism of action and pharmacokinetics; list the uses, adverse reactions (plus treatment of overdosage if applicable), and drug-drug interactions; and disadvantages of heparin

A

Mechanism of action:

  • acts in plasma to inhibit activated factors 2a, 10a (9a, 11a, 12a, 13a)
  • accelerates ATIII
  • LMWH binds 10a but not 2a; does not need to be monitored because doesn’t affect aPTT

Pharmacokinetics:

  • given IV
  • can give in pregnant women
  • 1st order renally eliminated
  • cont infusion
  • heparin: rapid onset of action
  • LMWH: 3-5hr onset
  • monitor with aPTT
  • eliminated renally

Uses:

  • prevent hypercoag
  • LMWH is preferred
  • treats coronary occlusion in unstable angina/acute MI
  • prevents VTE

Adverse reactions and treatment for overdose:

  • hemorrhage
  • thrombocytopenia
  • osteoporosis
  • use protamine for overdose (really + to neutralize really - heparin)

Drug drug interactions:
- inc bleeding with aspirin, ibuprofen, other antiplatelet agents

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83
Q

Describe the mechanism of action and pharmacokinetics; list the uses, adverse reactions (plus treatment of overdosage if applicable), and drug-drug interactions; and disadvantages of warfarin

A

Mechanism of action:

  • acts in liver to prevent synthesis of factors
  • blocks liver synth of vit k dep factors (2, 7, 9, 10)
  • onset delayed due to delayed turnover of existing clotting factors
  • protein C/S have shorter half lives so can actually cause coagulation early on

Pharmacokinetics:

  • 100% oral absorption
  • contraind in pregnancy
  • genetic polymorphisms can affect therapy
  • hepatic metabolism

Uses:

  • afib: prevents thromboemoblus
  • monitor with INR/PT
  • bridge with heparin for first few days

Adverse reactions and treatment for overdose:

  • hemorrhage
  • GI
  • contraind in pregnancy
  • if INR>10 then stop warfarin and give vitamin k; slow infusion if bleeding
  • prothrombin complex concentrate over fresh frozen plasma; or recomb factor 7a

Drug drug interactions:

  • inc PT with amiodarone, metronidazole, fluconazole, fluoxetine, rosuvastatin, aspirin
  • dec PT with barbiturates, carbamazepine, rifampin, vitamin k
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84
Q

Describe the mechanism of action and pharmacokinetics; list the uses, adverse reactions (plus treatment of overdosage if applicable), and drug-drug interactions; and disadvantages of dabigatran

A

Mechanism of action:

  • acts in plasma to inhibit thrombin (2a)
  • doesn’t require monitoring or dose adjustments

Pharmacokinetics:

  • oral
  • polar with bad bioavailability
  • prodrug is well absorbed by GI and converted
  • renally excreted

Uses:

  • reduce risk of stroke and systemic embolism in patients with afib
  • advantages over warfarin: lower stroke rate, no monitoring, no diet restrictions
  • disav over warfarin: twice daily dosing, shorter acting, dose adjustments for renal impairment

Adverse reactions and treatment for overdose:
- GI complaints

Drug drug interactions:
- fewer drug or food interactions than warfarin

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85
Q

Describe the mechanism of action and pharmacokinetics; list the uses, adverse reactions (plus treatment of overdosage if applicable), and drug-drug interactions; and disadvantages of rivaroxaban

A

Mechanism of action:

  • acts in plasma to inhibit factor 10a
  • doesn’t need monitoring
  • no antidote for rapid reversal of effect

Pharmacokinetics:
- oral

Uses:

  • prevent DVT
  • reduce risk of stroke and systemic embolism in patients with afib
  • adv over warfarin: lower stroke rate, no INR monitoring, no diet rest once daily dosing,
  • disad compared to warfarin: shorter acting, no antidote for reversal, apixaban required 2/day dosing, dose adjust for renal impairment

Adverse reactions and treatment for overdose:

  • bleeding
  • anticoag is difficult to reverse (FFP then PCC or r7a)
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86
Q

Describe the mechanism of action and pharmacokinetics; list the uses, adverse reactions (plus treatment of overdosage if applicable), and drug-drug interactions; and disadvantages of aspirin

A

Mechanism of action:

  • inhibits COX1 synth of TXA2 in platelets
  • TXA2 normally allows for GP2b/3a receptors, but dec so dec aggregation

Pharmacokinetics:

  • once orally in low dose daily
  • can be rapid onset
  • hepatic elimination

Uses:

  • acute MI (STEMI) plus an ADP antagonist
  • unstable angina (UA/NSTEMI) maybe with an ADP antagonist
  • percutaneous coronary intervention (PCI) plus ADP antagonist and maybe GP2b/3a inhibitor
  • 2ndary prev of MI

Adverse reactions and treatment for overdose:

  • bleeding risk with anticoag
  • rare with low doses
  • nausea, GI bleeding
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87
Q

Describe the mechanism of action and pharmacokinetics; list the uses, adverse reactions (plus treatment of overdosage if applicable), and drug-drug interactions; and disadvantages of clopidogrel

A

Mechanism of action:
- ADP receptor antagonist –> interferes with ADP induced platelet aggregation

Pharmacokinetics:
- once daily orally

Uses:

  • acute MI (STEMI): aspirin + clopidogrel
  • unstable angina/NSTEMI: aspiring and maybe clopidogrel
  • PCI: aspirin + clopidogrel

Adverse reactions and treatment for overdose:

  • upset GI, headache, dizziness, URI
  • bleeding
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88
Q

Describe the mechanism of action and pharmacokinetics; list the uses, adverse reactions (plus treatment of overdosage if applicable), and drug-drug interactions; and disadvantages of dipyridamole

A

Mechanism of action
- blocks phosphodiesterase breakdown of cAMP –> inc cAMP –> inc PGI2 –> inc vasodilation and anti-aggregatory

Pharmacokinetics:

  • orally 3-4x daily before meals
  • hepatic elimination

Uses: secondary prevention of MI with aspirin

Adverse reactions and treatment for overdose:

  • minimal
  • some dizziness and GI distress
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89
Q

Describe the mechanism of action and pharmacokinetics; list the uses, adverse reactions (plus treatment of overdosage if applicable), and drug-drug interactions; and disadvantages of abciximab

A

Mechanism of action:
- blocks GP2b/3a receptors on platelet –> prevents fibrinogen binding and dec aggregation

Pharmacokinetics:

  • cont IV infusion
  • rapid onset

Uses:
- percutaneous coronary intervention with aspiring and ADP antagonist

Adverse reactions and treatment for overdose:
- bleeding

90
Q

Describe the mechanism of action and pharmacokinetics; list the uses, adverse reactions (plus treatment of overdosage if applicable), and drug-drug interactions; and disadvantages of tPA

A

Mechanism of action
- inc formation of plasmin from plasminogen –> lyse thrombi

Uses:

  • acute MI
  • DVT
  • PE

Adverse reactions and treatment for overdose:
- hemorrhage

91
Q

Describe the mechanism of action and pharmacokinetics; list the uses, adverse reactions (plus treatment of overdosage if applicable), and drug-drug interactions; and disadvantages of reteplase

A

Mechanism of action:
- inc formation of plasmin from plasminogen –> lyse thrombi

Pharmacokinetics:

  • can be given as bolus
  • prolonged duration of action

Uses:

  • acute MI
  • DVT
  • PE

Adverse reactions and treatment for overdose:
- hemorrhage

92
Q

Compare DOAC vs Warfarin

A

DOAC:

  • generally preferred over warfarin for nonvalvular afib
  • doesn’t have variability in dosage req, no dietary rest, no INR monitoring

Warfarin

  • used in afib with valve issues
  • if already on warfarin and okay with monitoring
93
Q

Describe the steps contributing to the pathophysiology of the development of atherosclerosis and the progression to acute atherosclerotic cardiovascular disease (ASCVD)

A
  • LDL infiltrates into subendo space
  • LDL is modified (oxidized, glycosylated)
  • release of pro-inflammatory cytokines (TNFa, IL1, IL6, IFN) –> inc adhesion of monocytes due to CAM expression
  • monocytes recruited to clean up LDL
  • phagocytosis of LDL –> foam cell/activated macrophage
  • foam cells and T cells release MMP and degrade fibrous cap
  • plaque rupture –> ACS
94
Q

Discuss the physiology of lipid metabolism and the importance of cholesterol in the development of artherosclerotic cardiovascular disease (ASCVD)

A

Exogenous (from diet) lipid metabolism:
- package TG and CL from GI tract into chylomicron –> dump into lymph system –> taken up by vascular system –> hydrolyzed by LPL (lipoprotein lipase) that takes out TG and into skeletal muscle or fat cells –> remnant which is denser and smaller is taken up by liver

Endogenous:
- liver produces VLDL (like chylomicron) –> hydrolyzed by LPL –> IDL (intermediate density lipoprotein, sort of like remnant) –> LPL hydrolyzes more –> LDL taken up by LDL receptors on liver –> LDL endocytosed –> degraded in lysosome

HDL metabolism:
- have nascent HDL with no lipid in it –> LCAT accepts cholesterol –> mature HDL with cholesterol –> transfers lipids with VLDL and LDL –> HDL takes cholesterol from circulation

95
Q

Summarize the current guidelines for the screening and treatment of hypercholesterolemia in adults

A

Screening:

  • > 20yo should have fasting lipid panel done every 5yrs
  • LDL is the important one

LDL = total cholesterol - HDL - TG/5

  • if you have 0 or 1 risk factors, then LDL-C goal is
96
Q

What are major risk factors for ASCVD?

A
  • smoking
  • HTN
  • low HDL-C (50
  • obesity
  • insulin resistance
  • sedentary lifestyle
  • atherogenic diet
  • psychosocial factors
  • hyperTGemia
97
Q

What are the 4 major statin benefit groups?

A

1) known clinical ASCVD
2) LDL >=190mg/dl
3) diabetes (>40yo and LDL >70)
4) (>40yo and LDL >70) without ASCVD or diabetes who have 10yr risk >7.5%

98
Q

Describe the general pathophysiology of angina (imbalance between cardiac oxygen supply and demand) and characteristics of the three major types

A
  • angina is due to imbalance of cardiac supply and demand, most often due to atherosclerotic occlusion of coronary vessels

1) stable angina
- lumen narrowed by plaque
- innappropriate vasoconstriction

2) unstable angina
- plaque rupture
- platelet aggregation
- thrombus formation
- unopposed vasoconstriction

3) variant angina
- no overt plaques
- intense vasospasm

99
Q

Describe the precipitating causes of angina and their relation to the pathophysiology of angina

A

Stable angina:

  • results from fixed stenotic endothelialized atheromatous plaque –> inadequate O2 supply during times of O2 demand –> angina
  • reduce O2 demand with nitrates, CCBs, and beta blockers

Variant angina:

  • due to coronary vasospasm with/out plaque
  • O2 supply decreases due to vasospasm at rest
  • reverse/prevent vasospasm and inc supply with vasodilators (nitrates and CCBs)

Unstable angina:

  • rupture plaque –> thrombus occlusion
  • angina at rest with change in frequency, character, duration, and precipitating factors in patients with stable angina
  • aspirin, heparin, GP2b/3a inhibitors, angioplasty/bypass, fibrinolytics for clot
  • beta blockers for arrhythmias
  • morphine for pain
  • ACEIs, statins, beta blockers, aspirin, clopidogrel after MI
100
Q

List the mechanism and uses/effect on myocardial O2 supply and demand of nitroglycerin/nitrates

A

Mechanism:

  • nitrates are converted to NO at PM of VSMCs
  • NO activates guanylate cyclase –> inc cGMP –> activate phosphatase –> relaxation of smooth muscle by dec myosin phosphate

Uses/effect on O2 supply and demand:

  • reduction of LVEDP and systemic vascular resistance –> dec wall tension and dec O2 demand
  • treat acute angina
  • recommended if beta blockers are contraind in stable angina

Pharmacokinetics:
- sublingual due to low oral bioavailability

Adverse reactions:

  • due to vasodilation
  • headache
  • orthostatic hypotension
  • tolerance if continuous exposure

Target:

  • relax venous capacitance vessels –> dec preload and dec O2 demand
  • dilate coronary artery vessels –> inc O2 supply (helpful in variant angina)
101
Q

List the mechanism and uses/effect on myocardial O2 supply and demand of Ca channel blockers

A

Mechanism:

  • block LTCCs (more in arterioles than veins) –> prevents Ca into cell –> smooth muscle relaxation and vasodilation
  • dihydropyridines/nifedipine: more vascular relaxation than inotropic/chronotropic effects –> good vasodilation (which will actually in turn inc HR), but not good suppression of SA/AV node or suppression of contractility
  • verapamil/diltiazem have prominent effects on cardiac muscle –> okay vasodilation but even better suppression of SA/AV node and okay suppression of contractility)

Pharmacokinetics:

  • nifedipine: dec BP –> reflex SNS; avoid use
  • amlodipine is longer acting and has fewer symptomatic side effects
  • variable bioavailability

Uses:

  • long lasting decrease in peripheral vascular resistance –> dec O2 demand and coronary arterial tone
  • recommended initial therapy for vasospastic angina
  • long acting CCBs for stable angina if beta blockers contraind
  • anti-arrhythmic, anti-hypertensive, dec risk of subarachnoid hemorrhage, dec risk of premature labor

Adverse reactions:

  • cardiac depression more likely with verapamil or diltiazem
  • minor toxicities

Target:

  • block LTCCs –> reduce vasoconstriction in coronary and noncoronary vessels –> inc O2 supply and dec afterload
  • verapamil/diltiazem also dec HR and contractility –> dec O2 demand
102
Q

List the mechanism and uses/effect on myocardial O2 supply and demand of beta blockers

A

Mechanism:

  • result in dec HR, BP, and contractility –> dec O2 demand
  • not vasodilatory –> no reflex tachycardia really and does not help in vasospastic angina

Uses:
- first line therapy for stable angina unless contraind

Contraind:
- astham, peripheral vascular disorders, abrupt withdrawal –> sympathetic overactivity

Target:
- beta1 adrenergic receptor blocker in heart –> dec HR and contractility –> dec O2 demand

103
Q

List the major side effects and pharmacokinetic profiles of nitrate/nitrate products

A

Adverse reactions:

  • due to vasodilation
  • headache
  • orthostatic hypotension
  • tolerance if continuous exposure

Pharmacokinetics:
- sublingual due to low oral bioavailability

104
Q

List the side effects and relative cardiac vs. vascular action of Ca++ channel blockers [dihydropyridine class (nifedipine) vs. diltiazem vs. verapamil]

A

Adverse reactions:

  • cardiac depression more likely with verapamil or diltiazem
  • minor toxicities

Nifedipine:

  • 5/5 coronary artery vasodilation
  • 1/5 suppression of SA/AV node
  • 1/5 suppression of contractility
  • inc in HR due to reflex tachycardia

Diltiazem:

  • 3/5 coronary artery vasodilation
  • 4/5 suppression of SA/AV node
  • 2/5 suppression of contractility

Verapamil:

  • 4/5 coronary artery vasodilation
  • 5/5 suppression of SA/AV node
  • 4/5 suppression of contractility
105
Q

What factors control blood supply to heart?

A
  • major determinant is coronary blood flow
  • inc aortic pressure = inc coronary blood flow
  • inc HR = dec coronary blood flow
  • inc LVEDP = dec coronary blood flow
  • inc resistance = dec coronary blood flow
  • autoregulation is really important
106
Q

What factors control myocardial O2 demand?

A
  • contractility
  • heart rate
  • myocardial wall tension
107
Q

How do you manage angina?

A

1) primary prevention
- risk factor modification (HTN, diabetes, smoking, dyslipidemia)
- aspirin
- statins

2) pharmacotherapy
- restore balance between demand and supply (inc supply or dec demand)
- improve coronary blood flow with bypass or angioplasty or vasodilators
- reduce O2 demand with vasodilators or negative inotropic/chronotropic agents

108
Q

List the mechanism and uses/effect on myocardial O2 supply and demand of ranolazine

A

Mechanism:

  • failure of late Na current inactivation –> intracellular Na overload –> reversal of NCX –> intracellular Ca overload –> inc diastolic tension and imbalance between O2 supply and demand
  • ranolazine inhibits late Na current

Pharmacokinetics:
- variable bioavailability

Use in angina:

  • reduces symptoms of chronic stable angina and inc exercise capacity
  • sub for beta blockers

Adverse reactions:
- prolong QT interval

109
Q

Describe the effect of nitrates on HR, contractility, systolic pressure, and LV volume

A
  • inc HR (due to reflex tachycardia)
  • no effect on contractility
  • dec sys pressure
  • really decrease LV volume
110
Q

Describe the effect of beta blockers on HR, contractility, systolic pressure, and LV volume

A
  • really decrease HR
  • decrease contractility
  • dec sys pressure
  • inc LV volume
111
Q

Describe the effect of nifedipine on HR, contractility, systolic pressure, and LV volume

A
  • inc HR
  • little/no dec in contractility
  • really decrease sys pressure
  • little/no dec in LV volume
112
Q

Describe the effect of verapamil on HR, contractility, systolic pressure, and LV volume

A
  • dec HR
  • dec contractility
  • dec sys pressure
  • little/no dec in LV volume
113
Q

Describe the effect of diltiazem on HR, contractility, systolic pressure, and LV volume

A
  • really dec HR
  • little/no dec in contractility
  • dec sys pressure
  • little/no dec in LV volume
114
Q

What spectrum of ACS are nitrates beneficial for?

A
  • really good in stable, unstable, and variant angina

- good in MI

115
Q

What spectrum of ACS are CCBs beneficial for?

A
  • really good in stable and unstable angina
  • extremely good in variant angina
  • no effect on MI
116
Q

What spectrum of ACS are beta blockers beneficial for?

A
  • really good for stable and unstable angina
  • no effect on variant angina
  • extremely good for MI
117
Q

What spectrum of ACS is aspirin beneficial for?

A
  • extremely good for stable and unstable angina
  • no effect on variant angina
  • amazing for MI
118
Q

What spectrum of ACS are statins beneficial for?

A
  • extremely good for stable and unstable angina as well as MI
  • no effect on variant angina
119
Q

Define the role of secondary prevention strategies in reducing recurrent cardiac events and mortality

A
  • 2ndary prevention needed for patient with confirmed CAD or vascular equivalent (previous MI, previous revasc, angina)
  • prevent plaque rupture (which is unique to coronary arteries)
120
Q

List the various risk factors that contribute to recurrent cardiac events

A
  • aim for BP lower than 140/90

- lifestyle changes (dec fat and sodium in diet)

121
Q

Identify the guideline recommendations for both pharmacologic and lifestyle interventions to reduce cardiac risk, and which patients benefit from these recommendations

A

Pharmacologic:

  • antiplatelets (aspirin blocks COX production of TXA2 –> dec platelet agg; clopidogrel blocks P2Y12 receptors –> blocks binding of ADP –> dec act of GP2b/3a –> dec platelet agg)
  • beta blockers
  • RAAS inhibitors

Lifestyle:

  • weight management
  • exercise

Both:

  • BP control
  • manage lipids
  • manage diabetes
  • screen for depression
  • stop smoking
122
Q

What are the class I antiplatelet guidelines?

A
  • 81mg of aspirin is normal dose for all CAD patients
  • add clopidogrel in patients with ACS or PCI for one year
  • for post bypass, aspiring at 100mg
  • for post stroke, aspiring alone, clopidogrel alone, or aspiring+dipyridamole
  • for PAD, aspirin alone or clopidogrel alone
  • be careful if combining warfarin with aspirin
123
Q

What are class I and class IIa beta blocker guidelines?

A

Class I:
- beta blockers in all if EF lower than 40% and HF symptoms or MI/ACS in last 3yrs

Class IIa:

  • bb in all if EF lower than 40% even with no HF symptoms
  • all with any history of MI/ACS
124
Q

What are class I RAAS inhibitor guidelines?

A

ACEIs

  • all with EF lower than 40%, DM, HTN, CKD
  • ARBs for people who are ACEI intolerant
  • AA in post MI with EF lower than 40%, on BB, ACEI, and have HF and diabetes
125
Q

What are class I lipid guidelines?

A
  • **statins in all CAD patients
  • high dose in patients less than 75yo
  • mod dose if greater than 75yo?
126
Q

What are class I, IIa, and IIb guideliens for diabetes?

A

Class I:
- lifestyle modifications

Class IIa:
- metformin as a first line therapy

Class IIb:
- HbA1c less than 7%

127
Q

What are class IIa and IIb depression guidelines?

A

Class IIa:
- assessing for depression

Class IIb:
- treatment for depression does not improve cardiac outcomes, but beneficial for overall health

128
Q

What are class I smoking guidelines?

A

STOP IT

129
Q

What are class I weight control guidelines?

A
  • goal BMI is 18.5-24.9
  • goal waist circumference is less than 40in for men and less than 35 in for women
  • loss of 5-10% of body weight
130
Q

What are class I physical activity guidelines?

A
  • moderate to high intensity exercise for 30-60min/day

- 5-7x/week

131
Q

Identify the central role of monocytes and T-cells in atherogenesis and disease progression

A
  • monocytes engulf LDL and become foam cells
  • foam cells and T cells release MMPs to degrade fibrous cap –> rupture
  • dendritic cell antigen presentation –> T cell activation –> T cell expansion
  • Th1 response promotes IFN-gamma and atherosclerosis
  • Th17 may promote plaque instability and neoangiogenesis

Th1:

  • prothrombotic
  • EC activation
  • foam cell fomation
  • lesion formation and plaque vulnerability

Th2:

  • inc antibody prod
  • inc lipoprotein oxidation

Treg:

  • inc immune suppression
  • dec proinflam cytokines
  • dec lesion formation and dec plaque vulnerability
132
Q

Describe the role of biomarkers in cardiovascular diagnosis and treatment, with a focus on c-reactive protein (CRP)

A
  • CRP is shown to be associated with adverse outcomes and inc CV risk
  • statins lower cholesterol and CRP
  • JUPITER trial put people with high CRP but normal cholesterol on statins to see if any benefit
  • CRP is fairly stable over time so used reproducibly
133
Q

What are the major drivers of plaque instability?

A
  • macrophage apoptosis and necrosis –> promotes necrotic core
  • MMPs degrading fibrous cap
  • intra plaque hemorrhage
134
Q

What are the steps that allow atherosclerosis to progress to MI

A

1) lesion expansion
2) macrophage apoptosis and necrosis
3) weakening of fibrotic cap
4) plaque rupture

135
Q

What are the mechanisms of accelerated atherogenesis in AI diseases?

A

1) inc monocyte/macrophage activation
2) impaired endo vasodilatory function
3) proatherogenic lipoproteins
4) plaque instability

136
Q

Identify the prevalence and major risk factors for peripheral artery disease (PAD)

A

1) **diabetes
2) *smoking
3) hypertension
4) hyperlipidemia

137
Q

Describe the hemodynamic changes that occur in patients with claudication due to peripheral artery disease (relative to hemodynamic components that lead to a decrease in large vessel flow), including: the roles of length of the stenosis, radius of the stenosis, blood viscosity, and role of the atherosclerotic disease process on endothelial function as modulated by nitric oxide

A

Flow is determined by the equation:

Flow = deltaPpir^4/(8Lu)

  • inc length of stenosis = dec flow
  • inc radius of stenosis = inc flow
  • inc blood viscosity = dec flow
  • since deltaP is important, drugs that lower BP can decrease flow
  • multiple occlusions can have a significant effect
  • atherosclerosis –> oxidative stress –> endo dysfunction
138
Q

Describe the major risk factors for abdominal aortic aneurysm

A
  • AA contains fewer elastic lamellae than thoracic aorta

- vasa vasorum is less abundant in AA

139
Q

Describe the relationship between the size of an aortic aneurysm and the subsequent risk of rupture and identify the 5-year risk of rupture of a 5.5 cm abdominal aortic aneurysm

A
  • abd aorta >3cm –> aneurysm
  • 50% inc in size –> aneurysm
  • fusiform: entire vessel; more common
  • saccular: evagination of a segment
  • aneurysm is an elimination of supporting structures in medial and adventitial layers (collagen and elastin destruction)
  • inflammation occurs –> MMPs degrade wall
  • inc diameter = ince 5yr rupture risk
  • 5.5cm diameter = 25% risk over 5yrs
140
Q

List the key risk factors that initiate aortic dissection

A
  • uncontrolled hypertension (or dilation of aorta as an initiating event)
  • structural weakness in aortic wall
141
Q

For venous thromboembolism, list the components of Virchow’s triad and describe mechanistically how each component contributes to acute thrombosis

A

Virchow’s triad:

  • venous stasis: if sedentary, then muscle pump can’t bring venous blood back to heart –> pools in legs and coagulates –> thrombus
  • endo damage: seen in inflammation, DM, post surgery –> thrombus
  • hypercoaguable state –> post surgery, cancer, genetic disorders –> thrombus
142
Q

Describe the major sites of action in the clotting cascade of warfarin and heparins

A
  • vitamin k antagonist –> dec production of factors 2, 7, 9, 10
143
Q

What are the primary causes of morbidity and mortality due to aortic dissection?

A
  • complications from progression of dissection channel including branch vessel occlusion with end organ ischemia and external rupture with hemorrhage
  • dissection of ascending aorta is clinical emergency
  • most immediately lethal problem is external rupture with overwhelming hemorrhage at pericardial sac and left chest
  • next serious is occlusion of branch vessels –> stroke, spinal cord ischemia, renal failure
144
Q

How do you treat aortic dissection?

A
  • control pressure/time with beta blockers
  • control BP with ACEIs and CCBs
  • control pain
  • surgery
145
Q

Describe the Fick equation and how its components relate to the circulatory responses to dynamic exercise

A

CO*(a-vO2) = VO2

  • this says that the flow times the concentration of O2 entering the heart minus the concentration of O2 leaving the heart gives you the total O2 consumed by the heart
  • inc HR or SV is shown as an inc in CO
  • inc ability of the heart to extract O2 is shown as a larger difference between aO2 and vO2
146
Q

Describe the phases of the cardiac cycle and the effect of heart rate on ventricular filling and contraction. How does increasing the heart rate with exercise differ from artificially increasing heart rate on stroke volume?

A

Exercise:
- inc in SV due to peripheral vasodilation –> inc venous return –> venoconstriction –> inc SV

Pacemaker:
- dec in ventricular filling time –> dec in SV because don’t have the vascular effects

147
Q

Describe the heart rate response to exercise and the influence of the autonomic nervous system on heart rate during exercise

A
  • inc HR is directly proportional to exercise intensity until maximal exercise HR which is approximately 220-age
  • lower levels of exercise, inc in HR is due to parasymp withdrawal –> then followed by symp activity
148
Q

Describe the factors responsible for changes in stroke volume during exercise. What is the Frank Starling relationship? How does the stroke volume response during exercise differ between untrained persons and elite athletes?

A
  • SV inc by 40-60% during exercise
  • in untrained persons, stroke volume can go from 50 to 100 whereas it can go from 80 to 160 for elite athletes
  • mechanism is inc in EDV with inc starling forces at lower levels of exercise and inc contractility at higher levels of exercise
149
Q

Describe the cardiac output response to exercise in untrained and trained persons.

A
  • inc in CO is proportional to the metabolic rate and VO2 required during exercise
  • it requires 6L/min for each 1L/min inc in O2 uptake beyond resting conditions
  • inc in HR and SV –> inc in CO
  • > 50% VO2 max –> inc in HR –> inc in CO (except in elite athletes)
  • elite athletes can inc CO from 5L/min to 34 L/min compared to 22L/min in normal people
150
Q

Describe the response of blood pressure during exercise

A
  • there is a dec in vascular resistance but inc in CO maintains the BP
  • systolic BP inc due to inc CO and HR
  • little change in diastolic BP
151
Q

Explain how the redistribution of blood flow during exercise contributes to an increase in muscle blood flow

A
  • skeletal muscle goes from receiving 20% to 80% of blood flow during exercise
  • vasodilation of muscle bed and vasoconstriction of other organs
  • vasoconstriction is regulated by ergoreceptors and medulla
  • intensity of exercise/motor units recruited determines inc in CO
152
Q

Describe the concept of oxygen delivery and approaches to increase oxygen delivery.

A

O2 delivery = blood flow * arterial O2 content

blood flow = HR * SV

arterial O2 content = [Hb] * 1.34mlO2/gHb * %O2sat

153
Q

What is the role of the arterial-venous O2 content difference at maximal exercise? How does the increase in a-v O2 difference compare to the increase in cardiac output during exercise?

A
  • increase O2 extraction from blood during exercise –> increased a-vO2
  • usually increase in CO is much more than increase in a-vO2, but both contribute to O2 consumed
154
Q

How does the coronary circulation differ from the systemic circulation?

A
  • inc CO = inc coronary blood flow

- inc O2 extraction during exercise as well as inc CO –> inc O2 consumed

155
Q

Why can exercise be used to diagnose and risk stratify coronary artery disease?

A
  • can see effects of supply demand mismatch with exercise since you inc demand and se if heart can inc supply as a result
  • the more severe the coronary stenosis, the weaker the O2 supply
  • with exercise, see dec in coronary blood flow at 70% occlusion; but at 90% at rest
156
Q

What is rate-pressure product and how does it relate to MVO2?

A
  • RPP is HR * SBP = HR^2 * SV * SVR

- it is an index of myocardial O2 consumption

157
Q

What is the ischemic threshold and how can it be used to determine the severity of ischemia and responses to therapy?

A
  • ## RPP where signs of myocardial ischemia occur –> ischemia threshold
158
Q

What is the usual effect of exercise training on the ischemic (angina) threshold?

A
  • exercise training allows more intensity/higher workload before angina (shift right)
159
Q

What are the major circulatory adjustments to exercise?

A

1) inc in CO
2) redist of blood flow (dec flow to inactive organs and inc flow to skeletal muscle)
3) maintaining BP

160
Q

Name the four main regions of the heart present during the 4th week of development, and describe how the orientation of these regions shift during heart looping

A
  • truncus (becomes aortic and pulmonary valve outflow tract)
  • bulbus cordis (becomes RV)
  • primitive ventricle becomes LV
  • primitive atria (become atria)
  • loops to the right so that BC is right and PV is left
  • PA move backwards and upwards
  • septation begins
161
Q

Describe when and how the endocardial cushions grow to bissect the atrioventricular canal

A
  • 35-56days
  • at conus, we have dextrodorsal conal crest and sinistroventral conal crest grow inwards
  • at truncus, we have dextrosuperior truncal swelling and sinistroinferior truncal swelling grow inwards
  • aorticopulmonary septum at aortic sac
162
Q

Describe how and when the truncus arteriosus is subdivided into the pulmonary and aortic outflow tracts

A
  • at truncus, we have dextrosuperior truncal swelling and sinistroinferior truncal swelling grow inwards
  • also at 35-56days
163
Q

Describe the components of the embryonic heart that contribute to separation of the ventricles, and identify when this separation occurs

A
  • 26-28days
  • after looping, ventricles and atria are in right place
  • septation begins
  • see ventricular septum and ventricles are developing as outpouchings of the primitive areas
164
Q

Describe how and when the left and right atria are separated

A
  • during looping stage, atria come up posteriorly and sort of split
  • day 23-25
165
Q

Identify which aortic arch vessels are lost, and which are maintained by eight weeks gestation, and what are the anatomical names of the remaining vessels.

A
  • 1st, 2nd, and 5th aortic arches disappear
  • 3rd becomes carotid arteries
  • 4th becomes aortic arch or right brachiocephalic artery
  • 6th becomes ductus arteriosus and pulmonary arteries
166
Q

Identify two components of fetal cardiac circulation which are no longer patent after birth

A
  • ductus arteriosus: high resistance in lungs, so joins aortic outflow from left ventricle
  • ductus venosus: bypasses liver so oxy blood from placenta goes straight to right atrium
167
Q

Describe early cardiogenesis starting from fertilization

A
  • male and femal gametes fuse –> fertilization
  • cleavages –> morula
  • morula –> blastocyst
  • inner cell mass becomes embryonic disk with epiblast and hypoblast layers
  • early precardiac cells are in epiblast and on either side of primitive streak
  • epiblast cells give rise to intraembryonic mesoderm
  • precardiac cells are now in mesoderm and move cephalically and rotate
  • create this curve of cell clusters that will eventually be the CV system called cardiogenic area
  • cells migrate so that they are now ventral to forebran and foregut
  • form two endocardial tubes
  • two tubes form into one
168
Q

Describe fetal blood flow through the sinus venosus

A
  • umbilical vein: oxy blood from placenta
  • vitelline vein: nutrients from yolk sac
  • cardinal vein: drains deoxy blood from embryo
169
Q

Describe patent ductus arteriosus

A
  • DA connects aorta and pulmonary artery
  • usually closes functionally 10-15hrs after birth (inc in PaO2 –> contraction of smooth muscle in DA wall –> intimal thickening and protrusion into lumen)
  • anatomic closure in 2nd-3rd week of life (internal elastic membrane fragments –> hyaline mass occlusion of lumen)
  • > 98% of kids have DA closed by 1yo
  • can stay open with prostaglandins
170
Q

Discuss the embryologic development of the heart with attention to the formation of: ductus venosis; ductus arteriosis; interatrial septum; intraventricular septum; and division of the arterial trunk into aorta and pulmonary artery

A

a

171
Q

Outline the ways in which errors in these processes of embryonic development of the heart lead to congenital cardiac abnormalities

A

a

172
Q

Describe the hemodynamics, clinical features, diagnostic approaches, and natural history for: atrial septal defects; ventricular septal defects; tetralogy of fallot; coarctation of the aorta; and congenital aortic stenosis

A

a

173
Q

Describe the linkage and pathophysiology of pulmonary hypertension to some congenital cardiac abnormalities

A

a

174
Q

What is PDA?

A
  • patent ductus arteriosus
  • DA is persistence of left 6th aortic arch
  • PGs are vasodilatory and keep DA patent
175
Q

What is the magnitude of a shunt across a PDA based on?

A
  • the size of the PDA
  • relative resistances of the aorta and pulm artery
  • pressure differences between aorta and pulm artery
176
Q

What is the clinical presentation of PDA?

A
  • asymptotic if small PDA-
  • if moderate or large –> respiratory effects (lots of blood going to lungs), CHF, bowel ischemia, renal insuff, hemorrhage/stroke, death
  • pneumonias, difficulty breathing, hoarse cry
177
Q

What are physical exam findings of PDA?

A
  • wide pulse pressure
  • bounding pulse
  • inc work of breathing
  • murmur occasionally as a continuous machinery sound along LUSB
  • accentuated P2 if pulm HTN
  • diagnosed by history and physical exam, chest xray, echo
178
Q

What is involved in the management of PDA?

A
  • if asymptomatic neonate –> conservative management
  • if symptomatic neonate –> COX inhibitors (NSAIDs like indomethacin, ibuprofen, indocin) –> dec PG to close DA –> if not then surgery
  • if symptomatic older –> percutaneous occlusion
  • if asymptomatic older –> percutaneous closure if murmur
179
Q

How does ASD occur embryologically?

A
  • when forming septum between right and left atria, first have septum primum come down
  • left with ostium primum and ostium secundum
  • next, septum secundum comes down and covers foramen ovale and septum primum
  • if the ostium secundum is too big OR if the septum secundum does not cover completely –> ASD
  • basically have a flap that can open into the LA
180
Q

What is the magnitude of the shunt across an ASD based on?

A
  • size of the defect
  • relative inflow resistances of left and right ventricles
  • LA pressure usually > RA pressure
  • ASD is left to right if RV is thinner and more compliant than LV or if systemic vascular resistance is higher than pulm vascular resistance
181
Q

What are physical exam findings in ASD?

A
  • if large defect –> inc RR, sweating
  • 3/6 systolic ejection murmur at LUSB (excessive blood flow across pulm valve) and maybe a diastolic rumble at LLSB (excessive blood flow in diastole across tricuspid)
  • widely split second heart sound due to RV overload
  • diagnose with chest xray (see enlarged PA) or with echo
182
Q

What are complications of ASD?

A
  • inc pulm HTN
  • pulm vascular disease
  • atrial arrhythmias
183
Q

How do you manage ASD?

A
  • diuretic to relieve SOB

- close the hole qith a percutaneous device closure

184
Q

Describe the embryological origin of ventricular septum?

A
  • day 28-42
  • intraventricular septum grows towards based of heart as ventricles outpouch and develop
  • have 3 endocardial cushions (inf, sup, left, right) –> inf and sup merge together to form septum and create left and right atrioventricular canals
185
Q

What are the most common causes of VSDs?

A
  • perimembranous VSD
  • deficiency or lack of membranous portion of interventricular septum
  • rarer causes can be muscular VSDs
186
Q

What does the magnitude of a VSD shunt depend upon?

A
  • size of defect
  • systemic and pulm resistances
  • pulm or aortic stenosis
187
Q

What are the physiological consequences of VSD?

A
  • blood flows from left to right (PVR
188
Q

What is the clinical presentation of VSD?

A
  • asymptomatic until PVR falls after birth
  • large VSD –> respiratory distress and sweating and failure to thrive
  • small VSD –> tachypnea, sweating
189
Q

What are physical exam findings of VSD?

A

Large VSD:

  • active precordium
  • accentuated second heart sound
  • 3/6 harsh holosystolic murmur at LLSB due to flow across VSD
  • diastolic murmur due to inc flow across mitral valve

Small VSD:

  • normal second heart sound
  • 3/6 early systolic murmur
  • no diastolic murmur
  • if murmur gets louder, could mean closing VSD or low PVR
  • if murmur goes away could mean equalization of LV and RV pressure or inc PVR
190
Q

How do you diagnose VSD?

A
  • echo is gold standard

- ECG shows right axis deb and RVH and LVH

191
Q

How do you manage VSD?

A
  • manage symptoms in infancy (HF, pulm edema, treat with diuretics)
  • surgery if pulm vascular changes, poor growth, or secondary complications
192
Q

What is Eisenmenger’s syndrome?

A
  • large left to right shunt
  • inc pulm blood flow
  • pulm HTN
  • inc RV pressure
  • back up into RV
  • shunt reversal so pumps from right to left
  • cyanosis of clubbing due to poor oxygenation and inc workload of LV –> death
193
Q

What are the 4 things that comprise tetralogy of fallot?

A

cyanotic heart disease complex

1) RV outflow tract obstruction
2) RVH
3) dextraposition of aorta (aorta overrides VSD)
4) VSD

194
Q

What is the embryological basis of TOF?

A
  • abnormal development of conal crests –> infundibular septum displaced anteriorly, right, and superiroly
  • should be closing VSD but instead occludes outflow into pulm artery
  • aorta sits over the VSD
195
Q

What is the physiology in TOF?

A
  • RV and LV equalize pressure because VSD is so large

- since RV outflow is obstructed, pulm blood flow is determined by DA

196
Q

What is the difference between blue and pink tetralogy?

A

Blue:
- right to left shunt if RV outflow resistance is higher than systemic vascular resistance –> cyanosis

Pink:
- left to right shunt if RV outflow resistance is less than systemic vascular resistance –> no cyanosis

197
Q

What are Tet Spells?

A
  • hypoxic or hypercyanotic spells
  • blue on exam
  • dec intensity of murmur
  • altered consciousness/seizures
  • treat by increasing pulm blood flow –> inc SVR by bringing knees to chest or giving phenylephrine
198
Q

What is the clinical presentation of TOF?

A
  • blue baby with loud murmur

- cyanosis can worsen with DA closure

199
Q

How do you diagnose TOF?

A
  • physical exam shows tachycardia and cyanotic if blue tet, tachypneic and diaphoretic if pink tet
  • 3/6 short systolic murmur of pulm stenosis
  • ECG shows right axis deviation and RVH
200
Q

How do you manage TOF?

A
  • propranolol for tet spell prevention
  • surgical repair at 2-4mos
  • ductal dependency –> PGs for DA patency
201
Q

What happens in coarctation of the aorta?

A
  • ## localized intraluminal projection of a shelf from lateral, posterior, or anterior wall of aorta in the region of DA (usually opposite the DA)
202
Q

What kind of perfusion occurs as a result of coarctation of the aorta?

A
  • dec blood flow to lower extremities (bowel, leg muscles, kidneys)
203
Q

What are clinical presentations of coarctation of the aorta?

A
  • asymptomatic as newborn due to DA
  • 1-2 weeks as DA closes –> tachypnea, diaphoresis, poor feeding, shock and HF
  • **lack of femoral pulses
  • diagnose with absent femoral pulse, BP difference between UE and LE, chest xray
204
Q

How do you manage coarctation of the aorta?

A
  • keep on PGs until surgery

- angioplasty, surgery, stent

205
Q

Discuss the primary goals in cardiovascular disease prevention

A
  • primary prevention –> prevent onset of disease in person without symptoms
  • 2ndary prevention –> prevent death or exacerbation of disease in those who already have symptoms
206
Q

Recognize the public health benefits of blood pressure control

A
  • lowering SBP reduces the risk of stroke and MI and CV death at any age
  • for >60yo, target BP is
207
Q

Recognize public and community health approaches to cardiovascular disease prevention

A
  • shifting of curve to the left

- communities, schools, churches, etc.

208
Q

Recognize the relationship between depression, cardiovascular disease (CVD) risk, and cardiovascular disease (CVD) outcomes

A
  • depression predicts incident CVD
  • depression inc risk of CAD by 2x
  • depression is common in CV disease affected pops
  • depression predicts mortality after ACS
  • worse depression is, worse outcome
  • depression predicts declines in patient health status
209
Q

Appreciate the biological and behavioral mechanisms that may help explain the relationship between CVD and depression

A
  • depression is associated with physiologic derangements including ANS dysfunction, inc cortisol, platelet activation, endo dysfunction, inflammation
  • defect in serotonin signaling –> dysfunction of amygdala –> ANS dysfunction –> inflammation, endo dysfunction, platelet act
  • 2-4x less likely to adhere to meds, follow lifestyle recs, follow up
210
Q

Identify safe and effective screening and treatment strategies for depression in cardiovascular disease (CVD)

A
  • treatment –> dec platelet act, improved HR, dec inflam
  • IMPACT study showed 48% lower CVD risk over 5yrs in patients with depression and no CVD disease
  • team approach, engage patient, steps
  • ask 2 Qs: have you felt depressed in the past month and have you lost interest in doing things in the past month
  • SSRIs are first line as well as cognitive behavior therapy and exercise
211
Q

Define congenital heart disease

A
  • abnormality present at birth
  • genetically encoded usually but also could be environmental
  • 3-8wks gestation during heart development
  • 50% of symptoms show clinically in 1st year of life
212
Q

List 4 examples of left to right CHD shunt and which is most frequent

A
  • VSD (most common)
  • ASD
  • PDA
  • AVSD
213
Q

Define the underlying defect and process leading to Eisenmenger’s syndrome

A
  • if you have a large VSD, then more fluid is going to the right side of the heart
  • this ultimately causes RVH and pulm HTN because of all the extra fluid it is pumping
  • leads to build up in right sided pressure and turns into a R–>L shunt
214
Q

List 3 examples of right to left CHD and which is the most frequent cyanotic CHD

A
  • TOF (most common)
  • Transposition of great arteries
  • Truncus arteriosus
  • Total anomalous pulm venous connection
215
Q

List the 4 key features of TOF

A

PROVe it

  • Pulmonary stenosis
  • RVH
  • Overriding aorta
  • VSD
216
Q

Name 2 examples of obstructive CHD

A
  • coarctation of aorta

- aortic/pulm stenosis

217
Q

Define cyanosis

A
  • bluish color of blood from poor oxygenation
218
Q

Define association of coarctation with DA

A
  • a PDA can often present with coarctation

- hypoplasia of proximal descending aorta

219
Q

Distinguish adult variant coarctation from infantile variant coarctation

A
  • infantile: hypoplasia of arch

- adult: infolding in area of ligamentum arteriosum

220
Q

What are risk factors for congenital heart disease?

A
  • maternal diabetes 3x
  • rubella –> PDA
  • down syndrome
  • family history of defect in 1st degree relative

CVPR (4 decks)

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