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Cardiologia (lilly) > 6. Ischemic Heart Disease > Flashcards

6. Ischemic Heart Disease Flashcards

1
Q

what is the leading cause of death in industrialised nations?

A

atheroesclerosis

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2
Q

what is the most common manifestation of ischemic heart disease?

A

Angina pectoris

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3
Q

What does angina pectoris mean?

A

Strangling of the chest

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4
Q

what does angina mean?

A

uncomfortable sensation in the chest and neighbouring structures due to an imbalance between oxygen supply and demand.

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5
Q

Define ischemic Heart Disease

A

imbalance between myocardial oxygen supply and demand. Results in myocardial hypoxia and accumulation of waste metabolites most commonly caused by CAD.

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6
Q

Define stable angina

A

Chronic pattern of stable angina pectoris precipitated by physical activity or emotional upset, relieved by rest within a few minutes. Permanent myocardial damage does not result.

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7
Q

Define variant angina

A

anginal discomfort usually at REST. develops because of artery spasm rather than increase of oxygen demand. Also termed Prinzmetal angina.

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8
Q

Define silent ischemia

A

Asymptomatic episodes of myocardial ischemia. can be detected by EKG or other lab studies

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9
Q

Define unstable angina

A

Pattern of increased frequency and duration of angina episodes produced by less exertion or at rest; high frequency of myocardial infarction if untreated.

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10
Q

Myocardial Infarction

A

Region of myocardial necrosis caused by prolonged cessation of blood supply.

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11
Q

What are the Determinants of Myocardial oxygen Supply?

A
  1. oxygen content of the blood
  2. coronary blood flow
    - Coronary perfusion pressure
    - Coronary vascular resistance
    - external compression
    - Instrinsic regulation
    - local metabolites
    - endothelial factors
    - neural inervation
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12
Q

What determines oxygen content?

A
  1. hemoglobin concentration

2. degree of systemic oxygenation

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13
Q

Coronary blood flow formula

A

Q: coronary blood flow
P: vessel perfusion pressure
R: coronary vascular resistance

Q= directly proportional to P/R

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14
Q

The predominance of coronary perfusion takes place during:

A

Diastole

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15
Q

How can you approximate the coronaries perfusion pressure?

A

by the aortic diastolic pressure

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16
Q

what type of conditions can decrease coronary artery perfusion pressure?

A

Conditions that decrease aortic diastolic pressure e.g. hypotension or aortic valve regurgitation.

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17
Q

What modulates coronary vascular resistance?

A
  1. forces that externally compress the coronary arteries

2. factors that alter intrinsic coronary tone

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18
Q

What region is the most vulnerable to ischemic damage?

A

subendocardium, adjacent to the high intraventricular pressure.

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19
Q

how does external compression define coronary vascular resistance?

A

Compression during sistole augments the CVR especially in the subendocardium.

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20
Q

Can the heart increase oxygen extraction on demand?

A

NO, it can only augment the blood flow because on its basal state it already removes as much oxygen as posible.

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21
Q

What factors participate in the regulation of coronary vascular resistance?

A
  1. external compression

2. Factors that alter intrinsic coronary tone

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22
Q

What is the prime metabolic mediator of the vascular tone?

A

Adenosine

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23
Q

What are the factors that alter intrinsic coronary tone?

A
  1. metabolic factors
  2. endothelial factors
  3. neural innervation
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24
Q

What is inhibited in states of of hypoxemia?

A
  1. aerobic metabolism

2. oxidative phosphorilation in mitochondria

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25
Q

what comes as a consequence of the inhibition of aerobic metabolism and oxidative phosphorilation?

A

ATP cannot be formes therefore ADP and AMP accumulates in tissues. These are degraded into Adenosine.

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26
Q

What is Adenosine?

A

Adenosine is a potent vasodilator, it is though to be the prime metabolic mediator of vascular tone.

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27
Q

Mecanism by which Adenosine causes vasodilation

A

Adenosine decreases calcium entry into cells

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28
Q

Name all metabolites that act locally as vasodilators:

A
  1. Adenosine
  2. Lactate
  3. Acetate
  4. Hydrogen Ions
    5 CO2
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29
Q

Name endothelial-dependent vasodilators:

A
  1. Nitric Oxide (NO)
  2. Serotonin
  3. Histamine
  4. thrombin
  5. shear stress
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30
Q

What is another name for nitric oxide?

A

Endothelium derived relaxing factor (EDRF)

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31
Q

What is the effect of acetilcholine (Ach) in vessels?

A
  1. Vasocontriction in normal vessels

2. Vasodilation in vessels with intact endothelium surrounded by Smooth muscle.

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32
Q

What is the mecanism of action of the endothelium dependent vasodilators?

A

Their binding to endothelial cells catalyses the formation of NO form L-arginine. NO then diffuses to the vascular smooth muscle where it activates guanyl ciclase (G-cyclase) which forms cyclic guanine monophosphate (c-GMP) which results in smooth muscle relaxation due to reduction of cytosolic Ca+.

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33
Q

What agents can cause smooth muscle relaxation independent of the endothelium?

A
  1. sodium nitroprusside

3. nitroglycerin

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34
Q

mechanism of action of sodium nitroprusside and nitroglycerin:

A

provide exogenous NO production and activating G-cyclase and forming cGMP without endothelial participation.

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35
Q

When does IV infusion of Ach cause paradoxical vasoconstriction?

A

conditions of endothelial disfunction such as:
1. Atheroesclerosis.
or persons with certain cardiac risk factors:
1. elevated LDL
2. Hypertension
3. Smokers

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36
Q

what may be an early detector of later development of atheroesclerotic lesions?

A

Impaired release of NO.

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37
Q

Vasodilators produced by the endothelium:

A
  1. Nitric Oxide
  2. Prostacyclin
  3. Endothelium derived Hyperpolarizing Factor (EDHF)
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38
Q

Example of endothelium derived vasoconstrictor

A

Endothelin 1

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39
Q

What augments NO release from the endothelium?

A
  1. Ach
  2. thrombin
  3. products of aggregating platelets (serotonin and ADP)
  4. shear stress of blood flow
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40
Q

what is prostacyclin?

A
  1. Arachidonic acid metabolite
  2. vasodilator
  3. uses cAMP dependent mechanism
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41
Q

What is EDHF?

A
  1. vasodilator
  2. difusible to smooth muscle
  3. hyperpolarizes smooth muscle
  4. appears more important in small arterioles
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42
Q

What is Endothelin 1?

A

potent vasoconstrictor

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43
Q

At normal circumstances what type of neural innervation is more prominent?

A

Sympathetic

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44
Q

stimulation of alfa adrenergic:

A

vasoconstriction

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45
Q

Stimulation of B adrenergic:

A

Vasodilation

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46
Q

What happens with catecolamine stimulation of the heart?

A
  1. initial vasoconstriction due to alfa adrenergic-r stimulation
    2 vasodilation due to B adrenergic stimulation and accumulation of metabolites.
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47
Q

What are the three major determinants of myocardial oxygen demand?

A
  1. ventricular wall stress
  2. heart rate
  3. contractility
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48
Q

What are the syndromes of ischemic heart disease?

A
  1. ischemic heart disease
  2. angina pectoris
  3. stable angina
  4. variant angina
  5. silent ischemia
  6. unstable angina
  7. myocardial infarction
  8. X syndrome
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49
Q

what is the formula for wall stress?

A

wall stress= (PxR)/ 2h
P:IV pressure
R: Radius of the ventricle
H: Ventricular wall thickness

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50
Q

What increases wall stress?

A
  1. aortic stenosis
  2. hypertension
  3. mitral or aortic regurgitation
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51
Q

What decreases wall stress?

A
  1. Antihypertensive therapy
  2. nitrate therapy
    3 hypertrophied heart
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52
Q

how does nitrate therapy reduce wall stress?

A

By reducing LV filling and size

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53
Q

What increases the heart rate?

A
  1. physical exertion
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54
Q

What decreases the heart rate?

A

B blockers

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55
Q

What increases the contractility?

A

Cathecolamines

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56
Q

What decreases the contractility?

A

B blockers

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57
Q

What is the lowest pressure value of aortic percussion pressure that guarantees a constant rate of coronary flow?

A

60mmHg

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58
Q

recent study found that myocardial ischemia results from:

A
  1. fixed vessel narrowing

2. abnormal vascular tone

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59
Q

the hemodynamic significance of a stenotic lesion depends on:

A
  1. its length

2. the degree of vessel narrowing

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60
Q

the coronary arteries consist of:

A
  1. epicardial segments

2. arterioles

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61
Q

where can we usually find flow limiting plaques?

A

proximal vessels

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62
Q

On what depends the hemodynamic significance of a coronary artery narrowing?

A
  1. degree of stenosis

2. amount of compensatory vasodilation of distant resistance vessels

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63
Q

if stenosis narrows the lumen diameter

A

maximum blood flow is not altered

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64
Q

If stenosis narrows the lumen diameter >70%:

A
  1. resting blood flow is normal

2. maximum blood flow is reduced

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65
Q

If stenosis narrows the lumen >90%:

A

blood flow is inadequate to meet basal requirements

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66
Q

How can abnormal endothelial cell function contribute to the pathophysiology of ischemia?

A
  1. inappropriate vasoconstriction of the coronary arteries

2. through loss of normal antithrombotic properties

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67
Q

in normal persons, physical activity or mental stress cause:

A

vasodilation

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68
Q

what factors released form endothelial cells exert antithrombotic properties?

A
  1. NO

2. Prostacyclin

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69
Q

What are other causes of Myocardial isquemia apart from Endothelial disfunction and vessel narrowing?

A
  1. decreased perfusion due to hypotension
  2. severely decreased blood oxygen content (anemia/impaired oxygenation)
  3. profound increase in oxygen demand (tachycardia/aortic stenosis)
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70
Q

What pain receptors are activated by the metabolic products of the heart during ischemia?

A

C7 to T4

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71
Q

Which metabolic products are thought to activate pain receptors?

A
  1. lactate
  2. serotonin
  3. adenosine
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72
Q

what symptom can be found when there is elevation of the LV diastolic pressure due to ischemia?

A

Dyspnea

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73
Q

Arrhythmias during ischemias can be seen due to:

A
  1. accumulation of local metabolites

2. transient abnormalities of myocyte ion transport

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74
Q

The ultimate fate of the myocardium subjected to ischemia depends on:

A
  1. the duration of ischemia

2. severity of imbalance between oxygen supply and demand.

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75
Q

What is a stunned myocardium?

A

myocardial tissue that after suffering severe, acute, transient schema presents prolonged systolic function even after the return of normal blood flow.
The abnormalities following the ischemia are reversible and contractility gradually recovers.

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76
Q

Mecanism responsible for stunned myocardium

A
  1. myocite calcium overload

2. accumulation of oxygen-derived free radicals.

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77
Q

What is hibernating myocardium?

A

Tissue that manifests chronic ventricular contractile disfunction due to persistent reduced blood supply. Ventricular function can promptly improve with restored blood supply.

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78
Q

Stable angina is generally caused by:

A

a fixed obstructive atheromatous plaque

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79
Q

what is the pattern of symptoms of a stable angina?

A
  1. increased heart rate
  2. increased blood pressure
  3. increased contractility
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80
Q

what can worsen ischemia during an angina?

A

paradoxical vasconstriction

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81
Q

what is a fixed threshold angina?

A

an angina in which alterations in tone play a minimal role in the ischemia. The level of physical activity required to precipitate the angina is fairly constant.

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82
Q

What is a variable threshold angina?

A

vasoconstriction or vasospasm plays a mayor role. The same degree of physical exertion sometimes produces symptoms and sometimes doesn’t.

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83
Q

symptoms of unstable angina:

A

a patient with a history of chronic stable angina may experience a sudden increase in tempo and duration of ischemic episodes occurring with lesser degrees of exertion even at rest.

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84
Q

What are the acute coronary syndromes?

A
  1. unstable angina

2. acute MI

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85
Q

what is the mecanism of an acute coronary syndrome?

A

rupture of an unstable plaque and subsequent platelet aggregation and thrombosis.

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86
Q

what is a variant angina?

A

prinzmetal angina. Focal vasospasm in absence of overt atheroesclerotic plaques.

87
Q

What is a prinzmetal angina?

A

variant angina.

88
Q

what is the mechanism of a variant angina?

A

not well known but may be due to sympathetic activity with endothelial disfunction.

89
Q

When can variant angina occur?

A

It often occurs at rest.

90
Q

How can a silent isquemia be detected?

A
  1. continuos ambulatory EKG

2. Exercise stress testing.

91
Q

what percentage of patients with no symptomatic angina present silent ischemia?

A

2.5-10% of middle aged men.

92
Q

in who is silent schema most common?

A
  1. diabetics
  2. elderly
  3. women
93
Q

What is syndrome X?

A

patients with angina with no evidence of coronary stenoses in angiograms. May be related to inadequate vasodilatory reserve of the coronary resistance vessels.

94
Q

What may contribute to syndrome X?

A
  1. microvascular disfunction
  2. vasospasm
  3. hypersensitive pain perception.
95
Q

What clinical features of the angina should be taken in consideration for an accurate diagnosis?

A
  1. quality
  2. location
  3. accompanying symptoms
  4. precipitants
  5. frequency
  6. risk factors
  7. differential diagnosis
96
Q

What EKG abnormality is present in variant angina?

A

elevation of ST segment

97
Q

What EKG abnormality is present in Stable angina?

A

depression of the ST segment

98
Q

What is the “quality” of an angina?

A

it is usually described as:

  1. pressure
  2. discomfort
  3. tightness
  4. burning
  5. heaviness
99
Q

how long does an angina last?

A

always more than a few seconds but rarely more than 5-10minutes.

100
Q

What is the Levine sign?

A

when the patient clenches his fist over his sternum to describe an angina. He describes the constricting discomfort by the tight grip.

101
Q

What is the location of an anginal discomfort?

A
  1. difuse
  2. restroesternal/prechordial
  3. it can appear back, arms, neck, lower face, upper abdomen.
  4. it often radiates to the shoulder and inner portion of the arms (especially on the left side)
102
Q

What are the accompanying Symptoms of an angina?

A
  1. sympathetic (tachychardia, diaforesis, nausea)
  2. transient dysfunction of LV systolic contraction and diastolic relaxation
    3 dyspnea
  3. transient fatigue and weakness
103
Q

What are “anginal equivalents”?

A

WHEN ACCOMPANYING SYMPTOMS OF AN ANGINA PRESENT WITHOUT AN ANGINA.

104
Q

What are the precipitants of an angina?

A
  1. conditions that increase myocardial oxygen demand
    - physical exertion
    - anger
    - emotional excitement
  2. large meal/cold weather
105
Q

What type of angina doesn’t have precipitants?

A

variable angina/ prinzmetal angina

106
Q

What should you keep in mind when asking about the frequency of the angina?

A

The activities the patient has stopped doing to avoid precipitation of the angina. This may alter the frequency of presentation.

107
Q

What risk factors should we take in consideration as posible causes of the CAD leading to angina?

A
  1. cigarette smoking
  2. dyslipidemia
    3 HTA
  3. Diabetes
  4. family history of premature CAD
108
Q

What are the three main sources of recurrent chest pain?

A
  1. cardiac
  2. Gastrointestinal
  3. Musculoskeletal
109
Q

What are the cardiac causes of recurrent chest pain?

A
  1. myocardial ischemia

2. Pericarditis

110
Q

What are the gastrointestinal causes of recurrent chest pain?

A
  1. GERD
  2. peptic ulcer disease
  3. esophageal spasm
    4 Bilary colic
111
Q

What are the musculoskeletal causes of recurrent chest pain?

A
  1. costochondral syndrome

2. Cervical radiculitis

112
Q

What are the differentiating features of myocardial ischemia?

A
  1. restroesternal tightness/presure

2. lasts few minutes (

113
Q

What are the differentiation features of a pericarditis?

A
  1. sharp pleuritic pain that varies with position
  2. friction rub on auscultation
  3. last hrs-days
  4. EKG: difuse ST elevations and PR depression.
114
Q

What are the differentiating features of GERD?

A
  1. retroesternal BURNING
  2. precipitated by certain foods, worsened by supine position, unaffected by exertion
  3. Relieved by antacids
115
Q

What are the differentiating features of peptic ulcer disease?

A
  1. epigstric ache or burning
  2. occurs after meals
  3. unaffected by exertion
  4. relieved by antacids not nitroglycerin
116
Q

What are the differentiating features of an esophageal spasm?

A
  1. retrosternal pain accompanied with dysphagia
  2. precipitated by meals, unaffected by exertion
  3. may be relieved by nitroglycerin
117
Q

What are the differentiating features of a Biliary colic?

A
  1. constant deep pain in right upper quadrant; can last for hours
  2. brought by fatty foods, unaffected by exertion
  3. not relieved by antacids or nitroglycerin
118
Q

What are the differentiating features of the costochondral syndrome?

A
  1. sternal pain worsened by chest movements
  2. costochondral junctions tender to palpation
    3 relieved by anti-inflammatory drugs, not by nitroglycerin
119
Q

What are the differentiating factors of a cervical radiculitis?

A
  1. constant ache or shooting pains, may be in dermatomal distribution.
  2. worsened by neck motion.
120
Q

What will you find in physical examination of a patient DURING an anginal attack?

A
  1. augmented sympathetic response (increased blood pressure and heart rate, diaphoresis
  2. papilary muscle disfunction: mitral regurgitation
  3. decreased ventricular compliance: S4 gallop
  4. decreased systolic function: diskinetic apical impulse
  5. pulmonary congestion: rales
121
Q

What should you asses during the physical examination of a patient who has a history of angina?

A

Asses for signs of atherosclerosis in more accesible vascular beds.

  1. carotid bruits (cerebrovascular disease)
  2. femoral artery bruits/ diminished pulses in lower extremities (peripheral artery disease)
122
Q

What are the procedures used to confirm myocardial ischemia as the cause of angina?

A
  1. Electrocardiogram
  2. Stress Testing
    - standard exercise testing
    - nuclear imaging studies
    - exercise echocardiography
    - pharmacologic stress tests
  3. Coronary Angiography
  4. Noninvasive imaging of coronary arteries
123
Q

What can we find in the EKG of a patient during myocardial ischemia?

A
  1. transient horizontal or downsloping ST segment depression
  2. T wave flattening or inversion
  3. St elevations are occasionally seen: suggest more sever transmural ischemia or prinzmetal angina
124
Q

percentage of patients that have completely normal EKG in ischemia free periods?

A

50%

125
Q

What are the different types of stress testing?

A
  1. standard exercise testing
  2. Nuclear imaging studies
  3. Exercise Echocardiography
  4. Pharmacologic stress tests
126
Q

What is the target heart rate achieved during standard stress testing?

A

85% of the maximal predicted heart rate (MHR)

127
Q

What is the equation for the maximal predicted heart rate?

A

MHR= 220-px age

128
Q

When is the stress test considered positive?

A

The patients typical chest discomfort is reproduced or EKG abnormalities consistent with ischemia develop

(>1mm downsloping or horizontal ST depression)

129
Q

Sensitivity and specificity of standard stress testing?

A

sensitivity of 65%-70%

specificity of 75-80%

130
Q

When is the stress test considered markedly positive?

A
  1. ischemic EKG changes develop in first 3 min/persists 5 min after exercise has stopped
  2. St segment depression > 2mm
  3. systolic blood pressure fall abnormally during exercise
  4. high grade ventricular arrhythmia develop.
  5. the patient cannot exercise for at least 2 min because of cardiopulmonary limitations.
131
Q

patients with markedly positive tests are more likely to have?

A

Severe multivessel coronary disease.

132
Q

What medications can interfere with the utility of stress tests by blunting the patients ability to reach target heart rate?

A
  1. B blockers

2. Ca++ channel blockers (verapamil, diltiazem)

133
Q

If you want to determine whether ischemic heart disease is present via stress testing how long before the test should you suspend B blocker or Ca blockers?

A

24-48 hours before the test.

134
Q

What is the standard exercise test?

A

Patient exercises on a treadmill or a bicycle whilst having ECG and heart rate continuously monitored, blood pressure is checked at regular intervals.

135
Q

What stimulates endothelin 1?

A
  1. thrombin
  2. Angiotensin II
  3. Epinephrine
136
Q

When do we use Nuclear imaging studies with exercise testing to increase sensitivity and specificity?

A
  1. px with baseline ST abnormalities (LBBB or LV Hypertrophy)
  2. Px with (-) standard stress testing results but high clinical suspicion of ischemic disease.
137
Q

What radionuclides are used in patients during nuclear imaging studies?

A
  1. technetium 99m

2. thallium 201

138
Q

When is the radionuclide injected?

A

During peak exercise

139
Q

How do imaging studies work?

A
  • radionuclide accumulates in proportion to the perfusion of viable myocardial cells
  • poor perfusion areas appear as cold spots
  • images are taken after exercise to differentiate Transient ischemic areas from infected areas.
140
Q

Sensitivity and specificity of standard radionuclide exercise tests?

A

sensitivity: 80-90%
specificity: 80% specific

141
Q

Sensitivity and specificity of positron emission tomography (PET)

A

90%

142
Q

When do we use Exercise echocardiography?

A
  1. baseline St or T wave abnormalities

2. equivocal standard stress tests

143
Q

How does exercise echocardiography work?

A

LV contractile function is assessed by echography at baseline and immediately after exercise. It is posible if regions of ventricular contractile disfunction develop with exertion

144
Q

Sensitivity and specifity of exercise echocardiography?

A

sensitivity: 80%
Specificity: 90%

145
Q

When do we use pharmacological stress tests?

A

Patients who can’t exercise (arthritis)

146
Q

What agents are used in pharmacological stress tests?

A
  1. dobutamine

2. dipyridamole or adenosine

147
Q

effects of Dobutamine?

A

increases oxygen demand by stimulating heart rate and force of contraction.

148
Q

Effects of Dypiridamole

A

blocks destruction of adenosine, vasodilation results, healthy coronary arteries steal blood away from diseased segments.

149
Q

What is the gold standard for the diagnosis of CAD?

A

Coronary angiography

150
Q

In what cases is Cardiac Computed Tomography particularly sensitive?

A

For the detection of calcification

151
Q

mortality of a px with advanced stenose of a single coronary artery?

A

<4%

152
Q

mortality of a px with advanced stenosis of two vessels?

A

7-10%

153
Q

mortality of px with advanced stenosis of three coronary arteries?

A

10-12%

154
Q

mortality of px with stenosis of the left main artery?

A

15-25%

155
Q

What are the critical predictors of mortality in px with CAD?

A
  1. extent of impaired LV contractile function
  2. poor exercise capacity
  3. the magnitude of clinical anginal symptoms
156
Q

What are the goals of therapy in chronic ischemic heart disease?

A
  1. decrease frequency of anginal episodes
  2. prevent acute coronary syndromes
  3. prolong survival
157
Q

What risk factors should be addresses in treatment of coronary artery disease?

A
  1. smoking cessation
  2. cholesterol improvement
  3. blood pressure control
  4. obesity
  5. physical inactivity
158
Q

What is the treatment of an acute angina?

A
  1. cease physical activity

2. sublingual nitroglycerin

159
Q

How long does it take for nitroglycerin to take effect?

A

1-2 minutes

160
Q

How does nitroglicerin relieve angina?

pg 153

A

through vascular smooth muscle relaxation

  1. venodilation: decreases LV volume
  2. decreases myocardial oxygen consumption
  3. dilates coronary vasculature
161
Q

What agents are used in the treatment of recurrent angina attacks?

A
  1. organic nitrates
  2. B- blockers
  3. Ca++ Channel Blockers
  4. Ranolazine
162
Q

What is the first line of prevention of anginal attacks?

A

Pharmacological agents

163
Q

What is the goal of pharmacological therapy of anginal attacks?

A
  1. decrease cardiac workload

2. increase myocardial perfusion

164
Q

Examples of organic nitrates?

A

1, NITROGLYCERIN

  1. ISOSORBIDE DINITRATE
  2. ISOSORBIDE MONONITRATE
165
Q

when can organic nitrates be used?

A
  1. acute angina

2. before activity that induces angina

166
Q

What is the limitation of chronic nitrate therapy?

A

development of drug tolerance

167
Q

How can one overcome nitrate tolerance?

A

providing nitrate free intervals, usually during the night

168
Q

Side effects of nitrate therapy

A
  1. headache
  2. lighheadedness
  3. palpitations (vasodilation and reflex sinus taquicardia)
169
Q

How does B blockers reduce angina?

A

reducing myocardial oxygen demand

170
Q

Where can we find B1 and B2 Adrenergic receptors?

A

B1-Adrenergic: myocardium

B2-Adrenergic: blood vessels, bronquial tree

171
Q

What happens with the stimulation of B1 receptors by catecholamines or simpaticomimetics?

A
  1. increase heart rate

2. increased contractility

172
Q

What happens when B1 receptors are antagonized?

A
  1. decreased heart rate (improves perfusion)

2. decreased contractility (decreases oxygen demand)

173
Q

Apart from suppressing angina, what are B blockers also used for?

A
  1. prevent recurrent Mi after primary MI

2. Prevent primary MI in px with hypertension

174
Q

What are the side effects of B-Blockers?

A
  1. Broncospasm
  2. Fatigue
  3. Sexual disfunction
175
Q

In what patients should we be careful using B-Blockers?

A
  1. Asthmatics/EPOC
  2. decompensated LV heart failure
  3. insulin treated diabetic patients
  4. px with marked bradycardia
  5. certain types of heart blocks
176
Q

How does Ca++ channel blockers relieve angina?

A

antogonizing voltage gated L-type Ca++ channels

177
Q

What are the two types of Calcium Channel blockers?

A
  1. dihydropiridines

2. nondihydropiridines

178
Q

Name the dihydropiridines

A
  1. Nifedipine

2. Amlodipine

179
Q

Name the nonhidropiridines

A
  1. VERAPAMIL

2. DILTIAZEM

180
Q

Mecanism of action of the dihydropiridines

A

potent vasodilators

  1. decrease oxygen demand (arterial and venous dilation)
  2. increase myocardial perfusion ( coronary vasodilation)
181
Q

Mecanism of action of nondihydropiridines

A

Vasodilators (not as potent), (-) inotropy, (-) cronotropy

182
Q

What type of Calcium channel blockers are recommended in treatment of chronic angina?

A

ONLY long acting Ca channel blockers ( taken once a day)

183
Q

what two types of meds used to prevent recurrent ischemic episodes should we be cautious when using together?

A

B-blockers and nondihidropyridine Ca channel blockers (both (-) isotropy and (-) cronotropy)

184
Q

What is the fourth type of anti-ischemic therapy?

A

Ranolazine

185
Q

What is the mechanism of action of Ranolazine?

A

it inhibits the late phase of the action potential inward sodium current

186
Q

WHAT ARE THE BENEFITS OF RANOLAZINE?

A

it does not affect heart rate or blood pressure

187
Q

Mediacal treatment to prevent acute cardiac events

A
  1. antiplatelet therapy

2. Lipid regulating therapy

188
Q

What agents are used in platelet therapy?

A
  1. Aspirin
  2. Clopidogrel
  3. Angiotensin Converting Enzime (ACE) inhibitors
189
Q

What are the actions of Aspirin?

A
  1. INHIBITION OF PLATELET AGGREGATION

2. ANTI-INFLAMATORY

190
Q

What are the contraindication of aspirin?

A
  1. allergy

2. Gastric bleeding

191
Q

What does clopidogrel block?

A

platelet P2Y ADP receptor

192
Q

When should aspirin be continued indefinitely?

A

In all patients with CAD

193
Q

WHAT ARE THE BENEFITS OF LIPID REGULATING THERAPY ?

A
  1. lower lipids
  2. decrease vascular inflammation
  3. improve endothelial cell disfunction
194
Q

all patients with CAD should have their LDL cholesterol maintained at:

A

<100mg/dL

195
Q

px with CAD + risk factors (acute coronary sx, diabetes, smoking) should maintain there cholesterol:

A

<70mg/dL

196
Q

When is coronary revascularization pursued?

A
  1. Angina doesn’t respond to treatment
  2. unacceptable side effects
  3. High risk or coronary disease
197
Q

What are the two techniques used to accomplish mechanical revascularization?

A
  1. Percutaneus coronary intervention (PCI)

2. Coronary artery bypass graft (CABG)

198
Q

What is a percutaneus transluminal coronary angioplasty?

A

a procedure performed under fluoroscopy where a balloon tipped catheter is used to dilate a stenosed coronary.

199
Q

WHAT PERIPHERAL ARTERIES ARE USED IN PCI?

A
  1. femoral
    2 braquial
  2. radial
200
Q

What is the risk of MI during a PCI?

A

1.5%

201
Q

What is the risk of mortality in a PCI?

A

1%

202
Q

what percentage of patients that underwent a percutaneus transluminal coronary angioplasty (PTCA) develop recurrent symptoms 6 months after

A

1/3

203
Q

What are drug eluting stents for?

A

PREVENTING NEOINTIMAL PROLIFERATION

204
Q

What drugs are used in drug eluting stents?

A
  1. SIROLIMUS
  2. EVEROLIMUS
  3. PACLITAXEL
205
Q

Over what period of time d drug eluting stents release drugs?

A

2-4 weeks

206
Q

What are the side effects of drug eluting stents

A

Delay of endothelial coverage of the stent with risk of thrombosis

207
Q

What are the most common symptoms related with HT?

A
  1. flushing
  2. sweating
  3. blurred vision
208
Q

HT complicated by atheroesclerosis can manifest by?

A

carotid and femoral bruits

209
Q

Organ damage in HT can be attributed to

A
  1. increased workload of the heart

2. arterial damage resulting from the combined effects of elevated pressure itself and accelerated atheroesclerosis.

210
Q

What abnormalities of the vasculature can we find in HT px?

A
  1. smooth muscle hyperthrophy
  2. endothelial cell disfunction
  3. fatigue of elastic fibers
211
Q

how does chronic HT trauma to the endothelium promote atheroesclerosis?

A

by disrupting normal protective mechanisms, such as the secretion of NO.

212
Q

What are the mayor organs targeted by HT?

A
  1. heart
  2. Cerebrovascular system
  3. the kidneys
  4. the retina
213
Q

what are the main causes of death of untreated HT px?

A
  1. 50% CAD or congestive heart failure
  2. 33% stroke
  3. 10-15% complications of renal failure.

Cardiologia (lilly) (8 decks)

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