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Medicine 1 > Block 5 > Flashcards

Block 5 Flashcards

1
Q

Comprise the most prevalent serious disorders in industrialized nations

A

CARDIOVASCULAR DISEASES

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2
Q

Age-adjusted death rates for coronary heart disease have declined by _____ in the last four decades in US

A

2/3

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3
Q

Remain the most common cause of death: → 35% of all death → Almost 1 million death each year

A

CARDIOVASCULAR DISEASES

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4
Q

→ ¼ of cardiac deaths are?

A

sudden (sudden cardiac death)

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5
Q

Cardiovascular diseases was considered to be more common in?

A

men than in women

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6
Q

Percentage of all deaths due to CVD is higher among?

A

women (43%) than men (37%)

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7
Q

o Chest discomfort

A

Myocardial ischemia

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8
Q

Common symptoms of Heart Failure:

A

▪ Fatigue ▪ Peripheral Edema ▪ Dyspnea

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9
Q

→ Obstruction to blood flow

A

o Valvular Stenosis → heart failure

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10
Q

→ Abnormal cardiac rhythm or rate

A

o Palpitations o Dyspnea o Hypotension o Syncope

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11
Q

Dyspnea

A

→ Pulmonary disease, marked obesity and anxiety

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12
Q

Chest discomfort

A

→ Result from variety of non-cardiac and cardiac causes other than myocardial ischemia

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13
Q

Edema

A

→ Primary renal disease and hepatic cirrhosis

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14
Q

Syncope

A

→ Neurologic disorder

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15
Q

CHARACTERISTIC FINDINGS OF CARDIAC PATIENTS

A
  1. Dyspnea/Chest Discomfort 2. Heart murmurs 3. Elevated arterial pressure 4. Abnormal ECG, CXR, and other imaging 5. Risk factors for CAD
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16
Q

positive a wave on ECG

A

MI

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17
Q

Biomarker for cardiac disease

A

C-reactive protein

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18
Q

→ No limitation of physical activity → No symptoms with ordinary exertion → Mild form

A

Class I

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19
Q

→ Slight limitation of physical activity → Ordinary activity causes symptoms o Patient is walking on a flat surface and experience difficulty of breathing

A

Class II

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20
Q

→ Marked limitation of physical activity → Less than ordinary activity causes symptoms → Asymptomatic at rest

A

Class III

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21
Q

→ Inability to carry out any physical activity without discomfort → Symptoms at rest → Worst classification for the patient to have

A

Class IV

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22
Q

• Congenital Heart Disease • Ventricular Septal Defect • Perimembranous type • Qp:Qs Ratio = 1:2 (Measures pulmonary circulation and flow of blood in the circulation)

A

Functional Class II-B

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23
Q

• Ischemic Heart Disease • S/P anterior wall myocardial infarction • Congestive Heart Failure

A

Functional Class III-C

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24
Q

• Rheumatic Heart Disease • Mitral Stenosis(irreg cardiac rhythm) • Atrial Fibrillation • Pulmonary Hypertension (physiological dx)

A

Functional Class IV-E “worse final classification”

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25
Q

Mendellian transmission of single-gene defects

A

→ Hypertrophic cardiomyopathy, Marfan syndrome, long QT syndrome.

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26
Q

Failure by the noncardiologist to recognize important cardiac manifestations of systemic illnesses • Example: The presence of _______ in stroke.

A

mitral stenosis

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27
Q

Failure by the cardiologist to recognize underlying systemic disorders in patients with heart disease. • Example: ________ should be tested for in an elderly patient with atrial fibrillation and unexplained heart failure

A

Hyperthyroidism → Heart failure is just one of the clinical manifestations of hyperthyroidism.

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28
Q

Provide precise diagnostic information that is critical to clinical evaluation, which may be crucial in developing a therapeutic plan in patients with known or suspected CAD.

A

Cardiac catheterization and coronary arteriography

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29
Q

If the stress test is positive, request for?

A

Invasive coronary angiogram

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30
Q

Should not be carried out in lieu of a careful history in patients with chest pain suspected of having ischemic heart disease.

A

coronary arteriogram

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31
Q

Why should coronary arteriogram not be carried out in lieu of a careful history in patients with chest pain suspected of having ischemic heart disease?

A

Although coronary arteriography may establish whether the coronary arteries are obstructed, and if so the severity of the obstruction, the results of the procedure by themselves often do not provide a definite answer to the question of whether a patient’s complaint of chest discomfort is attributable to coronary arteriosclerosis and whether or not revascularization is indicated.

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32
Q

Asymptomatic or mildly symptomatic patients with valvular heart disease that is anatomically severe should be evaluated periodically, every _________, by clinical and noninvasive examinations.

A

6 to 12 months

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33
Q

Medical management for CAD

A

o Anti – anginal drugs o Antiplatelet or antithrombotic drugs o Statins

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34
Q

Percutaneous coronary intervention for CAD

A

Coronary angioplasty

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35
Q

Surgical revascularization

A

Coronary bypass surgery

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36
Q

Consist of an endothelial tube in contact with a discontinuous population of pericytes

A

Capillaries

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37
Q

Typically have thin medias and thicker adventitias

A

Veins

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38
Q

Consists of a prominent tunica media

A

Small muscular artery

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39
Q

Have a prominent media with smooth-muscle cells embedded in a complex extracellular matrix

A

Larger muscular arteries

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40
Q

Have circular layers of elastic tissue alternating with concentric rings of smooth-muscle cells

A

Larger elastic arteries

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41
Q

Smallest blood vessels

A

Capillaries

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42
Q

Consist of a monolayer of endothelial cells in close juxtaposition of occasional smooth muscle-like cells known as Pericytes

A

Capillaries

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43
Q

do not invest in the entire micro vessel to form a continuous sheath

A

Pericytes

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44
Q

the media can contain just a few layers of smooth-muscle cells

A

Veins

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45
Q

Have a Trilaminar structure

A

Arteries

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46
Q

→ Monolayer of endothelial cell → Continuous with those of the capillary trees

A

Tunica Intima

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47
Q

→ Middle layer → Layers of smooth-muscle cells

A

Tunica Media

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48
Q

In _____, the media can contain just a few layers of smooth muscle cells

A

veins

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49
Q

→ Consists of looser extracellular matrix → Occasional fibroblast, mast cells and nerve terminals

A

Tunica Adventitia

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50
Q

• have relatively thicker media relative to their adventitia

A

Smaller Arteries

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51
Q

• contain a prominent tunica media • Atherosclerosis commonly affects this type of muscular artery

A

Medium-size Arteries

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52
Q

• have a much more structural tunica media consisting of concentric bands of smooth-muscle cells interspersed with strata of elastin-rich extracellular matrix sandwiched between layers of smooth-muscle cells

A

Larger (elastic) Arteries

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53
Q

Veins: Tunica Media

A

contain a few layers of smooth muscle cells

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54
Q

Veins: Tunica Adventitia

A

(Some Veins) have thicker adventitia than intima

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55
Q

Arteries: Tunica Media

A

made-up of several layers of smooth muscle cells

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56
Q

Arteries: Tunica Adventitia

A

(Large Arteries) have their own vasculatures, the vasa vasorum, which nourishes the outer aspects of the tunica media

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57
Q

Often contains occasional resident smooth-muscle (SM) cells beneath the monolayer of vascular endothelial cells.

A

Intima

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58
Q

The embryonic origin of SM cells in arteries of the upper body is derived from?

A

neural crest

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59
Q

The embryonic origin of SM cells in arteries of the lower body is derived from?

A

mesodermal structures (somites)

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60
Q

_______ may also give rise to both vascular endothelial cells and SM cells.

A

Bone marrow

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61
Q

The cells of vascular intima

A

Endothelial cells (EC)

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62
Q

Forms the interface between tissues and blood compartment.

A

Endothelium

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63
Q

Regulates the entry of molecules and cells into the tissue in a selective manner.

A

Endothelium

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64
Q

Has the ability to serve as a permselective barrier.

A

Endothelium

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65
Q

Participates in the local regulation of the blood flow and diameter size of the blood vessel.

A

Endothelium

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66
Q

Vasodilators produced by the endothelium under physiologic conditions:

A

o Prostacyclin o Endothelium-derived hyperpolarizing factor (EDHF) o Nitric oxide (NO)

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67
Q

o Potent Vasoconstrictor o Occurs when there is Endothelial Dysfunction

A

Endothelin

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68
Q

Oxidative stress occurs when there is excessive production of reactive oxygen species, such as superoxide anion, by endothelial and SM cells under pathologic conditions such as excessive exposure to ________.

A

Angiotensin II

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69
Q

Oxidative stress may lead also to inactivation of?

A

NO

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70
Q

The endothelium produces more _________ if there is more endothelial dysfunction already.

A

The endothelium produces more vasoconstriction rather than vasodilation if there is more endothelial dysfunction already.

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71
Q

Contributes critically to inflammatory processes involved in normal host defenses and pathologic states.

A

Endothelial monolayer

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72
Q

The endothelial monolayer expresses _______ during infection and inflammatory process.

A

leukocytes adhesion molecules

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73
Q

Regulate thrombosis and hemostasis.

A

Endothelial monolayer

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74
Q

Both _____ and _____ limit and antagonize platelet activation and aggregation.

A

Both NO and prostacyclin limit and antagonize platelet activation and aggregation.

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75
Q

Through local generation of _____, the normal endothelial monolayer can promote the lysis of nascent thrombi.

A

plasmin

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76
Q

The endothelial cell surface contains ________ that furnish an endogenous antithrombin coating to the vasculature.

A

heparan sulfate glycosaminoglycans

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77
Q

It also participates actively in fibrinolysis and its regulation.

A

Endothelial cell surface

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78
Q

They express receptors for plasminogen activators and produce tissue-type plasminogen activator.

A

Endothelial cell surface

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79
Q

Homeostatic Phenotype of Endothelial Functions

A

o Vasodilation o Antithrombotic and Profibrinolytic o Anti-inflammatory o Anti-oxidant

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80
Q

Dysfunctional Phenotype of Endothelial Functions

A

o Impaired dilatation, vasoconstriction o Prothrombotic and Antifibrinolytic o Pro-inflammatory o Proproliferative o Prooxidant

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81
Q

Forearm circulation is assessed by performing occlusion of the ______ artery flow with BP cuff, after which the cuff is deflated.

A

brachial artery Assess the change in brachial artery diameter and blood flow using ultrasound (Doppler)

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82
Q

Use of agonists that stimulate release of endothelial NO

A

→ Acetylcholine → Methacholine

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83
Q

• The increase in vessel diameter size of at least 10%. • Increase in blood flow. • Reactive Hyperemia

A

Normal

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84
Q

• Endothelial dysfunction • Smaller increase in diameter (less than 10%) • In extreme cases - paradoxical vasoconstriction

A

Abnormal Results

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85
Q

Major cell type of the media layer of the blood vessels

A

VASCULAR SMOOTH MUSCLE CELL

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86
Q

→ Controls the Blood pressure → Regional blood flow → Left Ventricular afterload

A

Smooth Muscle Cell Contraction and Relaxation

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87
Q

→ Venous capacitance → Influence the venous return of both ventricles

A

Venous Smooth Muscle Cells

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88
Q

Proliferation and Migration of Arterial Smooth Muscle Cells contribute to development of?

A

Arterial Stenosis

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89
Q

Cerebral vascular disease

A

ischemic stroke

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90
Q

Coronary artery disease

A

Stable angina and Acute Coronary Syndrome

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91
Q

Angioplasty and stent deployment

A

Post-PCI restenosis (percutaneous coronary intervention)

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92
Q

The principal function of the vascular SM cells is to?

A

maintain vessel tone

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93
Q

Vascular SM cells contract when stimulated by a rise in?

A

intracellular calcium concentration after calcium influx through the plasma membrane and release from intracellular stores.

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94
Q

open during membrane depolarization

A

Voltage-dependent L-type calcium channels

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95
Q

Voltage-dependent L-type calcium channels are regulated by:

A

o Na+ , K+ -ATPase pump o Ca 2+ sensitive K+ ion channel

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96
Q

Vascular SM cell contraction is principally controlled by?

A

the phosphorylation of myosin light chain

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97
Q

The steady state is maintained by the balance between the actions of?

A

myosin light chain kinase & myosin light chain phosphatase

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98
Q

Myosin light chain kinase is activated by calcium through the formation of?

A

calcium-calmodulin complex

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99
Q

SM contraction is sustained due to increased myosin ATPase activity brought about by?

A

myosin light chain phosphorylation

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100
Q

_________, in contrary would reduce SM cells contractile force

A

Myosin light chain dephosphorylation

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101
Q

Both cAMP and cGMP _____ vascular SM cells

A

relax

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102
Q

Baroreceptors and chemoreceptors are found in?

A

within the aortic arch and carotid bodies

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103
Q

Thermoreceptors are found in?

A

the skin

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104
Q

Effect of NO

A

potent vasodilator

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105
Q

Process of growing new blood vessels that can occur in response to chronic hypoxia and tissue ischemia.

A

Angiogenesis

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106
Q

a signaling cascade is activated that stimulates endothelial proliferation and tube formation

A

Vascular Endothelial Growth Factor

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107
Q

About ¾ of the ventricle is composed of?

A

Individual striated muscle cells (myocytes/ cardiomyocytes) → Length: 60-140 um → Diameter: 17-25 um

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108
Q

• Multiple, rodlike crossbanded strands found in each cell that run the length of the cell and are, in turn, composed of serially repeating structures, the sarcomeres • Numerous mitochondria

A

Myofibrils

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109
Q

The sliding filament model for muscle contraction rests on: → The fundamental observation that?

A

both the thick and thin filaments are constant in overall length during both contraction and relaxation

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110
Q

During activation: → The actin filaments are propelled further into the ______

A

A band

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111
Q

In the process: → Describe the length of the A band, I band and Z line

A

The A band remains constant in length, whereas the I band shortens and the Z line move toward one another

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112
Q

It is the volume that decreases by about 70 milliliters as the ventricles empty during systole

A

Stroke Volume (SV)

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113
Q

amount of blood ejected by your left ventricle into the aorta during contraction in a single cardiac cycle

A

Stroke Volume (SV)

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114
Q

Stroke Volume (SV) =

A

Stroke Volume (SV) = (end diastolic volume) - (end systolic volume)

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115
Q

the volume of each ventricle that increases to about 110 to 120 milliliters during diastole

A

End-diastolic Volume

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116
Q

the remaining volume in each ventricle, about 40 to 50 milliliters,

A

End-systolic Volume

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117
Q

Cardiac Output (CO) =

A

Cardiac Output (CO) = (SV) x (Heart rate (HR)

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118
Q

Blood Pressure (BP) =

A

Blood Pressure (BP) = (CO) x PVR (peripheral vascular resistance)

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119
Q

3 DETERMINANTS OF VENTRICULAR STROKE VOLUME:

A
  1. Length of the muscle at the onset of contraction (preload) 2. Tension that the muscle is called upon to develop during contraction (afterload) 3. Contractility of the muscle (extent and velocity of shortening at any given preload and afterload)
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120
Q

Determines the: → length of the sarcomere at the onset of the contraction → The relation between the initial length of the muscle fibers → and the developed force has prime importance for the function of the heart muscle

A

Preload

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121
Q

“Starling’s Law” of the heart

A

the force of ventricular contraction depends on the end-diastolic length of the cardiac muscle

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122
Q

is sometimes used as a surrogate for the end-diastolic volume

A

Ventricular end-diastolic or filling pressure

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123
Q

The load that opposes the shortening of the muscles

A

VENTRICULAR AFTERLOAD

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124
Q

May be defined as the tension developed in the ventricular wall during ejection

A

VENTRICULAR AFTERLOAD

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125
Q

The extent/velocity of shortening of the ventricular muscle fibers at any level of preload and of myocardial contractility is ________ related to the afterload

A

inversely

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126
Q

Determinants of ventricular afterload:

A

→ Aortic pressure → Ventricular volume → Ventricular wall thickness

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127
Q

→ Indicates that the tension of the myocardial fiber is a function of the product of intracavitary ventricular pressure and the ventricular radius divided by the wall thickness

A

Law of Laplace

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128
Q

Determinants of Aortic Pressure

A

→ Peripheral vascular resistance → Physical characteristics of the arterial tree o The degree of stiffness of the arteries → The volume of blood it contains at the onset of ejection

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129
Q

EXERCISE • Interactions among 3 determinants of stroke volume

A

→ Increase (↑) in preload o Hyperventilation, pumping action of exercising muscle and vasoconstriction -increase in venous return and ventricular filling → Decrease (↓) in afterload o Arterial vasodilation in exercising muscles → Increase (↑) in contraction o Inc. in circulating catecholamines

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130
Q

Ventricular Preload: Lying Position

A

(↑) ventricular preload

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131
Q

Ventricular Preload: (↑) Intrathoracic pressure

A

can reduce (↓) preload

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132
Q

Ventricular Preload: Intrapericardial pressure

A

can also reduce (↓) preload

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133
Q

Ventricular Preload: (↑) venous tone= (↑) venous return

A

(↑) preload

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134
Q

Ventricular Preload: (↑) Pumping action

A

(↑) preload

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135
Q

Ventricular Afterload: Systemic vascular resistance = Arteriolar Constriction = (↑) arterial tone

A

(↑) afterload

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136
Q

Ventricular Afterload: Reduced elasticity of arterial tree (In case of atherosclerosis)

A

(↑) afterload

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137
Q

Ventricular Afterload: (↑)Elasticity

A

(↓) afterload

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138
Q

Ventricular Afterload: Arterial blood volume

A

(↑) afterload

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139
Q

Ventricular Afterload: Ventricular wall tension “law of laplace” (↑) of ventricular radius (dilated ventricle) ↓ (↑) ventricular tension

A

(↑) afterload

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140
Q

Qp:Qs Ratio- measures?

A

pulmonary circulation and flow of blood in the circulation

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141
Q

More sensitive index of cardiac function

A

EJECTION FUNCTION (EF)

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142
Q

Ratio of SV to end-diastolic volume

A

EJECTION FUNCTION (EF)

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143
Q

Normal value of ejection function

A

67 ± 8%

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144
Q

Systolic function

A

EJECTION FUNCTION (EF)

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145
Q

ELEVATED VENTRICULAR END-DIASTOLIC VOLUME • Normal value = ?

A

75 ± 20ml/m2

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146
Q

ELEVATED VENTRICULAR END-SYSTOLIC VOLUME • Normal value = ?

A

25 ± 7ml/m2

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147
Q

NON-INVASIVE TECHNIQUES OF MEASURING EJECTION FRACTION

A

• Echocardiography • Radionuclide scintigraphy (nuclear medicine) • Cardiac MRI

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148
Q

• Useful index of ventricular performance • Results are not dependent on the degree of preload and afterload

A

END-SYSTOLIC LEFT VENTRICULAR PRESSURE VOLUME RELATIONSHIP

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149
Q

Assessment of ventricular filling

A

DIASTOLIC FUNCTION

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150
Q

Increase in ventricular stiffness

A

→ Ventricular hypertrophy → Amyloid infiltration of the ventricle

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151
Q

Continuously Measuring The Velocity of Blood Flow Across The Mitral Valve Using Doppler Ultrasound

A

DIASTOLIC FUNCTION

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152
Q

4 causes of increase pressure in the right atrium and the jugular venous pressure:

A
  1. Heart failure 2. Fluid overload 3. Constrictive pericarditis 4. Cardiac tamponade
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153
Q

Jugular venous pressure is assessed by looking at what vein?

A

Right internal jugular vein visualized between the medial clavicle and the earlobe. It runs underneath the sternocleidomastoid muscle.

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154
Q

Is the external jugular vein medial or lateral to the internal jugular vein?

A

Lateral

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155
Q

Indirectly measures pressure in the right atrium and the venous system.

A

JVP

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156
Q

Increase right atrium (RA) pressure = ?

A

increase JVP

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157
Q

Why do we use the right internal jugular vein?

A

We use Right IJV because it is located most directly above the right atrium. It can give the best indication of what is happening in the right atrium.

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158
Q

How to visualize the JVP?

A

→ Have the patient sit on their back at angle 45 degrees and turn head slightly to the left. → Useful to shine light diagonally across patient’s neck so that you can see the change in shadows as you get the JVP pulsation. → Pulsation is like a wave in the neck with 2 pulses per heartbeat. More of a flutter underneath the SCM muscle. → Distinguished from carotid pulse in 2 ways: o 2 pulses per heartbeat o No palpable pulsation

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159
Q

Hepatojugular reflex

A

Press over the liver or right upper quadrant (RUQ) of the abdomen, cause temporary rise of JVP

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160
Q

How to measure the height of JVP?

A

→ On the sternal angle, measure vertically from this point and assess where JVP is. → On the vertical height from sternal angle to the level of JVP is the height of the JVP.

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161
Q

Normal JVP Height

A

Less than 3 cm

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162
Q

5 parts of JVP waveform

A
  1. A wave 2. X descent o 1st part of X descent o 2nd part of X descent 3. C wave 4. V wave 5. Y descent
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163
Q

Happening during ATRIAL CONTRACTION

A

A WAVE

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164
Q

What causes A wave?

A

→ Right atrium is contracting against blood that’s inside it then pushes blood into tricuspid valve to the right ventricle. Increase pressure of right atrium not only pushes blood downwards but also upwards. → Level of the blood in the IJV rises. This rise is the A WAVE.

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165
Q

Is caused by RELAXATION OF THE ATRIA, and the blood flows into the relax atria from the IJV and causes a drop of JVP.

A

1st X DESCENT

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166
Q

What causes the 1st X descent?

A

→ Is caused by RELAXATION OF THE ATRIA, and the blood flows into the relax atria from the IJV and causes a drop of JVP. → At the start of, X descent, there is also a blood that flows from the atria into the ventricles to complete the ventricular filling, leading to fall of JVP.

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167
Q

→ At the start of systolic contraction, the right ventricle contracts and squeezes blood out into the pulmonary artery. → This pressure pushes up against the close tricuspid valve and cause to bulge slightly into tha atria. → This pressure into the atria from that bulging tricuspid valve extend in SVC (superior vena cava) into IJV (Internal Jugular Vein) and creates rise in JVP called?

A

C wave

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168
Q

Is caused by the final parts of the Right VENTRICULAR CONTRACTION where it squeeze so small that creates space in the pericardium or the sack that fills the heart for the right ventricle to fill.

A

2nd X DESCENT

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169
Q

→ Ventricles become very small and create more space inside that sack so that atrium has space to fill out. → This sack is like a vacuum and ventricle shrinks and creates space inside the pericardium for atria to fill. So they expand and suck in blood and causing JVP to fall.

A

2nd X DESCENT

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170
Q

→ Happens when ATRIA RELAXES and right atrium starts to fill with blood. At this point tricuspid valve is still closed at the end of the systolic contraction of the ventricles. → So as the atria fills completely, this filling starts to occur higher up into the SVC, IJV and as a result JVP rises. It is called the?

A

V wave

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171
Q

→ Occurs when the tricuspid valve opens and all the blood flows from the right atrium into the right ventricle. This emptying of the right atria causes JVP to fall. → At this point, whole cycle restarts and the atria contracts and cause an a wave and so on.

A

Y DESCENT

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172
Q

It is cause by atrial contraction, causing atrial pressure to rise forcing blood flow both downward and upward into the JVP.

A

A WAVE

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173
Q

Starts with the relaxation of the atria and the blood flows back into the atrium.

A

1st X DESCENT

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174
Q

Caused by Right ventricular contraction causing the tricuspid to bulge into the right atria.

A

C WAVE

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175
Q

Caused by right ventricular contraction causing the right ventricles to take up less room and the atria to expand and fill the space left by the right ventricle and drain blood from IJV.

A

2nd X DESCENT

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176
Q

Caused by Right atrium filling up with blood and in turn the SVC and IJV filling with blood.

A

V WAVE

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177
Q

Caused by opening of tricuspid valve and emptying of the right atrium.

A

Y Descent

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178
Q

Absent A waves Example:

A

→ Atrial fibrillation. o The right atrium is not contracting in a coordinated way. The coordinated atrial contraction is what causes A waves

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179
Q

Large A waves Examples:

A

→ Right ventricular hypertrophy → Pulmonary hypertension → Pulmonary stenosis → Tricuspid stenosis o Cause by anything that makes flow from RA to RV more difficult because atria will be contracting against resistance and this will cause more blood to flow upwards because it can’t flow downwards.

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180
Q

Large V waves Example:

A

→ Tricuspid regurgitation - Right ventricular contraction will lead to blood flowing back thru the tricuspid valve and up into the right atrium, SVC and IJV - Will also cause loss of X descent because the ventricular contraction increases the pressure into the right atria rather than relieving it because the blood is trying to go back into the tricuspid valve to the RA.

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181
Q

Rarely palpable compared to carotid pulse. It has soft, bi-phasic, angulating quality with 2 elevation and inward deflection.

A

IJV

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182
Q

More vigorous thrust with single outward component.

A

carotid

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183
Q

Eliminated by light pressure in the vein just above the sternal and the clavicle

A

IJV

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184
Q

Not eliminated by pressure in vein at sternal end of clavicle

A

carotid pulsation

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185
Q

Height of pulsation of IJV changes with pulsation normally dropping as the patient _________ but in carotid it is unchanged.

A

becomes more upright

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186
Q

The height of pulsation usually _____ with inspiration in IJV while in carotid is not affected.

A

falls

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187
Q

Waves part of diastole

A

A and C wave is part of diastole

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188
Q

Waves part of systole

A

X and V wave is part of systole

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189
Q

Atrial contraction

A

A wave

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190
Q

Bulging of tricuspid valve

A

C wave

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191
Q

Atrial relaxation

A

X descent

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192
Q

Atrial filling

A

V wave

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193
Q

Followed by a drop in the pressure

A

Y descent

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194
Q

Best way to palpate carotid

A

→ Just below the caudal portion of the neck (rather than in the higher portion because it’s covered by the SCM muscle)

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195
Q

best heard carotid bruit

A

In the middle portion of the neck

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196
Q

Pressure within the thoracic vena cava just before the RA. The SVC and the connecting jugular veins act as a column of blood as which the CVP can be approximated by determining the JVP. This is done by measuring the elevation of the neck veins above the sternal angle and correlating it to the height of the blood column in cm of water.

A

Central Venous Pressure (CVP)

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197
Q

Best in examining jugular venous pressure because it is directly connected to the RA.

A

right side IJV

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198
Q

Can the external jugular vein be used in examining the central venous pressure?

A

The exam can also be performed in the EJV but they often branch at right angles which can interfere with the test results.

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199
Q

How to examine central venous pressure?

A

At the beginning of the test; → Patient should be recumbent with the head turned slightly to the left. The jugular veins are now at the same level as the RA and should be significantly distended under physiological conditions. → The jugular veins present with the regular pulse featuring a twin peak. The IJV pulsations are not readily observable because it lies deeper within the neck. Its pulsation, the weak, can be observed ventro-medial to the EJV. → The CVP or the height of the column above the RA can now be estimated by slowly raising patient’s upper body by 30 to 45 degrees. → As soon as the distention of the jugular vein starts to decrease halt the movement of the patient upper body and locate the most cranial point at which jugular vein is still distended. → The vein now functions a as nanometer that represent CVP. → Draw and imagine horizontal line toward the sternum starting at the most cranial point to at which the vein is still distended. → Since the sternal angle lies about 5 cm above the level of the RA, add those 5 cm to the measured distance. The sum roughly measures the CVP measured in cm of H2O

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200
Q

Normal CVP

A

4 to 10 cm of H2O

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201
Q

Is a CVP of 10 considered high?

A

If sum is greater that 10 cm the CVP is considered too high as seen in heart failure, hypovolemia or pulmonary embolism.

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202
Q

Lub

A

S1

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203
Q

Caused by the closing of the atrioventricular valves (the tricuspid and mitral valves) at the start of the systolic contraction of the ventricles.

A

S1

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204
Q

As the ventricles try to push blood out of the heart, the valves between the atria and the ventricles need to close to prevent blood from flowing back to the atria.

A

S1

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205
Q

Dub

A

S2

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206
Q

Caused by the closing or the semilunar valves (the pulmonary and aortic valves) once the systolic contraction is complete. This is to prevent blood from flowing back to the pulmonary arteries or the aorta into the ventricles.

A

S2

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207
Q

Lub de dub

A

S3

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208
Q

A third heart sound (S3) is heard roughly ___ second after the second heart sound.

A

0.1 second

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209
Q

Think of it as rapid ventricular filling causing the chordae tendineae to pull to their full length and twang like a guitar string.

A

S3

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210
Q

S3 is seen normally in?

A

This can be normal in young (15-40 years) healthy people because the heart functions so well that the ventricles easily allow rapid filling.

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211
Q

What does S3 indicate on older patients?

A

In older patients it can indicate heart failure, as the ventricles and chordae are stiff and weak so they reach their limit much faster than normal. Picture this like tight hamstrings in an old de-conditioned patient sharply tightening as they start to bend over.

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212
Q

Le lub dub

A

S4

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213
Q

A fourth heart sound (S4) is heard directly before ___.

A

S1

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214
Q

This is always abnormal and relatively rare to hear.

A

S4

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215
Q

 It indicates a stiff or hypertrophic ventricle and is caused by turbulent flow from an atria contracting against a non-compliant ventricle.  The ventricles are really stiff and the atria are trying to force blood in that causes a turbulent flow.

A

S4

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216
Q

“It’s also common to patients with hypertension, ischemic heart disease and coronary artery disease. ”

A

S4

You can hear S4 brought about by elevated left ventricular pressure

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217
Q

Significance of a loud S2 Is presence of?

A

pulmonary hypertension

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218
Q

How to use the stethoscope when listening to heart murmurs?

A

Auscultate with the bell of your stethoscope to better hear low pitched sounds and the diaphragm to listen to high pitched sounds. To remember this think of a child’s high-pitched screaming from their diaphragm versus a church bell giving a deep “bong”.

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219
Q

Aortic

A

2nd ICS Right Sternal border

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220
Q

Pulmonic

A

2nd ICS Left Sternal border

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221
Q

Tricuspid

A

5th ICS Left Sternal border

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222
Q

Mitral

A

5th ICS Mid-clavicular line (Apex area)

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223
Q

If you have a mitral regurgitation, you expect your ________ to dilate because of the regurgitated blood coming from the left ventricle coming back and forth to your left atrium. Because of that you have a dilated left ventricle. Likely the point of the maximum impulse is not on the 5th ICS (mitral area) but it would be on the?

A

left atrium 6th ICS left anterior axillary line

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224
Q

If you have aortic regurgitation, you have a dilated ________. But in this case of aortic regurgitation, it can be heard to your mitral going to your aortic valve. This refers to the _________ of the mitral valve going to your aortic area.

A

left ventricle “aortic sash area”

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225
Q

Remember when you’re dealing with aortic stenosis, you could also hear a systolic murmur. It starts in the mitral valve going towards the aortic area with radiation to your _______.

A

carotids

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226
Q

A murmur involving your atrial septum is usually located in the?

A

2nd or 3rd ICS left sternal boarder

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227
Q

A ventricular septal murmur (systolic), can be heard in the?

A

3rd or 4th ICS left sternal boarder

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228
Q

This is in the third intercostal space on the left sternal boarder and is the best area for listening to heart sounds (S1, S2, S3 and S4)

A

Erb’s Point

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229
Q

Special maneuvers can be used to emphasize certain murmurs: o mitral stenosis

A

Patient on their left hand side

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230
Q

Special maneuvers can be used to emphasize certain murmurs: o aortic regurgitation

A

Patient sat up, leaning forward and holding exhalation

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231
Q

Assessing a Murmur (SCRIPT): S

A

Site: Where your murmur is loudest?

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232
Q

Assessing a Murmur (SCRIPT): C

A

Character: soft/ blowing/ crescendo (getting louder)/ decrescendo (louder then quieter)

233
Q

Assessing a Murmur (SCRIPT): R

A

Radiation: can you hear the murmur over the carotids (AS) or left axilla (MR)?

234
Q

Assessing a Murmur (SCRIPT): I

A

Intensity: what grade is the murmur?

235
Q

Assessing a Murmur (SCRIPT): P

A

Pitch: Is it high pitched or low and grumbling? Pitch indicates velocity

236
Q

Assessing a Murmur (SCRIPT): T

A

Timing: Is it Systolic or Diastolic?

237
Q

Grade of Murmurs: 1

A

Difficult to hear

238
Q

Grade of Murmurs: 2

A

Quiet

239
Q

Grade of Murmurs: 3

A

Easy to hear

240
Q

Grade of Murmurs: 4

A

Easy to hear with palpable thrill

241
Q

Grade of Murmurs: 5

A

Can hear with stethoscope barely touching the chest

242
Q

Grade of Murmurs: 6

A

Can hear with stethoscope off the chest

243
Q

This patient has a harsh / soft / blowing, Grade …, systolic / diastolic murmur, heard loudest in the aortic / mitral tricuspid / pulmonary area, that does not / radiates to the carotids / left axilla. It is high / low pitched and has a crescendo / decrescendo / crescendo-decrescendo shape. This is suggestive of a diagnosis of ?

A

mitral stenosis / aortic stenosis

244
Q

Mitral stenosis causes?

A

left atrial hypertrophy

245
Q

Aortic stenosis causes?

A

left ventricular hypertrophy

246
Q

Mitral regurgitation causes?

A

left atrial dilatation

247
Q

Aortic regurgitation causes?

A

left ventricular dilatation

248
Q

Is when an incompetent mitral valve allows blood to lead back through during systolic contraction of the left ventricle.

A

Mitral regurgitation

249
Q

Mitral regurgitation results in ________ because the leaking valve causes a reduced ejection fraction and a backlog of blood that is waiting to be pumped through the left side of the heart.

A

congestive cardiac failure

250
Q

 It causes a pan-systolic, high pitched “whistling” murmur due to high velocity blood flow through the leaky valve.  The murmur radiates to left axilla.

A

Mitral regurgitation

251
Q

The radiation of your mitral regurgitation is usually at the __________ especially if it involves the anterior mitral valve leaflet.

A

back or at the axilla The non-quotation of the mitral valve causes the direction of the flow towards the back or the axilla.

252
Q

If you have a flailing posterior mitral valve leaflet, the direction of the flow is _______.

A

anteriorly Which means the pan-systolic murmur is best heard in the anterior portion or in the area of your tricuspid valve (4th ICS left parasternal boarder)

253
Q

You may hear a third heart sound in?

A

MITRAL REGURGITATION

254
Q

Causes of mitral regurgitation:

A

→ Idiopathic weakening of the valve with age → Ischaemic heart disease → Infective Endocarditis → Rheumatic Heart Disease → Connective tissue disorders such as Ehlers Danlos syndrome or Marfan syndrome

255
Q

“Burr”

A

mitral regurgitation

256
Q

The most common valve disease you will encounter.

A

Aortic stenosis

257
Q

Narrow Aortic Valve

A

Aortic stenosis

258
Q

It causes an ejection-systolic, high pitched murmur (high velocity of systole).

A

Aortic stenosis

259
Q

The high pitch murmur which is common in the erderly is sometimes called a “cooing murmur”

A

Aortic stenosis

260
Q

Diamond shaped murmur

A

Aortic stenosis

261
Q

This has a crescendo-decrescendo character due to the speed of blood flow across the value during the different periods of systole.

A

Aortic stenosis

262
Q

The differential diagnosis for aortic stenosis is?

A

hypertrophic cardiomyopathy

263
Q

The presentation looks like an aortic stenosis EXCEPT THAT IT DOES NOT RADIATE TO THE CAROTIDS because the obstruction is in the left ventricular outflow tract. IT DOESN’T INVOLVE YOUR AORTIC VALVE.

A

hypertrophic cardiomyopathy

264
Q

Flow during _____ is slowest at the very start and end and fastest in the middle.

A

systole

265
Q

Other signs of aortic stenosis?

A

→ The murmur radiates to the carotids as the turbulence continues up into the neck → Slow rising pulse → Narrow pulse pressure → Patients may complain of exertional syncope (light headedness and fainting when exercising) due to difficulty maintaining good flow of blood to the brain

266
Q

Causes of aortic stenosis?

A

→ Idiopathic age related calcification → Rheumatic Heart Disease

267
Q

“Burr Dub”

A

Aortic stenosis

268
Q

Aortic Valve Incompetent

A

AORTIC REGURGITATION

269
Q

Typically causes an early diastolic, soft murmur

A

AORTIC REGURGITATION

270
Q

Aortic regurgitation is also associated with a _________ pulse.

A

Corrigan’s pulse

271
Q

A Corrigan’s pulse is also called a?

A

collapsing pulse

272
Q

Is a rapidly appearing and disappearing pulse at carotid as the blood is pumped out by the ventricles and then immediately flows back through the aortic valve back into the ventricles.

A

Corrigan’s pulse

273
Q

Aortic regurgitation results in ______ due to a back pressure of blood waiting to get through the left side of the heart.

A

heart failure

274
Q

It can also cause an “Austin-Flint” murmur.

A

Aortic regurgitation

275
Q

This is heard at the apex and is an early diastolic “rumbling” murmur.

A

“Austin-Flint” murmur

276
Q

This is caused by blood flowing back through the aortic valve and over the mitral valve causing it to vibrate.

A

“Austin-Flint” murmur

277
Q

Causes of aortic regurgitation?

A

→ Idiopathic age related weakness → Connective tissue disorders such as Ehlers Danlos syndrome or Marfan syndrome

278
Q

“Lub Tarrr”

A

aortic regurgitation

279
Q

A wave that is produced by cardiac systole traversing peripheral direction in the arterial tree at a rate faster than the column of blood

A

ARTERIAL PULSE

280
Q

A wave being produce in the arteries which is transmitted in the arteries

A

Ventricular Systole

281
Q

A peripheral transferring wave is felt as the arterial pulse with three fingers:

A

→ Index → Middle → Ring

282
Q

Pulses that you can palpate:

A

→ Radial → – best suited for contour, volume and Brachial consistency → Carotid → Popliteal → Femoral → Posterior Tibial → Dorsalis Pedis

283
Q

Normal pulse rate?

A

Ranges between 60-100 bpm (beats per minute)

284
Q

Variations of pulse rate with age?

A

→ One week of age (Infant) – 140 bpm → One year of age – 120 bpm → Puberty – 70-80 bpm

285
Q

> 100 bpm

A

Tachycardia

286
Q

 Sinus rhythm → QRS in ECG is preceded by the P wave → Impulse originate in Sinus Node travels to the AV Node reaches Left Ventricle through the His and Purkinje Fibers

A

Tachycardia

287
Q

<60 bpm

A

Bradycardia

288
Q

 Sinus rhythm → QRS in ECG is also preceded by the P wave

A

Bradycardia

289
Q

Tachycardia sinus rhythm physiologic causes:

A

o Infancy o Early Childhood o Exercise o Excitement o Anxiety o Emotional Stress

290
Q

Bradycardia Sinus Rhythm physiologic causes:

A

o Athletes who undergo training o During sleep

291
Q

Tachycardia Sinus Rhythm pathologic causes:

A

o Cardiovascular causes  Congested Heart Failure  Acute Myocardial Infarction  Pulmonary Thromboembolism  or MyocarditisShock o Non-Cardiac causes  Fever  Anemia  Pregnancy  Thyrotoxicosis  Paget’s Disease  Beri-Beri (Vitamin B1 deficiency )  Hemorrhage  Hypotension

292
Q

Bradycardia Sinus Rhythm pathologic causes:

A

o Cardiovascular causes  Inferior Wall Myocardial Infarction  Sinus-Atrial Block  Post Cardiac Transplantation o Non-Cardiac causes  Myxedema  Chagas Disease  Hypothermia  Mental Depression

293
Q

Tachycardia Sinus Rhythm pharmacologic causes:

A

o Epinephrine o Isoproterenol o Ephedrine o Alcohol o Nicotine o Caffeine

294
Q

Bradycardia Sinus rhythm pharmacologic causes:

A

o Beta Blockers o Amiodarone o Propafenone o Lithium

295
Q

Regularly Irregular Pulse

A

→ Sinus Arrhythmia Pulsus Bigeminus → Pulsus Alternans Heart Block

296
Q

Irregularly Irregular Pulse

A

→ Atrial Fibrillation → Multifocal Atrial Tachycardia → Frequent Premature Ventricular Complexes

297
Q

→ Used in ancient times → A piece of glass with water inside, the rest of the air has been evacuated out to create a vacuum. → When pointed to a particular direction, the water would rush from one side to the other, hitting the bulb and makinga sound.

A

Water Hammer Pulse (Collapsing Pulse)

298
Q

 Water Hammer Pulse (Collapsing Pulse) Aortic Run-Off → Aortic Regurgitation

A

o Patent Ductus Arteriosus

299
Q

 Water Hammer Pulse (Collapsing Pulse) Aortic Run-Off → Aorto-Pulmonary Window

A

o Rupture of Sinus of Valsalva

300
Q

 Water Hammer Pulse (Collapsing Pulse) Cyanotic Congenital Heart Disease

A

→ Truncus Arteriosus → Pulmonary Atresia with Broncho-Pulmonary Collaterals → Tetralogy of Fallot with Blalock-Taussig Shunt

301
Q

 Twice Beating Pulse A. Anacrotic Pulse

A

→ Aortic Stenosis

302
Q

 Twice Beating Pulse B. Bisferiens Pulse

A

→ Aortic Regurgitation → Hypertrophic obstructive cardiomayopathy (HOCM) → Aortic Regurgitation and Aortic Stenosis → Hyperkinetic circulatory states → Patent ductus arteriosus

303
Q

 Twice Beating Pulse C. Dicrotic Pulse

A

→ Enteric fever → Cardiomyopathy → Hypovolemic Shock → Intra-arterial balloon pulsation

304
Q
A

Dicrotic pulse

305
Q
A

Bisferiens pulse

2 peaks before the dicrotic notch

306
Q
A

Bisferiens of HOCM

1 peak is taller, 2nd peak coincides with the dicrotic notch

307
Q

→ Variations in Left Ventricular Output Volume
→ Large wave from a large volume injected from the heart
→ Small wave with less volume injected from the heart
→ Result of left ventricular failure

A

Pulsus Alternans

308
Q

The pulse wave from the alternated (large and small) given the name?

A

“Pulsus Alternans”

309
Q
A

Pulsus alternans

310
Q

Normal inspiration in normal individuals blood pressure falls down but in __________, on inspiration blood pressure falls down exaggerated (more than 10 mmhg)

A

Pulsus Paradoxus

311
Q

Defined as Exaggeration of systolic fall of blood pressure by more than 10 mmhg.

A

PULSUS PARADOXUS

312
Q

On deep inspiration in a patient with tamponade:
o There is an increased flow in the right side of the heart
o There is also a pressure from the outside resulting in increased ventricular transmural pressure
o Shift of the septum from the right to the left to accommodate the increased blood volume
o The left ventricle becomes small because the inter-ventricular septum is pushed towards the left ventricle results to a exaggerated fall of systolic blood pressure.

A

PULSUS PARADOXUS

313
Q

CAUSES OF PULSUS PARADOXUS

A

 Cardiovascular
o Cardiac tamponade
o Effusive constrictive pericarditis
o Restrictive cardiomyopathy
o Massive pulmonary embolism
o Severe hypovolemic shock
 Pulmonary
o Chronic Obstructive Pulmonary Disease (COPD)
 Absence of Pulsus Paradoxus when there is presence of tamponade
o Atrial Septal defect (ASD)

314
Q

Type of pulsus paradoxus:

Due to Severe cardiac tamponade

A

Total Paradox

315
Q

Type of pulsus paradoxus:

o Due to positive pressure breathing with ventilators, Isorhythmic Atrioventricular Dissociation and Hypertrophic Obstructive Cardiomyopathy
o Means there is increased blood pressure during deep sleep inspiration

A

Reversed pulsus paradoxus

316
Q

VOLUME OF THE PULSE
 (delayed systolic peaking in a slow rising pulse)
o Caused by Aortic Stenosis

A

Pulsus Parvus et Tardus

317
Q

VOLUME OF THE PULSE:
o Caused by Aortic Regurgitation

A

Pulsus Magnus

318
Q

Hyperdynamic States (causes a high volume pulse)

A

o Pregnancy
o Thyrotoxicosis
o Beri-Beri
o Fever
o Paget’s Disease

319
Q

Radial pulse synchronicity can be abnormal in?

A

 Takayasu’s Arteritis
 Thoracic Outlet Syndrom
 Subclavian Steal Syndrome
 Chronic Atherosclerosis
 Coarctation of Aorta
 Dissection of Aorta

320
Q

CHARACTERISTIC PULSE IN VALVULAR HEART DISEASE:

AORTIC STENOSIS

A

 Pulvus Parvus et Tardus (slow rising pulse with delayed systolic peaking)
 Anacrotic Pulse
 Pulsus Alterans (left ventricular failure)
 Pulsus Bisferiens (severe aortic stenosis)

321
Q

CHARACTERISTIC PULSE IN VALVULAR HEART DISEASE:

AORTIC REGURGITATION

A

 Water Hammer Pulse
 Pulsus Bisferiens
 Pulsus Magnus

322
Q

Blood pressure in Aortic Regurgitation

A

Wide pulse pressure >70 mmHg

323
Q

Hill’s sign is seen in?

A

Aortic Regurgitation

324
Q

o Greater velocity of blood flow below lower limbs
o Greater gradient between posterior tibial and radial arteries

A

Hill’s sign

325
Q

Severity of Aortic Regurgitation:

60 mmHg

A

Severe

326
Q

Severity of Aortic Regurgitation:

40-60 mmHg

A

Moderate

327
Q

Severity of Aortic Regurgitation:

20-40 mmHg

A

Mild

328
Q

Other signs seen in aortic regurgitation:

A
  1. Landolfi’s Sign
  2. Becker’s Sign
  3. De Musset’s Sign
329
Q

Alternative dilation and constriction of the pupil

A

Landolfi’s Sign

330
Q

prominent retinal artery pulsation

A

Becker’s Sign

331
Q

Named after Alfred de Musset, a French philosopher who had a habit of synchronous nodding of head with his heartbeat

A

De Musset’s Sign

332
Q

Signs of Aortic Regurgitation in Head and Neck

A

 Corrigan’s sign
 Muller’s sign
 Minervini’s sign
 Logue sign

333
Q

dancing carotid pulsations

A

Corrigan’s sign

334
Q

pulsation of uvula

A

Muller’s sign

335
Q

pulsations of the tongue

A

Minervini’s sign

336
Q

pulsation of sterno-clavicular joint

A

Logue sign

337
Q

Signs of Aortic Regurgitation in Upper Extremity

A

 Locomotor brachialis
 Quincke’s pulse
 Palfrey’s sign

338
Q

dancing brachial pulsations

A

Locomotor brachialis

339
Q

pulsation of nail bed

A

Quincke’s pulse

340
Q

pistol shot over radial artery

A

Palfrey’s sign

341
Q

Signs of Aortic Regurgitation in Lower Extremity

A

 Hill’s sign
 Traube’s Sign
 Duroziez’s murmur

342
Q

pistol shot sounds over femoral artery

A

Traube’s Sign

343
Q

Three D’s of Duroziez’s murmur

A

→ Duroziez
→ Distal
→ Diastolic

344
Q

On placing the stethoscope in an inclined fashion, with the inclined towards the foot end, that is displaced distally, the patient will have a diastolic murmur. A systolic murmur will be normal because we are obstructing the artery with the stethoscope. However, if this murmur is also present in the diastolic phase, then this is called the __________ which is pathologic.

A

Duroziez murmur

345
Q

Signs of Aortic Regurgitation in Abdomen

A

 Rosenbach’s sign
 Gerhardt sign
 Dennision’s sign

346
Q

pulsation of liver

A

Rosenbach’s sign

347
Q

pulsation of spleen

A

Gerhardt sign

348
Q

pulsation of the cervix

A

Dennision’s sign

349
Q

Case: A 78 year old male presents complaining of dyspnea on exertion and exertional angina for the past 3 months. On exam, you note a 2/6 systolic murmur when your stethoscope is placed in the apical area. Which of the following is the correct murmur?

 Step 1: Know if it is diastolic or systolic:

A

Systolic

350
Q

Case: A 78 year old male presents complaining of dyspnea on exertion and exertional angina for the past 3 months. On exam, you note a 2/6 systolic murmur when your stethoscope is placed in the apical area. Which of the following is the correct murmur?

Step 2: Know the location of the murmur:

A

Apical

351
Q

 Step 1: Know if it is diastolic or systolic: Systolic
 Step 2: Know the location of the murmur: Apical

Basing on the picture above and the given data, it is now obvious that the murmur is of the _____ area.

A

mitral area

352
Q

the only time you hear this is when blood flows across the mitral valve when the left atrium is trying to throw blood into the ventricles as it fills that ventricle during diastole

A

Mitral stenosis

353
Q

blood ejects out of the left ventricle and has the potential of going back across the mitral valve if it will regurgitate back to the left atrium which is called a?

A

mitral regurgitation

354
Q

Systolic Murmurs

A

Mitral Regurgitation

Tricuspid Regurgitation

Aortic Stenosis

Pulmonic Stenosis

355
Q

Diastolic murmurs

A

Mitral Stenosis

Tricuspid Stenosis

Aortic Regurgitation

Pulmonic Regurgitation

356
Q

Mnemonics: MRS. ASS

A

→ Mitral Regurgitation – Systolic
→ Aortic Stenosis – Systolic

357
Q

Murmurs are louder during:

A

→ Right sided murmurs in Inspiration
o RINspiration
→ Left sided murmurs in Expiration
o LEXpiration

358
Q

o heart becomes hypertrophied and the septum bulges and blocks the outflow tract
o normally more blood flow across the valve or into the heart makes the murmur louder but in __________, more blood or pressure in the heart actually pushes the septum back to its normal physiologic condition and re-opens the outflow tract obstruction

A

Hypertrophic Obstructive Cardiomyopathy (HOCM)

359
Q

o prolapsing and blocking normal blood flow
o more blood going to the heart and returning the mitral valve leaflets back into their normal position
o you don’t hear the midsystolic click that goes along with the mitral valve prolapse

A

Mitral Valve Prolapse (MVP)

360
Q

→ Done every time you increase preload to get a louder murmur during auscultation
→ more blood is going to flow through the heart and more blood flows over a valve whether it is stenotic or regurgitant

A

Maneuvers: Squatting / Leg raising

361
Q

HOCM – less blood flow, less blood is there to push the septum back to its normal position so the sounds are louder or worse

A

Decreased preload

362
Q

MVP – less blood to return the mitral valves back to their normal position

A

Decreased preload

363
Q

→ Used to decrease decrease preload
→ Tell the patient bear down and pretend like having a bowel movement
→ this prevents blood from returning to the heart aka decreases preload

A

Maneuver: Valsava

364
Q

means more pressure is being exerted upon the left ventricle as it tries to eject the blood out of the heart

A

Increased afterload

365
Q

→ used to increase afterload
→ tell the patient to squeeze their left hand

A

Maneuver: Hand grip

366
Q

regurgitant murmur becomes louder

A

Increased afterload

367
Q

HOCM and MVP on the other hand has softer murmurs

A

→ in increased afterload, HOCM and MVP have more pressure propping the septum and those valve leaflets back into its normal position respectively
→ softer HOCM and MVP means that murmur is getting better; you don’t hear it as much because there’s less mechanical issue since there is more pressure returning to the heart to its physiologic position

368
Q

achieved by using a drug called amyl nitrate

A

Decreased afterload

369
Q

In HOCM, because less pressure is forcing that septum back into its normal position, the outflow tract gets obstructed and murmur gets worse or louder

A

Decreased afterload

370
Q

In MVP, because less pressure is being forced upon those mitral valve leaflets, the mitral valve is going to prolapse more and get worse or louder

A

Decreased afterload

371
Q

Cresendo-Decresendo

A

AORTIC STENOSIS

372
Q

Present in Old patients (70 years old or older)

A

AORTIC STENOSIS

373
Q

SAD- Syncope, angina, dyspnea

A

AORTIC STENOSIS

374
Q

Calcified valve- deposits of calcium crystal present around the aortic valve resulting to decrease in space

A

AORTIC STENOSIS

375
Q

Radiates to the carotids

A

AORTIC STENOSIS

376
Q

Holosystolic- same volume throughout; continuous murmur

A

MITRAL REGURGITATION

377
Q

History of Rheumatic fever

A

MITRAL REGURGITATION

“Rheu-mitral”

378
Q

Radiates to the axilla

A

MITRAL REGURGITATION

379
Q

Holosytolic- murmur between S1 and S2

A

TRICUSPID REGURGITATION

380
Q

History of Intravenous Drug Abuse-

A

TRICUSPID REGURGITATION

“Want to TRI some drugs?”

381
Q

damage is primarily on the tricuspid valve due to presence of pathogens in the blood due to intravenous drug abuse

A

TRICUSPID REGURGITATION

382
Q

in the Philippines, common cause of Tricuspid regurgitation is?

A

severe pulmonary hypertension and rheumatic heart disease (due to infective endocarditis)

383
Q

Opening snap- hard to hear

A

MITRAL STENOSIS

“Operating System is MicroSoft” (the OS is MS)

384
Q

Family History of sudden cardiac death

A

HYPERTROPHIC OBSTRUCTIVE MYOPATHY

385
Q

Similar to other murmurs- maneuvers give it away

A

HYPERTROPHIC OBSTRUCTIVE MYOPATHY

386
Q

HYPERTROPHIC OBSTRUCTIVE MYOPATHY with decreased preload:

A

→ Louder (worse) with decreased pre-load-
o less blood going to the heart, septum can push over more and obstruct more which means the murmur is louder

387
Q

HYPERTROPHIC OBSTRUCTIVE MYOPATHY with decreased afterload:

A

→ Louder (worse) with decreased afterload-
o less pressure forcing the septum over which means the septum is going to block the outlet so the murmur gets louder

388
Q

HYPERTROPHIC OBSTRUCTIVE MYOPATHY with increased preload:

A

→ Softer (better) with increased pre-load-

o Have the patient do some leg raising or squatting so more blood goes back to the heart. More blood will force the septum push into the side and make the murmur better or softer

389
Q

HYPERTROPHIC OBSTRUCTIVE MYOPATHY with increased afterload:

A

→ Softer (better) with increased afterload-
o have the patient do some handgrip of squeeze their left hand making the heart pump against a greater pressure which means more pressure is going to force the septum back to its normal position which makes it sound softer or better

390
Q

 Midsystolic click
o Young woman with psychiatric history- young women who are anxious and depressed
o Myxomatous valve disease

A

MITRAL VALVE PROLAPSE

“to win MVP, your team has to click”

391
Q

<60- junctional rhythm

A

Tachycardia and or Ventricular Tachycardia

392
Q

below 60 but not less than 40 bpm

A

Sinus bradycardia-

393
Q

o Below 40 bpm

A

2nd degree AV block or complete heart block

394
Q

For patients experiencing syncopal attacks/ near syncope, dizziness, and HR is below 60/min, request for a ________ to find out if you are dealing with a pathologic type of bradyrrythmia

A

holter monitor

395
Q

Atrial fibrillation- can be seen in patients with ?

A

Mitral Stenosis, Dilated Cardiomyopathy, Hyperthyroidism

396
Q

can be seen in young normal individuals; no treatment needed

A

Sinus arrhythmia

397
Q

A midsystolic nonejection sound (C) occurs in ______and is followed by a late systolic murmur that crescendos to the second heart sound (S2).

A

mitral valve prolapse

398
Q

_________ decreases venous return; the heart becomes smaller; C moves closer to the first heart sound (S1), and the mitral regurgitant murmur has an earlier onset.

A

Standing

399
Q

With prompt ________, venous return and afterload increase; the heart becomes larger; C moves toward S2; and the duration of the murmur shortens. The systolic murmur of hypertrophic obstructive cardiomyopathy behaves similarly.

A

squatting

400
Q

Peripheral cyanosis:

A

Congenital Heart Disease/Heart Failure

401
Q

Splinter Hemorrhages:

A

Infective endocarditis

402
Q

Xanthomata:

A

Hypercholesterolemia

403
Q

Tar Staining:

A

Smoking

404
Q

Finger Clubbing:

A

Infective endocarditis and Congenital heart disease

405
Q

Schamroth’s window test:

A

lost with finger clubbing

406
Q

Capillary refill time:

A

less than 2 seconds is normal

407
Q

Assess for radio-radial delay:

A

aortic coarctation

408
Q

Assess for a collapsing pulse:

A

aortic regurgitation

409
Q

Auscultate the carotid arteries to detect bruits

A

o Patient should hold their breath upon auscultation
o Palpate the carotid pulse if no bruits identified

410
Q

Xanthelasma and Corneal Arcus:

A

Hyperlipidemia

411
Q

Conjuctival Pallor:

A

Anemia

412
Q

Radiation of an ejection systolic murmur is often heard in ?

A

aortic stenosis

413
Q

Aortic murmurs- (patient sits up)
o will get louder with ______

A

expiration

414
Q

Mitral murmurs- (rolls on left side)
o Will get louder with ______
o Auscultate the _____ listening for radiation of a mitral murmur

A

expiration

axilla

415
Q

Assess for sacral edema-

A

o Right ventricular failure

416
Q

 Assess for pedal edema

A

o Right ventricular failure

417
Q

CORONARY ARTERY DISEASE:

Cerebrovascular

A
  • Ischemic stroke
  • Transient ischemic attack
418
Q

CORONARY ARTERY DISEASE:

Coronary artery

A
  • Myocardial infarction
  • Angina
419
Q

CORONARY ARTERY DISEASE:

Peripheral

A
  • Intermittent claudication
  • Rest pain
  • Gangrene
  • Necrosis
420
Q

supplies the anterior portion, the
atrioventricular septum and the apex

A

left anterior descending artery

421
Q

supplies the lateral portion of the heart

A

Left main coronary artery

422
Q

→ supplies the inferior posterior portion of the
heart
→ supplies right portions of the heart as well as
the inferolateral portions

A

Right coronary artery

423
Q

Generally refers to atherosclerosis of the
coronary arteries that may result in significant
obstruction to coronary blood supply leading to
myocardial ischemia.

A

Coronary artery disease

424
Q

Refers to a condition in which there is an
imbalance between the oxygen supply and
oxygen demand of the myocardium usually due to
severe fixed or dynamic obstruction of the
myocardial blood supply, or an increase in
myocardial oxygen requirements or both.

A

Myocardial ischemia

425
Q

most common cause of life threatening illness

A

ISCHEMIC HEART DISEASE

426
Q

Major determinants of myocardial oxygen demand

A

• heart rate
• myocardial contractility
• myocardial wall tension (stress)
In managing patients with ischemia, reducing the
determinants will improve blood supply.

427
Q

Oxygen carrying capacity of the blood

A
  • Inspired oxygen
  • pulmonary function
  • hemoglobin concentration
428
Q

3 sets of coronary arteries regarding coronary
resistance flow

A

• large epicardial arteries (R1)
• prearteriolar vessels (R2)
• arteriolar and intramyocardial capillary vessel
(R3)

429
Q

Occurs when too much cholesterol, triglyceride or
lipid substances are deposited in the arterial wall.

A

ATHEROSCLEROSIS

430
Q

Obstruction is significant if more than
___% involving the left vein, also Left circumflex
and right coronary artery obstruction is significant
if more than ____%.

A

Obstruction is significant if more than
50% involving the left vein, also Left circumflex
and right coronary artery obstruction is significant
if more than 70%.

431
Q

But a _____% luminal obstruction
is enough to have ischemia, at rest is okay but if
you increase workload that can result to
myocardial ischemia.

A

50%

432
Q

major site of
atherosclerotic disease

A

Epicardial coronary arteries

433
Q

sub intimal collections of
fat, smooth muscle cells, fibroblasts and
Intracellular matrix

A

atherosclerotic plaque

434
Q

CASCADE OF MECHANISMS AND
MANIFESTATIONS OF ISCHEMIA

A
  • endothelial and microvascular dysfunction
  • decreased sub endocardial perfusion
  • altered metabolism/abnormal ST segment
  • micro-infarction/myocardial fibrosis
  • diastolic dysfunction
  • decreased segmental perfusion
  • regional wall motion
  • systolic dysfunction
435
Q

o Clenched fist
o squeezing
o Central substernal chest discomfort

A

Levine’s sign:

436
Q

Normal ABI (ankle-brachial index)

A

< 0.8

437
Q

HOW TO
OBTAIN ABI:

A

get systolic pressure of
dorsalis pedis and systolic pressure or
brachial artery.
Usually, LE would have higher systolic
blood pressure compared to UE. For
example: systolic pressure sa imo upper
arm is 100, the systolic pressure in your
dorsalis pedis would be above 100 —
normal
In opposite, dorsalis pedis systole is 90 and
brachial index is above 100 or 110, that’s
significant. You have presence of arterial
occlusive disorder.

438
Q

Cause of Increase demand for Oxygen by the heart
muscle

A

→ increase in heart rate
→ increase in contraction
→ increase in blood pressure

439
Q

Cause of inadequate supply of Oxygen to the heart

A

Either due to:

1) Atherosclerosis
2) Spasm of the coronary artery
- Which is the Prinzmetal angina

440
Q

Emergency medications for angina pectoris

A

• Nitroglycerin gr 1/150 tablet
• Isordil 5 mg
→ one tablet sublingual
→ Iban na ginahatag spray. You give that every 5
minutes. Mas dasig ang spray. Diri sa
Philippines, indi available ang spray.
→ Butang mo under the tongue. After 5 minutes,
stop it. After 5 minutes, repeat it if may chest
pain pa. After 5 minutes, liwat. After 3 tries and
the px is still having chest discomfort, tell the px
“go to the hospital and probably you’re dealing
already with acute coronary syndrome.

441
Q

Warning to patients who take Emergency Nitrates

A

Headache

Hypotension

442
Q

Anti-Anginal Agents

A

Nitrates

Beta blocker

Calcium channel blocking agent

443
Q

Administration of *trace amount of molecule, *labeled with radionuclide, to provide diagnostic information and assess therapeutic response long before changes can be seen at anatomical level

A

Nuclear Medicine

444
Q

Simply an unstable nuclide or nuclear species that undergoes radioactive decay.

A

Radionuclide

445
Q

Radionuclide signal is for _____detection

A

external

446
Q

the biological distributor

A

Pharmaceutical

447
Q

= Radiopharmaceutical

A

Suitable Radionuclide + Specific Pharmaceutical

448
Q

detects or captures what is happening with the organ of interest because it traces the radiation being emitted by the unstable radionuclide; This produces the images

A

Gamma camera

449
Q

Unstable nuclides → Stable

A

Radioactive Decay

450
Q

→ A device which narrows a beam of particles or waves
→ To narrow can mean either to cause the direction of motion to become more aligned in specific direction or to cause the spatial cross section of the beam to become smaller
→ It also removes the energy that is not needed and not in the path
→ It only absorb the specific energy to produce the specific structure or images

A

“Collimator”

451
Q

Gamma emissions must be of suitable energy between __________ (ideal of gamma camera)

A

50-200 KeV

452
Q

Desirable Characteristics of Radionuclide

A
  1. Gamma emissions must be of suitable energy between 50-200 KeV (ideal of gamma camera)
  2. Effective half-life and bio distribution is long enough and suitable for its intended use
  3. Do not emit particulate particle
453
Q

Nuclear Medicine Imaging
 Two broad classes:

A

→ Single Photon Emission Tomography (SPECT)
→ Positron Emission Tomography (PET)

454
Q

It is similar to a conventional nuclear medicine planar imaging using a gamma camera (scintigraphy) but is able to provide true 3D information. This information is typically presented as cross-sectional slices through the patient but can be freely reformatted or manipulated as required.

A

SPECT Imaging
 Single Photon Emission Computer Tomography

455
Q

Radionuclides use that decay by positron emission.

A

Positron Emission Tomography

456
Q

one particular angle

A

Planar

457
Q

collected from many angles around the patient

A

Tomographic

458
Q

depth information

A

Cross-sectional images

459
Q

positive electron released from the nucleus wherein it interacts with the electrons of the tissue. They undergo annihilation and produce energy wherein the gamma camera captures.

A

Positron

460
Q

Advantages of Functional Imaging (Scintigraphy)

A

 Early diagnosis
 Increased test sensitivity
 Directly demonstrates effects of therapy
 Complements anatomical imaging

461
Q

Indications of MPI (MYOCARDIAL PERFUSION IMAGING)

A
  1. Suspected with Coronary artery disease (CAD)
  2. Symptomatic patients with pretest probability of CAD 15%-85% with LVEF of >50%; or in patients unable to exercise adequately with ECG characteristic such as Left bundle branch block.
  3. Pretest probability 66-85% for CAD or LVEF <50% without typical of angina.
  4. Patients with known CAD diagnosed by an anatomical imaging modality in whom the functional significance of the stenosis should be determined.
  5. To exclude ischemia as a trigger for rhythm disorders.
  6. Patients with persistent symptoms after revascularization procedures.
  7. Patients with >3 risk factors who will undergo high risk surgery.
  8. To assess viability of dysfunctional myocardium; sometimes followed by viability testing with FDG.
  9. Patients with Agatston calcium score of >400 and any risk.
462
Q

Contraindications of MPI

A

 Pregnancy
 Unstable angina pectoris and recent Myocardial Infarction (MI) less than 4 days are contraindicated to stress MPI.

463
Q

O2 supply below the metabolic requirements because of inadequate blood circulation cause by coronary stenosis.

A

Myocardial Ischemia

464
Q

Necrosis of myocardial tissue as a result of coronary occlusion.

A

Myocardial Infarction

465
Q

Necrosis involves all layers from endo to epicardium.

A

Transmural Infarction

466
Q

Necrosis involves only muscles adjacent to endocardium.

A

Subendocardial Infarction

467
Q

late result of infarction.

A

Myocadial scar

468
Q

Chronic ischemia with decreased blood flow and down regulation of contractility. Reversible with restoration of blood flow. No perfusion on rest imaging poor ventricular contraction. Improved perfusion given a long recovery between rest-rest imaging or delayed reinjection T1 201.

A

Hibernating Myocardium

469
Q

myocardium with persistent contractile dysfunction despite restoration of perfusion after a period of ischemia; usually improves with time. Normal perfusion imaging. Poor ventricular contraction. Uptake by FDG metabolic imaging.

A

Stunned Myocardium

470
Q

2 clinical reasons for selecting MPI:

A

→ The desirability of highly sensitive test for detecting ischemia over time bec of the presence of coronary angioplasty or restenosis.
→ Extent & severity of ischemia of potential residual ischemia may help govern the indication for repeat intervention.

471
Q

MPI Basic Concepts

A

 A tracer must be delivered to the myocardium
 A viable, metabolically active myocardial cells must be present to localize the tracer
→ HEALTHY = (+) UPTAKE
→ INFARCTED = (-) UPTAKE

472
Q

Myocardial Perfusion agents

A

→ Thallium
→ Technetium (Tc99m) + Sestamibi
→ Technetium (Tc99m) + Tetrosfosmin

473
Q

Infarct Myocardium Scintigaphy agents

A

Technetium (Tc99m) Pyrophosphate

474
Q

Radionuclide Ventriculography

A

Technetium (Tc99m) + RBC

475
Q

Biokinetic properties similar but not identical to potassium.

A

Thallium (TL)

476
Q

Images immediately after injury- flow dependent initial distribution- regional myocardial blood flow.

A

Thallium (TL)

477
Q

Delayed images (2-24 hours)- distribution of K+ pool- myocardial viability

A

Thallium

478
Q

Principle is that it is not static over time

A

Thallium

479
Q

 Redistribution
→ Filling in of the myocardial perfusion defect occurring shortly (between 3-5 hours) after injection is related to 2 factors.

A

Thallium

480
Q

 Negative charge cross the membrane and affinity with mitochondria.
 Distribution remained relatively fixed over time, reflecting the distribution of myocardial blood flow at the time of injection and is frozen over time- can be imaged for several hours.
 2 separate injections are required (during rest and exercises)

A

Tc-99m SESTAMIBI

481
Q

Manifestations of Myocardial Ischemia:

EKG

A

→ Ion flux across cell membrane is impaired, therefore produces ST segment depression.

482
Q

Manifestations of Myocardial Ischemia:

Perfusion Scintigraphy

A

→ Decrease in regional flow produces cold defect area on scintigraphy

483
Q

Manifestations of Myocardial Ischemia:

Radionuclide Ventriculography

A

→ Regional wall motion abnormality or fall in left ventricular ejection fraction
More on functional imaging; Way better than 2d-echo; Invasive and very expensive.

484
Q

Pharmacologic Stress Study
 Indications:

A

→ Inability to exercise (can’t walk, obese, pain in the body)
→ Inadequate exercise heart rate or workload
→ Left bundle branch block or ventricular pacemakers

485
Q

→ An indirect vasodilator
→ Blocks cellular absorption of Adenosine increase concentration of Adenosine (vasodilation)

A

Dipyridamole or persantine

486
Q

Dipyridamole Infusion Protocol

A

o 0.142 mg/kg/min is infused for 4 mins.
o Maximal vasodilation after the 4th min
o Tracer is injected after the 4th min

487
Q

Side Effects of Dipyridamole or persantine

A

o HA, flushing, nausea, angina
o Reversed quickly by IV Aminophylline which blocks Adenosine receptors

488
Q

Ischemia may be induced by __________ (inc. bld flow in NL CA steals bld away from vasc. bed supplied by stenotic CA

A

CORONARY STEAL

489
Q

an endogenous vasodilator

A

Adenosine

490
Q

Adenosine Infusion Protocol

A

o 40 ug/kg/min is infused via infusion pump for 6 minutes
o Radiotracer is injected on the 5th minute
o Has more potent and consistent vasodilatory effect than Dipyridamole

491
Q

Side effects of adenosine:

A
  • more common (75%)
    o HA, nausea, flushing, chest pain, AV blocks
    o Reversed instantaneously by terminating the infusion
492
Q

→ Sympathomimetic agent increase myocardial oxygen demand by increasing HR and BP even flat in bed
→ Used for patients with contraindication to Dipyridamole or Adenosine (BA, COPD, patients taking Xanthine derivatives and those who have consumed caffeine)

A

Dobutamine

493
Q

 The computer acquires imaging data synchronous with the ECG R wave
 Arrythmic beats are filtered out of the data collection cycle
 The R-R interval is usually divided into 8 – 16 frames
 Enable to display sequential gated images in a cinematic display to assess tracer distribution, regional wall motion, Ejection Fracton, wall thickening.
 It permits 3D display of the myocardium

A

Gated SPECT Imaging Acquisition

494
Q

 IMAGE RECONSTRUCTION
 Filtered back projection
 Filtering – to correct for reconstruction artifacts, suppress noise and enhance image quality

A

Tomo SPECT Imaging

495
Q

short axis view

A

Apex to base

496
Q

horizontal/ long axis view- from inferior going upward

A

Coronal view

497
Q

from septum to lateral- vertical long axis view

A

Sagittal cut

498
Q

Gold standard in viability study-

A

PET

499
Q

Polar Map Circumferential Profiles
→ Advantage

A

o provides graphic display of the relative distribution of the tracer uptake in the myocardium and the degree of perfusion abnormality in comparison to a normal reference data base

500
Q

Polar Map Circumferential Profiles disadvantage:

A

o unable to distinguish between true perfusion defects and artifacts

501
Q

Glucose analog transported into the cell by glucose transporter (GLUT) express on the cell membrane, phosphorylated by the enzyme hexokinase and trapped. (Half-life 1 hour and 10 mins)

A

Fluorodeoxyglucose (FDG)

502
Q

GOLD STANDARD study to detect viable myocardium considered for revascularization in order to predict outcome benefit and for correct stratification and guide further treatment.

A

Positron Emission Tomography (PET)

503
Q

 Assess regional and global wall motion
 predictor of long term outcome of MI
 Cardiac chamber volumes and morphology
 distinguish systolic from diastolic CHF
 Ventricular systolic and diastolic function indices including LV and RV EF-prognosis value.
 evaluation of patient undergoing chemotherapy in monitoring cardiotoxicity induced by chemo agents.

A

Equilibrium Radionuclide Angiocardiography

504
Q

 To calculate LV and RV EF. (More on RV EF)
 Assess wall motion abnormality
 Quantify left to right cardiac shunt.
 Measure cardiac output and absolute ventricular chamber volume.
 Evaluate diastolic volume.

A

First Pass Radionuclide Ventriculography

505
Q

All of the ff are important in xray
A. Projection
B. Inspiration
C. Rotation
D. artifact

A

B. Inspiration

506
Q

A good inspiraroty film should be:
A. Below the 9th rib
B. Above the 10th rib
C. At the level of 12th rib
D. Equidistant clavicles

A

B. Above the 10th rib

507
Q

pulmonary artery supply deoxygenated blood in this chamber?
A. R atrium
B. R ventricle
C. L atrium
D. L ventricle

A

B. R ventricle

508
Q

Pulmonary veins drain blood into what chamber?
A. RA
B. LA
C. RV
D. LV

A

B. LA

509
Q

Which chamber does the blood to the aorta come from?
A. RA
B. LA
C. RV
D. LV

A

D. LV

510
Q

Projections of chest heart radiograph?(ang major ata na ginagamit)
A. PA
B. PA lateral
C. AP
D. AP lateral

A

A. PA

511
Q

What projection will show retrocardiac fullness
A. PA
B. AP
C. Lateral
D. Oblique

A

C. Lateral

512
Q

most posteriorly and superiorly located in chest PA xray

a. RA
b. LA
c. RV
d. LV

A

b. LA

513
Q

What cardiac chamber forms the right cardiac border in PA view?
A. Right atrium
B. Left atrium
C. Right ventricle
D. Left ventricle

A

A. Right atrium

514
Q

It forms the left border of the heart in chest PA
A. Left ventricle
B. Left atrium
C. Right Ventricle
D. Right atrium

A

A. Left ventricle

515
Q

Normal cardiothoracic ratio on PA–

A

0.5

516
Q

signs of cardiomyopathy-

A

water bottle sign

517
Q

Most common cardiomyopathy
A. Restricted cardiomyopathy
B. Constricted cardiomyopathy
C. Hypertrophic cardiomyopathy
D. Dilated cardiomyopathy

A

D. Dilated cardiomyopathy

518
Q

Which is not a mogul of the heart at the left mediastinal outline?
A. Aortic knob
B. Pulmonary artery
C. Left atrial appendage

D. Left hemidiaphragm

A

D. Left hemidiaphragm

519
Q

Heart mogul commonly unseen but when seen denotes prominence/enlargement.

A

Ans. Left atrial appendage

520
Q

Not true in ABI
A. most powerful indicator of LVH
B. Ankle>Branchial
C. Diagnosis fir peripheral art. Disease
D. Normal 0.70

A

D. Normal 0.70

521
Q

Which is not true about A Wave - ang answer ko lang ang A wave ha - para atrial contraction that pushes blood from RA to RV -may choice to nga wave after P wave( confirm lng kung amo ni ang answer)

(INCOMPLETE CHOICES)

A
522
Q

Which is true about V wave?

A

Ans. Ventricular filling

523
Q

Not have LV heave
A. Mitral stenosis
B. Aortic stenosis
C. Mitral regurgitation
D. Aortic regurgitation

A

A. Mitral stenosis

524
Q

RV heave -

A

atrial septal defect

525
Q

Pulsus parvus et tardus

A
  • Aortic stenosis
526
Q
A

Cardiac Tamponade

527
Q
A

Aortic Regurgitation

528
Q
A

LV Systolic dysfunction

529
Q

Soft S1 sound

A

Coronary Artery Disease

530
Q

Loud Second Heart Sound

A

Hypertension

531
Q

Mid systolic clicks

A

Mitral Valve Prolapse

532
Q

hypertrophic cardiomyopathy

A

increased murmur when standing

533
Q
A

crescendo decrescendo midsystolic murmur radiating to neck

534
Q
A

holosystolic murmur at 2nd ICS

535
Q
A

diastolic blowing murmur, located at 2nd and 3rd ICS

536
Q

PDA

A

continuous murmur at pulmonic area

537
Q

Ventricular septal defect

A

Holosystolic murmur heard best at 3rd-4th midclavicular ics

538
Q

18 yo female, chest discomfort. LV heave @ 6th ICS LAAL, holosystolic murmur @ 4th & 5th ICS MCL. Diagnosis
A. Mitral regurgitation
B. VSD
C. ASD
D. Hypertrophic cardiomyopathy

A

B. VSD

539
Q

Mitral Regurgitation -

A

radiates to the axilla

540
Q

40 yo male (+) dyspnea, bipedal edema, RV heave, apex at 5th ICS LMCL, grade3/6 systolic murmur @ 3rd and 4th ICS left parasternal, diastolic rumbling murmur at apex. Give the diagnosis:
A. Mitral regurgitation and tricuspid regurgitation
B. Mitral Valve Prolapse and Aortic Regurgitation
C. Tricuspid Stenosis and Mitral Regurgitation
D. Aortic Regurgitation and Mitral Regurgitation

A

C. Tricuspid Stenosis and Mitral Regurgitation

541
Q
A

True

542
Q

HOLTER recorder basically used to detect ischemic diseases and cardiac arrhythmia.

(True or False)

A

True

543
Q

Radiology does not include the shadow of the heart.

A

-False

544
Q

Doppler Flow shows color flow directions of blood flow and shunts

(True or False)

A

True

545
Q

Color coding is used in the direction of the blood flow.

(True or False)

A

True

546
Q

Red color indicate blood flow away from the tracer. -

(True or False)

A

False

547
Q

Holter is used to detect asymptomatic cardiac arrthymia-

(True or False)

A

True

548
Q

Holter can be used to identify/detect asymptomatic ST segment elevation -

(True or False)

A

True

549
Q

Made up of smooth muscle cells.
A. Media
B. Intima
C. Adventitia
D. Pericytes

A

A. Media

550
Q

Consists of loose extracellular matrix -

A

Adventitia

551
Q

Monolayer of Endothelial cells
A. Media
B. Intima
C. Adventitia
D. Pericytes

A

B. Intima

552
Q

Forms an interface between tissue and blood component.
A. Extracellular matrix
B. Intima
C. Endothelium
D. Capillary

A

C. Endothelium

553
Q

Type of vessel that has few layers of media:

A

Vein

554
Q

Type of blood vessel that is commonly affected by atherosclerosis.
A. Capillaries
B. Veins
C. Medium-sized arteries

D. Elastic arteries

A

C. Medium-sized arteries

555
Q

Type of vessel that has prominent tunica media

a. Veins
b. Capillary
c. Medium size artery
d. Elastic artery

A

c. Medium size artery

556
Q

Embryonic origin of smooth muscle of the upper body parts. -

A

neural crest

557
Q

Embryonic origin of smooth muscle of lower body parts. -

A

Somites

558
Q

Reactive oxygen species produced by endothelium:
A. Phosphorylation of myosin light chain
B. Oxidative stress
C. Responsive oxygenation
D. Sympathetic activation

A

B. Oxidative stress

559
Q

It is used to assess noninvasively endothelial dysfunction.
A. Methacholine
B. Doppler study
C.
D.endothelin

A

B. Doppler study

560
Q

It is an agonist used to assess endothelial function invasively.

A

A. Methacholine*

561
Q

Normal endothelium function after clinical assessment
A. Decrease blood flow
B. Paradoxical vasoconstriction
C. less than 10%
D. Reactive hyperemia

A

B. Paradoxical vasoconstriction

562
Q

NO is associated with what type of ANS

a. sympathetic
b. parasympathetic
c. nonadrenergic

A

nonadrenergic

563
Q

A potent vasoconstrictor that endothelium produce
A. NO
B. Prostacyclin
C. Endothelin

A

C. Endothelin

564
Q

What is the principal function of vascular smooth muscle cells
A.
B. To maintain vessel tone
C.
D. Improve blood flow

A

B. To maintain vessel tone

565
Q

Not a determinant of aortic pressure
A. Peripheral Vascular Resistance
B. Degree of stiffness of arteries
C. Hyperventilation
D. Volume of blood on onset of ejection

A

C. Hyperventilation

566
Q

Length of muscle before the onset of contraction?
A. Afterload
B. Contractility
C. Wall stress
D. Preload

A

D. Preload

567
Q

Nuclear Medicine
A. Used unsealed radionuclide for … theranostic
B. Uses sealed radionuclide for… Theranostic
C. pure therapeutic
D. Uses safe radionuclide? (lipat ko kay kalaba)

A

A. Used unsealed radionuclide for … theranostic

568
Q

The advantages of functional imaging (scintigraphy):
A. Early diagnosis, increased test sensitivity and complements anatomical imaging

B. Indirectly demostrates effects of therapy

C.
D. AOTA

A

A. Early diagnosis, increased test sensitivity and complements anatomical imaging

569
Q

Basic principle of nuclear medicine
A. Radiotracer must be delivered to the myocardium with the viable myocardium extracting the tracer
B. Radiotracer must be delivered to the myocardium with the non-viable myocardium extracting the tracer (Only 2 choices were given)

A

A. Radiotracer must be delivered to the myocardium with the viable myocardium extracting the tracer

570
Q

Clinical Application of Myocardial Perfusion test?
A. Diagnosis of Myocardial Ischemia
B. To know location, duration and severity of Myocardial Ischemia
C. Planning for PTCA by identifying lesions.
D. AOTA

A

D. AOTA

571
Q

Indication of exercise stress imaging?
A. Inability to exercise
B. Inadequate exercise heart rate or workload
C. Left bundle branch block
D. Aota

A

D. Aota

572
Q

Contraindications in taking Adenosine and Dypiridamole
A. Asthma
B: 2nd or 3rd deg AV block
C. Systolic BP of 90 or less
D. AOTA

A

D. AOTA

573
Q

Contraindications in using Dobutamine.
A. Recent acute coronary syndrome
B. Severe Aortic stenosis
C. Left ventricular outflow tract obstruction
D. All of the above

A

D. All of the above

574
Q

Adenosine is a potent vasodilator that increases cgmp and camp-

(True or False)

A

True

575
Q

Perfusion scintigraphy: decrease regional blood flow produces cold defect in areas of scintigraphy. -

TRUE or FALSE

A

TRUE

576
Q

True or false Mechanism of ischemia Radionuclide ventriculography: regional wall motion abnormality or fall in left ventricular ejection fraction.

(TRUE or FASLE)

A

TRUE

577
Q

True or false: perfusion-like scintigraphy detect abnormal motion cold defect TRUE
85. True or false Adenosine is a potent vasodilator that forms adenyl cyclase and camp

(TRUE or FALSE)

A

TRUE

578
Q

True or False Dipyridine block the cellular uptake of adenosine

TRUE or FALSE

A

TRUE

Medicine 1 (7 decks)

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