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Cardiopulmonary > Test 1 > Flashcards

Test 1 Flashcards

1
Q

why is the heart a hollow muscular organ?

A

It needs to be hollow and muscular to be able to pump blood through.

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2
Q

Where is the heart located in the body?

A

middle thoracic cavity.

2/3 of its mass is found to left of midline of sterum.

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3
Q

What surrounds the heart?

A

pericardial sac

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4
Q

What forms the apex of the heart?

A

It is formed by the tip of left ventricle

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5
Q

What forms the base (top) of the heart?

A

Approximately at the level or the 2nd costal cartilages

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6
Q

What makes up the anterior surface of the heart?

A

It consists primarily of the right ventricle

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7
Q

What are the dimensions of the heart?

A

5 inches (12cm) long
3 1/2 inches (9cm) wide
2 1/2 inches (6cm) thick
About the size of a fist

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8
Q

What are the 4 chambers of the heart?

A

Upper two chambers: Right and Left Artria

Lower two chambers: Right and Left Ventricle

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9
Q

What chamber of the heart are considered “work horses”?

A

Left ventricle

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10
Q

What moves venous blood to the pulmonary circulation?

A

Right ventricle. Blood goes to lungs for gas exchange.

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11
Q

What moves arterial blood to the systemic circulation?

A

Left ventricle. Blood is pumped everywhere except lungs

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12
Q

What completely separates the right and left atria?

A

Interatrial septum

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13
Q

What is the depression called in the interatrial septum that is a remnant of foramen ovale?

A

Fossa ovalis

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14
Q

True or False.

The atria are thin-walled, less muscular chambers that receive blood.

A

True

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15
Q

Failure of the foramen ovale to close prior to birth results in?

A

patent foramen ovale

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16
Q

Term used to describe an interatrial septum that fails to develop properly is called?

A

Atrial septal defect

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17
Q

What do the right and left ventricles do?

A

pump blood to the lungs and systemic circulation

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18
Q

What separates the right and left ventricles?

A

interventricular septum

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19
Q

What are the most common congenital cardiac abnormalities?

A

VSD-ventricle septal defects. Found in 30-60% of all new borns with a congenital heart defect, or about 2-6 per 1000 births.

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20
Q

How can VSD (ventricle septal defect) be acquired?

A

They can be formed within a few days after a myocardial infarction due to macrophae remodeling of dead heart tissue before scar tissue forms.

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21
Q

How does the heart pump blood?

A

it must contract forcefully and overcome aortic and pulmonary pressures in order to pump blood.

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22
Q

How much blood does each ventricle hold?

A

150 ml (end diastolic volume) when full and normally ejects only half of this volume (70-80 ml) with each contraction (stroke volume).

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23
Q

What is ejection fraction?

A

SV/EDV(100%) - should be at least 50%. Anything less may suggest heart problems i.e. congestive heart failure, etc.

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24
Q

What are the 3 layers of the heart?

A

Endocardium, Myocardium and Epicardium (visercal pericardium)

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25
Q

What layer the of the heart makes up the majority?

A

Myocardium

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26
Q

What lies between the edpicardium and parietal pericardium?

A

pericardial space

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27
Q

What is the inner most layer of the heart? And what does it consist of?

A

Endocardium. Lines the inner chambers, valves, chordae tendineae, and papillary muscles.q

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28
Q

What is the middle layer of the heart? And what does it consist of?

A

Myocardium. Thick, muscular layer that is responsible for pumping. It is not capable to regeneration (hyperplasia). But it is capable of hypertrophy.

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29
Q

What is hypertrophy?

A

a growth in tisses (size) but not an increase in number of cells.

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30
Q

What is hyperplasia?

A

a growth in the number of cells that causes a growth in the size of tissue

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31
Q

Cardiac muscle cells consist of?

A

cylindrical branching cells, single central nucleus, intercalated discs.

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32
Q

What is the outer/external layer of the heart? And what does it consist of?

A

Epicardium (visercal pericardium). Very thin layer with blood capillaries, lymph capillaries, nerve fibers, and epicardial fat,

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33
Q

How much does fat contribute to the surface of the heart?

A

Epicardial fat cover approx 60-80% of the heart’s surface and constitutes 20% of total heart weight. It is present aloing the distribution of the coronary arteries, over the right ventricle especially along the right border, anterior surface and at the apex.

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34
Q

What does epicardial fat provide for the heart?

A

Fat provides fatty acids to cardiac muscle as a local energy source in times of high demand.

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35
Q

What is the relationship between epicardial fat and general body adiposity?

A

Clincial imaging have demonstrated a strong direct correlation between epicardial fat and abdominal visceral adiposity. It is suggested there is a role for epicardial fat in the pathogenesis of CAD. (blocks vessels)

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36
Q

What is the rough outer layer of the heart?

A

parietal pericardium. Not really considered a “part” of the heart.

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37
Q

Where does the pericardial space/cavity lie?

A

It lies between the pariteal and visceral pericardial layers.

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38
Q

How much fluid is normally contained in the the pericardial sac? What function does the fluid serve?

A

10ml. It acts as a lubricant, preventing friction as the heart beats. It diffuses heat into fluid and keeps it cool.

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39
Q

What are the major heart valves?

A

2 atrioventricular (AV) valves and 2 semilunar valves

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40
Q

What are the functions of the heart valves?

A

to ensure blood flow in ONE direction through the heart chambers and to prevent backflow (regurgitation) of blood.

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41
Q

What separates the atria from the ventricles?

A

Tricuspid and mitral (biscuspid) valve

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42
Q

What lies between the right and atrium and right ventricle?

A

tricuspid valve

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43
Q

What does the tricuspid valve consist of?

A

3 separate leaflets

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44
Q

Which is larger in diameter, Tricuspid or Mitral valve?

A

Tricuspid valve- it is larger but also thinner than mitral valve.

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45
Q

How many cusps does the mitral valve have?

A

Mitral (bicuspid) valve has 2 cusps.

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46
Q

What lies between the left atrium and left ventricle?

A

Mitral (bicuspid) valve.

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47
Q

What are “heart strings”?

A

They are chordae tendineae which originate from papillary muscles. They serve as anchors in the closed position. If not anchored they would be blown upward into the atria (umbrella).

When papillary muscles contract they pull the vanes of the valves inward toward the ventricles to prevent their bulging too far backward toward the atria during ventricular contraction

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48
Q

How many cusps do semilunar valve have and what is their function?

A

3 moon shaped cusps that prevent backflow from the aorta and pulmonary arteries into the ventricles during ventricular diastole.

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49
Q

What is the pulmonic valve?

A

a valve that separates the right ventricle from the pulmonary trunk

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50
Q

What is the aortic valve?

A

a valve that separates the left ventricle from the aorta

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51
Q

What is the first heart sound associated with?

A

S1 is associated with the closure of tricuspid and mitral (AV) valves. Often referred to as “lub” in “lub-dup”

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52
Q

What is the second heart sound associated with?

A

S2 is associated with closure of pulmonic and aortic (semilunar) valves. “dup” in “lub-dup”

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53
Q

How does the blood flow through the heart?

A

The right atrium receives deoxygenated blood from the superior and inferior vena cava and coronary sinus -> tricuspid valve-> right ventricle->pulmonic valve-> pulmonary trunk -> pulmonary arteries -> lungs (pulmonary capillaries) -> oxygenated blood travels through pulmonary veins-> left atrium -> mitral valve -> left ventricle -> aortic valve -> aorta -> systemic circulation

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54
Q

What is acute pericarditis?

A

Inflammation of the pericardial layer lasting less lasting less than 2 weeks. Often, infections in origin (viral, bacterial or fungal), but can be due to autoimmune (RA, SLE) trauma, drug toxicity.

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55
Q

What are the manifestations of acute pericarditis?

A

consists of a triad of chest pain (abrupt, precordial, sharp), friction rub (rubbing and friction between the inflamed pericardial surfaces) and ECG changes.

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56
Q

Is acute pericarditis life threatening?

A

Not normally life threatening and treatment of the cause is needed (antibotics, antifungals, etc)

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57
Q

Whay is an expanded pericardial sac harmful?

A

the pericaridal sac does not tolerate sudden increases in heart size or amount of fluid in the pericardial sac

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58
Q

What is meant by pericardial effusion?

A

It refers to the accumulation of excess fluid (exudate) in the pericardial sac. The amount of fluid, rate at which it accumulates, and the elasticity of the pericardium determines the effect of effusion has on the cardiac function.

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59
Q

What can happen if the pericardial sac experiences sudden increase in heart size or increase in fluid?

A

Fluid around the heart can compress the heart wall
The heart cannot expand to fill with blood
backup into systemic circulation
decreased blood flow to lungs
decreased output of oxygenated blood to the body

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60
Q

What is serous pericarditis?

A

it is associated with sustemic lupus erthematosus (SLE), rhematic fecver, and a variety of viral infections.

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61
Q

What produces clear, straw-colored, protein rich exudate containing small numbers of inflammatory cells?

A

Serous pericarditis

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62
Q

What produces a fibrin-rich exudate?

A

Fibrinous pericarditis

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63
Q

Uremia, Myocardial infarction or acute rheumatic fever can cause?

A

fibrinous pericarditis

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64
Q

What is uremia?

A

uremia is caused by increase of urea in the blood. The liver makes urea and the kidney gets rid of it. During kidney failure, kidneys have a difficult time ridding our body of urea and it builds up in the blood.

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65
Q

what are 2 types of pericarditis?

A

Purulent and hemorrhagic

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66
Q

What type of pericarditis is almost always caused by a bacterial infection?

A

Purulent pericarditis. is produces a grossly cloudy exudate

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67
Q

What type of pericarditis results from tumor invasions of the pericardium, but can also result from TB or other bacterial infections?

A

hemorrhagic pericarditis

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68
Q

An increase in pericardial sac pressure caused by an accumulation of fluid or blood in the pericardial sac, that results in reduced ventricular filling and subsequent hemohynamic compromise is considered what?

A

cardiac tamponade

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69
Q

what is caridac tamponade?

A

it is a medical emergency. the overall risk of death depends on the speed of diagnosis, the treatment provided, and the underlying cause of the tamponade.

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70
Q

What is pericardiocenteses?

A

a procedure done to relieve the pressure of excess fluid/blood in the pericardial space. This is done in 2 ways: subxiphoid approach or parastenal approach. A large needle is inserted into the sac and fluid is released and pressure is decreased

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71
Q

What are considered myocardial diseases?

A

Disorders originating from within the myocardium, but not from cardiovascular disease.

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72
Q

What are the 2 majors forms of myocardial disease?

A

myocarditis and primary cardiomyopathies

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73
Q

Inflammation of the heart muscle (and conduction system), without evidence of a heart attack is considered what?

A

myocarditis

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74
Q

What causes myocarditis?

A

The heart becomes thick and swollen. It often presents as biventricular heart failure in yound persons who do not have valvular, rheumatic, or congenital heart disease.

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75
Q

What are the causes of myocarditis?

A

1 cause is viral, followed by drug toxicity (cocaine), then autoimmune diseases.

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76
Q

What are primary cardiomyopathies?

A

diseases of the heart muscle that are non-inflammatory and are not associated with hypertension, CHD, valvular disease, or CAD.

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77
Q

What are the symptoms of primary cardiomyopathies?

A

onset is often silent, and symptoms do not occur until the disease is well advanced. Maybe detected with PE (particularily in athletes)

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78
Q

How is primary cardiomyopathies diagnosed?

A

Is suspected when a young, previously healthy, normotensive person experiences cariomegaly and heart failure.

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79
Q

what are the 3 types of primary cardiomyopathies?

A

dilated, hypertrophic, and restrictive

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80
Q

What is the most common form of cardiomyopathy?

A

Dilated cardiomyopathy. it is progressive cardiac hypertrophy and dilation and impaired pumping abilty in one or both ventricles. Initial manifestations are those related to heart failure.
there is no cure other than transplant, recommend rest and limited activity so hopefully the heart can remodel itself.

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81
Q

Mural thrombi is associated with what cardiopyopathey?

A

dilated cardiomyopathy. they are common and may be a source of thromboemboli. Since blood isn’t being pumped sufficently it can collected and from a clot on the wall of the heart. This clot can break free and travel causing an embolism.

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82
Q

What are the causes of dilated cardiomyopathy?

A

most are idiopathic. infectious myocarditis, alcohol abuse.

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83
Q

What type of cardiomyopathy is characterized by ventricular hypertrophy and impaired diastolic ventricular filling?

A

Hypertrophic cardiomyopathy

84
Q

What type of cardiomyopathy is often inherited as autosomal dominant?

A

Hypertrophic Cardiomyopathy
persons remain stable for many years and gradually acquire more symptoms as the disease progresses, but for others it may result in left ventricular outflow obstruction, placing the patient in danger of syncope and even sudden death. Often occurs unexpectedly in young athletes

85
Q

what is the least common type of primary cardiomyopathy?

A

restrictive cardiomyopathy and cause is unknown may be associated with variousd infiltrations

86
Q

What is characterized by the ventricular filling becoming resticted because of excessive rigidity and stiffness of the ventricular walls?

A

restrictive cardiomyopathy

87
Q

What 2 independent factors are normally present in infective endocarditis?

A
  1. damaged endocardial surface (presence of valvuare disease, prosthetic heart valves, or congenital heart defects that provide an environment conducive to bacterial growth)
  2. a portal of entry by which the organism gains access to the vasculature (innocuous oral lesion, upper respiratory tract infection, skin lesion, dental procedure). Can also develop in normal hearts of IV drug users.
88
Q

what bacteria is responsible for about 50% of infective/bacterial endocarditis?

A

Staphylococcus aureus

89
Q

What are the characteristics of IE?

A

large, soft, friable, easily detached vegetations consisting of fibrin and intermeshed inflammatory cells and bacteria. May cause ulcerations, often with perforation of the valve cusps or rupture of one of the chordae tendinae.

90
Q

Which valve is most frequently involved in IE?

A

mitral valve

91
Q

What can happen if vegetations fragment?

A

a distal embolization can occur almost anywhere in the body and can result in septic infarcts int eh brain or in other organs

92
Q

What is the prophylatic regimen for those who are at risk of IE?

A

primary antibotic is amoxicillin, 2g orally 30-60 minutes before the procedure.
patients who are allergic to “cillins” can be treated with cephalexin (2g) or azithromycin or clarithromycin (500mg)

93
Q

Thick filaments?

A

Myosin

94
Q

Thin filaments?

A

Actin, tropomyosin and troponin

95
Q

What is a basic 3-lead electrocardiogram (ECG)

A

Four electrodes are placed on both of the arms and on left leg. Minute potential difference recorded between the electrodes on the person’s left arm (LA) and right arm (RA) is called lead 1 of the ECG.
the other limb leads are recorded between the RA and LL (lead II) and LA and LL (lead III)

96
Q

What type of basic lead is normally used?

A

Lead II-which is characterized by the view of electrical activity of the heart

97
Q

What is a 12-lead electrocardiogram (ECG)?

A

10 electrodes are used: 6 precordial (chest) electrodes that give 6 views (v1, v2, v3, v4, v5, v6). 4 limb electrodes are used (RA, LA, RL and LL-> give 6 views- I, II, III, aVL, aVF and aVR)

12 angles of electroactivity

98
Q

Why are 12-lead ECG’s recorded from 6 chest electrodes?

A

because the heart surfaces are close to the chest wall, each chest electrode records mainly the electrical potential of the cardiac musculature immediately beneath that electrode. Therefore, relatively small abnormailities in the ventricles, particularily in the anterior ventricular wall, can cause marked changes in the ECG’s recorded from individual chect electrodes.

99
Q

True or False. ECG measure action potentials?

A

False. They capture electroactivity caused by action potentials and not by mechanical events. Contraction are not measured.

100
Q

What does the ST segment measure?

A

it measures the end of the QRS complex to the onset of the T wave.

101
Q

What does the ST interval measure?

A

The end of the QRS complex to the end of the T wave

102
Q

What does the QT interval measure?

A

The onset of QRS complex to the end of the T wave.

103
Q

What is the P wave?

A

it is the depolarization of the atria. (can assume contraction is happening)

104
Q

What is the QRS complex?

A

it is the depolarization of the ventricles

105
Q

What is the T wave?

A

It is the repolarization of the ventricles

106
Q

What is the PQ segment?

A

It is the time when the impulse is traveling through the AV node, bundle of HIS, and bundle branches

107
Q

What is the PR interval?

A

It is the onset of the P wave to the middle of the QRS complex

108
Q

What is a normal sinus rhythm (NSR)?

A

heart rate: 60-100bpm
regular heart rhythm
P waves are uniform in appearance, positive (upright) in lead II, one precedes each QRS complex
Pr interval is WNL for age and constant from beat to beat (.12-.20 sec)
QRS duration is .10 sec or less

109
Q

Who are the latent pacemakers?

A

AV (40-60 bpm) node and Purkinje fibers (15-40bpm). They are next in line to the “king” Sa node pacemaker. They may exhibit automaticity and override SA node if it is suppressed.

110
Q

What node is the normal pacemaker of the heart?

A

SA node

111
Q

What factors affect heart rate?

A

Negative chronotropic effects to the parasympathethic and the positive chronotropic effects to the symapthetic nervous system.

112
Q

What is [parasympathetic nerve innervates the SA node, atria and AV node?

A

Parasympathetic functions of vagal nerve (CN10)

113
Q

What parasympathetic nervous system neurotransmitter acts on the SA node, atria and AV node?

A

Acetylcholine (Ach)

114
Q

What neurotransmitter acts on muscarinic receptors?

A

Acetylocholine (Ach)

115
Q

What is the negative chronotropic effect?

A

It is when the heart rate decreases the rate of phase 4 depolarization causing fewer action potentials to occur per unit time because the threshold potential is reached more slowly and less frequently.

116
Q

What happens to the mechanism in the negative chronotropic effect?

A

The mechansim is decreased I(f), the inward Na+ current that is responsible for phase 4 depolarization in the SA node.
(HR)(SV) =CO

117
Q

What sympathetic nerve innervates the SA node,atria, AV node and ventricles?

A

T1-T4

118
Q

What sympathetic nervous system neurotransmitter acts on the B1 receptors?

A

norepinephrine (NE)

119
Q

What does the positive chronotropic effect do?

A

It increases the HR by increasing the rate of phase 4 depolarization causing more action potentials to occur per unit of time because the threshold potential is reached more quickly and frequently.

120
Q

What is the mechansim of the positive chronotropic effect?

A

The mechanism is increased I(f), the inward Na+ current that is responsible for phase 4 depolarization in the SA node.
(HR)(SV) =CO

121
Q

What other factors affect heart rate?

A 
hormones like epinephrine/norepinephrine from the adrenal medulla exert similar effects as the SNS (important during exercise and excitement).
thyroid hormones (T3 and T4) can elevate heart rate, ions such as K+ can cause hyperkalemia or hypokalemia both decreasing HR. Also, age, gender, physical fitness and body temperature also influence resting HR.
122
Q

Any time you see “itis” that means?

A

inflammation

123
Q

If you have inflammation means that you had some type of?

A

injury: some kind of trauma, infection, autoimmune disorder, drug reaction.

124
Q

Inflammation of the pericardium (heart sac) is called?

A

Pericarditis: both the parietal (layer towards lungs surface) and the epicardium (visceral pericardium) are inflamed.

125
Q

Acute pericarditis lasts for about?

A

2 weeks or less.

126
Q

What are the steps in cardiac muscle excitation-contraction coupling?

A
  • A cardiac muscle cell (myocyte) action potential spreads from the sarcolemma into the T tubules.
  • during the plateau phase of the this AP, Ca+2 channels open and Ca+2 enters the cell from the ECF.
  • This Ca+2 entry triggers the release of Ca+2 from the sacroplasmic reticulum.
  • As a result of Ca+2 release, ICF (Ca+2) rises significantly.
  • Ca+2 binds to troponin C and tropomyosin is moved out of the way, removing the inhibition of actin and myosin binding.
  • actin and myosin bind, the thick and thin filaments slide past each other and the heart muscle cell contracts. (the magnitude of the tension that develops is proportional to the ICF (Ca+2)).
  • relaxation occurs when Ca+2 is reaccumulated by the sarcoplasmic reticulum and moved from the ICF back to the ECF.
127
Q

What are the symptoms of pericarditis?

A

chest pains, friction rub (rubbing and friction between the inflamed pericardium surfaces against the sternum, and ECG changes.

128
Q

Is acute pericarditis usually easily treated?

A

Yes

129
Q

Pericardial effusion?

A

Accumulation of excess fluid (exudate) in the pericardial sac. Pericardial sac does not tolerate sudden increases in the heart size or the amount of fluid. It creates pressure which compresses the heart wall and prevents heart from expanding. This is where pericarditis goes wrong.

130
Q

To determine what type of pericarditis you may have, the Dr. will analyze the fluid in the pericardial sac. What is serous pericarditis and what may cause it?

A

Clear, straw colored, protein rich exudate (excess fluid) containing small number of inflammatory cells (WBCs). Associated with SLE, rheumatic fever, and viral infections.

131
Q

Fibrinous pericarditis and what causes it?

A

Fibrin rich exudate. May be caused by uremia, myocardial infarction, or acute rheumatic fever.

132
Q

How does the cardiac contractions spread?

A

contractions spread downward from SA node-> AV node-> Bundle of HIS-> towards apex of heart in Purkinji fibers and upward along side of ventricles.

133
Q

Purulent pericarditis is almost always caused by?

A

Bacterial infection

134
Q

A bloody exudate means you have _____ pericarditis.

A

Hemorrhagic pericarditis

135
Q

Causes of hemorrhagic pericarditis?

A

Tumors, invasion of pericardium, TB, or other bacterial infections.

136
Q

An increase in pericardial sac pressure caused by an accumulation of blood in the pericardial sac, resulting in reduced ventricular filling and subsequent hemodynamic compromise is called?

A

Cardiac tamponade

137
Q

Is cardiac tamponade a serious threat?

A

Yes. It is a medical emergency. The risk depends on the speed of diagnosis, the treatment provided and the underlying cause of the tamponade

138
Q

what make up thick filaments?

A

myosin

139
Q

What make up thin filaments?

A

Actin, tropomyosin and troponin

140
Q

What are the 3 components that make up troponin?

A

I, C and T

141
Q

What is the sliding fliament theory and cross bridge cycling?

A

-ATP present on the S1 subfragment is hydrolyzed and the complex binds to the active site on actin.
-Pi is released resulting in a conformational change altering the S1 subfragment.
-ADP is also released and the thin filament is dragged toward the center of the sarcomere (powerstroke).
-A new ATP moleucule binds to the S1 subfragment which causes the release of the bond between actin and myosin.
This theory is used by skeletal muscle cells for contraction

142
Q

What are the steps in cardiac muscle excitation-contraction coupling?

A
  • A cardiac muscle cell (myocyte) action potential spreads from the sarcolemma into the T tubules.
  • during the plateau phase of the this AP, Ca+2 channels open and Ca+2 enters the cell from the ECF.
  • This Ca+2 entry triggers the release of Ca+2 from the sacroplasmic reticulum.
  • As a result of Ca+2 release, ICF (Ca+2) rises significantly.
  • Ca+2 binds to troponin C and tropomyosin is moved out of the way, removing the inhibition of actin and myosin binding.
  • actin and myosin bind, the thick and thin filaments slide past each other and the heart muscle cell contracts. (the magnitude of the tension that develops is proportional to the ICF (Ca+2)).
  • relaxation occurs when Ca+2 is reaccumulated by the sarcoplasmic reticulum and moved from the ICF back to the ECF.
143
Q

Pericardiocentesis

A

To treat cardiac tamponade Dr. will inject syringe into pericardium to withdraw the excess fluid. Either the subxiphoid approach (safer) or the parasternal approach (b/w ribs).

144
Q

Disorders originating from within the myocardium but not from cardiovascular disease is?

A

Myocardial disease.

145
Q

Two major forms of myocardial disease?

A

Myocarditis and primary cardiomyopathies

146
Q

Myocarditis?

A

Inflammation of myocardium not due to heart attack but bc something else like a viral infection (#1 cause), drug toxicity (cocaine) or autoimmune disease (rare). Presents as biventricular heart failure in young pp. who don’t have valvular, rheumatic, or congenital heart disease.

147
Q

Primary cardiomyopathy?

A

Non inflammatory disease of heart muscle not associated with hypertension, congenital heart disease, valvular disease or coronary artery disease.

148
Q

Symptoms of primary cardiomyopathy?

A

Onset is often silent, and symptoms don’t occur until disease is advanced.

149
Q

Primary cardiomyopathy often seen in?

A

Athletes. Diagnosis is suspected when young previously healthy person without hypertension experiences heart failure and cardiomegaly.

150
Q

What are the different types of cardiomyopathy?

A

Dilated (ventricles stretched out = walls are thinner), hypertrophic (left ventricle wall is abnormally thick), or restrictive (walls are a little thick but very rigid).

151
Q

__________cardiomyopathy is a primary cardiomyopathy in which thrombus/thromboemboli can occur

A

Dilated.

152
Q

Causes of dilated cardiomyopathy?

A

idiopathic, infectious myocarditis, alcohol.

153
Q

Impaired pumping ability in one or both ventricles, progressive cardiac hypertrophy and dilation?

A

Dilated cardiomyopathy

154
Q

Ventricular hypertrophy and impaired diastolic ventricular filling is?

A

Hypertrophic cardiomyopathy (a type of primary cardiomyopathy)

155
Q

Cause of hypertrophic cardiomyopathy?

A

Often genetic: inherited as an autosomal dominant characteristic. Several genes linked to the disorder

156
Q

Why is hypertrophic cardiomyopathy dangerous?

A

Can result in ventricular outflow obstruction, placing patient in danger of syncope (fainting) and sudden death. Seen in young athletes.

157
Q

What are some of the important differences and similarities between skeletal and cardiac muscle?

A

They both have striated muscle, thick and thin filaments. Cardiac muscle is NOT voluntary and is less dense in sarcoplasmic reticulum than skeletal muscle. Cardiac muscle has intercalated discs and a tremendous amount of mitochondria compared to skeletal muscle.

158
Q

How are skeletal and cardiac muscle cells different in one another?

A

Skeletal cells are independent of one another both structurally and functionally. But in cardiac cells the plasma membrane interlock at dark staining junctions (intercalated discs).

159
Q

Describe the function of desmosomes in cardiac muscle cells.

A

desomosomes prevent adjcent cardiac cells from separating during contraction

160
Q

Describe the function of gap junctions in cardiac muscle cells.

A

Gap junctions allow ions to pass freely from cell to cell, directly transmitting the depolarizing current across the entire heart.

161
Q

What is functional synctium?

A

When the entire myocardium behaves as a singel coordinated unit because the cardiac fibers are electrically coupled by the gap junctions.

162
Q

How does the cardiac contractions spread?

A

contractions spread downward from SA node-> AV node-> Bundle of HIS-> towards apex of heart in Purkinji fibers and upward along side of ventricles.

163
Q

Least common form of primary cardiomyopathy?

A

Restrictive cardiomyopathy.

164
Q

In this type of primary cardiomyopathy ventricular filing is restricted b/c of excessive rigidity and stiffness of the ventricular walls.

A

Restrictive cardiomyopathy

165
Q

Infective endocarditis is due to a ____ infection

A

bacterial

166
Q

Endocarditis is a life threatening condition of the endocardial surface of the heart including the heart valves. What 2 factors are normally required for endocarditis?

A
  1. Damaged endocardial surface (valvular disease, prosthetic valves, or congenital heart defects to allow environment for bacterial growth.
  2. A way for bacteria to get into our bodies (skin lesion, oral lesion, upper respiratory tract infection)
167
Q

This bacteria is the cause of endocarditis (50%) of the time

A

Staphylococcus aureus

168
Q

Infective endocarditis usually appears in what kind of patients?

A

normal hearts of IV drug users or in the heart of pp with pre-existing heart lesions.

169
Q

Characteristics of bacterial endocarditis?

A

soft, large, friable easily detached vegetation consisting of fibrin and intermeshed inflammatory cells and bacteria. May cause ulceration and perforation of the valve or rupture of chordae tendinae. Embolization may occur if vegetation breaks off and can cause infarcts in brain or other organs

170
Q

What valve is most frequently involved in endocarditis?

A

mitral (bicuspid)

171
Q

The primary antibiotic given to people with infective endocarditis while undergoing dental procedures is?

A

Amoxcillin (type of penicillin): 2g orally 30-60 minutes before the procedure

172
Q

Patients who are allergic to penicillin can be treated with what other three antibiotics?

A

Cephalexin (2g) or Azithromycin or Clarithromycin

173
Q

What does the cardiac troponin complex consist of?

A

It consists of 3 proteins:
Cardiac troponin C (cTnC)-binds Ca+2
cardiac troponin I (cTnI)-inhibitory
cardiac troponin T (cTnT)-tropomyosin binding

174
Q

How do skeletal and cardiac troponin complexes differ?

A

They differ from each other in amino acid sequences in T and I troponin isoforms.

175
Q

What is Angina?

A

Chest pain from myocardial ischemia most commonly from atherosclerosis. Angina is often related to exertion, emotion, eating, or cold. It is usually short lived and relieved by NTG (vasodialator). Cell death does not occur because the supply and demand for oxygen becomes equal again before there is permanent damage to the myocardium.

176
Q

What is myocardial infarction?

A

Chest pain from myocardial ischemia most commonly from atherosclerosis. It occurs spontaneously, is more long-lasting compared to anginal pain and is not relieved by NTG. Cell death occurs because the supply and demand for oxygen remains mismatched for an extended time and myocardial tissue becomes hypoxic. Death can result if enough cells die before the supply and demand for oxygen is equal or it there are subsequent complications following initial survival.

177
Q

What cardiac isoforms are specific for cardiac injury but not in the blood of healthy people?

A

Troponin 1 (cTnI) or T (cTnT) are frequently assessed in the blood to determine if a heart attack has happened.
Both arise 2-6 hours after injury.
Both peak in 12-24 hours.
cTnI can stay elevated for 5-8 days and cTnT can stay elevated for 5-14 days.

178
Q

The appearance of the cardiac action potential on an ECG depends on?

A

WHERE the AP is measured.

179
Q

What are the two types of action potentials?

A

non-pacemaker or fast response action potential and pacemaker or slow response action potentials

180
Q

How is a non-pacemaker (Fast response) action potential defined?

A

It occurs in the atria, ventricles and purkinje fibers and undergo rapid depolarization.

181
Q

How is a pacemaker (slow response) action potential defined?

A

It occurs in the SA node and AV node and undergoes slow depolarization

182
Q

What is the phase 0 (rapid depolarization) in fast response?

A

It is the upstroke of the AP where fast Na+ channels open and several types of K+ channels close.

183
Q

What is phase 1 (early/initial repolarization) in fast response?

A

It is the transient outward current as K+ channels open and fast Na+ channels close.

184
Q

What is Phase 2 (Plateau phase) fast response?

A

It is a long lastiong (L-type) Ca+2 channels open leading to inward Ca+2 movement causing an efflux of K+ through several types of K+ channels.

185
Q

What is the key difference between excitation-coupling in skeletal muscle and cardiac muscle?

A

Excitation-contraction coupling in skeletal muscle does not require influx through L-type Ca+2 channels. Cardiac contraction has an absolute requirement for Ca+2 influx through these channels during the AP.

186
Q

Does the amount of Ca+2 entering the cardiac muscle cell during an AP promote actin-myosin interaction?

A

No the AP is too small. The influx of Ca+2 only services as a trigger to induce Ca+2 release from the sarcoplasmic reticulum (Ca+2-induced calcium release= CICR). Which promotes actin-myosin interaction and hence contraction; occurs via rynanodine receptors (RyR2).

187
Q

What can alter Ca+2 conductance?

A

Norepinephrine increased conductance, whereas Ach, Beta blockers and Ca+2 channel blockers decrease the conductance.

188
Q

How much time does the heart spend in Systole and Diastole?

A

2/3 of its time is spent in Diastole and 1/3 of its time in Systole.

189
Q

What is phase 3 (late or final repolarization) fast response?

A

It is the continual efflux of K+ through several types of K+ channels and which causes L-type Ca+2 channels to eventually close

190
Q

What is phase 4 (RMP) fast response?

A

The K+ channels remain open and Ca+2 extrusion mechanisms become highly active.

191
Q

What is the effective (or absolute) refractory period?

A

a 2nd AP absolutely cannot be inititated no matter how large a stimulus is applied.

192
Q

What is a refractory period?

A

Once a fast response AP has been initiated, the depolarized cell is no longer excitable until the cell is partially repolarized.

193
Q

What is the relative refractory period?

A

a 2nd AP may be evoked only when the stimulus is sufficiently strong (suprathreshold).

194
Q

Describe the action of the Sinoatrial (SA) node.

A

It is the normal pacemaker of the heart, it has an unstable RMP. The SA node exhibits phase 4 depolarization or automaticity (the ability to initiate its own depolarization).

195
Q

What is the Phase 0 of slow response cardiac AP?

A

it is the upstroke of AP and is caused by an increase in Ca+2 conductance. The ionic basis for phase 0 in the SA node is very different from that in the ventricles, atria and Purkinje fibers (where it is the result of an inward Na+ current).

196
Q

What happens in the phase 1 and 2 in a slow response Cardiac AP?

A

These two phases are skipped and do occur.

197
Q

What happens in Phase 3 slow response cardiac action potentials?

A

repolarization occurs and is caused by an increase in K+ conductance. THis increase results in an outward K+ current that causes repolarization of the membrane potential.

198
Q

What is Phase 4 in a slow response cardiac AP?

A

SLOW depolarization occurs and accounts for the pacemaker activity of the SA node (automaticity). It is caused by an increase in Na+ conductance which results in an inward current called I(f).

199
Q

When is I(f) turned on?

A

it is turned on by repolarization of the membrane potenital during the preceding AP.

200
Q

Define heart rate.

A

HR is the number of times the SA node discharges per minute.

201
Q

What is conduction velocity?

A

(CV) is the time required for excitation to spread throughout cardiac tissue.

202
Q

Where is Conduction velocity (CV) the fastest?

A

in the Purkinje system.

203
Q

Where is Conduction velocity (CV) the slowest?

A

It is the slowest in the AV node (seen as the PR interval on the ECG). This allows time for ventricular filling before ventricular contraction. If conduction velocity through the AV node is increased, ventricular filling may be compromised.

204
Q

What chronotropic effects are produced on the heart?

A

They produce a change in heart rate which are reflected on the ECG by changes in the R-R intervals.

  • negative chronotropic effect decreases the heart rate by decreasing the firing rate of the SA node
  • positive chronotropic effect increases heart rate by increasing the firing rate of the SA node.
205
Q

What dromotropic effects are produced on the heart?

A

They produce changes in conduction velocity, primarily in the AV node.

  • negative dromotropic effects decreases conduction velocity through AV node, slowing down the conduction of AP from the atria to the ventricles and increasing the PR interval. The mechansim of the negative dromotropic effect is decreased inward Ca+2 current and increased outward K+ current
  • positive dromotropic effect increases conduction velocity through the AV node, speeding the conduction of AP’s from the atria to the ventricles and decreasing the PR interval
206
Q

What kind of effect are affected by the parasympathetic effects on conduction velocity?

A

Negative chronotropic and dromotropic effects.

207
Q

What are the chronotropic and dromotropic effects on the sympathetic conduction velocity?

A

Postive chronotropic effects increase the heart rate by increasing the rate of phase 4 depolarization causing more AP because the threshold potential is reached more quickly and more frequently. The mechansim of the positive chronotropic effect is increased I(f), the inward Na+ current that is responsible for phase 4 depolarization in the SA node.
Positive dromotrophic effect increases the conduction velocity through the AV node causing AP’s conduct more rapidly from the atria to the ventricles, and ventricular filling may compromised. This decreases the PR interval. The mechansim of the positive dromotropic effect is increased inward Ca+2 current

Cardiopulmonary (1 decks)

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