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NRP511 > Cardiac 2 > Flashcards

Cardiac 2 Flashcards

1
Q

What valves are open/closed during diastole?

A

Open: AV valves
Closed: Semilunar valves

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2
Q

What area of the heart is filling/emptying during diastole?

A

Filling: Ventricles
Emptying: Atria

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3
Q

What electric activity corresponds to diastole?

A

T wave

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4
Q

What heart sound occurs during diastole?

A

S2 (Closure of semilunar valves)

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5
Q

What valves are open/closed during systole?

A

Open: Semilunar valves
Closed: AV valves

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6
Q

What area of the heart is filling/emptying during systole?

A

Emptying: Ventricles

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7
Q

What electric activity corresponds with systole?

A

The QRS complex

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8
Q

What heart sound occurs during systole?

A

S1 (closure of AV valves)

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9
Q

The greater the preload the greater the _______.

A

Cardiac Output

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10
Q

An increase in contractility is demonstrated on a Frank-Starling diagram by:

A

Increased cardiac output for a given EDV

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11
Q

Walk through the conduction system of the heart beginning with SA node.

A

SA node –> atrial conducting fibers –> AV node –> Bundle of His–>Bundle branches (R/L) –>Purkinje fibers

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12
Q

What is the pacemaker of the heart? What does it normally set the rate to?

A

SA node

60-100bpm

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13
Q

What is CN X’s affect on HR?

A

Slows the rate (parasympathetic)

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14
Q

What corresponds to the SA and AV nodes firing?

A

The SA node causes the atria to contract and the AV node causes the ventricles to contract

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15
Q

What does the the P wave correspond to?

A

Atrial contraction (depolarization)

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16
Q

What does the QRS complex correspond to?

A

Ventricular contraction (depolarization)

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17
Q

What does the T wave correspond to?

A

Ventricular relaxation (repolarization)

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18
Q

What does the U wave correspond to?

A

The repolarization of the Purkinje fibers

Often not visible, best seen on leads V2 and V3

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19
Q

What does the PR interval represent?

A

atrial, AV node, and Purkinje depolarization

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20
Q

The physiologic function of the relatively slow conduction through the AV node is to allow sufficient time for:

A

Ventricular filling

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21
Q

Name the three layers of the artery from innermost to outermost:

A
  1. Tunica intemae
  2. Tunica media
  3. Tunica adventitia
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22
Q

How do the anatomy of the veins and arteries contribute to different functions?

A
  • Arteries are muscular, thick, and elastic. They are able to sustain higher pressures
  • Veins are muscular, thin, and elastic. They contain semilunar valves to direct flow.
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23
Q

What factors determine blood flow? (2)

A
  1. Pressure (force exerted)

2. Resistance (opposition to force)

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24
Q

Blood pressure = ______ x ________

A

Cardiac Output x Peripheral Resistance

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25
Q

What are some genetic and environmental factors that could lead to hypertension?

A
  • Defects in renal Na homeostasis
  • Functional vasoconstriction
  • Defects in vascular smooth muscle and growth structure
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26
Q

What can preload be equated to?

A

EDV

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27
Q

What is afterload?

A

The pressure during ejection that the LV must overcome to eject.

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28
Q

What three factors make up Vichrow’s triad and what do they result in?

A
  1. Endothelial (intimal) injury
  2. Venous stasis
  3. Hypercoagulability

=THROMBOSIS

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29
Q

What is shock?

A

An imbalance between oxygen supply and oxygen demand at the cellular level.

=hypoperfusion and impaired cellular oxygen utilization

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30
Q

What are the four major types of shock?

A
  1. Cardiogenic
  2. Obstructive
  3. Hypovolemic
  4. Distrubutive
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31
Q

What is the pathogenesis of cardiogenic shock?

A

Blood pump problem; inadequate CO despite sufficient vascular volume

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32
Q

What is the pathogenesis of obstructive shock?

A

Blood flow problem; circulatory blockage such as a large PE or cardiac tamponade= disrupts CO

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33
Q

What is the pathogenesis of hypovolemic shock?

A

Blood volume problem; Loss of blood volume as a result of hemorrhage or excessive loss of extracellular fluids

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34
Q

What is the pathogenesis of distributive shock?

A

Blood vessel problem; greatly expanded vascular space because of inappropriate vasodilation

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35
Q

Acyanotic congenital heart defects cause what type of shunt. Give examples.

A

L –> R shunt

ASD, VSD, PDA, CoA, PS, or AS

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36
Q

Cyanotic congenital heart defects cause what type of shunt? Give examples?

A

R–>L shunt

Tet, d-TGA, Truncus, TA

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37
Q

______ delivers oxygenated blood to the fetus in fetal circulation.

A

Umbilical vein

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38
Q

What are the four components of a Tet?

A
  1. Large VSD
  2. Overriding Ao (over VSD instead of LV)
  3. RV hypertrophy
  4. PS or PA
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39
Q

What is Kawasaki Disease?

A

A mucocutaneous lymph node syndrome. Acute, self limiting systemic vasculitis that may result in cardiac sequalae.

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40
Q

What is pediatric systemic hypertension defined as?

A

SBP and DBP >95th percentile for age and gender on at least three occasions.

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41
Q

What are some underlying disease that could cause HTN in pediatric patients?

A

Renal disease
CoA
Adrenal tumors
Space occupying lesions of the cranium

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42
Q

What are some complications of shock?

A 
DIC
Acute Renal Failure
ARDS
MODS
GI Ischemia
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43
Q

What are the three clinical stages of shock?

A
  1. Compensated (homeostatic mechanisms)
  2. Progressive (hypotensive, immediate intervention)
  3. Refractory (unresponsive to treatment)
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44
Q

When can S3 be heard?

A

Abnormal
Dilated heart
Also known as the Kentucky gallop

d/t: Increased blood volume, stiff chordae tendinae, HF (more volume at end of systole)

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45
Q

When can S4 be heard?

A

Abnormal
Stiffened ventricle/restrictive cardiomyopathy
“Atrial kick”
Also known as the Tennessee gallop

d/t:
Turbulent blood flow against stiffened ventricular walls
Hypertrophy
Atrial contraction attempting to overcome hypertrophic ventricle

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46
Q

What happens during atrial systole?

A

An atrial contraction causes a small amount of additional blood into the ventricles

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47
Q

What is End diastolic volume and what is a normal amount.

A

The maximum amount of blood in the ventricles which occurs at the end of ventricular relaxation.
~135ml

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48
Q

What is happening during isovolumic ventricular contraction?

A

1st phase of ventricular contraction
Pushes AV valves closed but does not create enough pressure to open semilunar valves
Volume in heart stays the same (isovolumic)

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49
Q

What is happening during ventricular ejection?

A

As ventricular volume rises and exceeds pressure in the arteries the semilunar valves open and blood is ejected

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50
Q

What is End Systolic Volume and what is a normal amount?

A

Minimum amount of blood in ventricles at the end of systole.
~65ml

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51
Q

What is happening during isovolumic ventricular relaxation?

A

As ventricles relax pressure in the ventricle drops causing the semilunar valves to snap shut
Volume in the heart stays the same (isovolumic)

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52
Q

What is the rate of rhythmic discharge of the cardiac cells determined by?

A

Influx of Na and Ca versus the efflux of K

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53
Q

Spread of an action potential over cardiac muscle cell surfaces results in ___________.

A

myocardial contraction

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54
Q

What ion concentration difference across the cell membrane is the primary determinant of the resting membrane potential?

A

Potassium

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55
Q

What happens during phase 0 of an cardiac action potential?

A
  • Membrane potential of the cardiac cell approaches threshold and voltage gated Na channels open
  • Na rushes into cell causing depolarization

(Class I antidysrhythmics block voltage gated channels- quinidine, lidocaine)

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56
Q

What happens during phase 1 of a cardiac action potential?

A
  • Na channels close
  • K channels open and K leaves cell
  • Cell becomes more positive (repolarizing)
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57
Q

What happens during phase 2 of a cardiac action potential?

A
  • Plateau phase (little change in membrane potential)
  • Influx of Ca and efflux of K
  • This phase is reduced in atrial cells

(Ca channel blockers are used to inhibit this Ca influx. Beta blockers also reduce Ca influx)

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58
Q

What happens during phase 3 of a cardiac action potential?

A
  • Rapid return to resting membrane potential
  • Closure of slow Ca channels and more rapid efflux of K
  • Latter phase known as the relative refractory period
  • Na channels may be induced to open by a larger than normal depolarization stimulus; could cause Vfib

(Class III agents like amiodarone increases the refractory period by inhibiting K channels)

59
Q

What happens during phase 4 of a cardiac action potential?

A
  • The time between action potentials
  • No change in membrane voltage; resting membrane potential
  • Flat in ventricular cells
  • Sloping in pacemaker and conduction system cells that automatically depolarize
60
Q

Why are the cells in the SA node the heart’s pacemaker cells?

A

They have the fastest rate of spontaneous depolarization

61
Q

Sympathetic action on the heart :

A
  • Increased HR
  • Increases speed of conduction
  • Increases force of contraction
  • Relaxes more quickly

via release of NE= increases cAMP

62
Q

Sympathetic action on the blood vessels:

A

Causes vasoconstriction

63
Q

Parasympathetic action on the heart:

A
  • Decreases HR
  • Decreased speed of conduction

via CN X/vagus nerve and release of Ach=binds to muscarinic receptors and decreases cAMP and increases K leak (makes it harder to depolarize cell)

64
Q

What do the specialized sensory nerve endings called baroreceptors do and where are they located?

A
  • Located in the carotid bodies and Ao arch
  • Decrease HR in response to high BP

Transmits info to the CNS by way of the Glossopharyngeal (IX) and Vagus (X) nerves

-Affects contractility to regulate SV

65
Q

A decrease in blood pressure causes:

A

parasympathetic inhibition and cardiac sympathetic activation to increase HR

66
Q

An increase in blood pressure causes:

A

parasympathetic activation and sympathetic inhibition to decrease HR

67
Q

What is the Bainbridge reflex?

A

Suppression of parasympathetic influence and an increase in heart rate d/t atrial or ventricular overdistention

68
Q

CO= (2)

A

HR x SV

69
Q

Q(flow)=

A

change in P/ R

Ohm’s law

70
Q

CO= (3)

A

MAP-CVP/TPR

MAP-CVP= change in P
TPR=SVR

71
Q

Explain the Frank-Starling law of the heart (length-tension relationship).

A

An increase in resting muscle fiber length results in a greater development of muscle tension. Preload determine ventricular muscle fiber length.

An increase in preload results in a greater force of contraction and a larger stroke volume.

72
Q

Arterial pressure is affected by:

A

CO
SV
Arterial compliance
Peripheral resistance

73
Q

What does the dichrotic notch represent?

A

Ao valve closing and beginning of diastole

74
Q

Should pressure be high or low in the RA?

A

Low, to allow passive flow back to the heart

75
Q

What 3 factors affect contractility?

A
  1. The amount of contractile proteins in the muscle cells
  2. The availability of ATP
  3. The availability of free Ca ions in the cytoplasm
76
Q

What three factors determine Stroke Volume?

A
  1. Preload
  2. Contractility
  3. Afterload
77
Q

Any factor that increased the HR, preload, contractility, or afterload will:

A

Increase the workload of the heart

78
Q

What is the heart’s endocrine function?

A

Secretion of natriuretic peptides

ANP/BNP= enhanced excretion of Na and H2O in the kidneys

79
Q

What is ANP?

A

Atrial natriuretic peptide
Synthesized by the atrial myocytes and released in response to atrial stretch occurring when blood volume becomes excessive

80
Q

What is BNP

A

B-type natriuretic peptide

Produced by ventricles when they are chronically overdistended (congestive HF)

81
Q

How might poor myocardial oxygen delivery be evident on an EKG?

A

ST elevation or depression

T wave abnormalities

82
Q

What are the 2 major determinants of coronary vascular resistance?

A
  1. Coronary artery diameter

2. Varying degrees of external compression d/t myocardial contraction and relaxation.

83
Q

What is pressure through the coronary arteries determined by?

A

Aortic BP

RAp

84
Q

Why do blood vessels dilate?

A

Protection; decrease in turbulent flow

NO, ANP, prostacyclin cause this

85
Q

Why do blood vessels constrict?

A

Prevent diuresis in hypotension

ADH(Vasopressin) and A-I/A-II

86
Q

What is atherosclerosis?

A

The hardening of the arteries d/t plaque formation

87
Q

What is an atheroma/plaque made of?

A

A lipid core covered by a fibrous cap

88
Q

What initiates the formation of a plaque?

A

Injury to the coronary artery endothelium

89
Q

What is contained in the fibrous cap of a plaque?

A

SMC, macrophages, foam cells, lymphocytes, collagen, elastin, proteoglycans, and intra and extracellular lipid

90
Q

What is contained in the necrotic center of a plaque?

A

Cell debris, cholesterol crystals, Ca, foam cells (macrophages that phagocytose oxidized LDL become necrotic d/t no blood supply)

91
Q

What are the four main steps that produce atherosclerosis?

A
  1. Endothelial dysfunction (injury –>inflammation)
  2. Oxidized LDL (increases inflammation)
  3. Foam cell formation (deposition into cell wall
  4. SMC migration, proliferation and secretion
92
Q

What region of a plaque is clot formation most common?

A

The ‘shoulder’ region (small out-pouching)

93
Q

What is the difference between primary and secondary hypertension?

A

Primary HTN is idiopathic, secondary HTN is attributable to a specific identifiable cause.

94
Q

What is malignant hypertension?

A

Also known as hypertensive crisis

Sudden increased in either or both systolic and diastolic pressure that causes signs of end organ failure.

95
Q

What are complications associated with preeclampsia?

A 
Preterm labor
Abruptio placentae
DIC
Hemorrhagic stroke
Liver failure 
ARF
96
Q

What is an Aortic Aneurysm?

A

Saclike enlargement in the wall of the aorta that is often associated with atherosclerosis

97
Q

What happens in a ruptured aortic aneurysm?

A

Internal hemorrhage. Blood moves to extravascular space

98
Q

What happens during dissection of an aortic aneurysm?

A

Bleeding into the vascular wall through a tear in the inner layer of the vessel (intima)

99
Q

What are the critical factors in meeting the cellular demands (O2 delivery) of the heart?

A
  1. Coronary perfusion

2. Myocardial workload

100
Q

What is stable or classic angina described as?

A

Predictable onset of ischemia with activity that subsides with rest. Caused by stenosis of coronary arteries

101
Q

When does ischemic heart disease occur?

A

When there is an imbalance in myocardial oxygen demand and supply

102
Q

What happens during an acute MI?

A

Plaque rupture and subsequent clot formation that causes complete occlusion and irreversible damage to the myocardial cells resulting in necrosis.

103
Q

What is the most common EKG change seen with MI?

A

ST elevation (STEMI)

104
Q

What lab values should be obtained in the individuals suspected of having an NSTEMI?

A

CK-MB (fall to normal within 48hrs)

Troponin I and T (remain elevated for 4-7days)

105
Q

What is chronic ischemic cardiomyopathy?

A

Ischemic heart disease with congestive heart failure. Progressive degeneration of the myocardium with angina or MI

106
Q

What are some management options of coronary artery occlusion?

A

Thrombolysis
Percutaneous transluminal coronary angioplasty
Placement of a stent
CABG

107
Q

What is valvular stenosis?

A

Inability of the valve to open completely (hard/stiff valve)

108
Q

What is valvular regurgitation?

A

(Insufficiency) Inability of the valve to close completely. Causes back-flow (floppy valve)

109
Q

What are the most common causes of valvular stenosis?

A

Postinflammatory scarring from rheumatic heart disease (MV) and valvular calcification associated with aging (AoV)

110
Q

If untreated mitral stenosis can lead to:

A

Chronic pulmonary HTN, RV hypertrophy, and R sided heart failure.

111
Q

What are the s/s of mitral stenosis d/t?

A

Congestion of blood volume and increased pressure in the LA and pulmonary circulation. Decreased SV of the LV d/t deficient filling

S/s are exacerbated by any condition that further decreases LV filling (ex-afib)

112
Q

What are the s/s of mitral stenosis?

A

Secondary to pulmonary congestion: DOE, orthopnea, cough, paroxysmal nocturnal dyspnea, abnormal breath sounds, and poor arterial oxygenation.

Secondary to reduced LV SV: fatigue, poor activity tolerance, and weakness

113
Q

What does mitral stenosis sound like?

A

Low-pitched diastolic rumble (at apex)

Loud S1

114
Q

What is represented by giant V waves on an atrial pressure monitor?

A

Mitral regurg. Elevation of LA volume and pressure of regurgitant flow in systole.

115
Q

Severity of mitral regurg is dependent on:

A
  1. The amount of LV SV that is reguritant

2. Afterload

116
Q

What is the sequelae of mitral regurg?

A

Dilated LA and LV and LV hypertrophy to compensate for the extra volume it is required to pump.

117
Q

What does mitral regurg sound like?

A

Pansystolic murmur that radiates towards axilla and has a high pitched blowing character

118
Q

Mitral regurg is almost always due to:

A

Rheumatic fever (and almost always associated with MS)

119
Q

A mitral valve that balloons into the LA during ventricular systole is called:

A

mitral valve prolapse (autosomal dominant, females, assoc w/ Marfans)

2mm or more of displacement of the valve leaflets above annulus on echo is diagnostic.
Could trap blood in ballooned area

120
Q

What does mitral prolapse sound like?

A

Mid-systolic click or systolic murmur.

121
Q

What is the most common cause of non-rheumatic Aortic valve stenosis?

A

Progressive calcifications of a congenitally abnormal bicuspid aortic valve

122
Q

What is characteristic of the LV in patients with Aortic Stenosis?

A

High LV- Ao pressure gradient during ejection to overcome the stenotic valve

Leads to LV hypertrophy and left-sided failure (eventual)

123
Q

What is the transvalvular pressure gradient and valve orifice size in aortic stenosis?

A

> 50mmHg

<1cm squared

124
Q

What are the common s/s of aortic stenosis?

A

d/t decreased cardiac output: syncope, fatigue, low SBP, faint pulses.
critical stenosis: angina
pulmonary complications come later

125
Q

What does aortic stenosis sound like?

A

Harsh, midsystolic crescendo-decrescendo
R second intercostal space transmitted to neck

HR is usually slow to along for long ejection and a prominent S4 is heard

126
Q

When does the backflow of aortic regurg happen?

A

During diastole blood leaks back from aorta to LV

127
Q

What is chronic aortic regurg associated with?

A

Prior rheumatic fever

Persistent systemic hypertension

128
Q

What is acute aortic regurg associated with?

A

Infective endocarditis
Trauma
Dissection of a thoracic aneurysm

129
Q

Aortic regurg could be secondary to (anatomic):

A

Abnormal aortic valve
Dilated aortic root
Degenerative changes d/t aging

130
Q

What does aortic regurg sound like?

A

Faint blowing in diastole

L sternal border, aortic area, apex

131
Q

Symptoms of L heart failure include:

A

Problem is in the system, symptoms are in the lungs

Dypsnea
S3
Crackles

132
Q

Symptoms of R heart failure include:

A

Problem is in the lung, symptoms are in the system

JVD
Peripheral edema
Hepatomegaly

133
Q

Hyperlipidemia is characterized by:

A

increased LDL

decreased HDL

134
Q

What are 3 common diseases affecting heart structure?

A
  1. Pulmonary HTN
  2. Aortic stenosis
  3. Mitral incompetence
135
Q

What is dilated cardiomyopathy?

A

A progressive dilation of one or both ventricles and affects systolic function (high ESV=increased workload). Weakened muscle wall over time

136
Q

What protein is associated with the genetic component of dilated cardiomyopathy?

A

Dystrophin (important in contractile function of the muscle=systolic dysfunction= higher ESV= dilation)

137
Q

What is hypertrophic cardiomyopathy?

A

Asymmetric hypertrophy of the LV leading to diastolic disfunction and outflow obstruction

138
Q

What is the pathophysiology of hypertrophic cardiomyopathy?

A

Hypertrophy causes a stiff walled ventricle that leads to inability to fill, a decreased EDV, and may lead to intermittent ventricular outflow obstruction as well as MR

Hereditary component (sarcomeric contractile proteins)
Impaired filling during systole could lead to ventricular arryrthmias and death
139
Q

Describe restrictive cardiomyopathy.

A

Decrease in ventricular compliance causing decreased filling in diastole with normal but inadequate systole

140
Q

Common causes of restrictive cardiomyopathy:

A

endomyocardial fibrosis
cardiac amyloidosis

stiff and inelastic ventricle that only fills with great effort (LA working harder)

141
Q

What causes congestive heart failure in the forward direction?

A

Systemic hypertension
MV/AV disorder
Ischemic heart

142
Q

What causes congestive heart failure in the backward direction?

A

Venous backup

143
Q

What does pulmonary hypertension often cause?

A

Cor pulmonae (right sided heart failure)

144
Q

How is hypertrophic cardiomyopathy sometimes treated with respect to afterload?

A

In some cases an increase in afterload will prevent the further obstruction of the MV and LVOT

NRP511 (23 decks)

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