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Pt.2 PHRM/PHYS/NS > week 5: heart failure/dysrhythmias > Flashcards

week 5: heart failure/dysrhythmias Flashcards

1
Q

what is the definition of heart failure?

A

when the heart’s ability to pump blood has been compromised leading to ↓ CO

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2
Q

why can heart failure occur?

A

Due to impaired cardiac pumping or filling, or both
two major: pump or sqeezing action of heart muscle
lack of heart filling - either stiff heart or smaller than normal

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3
Q

true or false due to heart failure?
Results in accumulation of fluid in lungs and/or the periphery
* Can be acute or chronic
* Major reason for hospital admission in adults over 65 years

A

true

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4
Q

what can heart failure also be called?

A

pump failure - when heart is not pumping correctly

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5
Q

what is one thing to remember about heart failure? think CO

A

Co = SV x HR
CO should be 3-6L/min

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6
Q

what are the five factors affecting CO?

A

cardiac contractility
heart rate
preload
afterload
blood volume

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7
Q

what does r side heart failure back up to ?

A

systemic circulation

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8
Q

what does l side heart failure back up to?

A

pulmonary circulation

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9
Q

what does heart failure affect (just checking if you get it)

A

cardiac functioning

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10
Q

what are the risk factors of developing heart failure?

A
  • CAD
  • HTN
  • DM
  • Smoking
  • Obesity
  • High cholesterol
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11
Q

why is CAD and HTN bolded as risk factors of HF?

A

CAD: obstruction in the coronary arteries, reduces blood flow to myocardial - can lead to cardiac tissue damage which affect the pumping function of the heart

HTN: afterload - increase in resistance against heart pumping action - thickening of ventricle wall - leads to dysfunction

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12
Q

what does DM, smoking, obesity and High chlosterol cause - related to HF?

A

atherosclerosis - triggers an inflammatory response

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13
Q

what are the chronic causes of HF?

A

CAD - contractility
Cardiomyopathy - disease to the myocardial, many different kinds, contractility
HTN - afterload, systemic - right sided - high pressur eand higher workoad
Pulmonary disease - afterload
Valvular Disease - valves become tight - stenosis, loose dont close properly

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14
Q

what are the acute causes of HF?

A

Acute MI- contractility
Myocarditis - contractility, inflammation of the heart in response to an infection
Hypertensive crisis - aftrload, bp goes up quickly
Rupture of papillary muscle (preload increasing filling pressure and backflow into chambers of heart) - leads to regurgitation of backflow
Dysrhythmias - HR

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15
Q

what is ejection fraction?

A

percentage of end-diastolic blood volume that is ejected during systole
blood is left behind, below 40% ejection is not providing enough blood- may be in heart failure

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16
Q

what is normal ejection fraction (EF)?

A

50-70% - it I s a misconception that all the blood in the heart gets pumped out

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17
Q

what is an important measurement we use to determine the functioning of the heart amount of blood every time it beats

A

ejection fraction

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18
Q

___ means contraction, so when we are talking about heart failure that is caused by pump problems. This would include conditions where the muscle is destroyed. Name these type of conditions

A

systole, and conditions such as myocardial ischemia, cardiomyopathy, or long standing HTN can be an example.

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19
Q

Name the two characteristic of pathology of heart failure

A

HF with Reduced EF ( systolic dysfunction )
HF with Preserved EF ( diastolic dysfunction )

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20
Q

what is the most common form of HF ? and what does this do ?

A

the most common form is HF with reduced EF ( systolic dysfunction )

the heart is unable to pump blood effectively

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21
Q

LV cannot contract strongly enough to pump blood into aorta: this undergoes which pathology of heart failure ?

A

HF with Reduced EF ( systolic dysfunction )

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22
Q

True or False. HF with reduced EF ( systolic dysfunction ) : EF usually less than 40%.

A

true

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23
Q

What is HF with Preserved EF ( Diastolic dysfunction )

A

inability of ventricles to relax and fill during diastole

decreased filling results in decreased SV

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24
Q

This is high filling pressure to to poorly complaint ventricles and ventricular hypertrophy common.

A

HF with preserved EF ( diastolic dysfunction )

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25
Q

what is a pumping problem and what is a filling problem ?

A

HF with reduced EF ( systolic dysfunction ) and HF with preserved EF ( diastolic dysfunction )

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26
Q

Why is dialostic dysfunction more complicated than HF with reduced EF ( systolic dysfunction ) ?

A

cardiac muscle is working but cannot relax, reduced cardiac output and stroke volume

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27
Q

what is a mixed HF ?

A

both systolic and diastolic dysfunction, the patient with combination have extremely low ejection fraction less than 35 %- poor cardiac output

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28
Q

HF : compensatory mechanisms ( what are the different kind of mechanisms )

A

SNS activation
neuro hormonal response ( RAS )
ventricular dilation
ventricular hypertrophy

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29
Q

The release Catecholamines, in which increases this mechanism, most immediate mechanism that will come to rescue

A

SNS activation

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30
Q

What happens when the heart rate becomes too rapid?

A

the heart ability to fill during diastole is limited and cardiac output is decreased. Increase in arterial vasoconstriction tightening of the vessels, affect the SV because it increase afterload.

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31
Q

briefly explain the HF : compensatory mechanisms

A

SNS activation : increase in heart rate, increase in contractility , peripheral vasoconstriction

Neuro hormonal Response ( RAS ) : NA/ Water retention, increase periph vaso. , ADH causes water retention

ventricular dilation : enlargement of the heart chambers ( usually LV ) , muscle fibers of heart stretch ( initially good but over time stretch too far and decrease CO )

ventricular hypertrophy : increase muscle mass and ventricular wall thickness

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32
Q

why would neuro hormonal response be a bad thing in the long run ?

A

helping us in the moment but in the future it is actually increasing our fluid overload

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33
Q

ventricular dilation is poor conduction that can lead to dysthymias, is this true or false.

A

true

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34
Q

when the chamber wall thickens - there is less room for filling during diastole

A

this is true

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35
Q

cardiac hormones release by the heart if it’s under stress or what state ? this causes strecth and causes diuresis ( increase peeing, widening of the vessels and work against the raas system.

A

heart failure

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36
Q

ADH is also referred to as

A

vasopressin

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37
Q

what does vasopressin mean

A

causes fluid retention, with this blood volume increase venous return to the heart goes up, high preload

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38
Q

what happens if u have constantly high preload

A

causes stretches to accomodate to the end of diastole ventricular dilation

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39
Q

although the enlargement of the chambers how can it contribute to not being helpful?

A

at some point becomes over stretched and cardiac output will drop off

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40
Q

ventricular hypetrophy is common where ?

A

long standing HTN and the muscle grows to meet the increased workload demands

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41
Q

types of heart failure : acute vs chronic and left vs. right sided

A

acute comes quickly ( pulm edema) and chronic happens over years ( neuro- hormonal activation)
acute on chronic heart failure
both are equally life threatening

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42
Q

types of heart failure :
left vs right sided

A

left sided HF symptoms due to decrease CO or pulmonary congestion

right sided HF symptoms related to increase systemic venous congestion

failure of one pump will eventually cause other pump to fail = biventricular failure

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43
Q

what is the classic symptom of acute heart failure is the development of ?

A

flash pulmonary edema

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44
Q

what are the compensatory of chronic patients ? can you name an example for this ?

A

associated with neuro hormonal activation to compensate to maintain cardiac output, for example , result of long standing hypertension ( standing against that resistance, lead to HF)

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45
Q

what does the right side receive and where does it go , what happens when the right side fails ?

A

right side received deoxygenated blood from the body and brings it to pulmonary circulation
when the right side fails there is a backup of blood into the peripheral veins - venous circulation

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46
Q

As the pressure rises in the veins, fluid begins to leak into the interstitial which occurs all over the body, is this true or false?

A

this is true

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47
Q

right sided heart failure head to toe : ** hint this is referring to fluid over load **

A

jugular vein distention
swollen hands and fingers
anorexia and nausea
distended abdomen
enlarged liver and spleen
polyuria at night
dependent edema

a person can also develop ascites and not being hungry ( feeling full )

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48
Q

what are the general symptoms of right sided heart failure ?

A

weight gain and increased BP

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49
Q

Right sided heart failure is usually referring to

A

referring to that accumulation of fluid everywhere

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50
Q

left sided heart failure
Decreased CO

A

fatigue/weakness
confusion, restless
tachycardia
angina
oliguria
pallor, weak
peripheral pulses
cool extremities

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51
Q

faitgue/weakness and confusion/restless is more common in older adult when it comes to left sided heart failure

A

yes this is true

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52
Q

left sided heart failure what does it relate to ?

A

relate to decreased perfusion to the tissues, not receiving adequate blood flow

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53
Q

left sided heart failure :
pulmonary congestion

A

cough
dyspnea : orthopnea , paroxysmal nocturnal dyspnea
crackles/wheezes
frothy, pink tinged sputum
s3/s4 gallop

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54
Q

what is paroxysmal nocturnal dyspnea ?

A

waking up at night suddenly SOB ( suffocation )

55
Q

where is the cardiac electrical system found ?

A

this is found in the right atrium - the SA node

56
Q

what part of the heart has the ability to depolarized ?

A

Sa node have the ability to depolarized, depolarization means that the cell goes form neg. charged to becoming positive resulting in a contraction.

57
Q

name the characteristics of the cardiac electrical system

A

impulse is iniated in SA node

travels down atria to AV node ( signal is delayed for ventricular filling )

signal then travels down bud;le of his to L and R bundle of branches and purkinje fibers

58
Q

why is the impulse delayed?

A

it allows for increase ventricular filling so that tricuspid will remain open for longer ( stronger contractions moving forward )

59
Q

The atria and ventricle are isolated from each other, what is the only way a signal can pass from atrium toventricle ?

A

through an AV node

60
Q

what are the properties of cardiac cells : ACCE

A

automacity
contractility
conductivity
excitability

61
Q

The atrium depolarize via what ?

A

ventricles

62
Q

what is the ability to transmit an impulse called ?

A

conductivity

63
Q

The electrocardiogram : what is it ?

A

when electrolodes are place on the skin, an electrical signal of the entired heart is observed ( EKG )

64
Q

what signs can an ecg give u

A

ecg can give a lot of signs of muscles not getting enough blood, it can tell cardiac muscle is thicker than normal

65
Q

what else can ecg pick up ?

A

electrolytes imbalances ( potassium imbalances )

66
Q

what type of abnormalities can and EKG see?

A

EKG can detect abnormalities in cardiac conduction, ischemia, infraction, hypertrophy, and electrolyte imbalances

67
Q

how are waveforms form in EKG ?

A

waveforms are produced by charged ions moving across membranes of myocardial cells

68
Q

At rest what is the inside of the cell’s charge ?

A

negative

69
Q

What happens when the cell is stimulated ?

A

there is a change in charge, from neg. to pos. ( depolarization )

70
Q

where is the wave that corresponds with atrial repolarization?

A

it occurs with the ventricular depolarization - it gets hidden in the QRS complex

71
Q

the movement of the impulse and subsequent depolarizaition of the atria and ventricles from the SA Node all the way to the purkinje represents as what wave ( s )

A

P WAVE, QRS complex, and T WAVE
the corresponding mechanical activity is contraction of atria followed by contraction of ventricle - the heartbeat

72
Q

what does the action potential represent ?

A

represents the change in voltage across the single cell due to impulse

73
Q

how does action potential occurs ?

A

when the charge across the membrane changes from neg. to pos., the changes in charge is due to the movement of ions in and out of the voltage gated channels.

74
Q

ECG waveform represents ……

A

an impulse moving through the entire heart

75
Q

how many phases can depolarization of a cell divide ?

A

4 phases

76
Q

Conduction on ECG : what is NSR

A

a term used to describe a normal ECG rate and rhythm, generated in the sinotrial node

77
Q

Sa node cells depolarize faster than other cardiac cells, what does this mean ?

A

it sets the pace of conduction

78
Q

ONLY an impulse from where will derived a coordinated cardiac cycle with good stroke volume

A

SA NODE

79
Q

what are the ‘backups’ if the SA node is not functioning properly ( intrinsic rates )

A

AV/junctional
ventricular and purkinje fibers ( this is not fast enough to maintain CO )

80
Q

what are the two types of ECGs

A

12 lead ECG
continuous cardiac monitoring

81
Q

what is the 12 lead ECG

A

10 electrolodes placed on chest and limbs, giving 12 views of the heart

  • diagnostic ( rhythm, ST elevation )
82
Q

what is the continous cardiac monitoring ?

A

3 electrolode placed on chest

gives 5 views of heart

monitor rhythym , ST elevation ( changes or diagnosis always made with 12 lead )

83
Q

12 lead is used for what? and telemetry is used for …?

A

to diagnose
and telemetry is used for monitoring

84
Q

if pateint is in risk of low ischemia and low cardaic output then we can identify as t changes quickly and intervene
any changes can be confirmed with ….

A

12 lead ECG

85
Q

acute cardiac symptoms or heart rate has suddenly become irregular, what are we utilizing in term of ecg ?

A

12 lead ecg

86
Q

ECG analysis w, another word for leaders in ( 12 lead ECG ) is what ?

A

views

87
Q

when we are looking at the ECG what are we looking at ? and what does those specific changes lead to or indicate?

A

we are looking at the angle of the heart, and those specific changes indicates problem with the coronary artery ( or oxygenated blood )

88
Q

if there is an ST eleavtion , what does this tell you ?

A

obstruction in the artery ( most liely )

89
Q

what does the 12 different leads or views help us diagnose ?

A

helps diagnose location of the MI or determine where blockages are happening

90
Q

why would you want to print a telemetry result out?

A

tells you the patients baseline rhythm so we can compare if it changes

91
Q

the st segment - review

what is a st segment depression

A

ischemia caused by partial occulusion of ca coronary artery : unstable angina and non stemi

92
Q

what is st segment elevation ?

A

complete occlusion of the coronary artery, the entire thickness of the myocardium becomes ischemic : stemi

93
Q

Potassium Imbalances and ECG changes , what does this effect?

A

effects the myocardium resting potential and ability to repolarize

94
Q

what is the important electrolyte in part of the depolarization and repolarization

A

potassium

95
Q

K imbalances tend to _____ through the AV node and the myocytes

A

slow impulse conduction

96
Q

what are the characteristics of hypokalemia in ecg changes

A

prolonged PR
depressed ST
low or inverted T
appearance of U
increase in QT ( which predisposes to torsade de pointe )

97
Q

name the characteristics of hyperkalemia in ecg

A

diminished or absent P
widening of the QRS
characteristic peaked T
cells become unexcitable
can rapidly progress to VT or VF and cardaic arrest

98
Q

what is a lethal rhythm

A

torasde de pinte ( increase in QT )

99
Q

characteristics peaked T in hyperkalemia can put the PT for risk lethal what?

A

arythmias

100
Q

what type of wave is the depolirazation of atria

A

P wave

101
Q

ST segment of depression is caused by

A

ischemia

102
Q

T wave can be affected by …?

A

low potassium ( lower than normal or inverted )

103
Q

U wave is unique to what characteristic ?

A

hypokalemia ( low potassium )

104
Q

Q and T - is related to

A

this is related to slowing the conduction when we have low intervals

105
Q

Sinus Rhythym :
what is the description
clinical associations

A

description : normal conduction
clinical associations : healthy adults

106
Q

Sinus rhythm : ECG characteristics
clinical significance
treatment

A

rate 60-100 beats/min, regular, p wave precedes each QRS, PRI normal, QRS complex normal
none
none

107
Q

true or false. each beat should be equal distant apart this is our heart rate when the beats is equal it is considered normal

A

true

108
Q

true or false. always have a visibly P wave that is upright and comes before QRS complex, there should be a P wave for every WRS in the strip.

A

true

109
Q

The QRS complex should always be narrow, it should always be followed by a rounded and upright T wave , we do not want to see U wave. Is this a true statement?

A

true

110
Q

Sinus Bradycradia: what can impact this and what condition?

A

PNS , and hypothyrodism

111
Q

Cardiac muscle is strong therefore you have a higher stroke volume and do not need the heart rate to be as high ( sinus bradycardia ) when u are an athlete

A

yes this is true

112
Q

What is the description for sinus bradycardia

A

same conduction pathway as SR but SA node fires at a rate below 60 beats/ min

113
Q

sinus bradycardia : clinical associations

A

may be normal in aerobically trained athleetes, secndary to medications, vegal stimulation, hypothermia, hypothyrodism , increase CP , Inferior Mi

114
Q

sinus bradycardia : ecg characteristics and clinical significance

A

rate below 60 beats/min, regular , p wave precedes each QRS, PRI normal, QRS complex normal

if patient does not tolerate low heart rate may become pale, col skin, hypotensive, weak, angina dizziness, confusion , SOB

115
Q

sinus bradycardia , do u have low or high co

A

low

116
Q

sinus bradycardia how is the conduction pathway

A

conduction pathway is normal, the wave patterns follow the same rules develops fast rhythms because of SNS inhibition

117
Q

Sinus tachycardia description

A

same conduction pathway as SR but SA node fires at a rate above 100 beats/min ( vagal inhibition or SNS )

118
Q

what is the clinical associations of sinus tatchycardia

A

stress, exercise, pain, hypotension, hypovolemia, anemia, hypoxia, hypoglycemias, MI, heart failure

119
Q

ECG characteristics of sinus tatchycardia

A

rate above 100 beats/min, regular, p wave precedes each QRS, PRI normal, QRS complex normal

120
Q

what is the clinical significance of sinus tatchycardia and treatment

A

Clinical Significance: patient may develop dizziness, dyspnea and hypotension Treatment: based on cause

121
Q

true or false. Sinus tatchycardia shortens the time of filling during the diastole period. ( less to feed the muscle )

A

this si true

122
Q

coronary arteries fill during diastole which is shortened with increased HR can lead to what ?

A

angina

123
Q

what is atrial fibrillation ?

A

total disorganization of atrial activity cause by multiple ectopic foci, loss of atrial contraction, most common dysrthmia, may be chronic or acute

124
Q

what is the clinical associations of atrial fibrillation

A

occurs in patients with underlying heart disease, throtoxios, alcohol intox, caffeine use, electrolyte imbalances, stress

125
Q

atrial fibrillation ecg characteristics :

A

atrial rate may be up to 600 bpm, ventricular rate varies between 50 - 180 ( irregular ) , p waves replaced by wavy baseline

126
Q

what is the clinical significance of atrial fibrillation

A

decrease in CO ( loss of atrial kick and rapid ventricular response ) thrombus may be form because of stasis ( stroke risk increase 3-5 times )

127
Q

we have a situation where there is decreased time time for ventircular during the time for diastole ( this drops co even more )

A

atrial fibrillation

128
Q

statis ( the blood is just sitting there ) - increase risk of blood ( stroke ) what is this being reffered to ?

A

multiple ectopic foci

129
Q

atrial tatchycardia , what occurs here

A

we are going to see rapid atrial contraction, many p waves in a row

atrial wave is so fast, and its almost not distinguish ( can be 600 waves per minute )

130
Q

where are the impulses coming in a trial fibrillation

A

impulses are coming all the way from the atrium

131
Q

there are multiple ectopic foci - these are impulse coming outside of where ?

A

sinotrial node ( stimulated so fast there is no time for normal contraction )

132
Q

After Mi or longstanding heart failure ( alcohol or caffeine or stress , electrolyte imbalances can lead to ______ )

A

AFIB

133
Q

not getting real contraction - not efficiently moving forward, this can be chronic or acute. This is so fast we arent able to do anything with the P wave

A

AFIB, we will notice they are not distance apart ( irregular rhythm ) because of occlusion going through av node at a irregular rate

the ventricular responses is faster or slower sometimes

Pt.2 PHRM/PHYS/NS (14 decks)

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