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Cardiology (inpatient) > congestive heart failure > Flashcards

congestive heart failure Flashcards

1
Q

Where is the only vein-capillary-vein system located in the body?

A

hypothalamus

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2
Q

what part of the body holds the most blood at any given time?

A

VEINS!

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3
Q

What are things that contribute to resistance of w/in yo body

A

1) blood viscosity (effected by volume and # of RBC)
2) total blood vessel length

3) blood vessel diameter

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4
Q

what is the biggest contributor to minute-to min control of resistance in the vascular system?

A

Blood vessel diameter

R= 1/(r^4)

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5
Q

can the heart heal itself?

A

yes, but very slowly- only 1% of heart muscle cells are replaced per year

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6
Q

how are electrical currents spread w/in the myocytes?

A

via gap junctions

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7
Q

what does atrial natriuretic peptide do?

A

regulates the concentration of sodium in the extracellular fluid

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8
Q

What part of the heart does the sympathetic fibers innervate?

A

the entire heart muscle, and node cells

releases NE

**the receptors will also bind to the neuroendocrine hormone epinephrine from the adrenal gland

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9
Q

what part of the heart does the pSNS innervate?

A

the SA-AV node, released acetylcholine

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10
Q

what is the inherent rate of the SA node?

A

100 bpm, but it is moderated by the nervous system

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11
Q

what part of the heart conduction system has a .1s delay>

A

the AV node- allows the atrai to contract and totally fill the ventricles

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12
Q

What to the purkinje fibers do?

A

supply the papillary muscles-tell them to contract before the rest of teh ventricles to hlep prevent backflow through the valves

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13
Q

why is the refractory period for heart cells important?

A

long refraction means the cell won’t fire again until its last contration is almost relaxed away- lets its empty completely

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14
Q

arrhythmia

A

uncoordinated atrial and ventricular contractions caused by a defect in the conduction system.

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15
Q

Fibrillation

A

: a rapid and irregular (usually out of phase) contraction where the SA node is no longer controlling heart rate.

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16
Q

ventricular fib

A

is more life threatening. The ventricles pump ineffectively and without filling. If the heart’s rhythm is not rapidly reestablished then circulation stops and brain death occurs

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17
Q

ectopic focus

A

abnomral pacemaker that takes over the conduction system- usually bc it goes faster than the SA node

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18
Q

Extrasystole

A

premature conractions, can be atrial or ventricular

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19
Q

total block

A

ventricles beat at their intrinsic rate- too slow to maintain circulation

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20
Q

partial block

A

AV impulse isslow, but it does get through

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21
Q

coronlary ostia

A

openings to coronary vessels- blood falls back into them during dicrhotic notch- heart is the FIRST THING to get oxygenated b/c of these

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22
Q

Cardiac Output

A

amount of blood pumpled out of each ventricle in one minute

CO=HR X SV

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23
Q

what is the normal cardiac output?

A

5.25 L/min

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24
Q

what is the most common way your body varies CO?

A

Via heart rate

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25
Q

what are things that increase heart rate?

A

positive chronotropic factors

-sympathetic NS

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26
Q

what are things that decrase heart rate?

A

PSNS

negative chronotropic factors

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27
Q

what is SV?

A

the diff bw end diastolic volume (after ventricles have completely filled) and end systolic volume (after ventricles have completely emptied)

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28
Q

what is the average amount of blood that gets pumped out?

A

60% of blood that was in the chamber (avg 70 ml)

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29
Q

inotropy

A

how wll the heart is working - muscle contractions

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30
Q

Starlings Law and SV?

A

the critical factor controlling SV is PRELOAD

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31
Q

preload

A

degree to which the cardiac muscle cells are stretched before they contract

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32
Q

is there an optimal Length/tension for preload?

A

yes! you want maximal force generation

-underextension limits force, but overextension leads to inefficient pumping

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33
Q

what is the most important factor in causing increased preload?

A

the amount of blood inthe ventricles by the end of diasole

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34
Q

what is the amount of blood in the ventricles controlled by?

A

venous return and the amount of time b/w ventricular contractions (diastole)

** anything that incrases venous return or slows heart rate increases EDV

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35
Q

Frank-Starling mechanism

A

the higher the EDV, the higher the SV

But there is a limit to how high the SV will go. at some pt, increased EDV doesnn’t help much

think-larger EDV =stronger contraction= lareger SV w/ same amount of residual volume

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36
Q

how can the ventricle be emptied better for increased SV?

A

“squeez force” contract dat shit

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37
Q

How does the SNS control stroke volume?

A

by increased the force of each ventricular contraction at any given SV

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38
Q

What is Ejection Fraction

A

expressed as a %- normally avgs btw 50-75 %

EF=SV/EDV

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39
Q

what can EF measure?

A

contractility via SV

*increased contractility=increased EF

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40
Q

preload definition?

A

is proportional to the amount of ventricular myocardial fiber stretch just before systole (EDV).

Preload ~ Starling’s “length”

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41
Q

afterload definition?

A

pressure that the ventricles must overcome to force open the aortic and pulmonary valves.

Afterload ~ how much tension the heart must create to do its job (systemic high bp ex)

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42
Q

what is the ideal situation for the heart to work its best?

A

high preload and low afterload

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43
Q

what can increase afterload?

A

anything that increases systemic or pulmonary arterial pressure (ex. HTN)

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44
Q

do arteries need to be more elastic or compliant?

A

Elastic! they are often called pressure reservoirs bc of their elastic recoil

they need to keep the pressure high

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45
Q

Veins: more elastic or compliant?

A

they need to be more compliant

-higher the compliance ofa structure, the more it can be stretched w/o a corresponding increased in pressure

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46
Q

V vs P: vein and artery

A

at low pressures, venous compliance is 10-20 times greater than arterial compliance, but arterial and venous compliance are similar at high pressures

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47
Q

is pulmonary pressure higher or lower than systemic pressure?

A

LOWER!

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48
Q

what would happen if pressure to the lungs when way up?

A

Trauma to smaller vessels of the lungs;
inflammation and repair;
narrowing of these vessels as they heal;
increased resistance of blood flow to the lungs.

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49
Q

systolic pressure

A

max pressure at Systole

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50
Q

diastolic pressure

A

min pressure at diastole

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51
Q

pulse pressure

A

systolic-diastolic

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52
Q

what is MAP?

A

Diastolic + 1/3 of the pulse pressure

53
Q

what are you hearing when you listen to someones bp?

A

turbulence- a little blood can get through. so when it goes under diastolic pressure- there will be no sound of turbulence bc vessel is completely open

54
Q

arterioles

A

smallest arteries- their function is controlled by neural, hormonal, and local chemicals

  • muscularis!
  • change their diameter via autoregulation
55
Q

what are some local controls of arterioloar radius?

A

pH

  • if an organ becomes morme metabolically active, its CO2 increased and O2 decreases
  • resulting pH change leads to the dilation of the arteriolies

and vice versa

56
Q

continuous capillaries?

A

most common and allow passage of fluids and small solutes

-skin and muscle

57
Q

fenestrated capillaries

A

more permeable to fluids and solutes than continuous capillaries

  • allow more rapid transfer of substances
  • kidneys, intestins, endocrine
58
Q

sinusoidal caps

A

leaky- allows large molecules to pass btw the blood and surrounding tissues

-liver, bone marrow, lymphatics

59
Q

at what part of the capillary does osmotic pressure have more of an effect?

A

the distal end! bc blood is more concentrated there

60
Q

what are the two main roles of lymphoid tissues?

A
  1. house and provide a proliferation for lymphocytes

2. give a surveillance site to examine and clean the lymph fluid

61
Q

venous system: componenets?

A

3 main layers (tunics)

veins also have less smooth muscle and elastin than arteries

-veins also highly distensible- called “capacitance vessels”

62
Q

what is the blood pressure in veins?

A

15 mmgh

63
Q

what helps veins move blood back to the heart?

A
  1. respiratory pump

2. muscular pump

64
Q

heart failure

A

inadequate pump function of the heart, which leads to congestion resulting from a back up of fluid in the lungs and peripheral tissues

65
Q

what are the general etiologies of left heart failure?

A

1) inappropriately lrge workload on the heart
2) restricted ability of the heat to fill
3) loss of heart muscle cells
4) poor ability of myocytes to contract

66
Q

wwhat can cause the restricted ability of the heart to fill?

A

pericardial dz, Mitral stenosis, infiltrative “fibrotic” heart dz (amyloid)

67
Q

what can cause the loss of heart muscle cells?

A

cells died in heart attack

68
Q

what can decrease the myocytes ability to contract?

A

poisons, infxns, mutuations of myocyte protines

69
Q

what can cause an increased workload on the heart?

A

valves that regurg- M/A

pushing against too much systemic pressure

  • HTN
  • AS
  • asymmetric septal hypertrophy
70
Q

what happens in systolic left heart dysfuction?

A

pressure-volume line shifts to the right

  • ventricle stops pumping out earlier (at a higher pressure reading) than is normal
  • isovolumetric relaxation hit faster than normal
  • reduced EF
71
Q

how does your heart try to compensate for this? (systolid L heart dysfxn)

A

1) increase LV volume by increasing the overall size of the LV via muscle mass and chamber size
* gives the LV more “contents” to push out

72
Q

more ways your heart compensates for systolic L heart dysfxn?

A

1) improve contractility by pumping catecholamines (epei or dopamine) “diggin deep”
3) improving preload (just shove more in there)

73
Q

diastolic left heart failure

A

diastolic curve shifts to the right

-ventricle reaches a max pressure that it can handle at a lower volume than normal

**the ventriculare hypertrophy that initially can make the heart pump better in systole can eventually lead to dysfxn in diastole

74
Q

symptoms of right-sided heart failure

A

-dependent edema
-JVD
-abdominal distention
-hepatomegaly
splenomegaly
-anorexia, N
-weight gain
-nocturnal distress

75
Q

left sided heart failure sx

A

dyspnea

  • tachypnea
  • crackles in lungs
  • dry hacking cough
  • paroxysmal noctural dyspnea
76
Q

what is a common cause of right heart failure?

A

chronic lung dz

cor pulmonale (enlargement of the right ventrical due to high BP in the lungs)

77
Q

how does Right heart failure lead to left heart failure

A
  • normally, the interventricular septum is usually bowed toward the thinner walled and lwoer pressure right ventrilce
  • when R V pressure increases relative to the left, the IV septum can bow to the left and prevent efficient filling of hte LV
  • lead to even More pulm congestion
78
Q

what does SOB happen with heart failure?

A

1) pulmonary source (lung dz)
2) Right heart source (enlarged liver presseing agains diaphragm limiting lung volume)

3) left heart source
(decreased ability to pump blood has led to pulmonary edema)

79
Q

ventricular hypertrophy: concentric growth

A

even grown of a ventrical w/o overall enlargment- wall of ventricle are thickened and volume is diminished

*sarcomeres added in parallel (increase width)

80
Q

ventricular hypertrophy: eccentric growth

A

even growth of a ventricle w/ heart enlargment

  • ventricle size and volume both increase
  • increase myocyte cell lenthg
  • more rapid change
81
Q

what is concentric hypertrophy causes by?

A

HTN, aortic constriction

82
Q

what is eccentric hypertrophy caused by?

A

valve dz

83
Q

JVD

A

right sided heart failure

84
Q

what is the classic wave form of JVP?

A

a, c, and v

a=atrial wave
c=contraction (ventricular wave)
v=filling wave

85
Q

what are RF for CHF?

A

CAD, MI, smoking, HTN, obesity DM, valvular heart dz, cardiomyopathy

86
Q

what is CHF

A

clinical syndrome characterized by abnormal retention of water and sodium

87
Q

causes of diastolic HF

A

restrictive, infiltrative cardiomyopathies (amyloidosis, sarcoidosis), pericardial effusion, hypertrophic card, MI, HTN

88
Q

systolic HF etiology

A

dialated cardiomopathies, MI, Ischemic heart dz, chronic HTN

89
Q

high output HF

A

anemia, hyperthyroidism, AV fistula, Beriberi (thiamine deficiency) Paget dz

90
Q

systolic dysfunction

A

HF w/ decreased or impaired EF (HFrEF)

<40%

91
Q

diastolic dysfxn

A

diastolic HF w/ normal or perserved EF

HFpEF >50%

92
Q

what does CFH affect?

A

left atrial pressure, CO

93
Q

what are some PE findings of HF?

A

tachypnea, JVD, hepatojuglar reflux, pulm rales or crackles, wheezing, pleural effusion,

-lateral displacement of apical impulse

cyanosis, anasarca, hypotension, cheyne-stokes
ascites

94
Q

anasarca

A

peripheral edema

95
Q

what causes the S3 sound

A

oscillation of blood back and forth between the walls of the ventricles initiated by the inflow of blood from the atria.

96
Q

what is the confusion and unconsciousness caused by in HF?

A

the decreased O2 to brain

97
Q

when might one hear the S4 sounds?

A

diastolic HF

98
Q

what are the predominant features of RHF?

A

anasarca and hepatomegaly

99
Q

what cuases the cold and clammy skin associated with heat failure?

A

sympathetic activity

100
Q

what is another randome x of HF

A

nocturia

101
Q

what to expect BP wise

A

hypotension and narrow pulse pressure

BP can be high, normal , or low

102
Q

diagnostic studies: labs

A
  • anemia
  • renal insufficiency
  • hyper kalemia
  • hyponatremia
  • elevated liver enzymes
103
Q

what is the most useful imaging study?

A

Echo- assess size and function of the chambers, valve abnormalities, pericardial effusion, shunting, and segmental wall abnormality

104
Q

what would a chest xray show?

A

cardiomegaly, bilateral or right-sided pulmonary effusion, perivascular or interstitial edema, venous dilation and cephalization, alveolar fluid

105
Q

what are kerley B signs?

A

horizontal lines less than 2cm long, commonly found in the lower zone periphery. These lines are the thickened, edematous interlobular septa. Causes of Kerley B lines include; pulmonary edema, lymphangitis carcinomatosa and malignant lymphoma, viral and mycoplasmal pneumonia, interstital pulmonary fibrosis, pneumoconiosis, sarcoidosis.

106
Q

NYHA class I

A

cardiac dz but no limitations, asx

107
Q

when is stress imaging or radionuclide angiography needed?

A

to assess the cause of severity of the dz

108
Q

what other cardiac labs may be elevated?

A

BNP or N-termial pro-BNP may be elevated

creatine kinase mB and troponins should also be tested to evaluate for new MI

109
Q

what is something taht should be looked at in older population that present w/ Hf?

A

thyroid test

110
Q

Class II

A

Cardiac disease slight limitation with ordinary activities, symptoms with ordinary activities

111
Q

Class III

A

Cardiac disease marked limitation; symptomatic with less than ordinary activities

112
Q

Class IV

A

Cardiac disease inability to perform any physical activity without symptoms. Symptoms at rest

113
Q

tx of HF-non-pharmacologic

A

progressive aerobic exercise,low-sodium diet, tobacco and alcohol stopping, stress reduction

114
Q

initial pharmacologic methods

A

early initiation of ACE I

2cd: ARB, BB, aldosterone agonists

115
Q

How does ACEI help?

A

decreases let ventricular wall stress, slows mycardial remodeling and fibrosis

116
Q

BB?

A

improve EF, reduce Left ventricular dilation, and reduce the incidence of arrythmias

117
Q

reduced EF heart failure?

A

systolic (enlarged ventricles fill w/ blood and pump out less than 40-50%)

118
Q

non-reduced EF heart failiure

A

diastolic (stiff ventricles fill with less blood than normal- vetricles pump out about 60% of the blood, vut the amount may be lower than normal

119
Q

what are some meds that cn worsen HF

A 
NSAIDSNSAIDs
Some anesthesia and chemotherapy meds
TZDs
CCBs
Saxagliptin and sitagliptin
Flecainide, disopyramide, sotalol, dronedarone
Alpha blockers, minoxidil
Itraconazole, ampho B
120
Q

More meds that worsen HF?

A 
Carbamazepine, pregabalin
TCAs, citalopram, clozapine, lithium
Bromocriptine, pergolide, pramipexole
Albuterol, bosentan, epoprostenol
TNF-alpha inhibitors
Chloroquine, hydroxychloroquine
121
Q

Stage A tx

A

high risk for HF but no damage or sx

*get yo house in order

122
Q

Stage B tx

A

damage, but no sx

  • ACEI or ARB (all pts w/ rEF)
  • BB (all pts w/ rEF)
  • statins
123
Q

when can you use CCB?

A

preferably amlodipine- used only to tx associated angina or HTN

124
Q

ARni?

A

sacubitril/valsartan
aRB + neprilsyn inhibitor

neprilysin- breaks down natriuretic peptides–> vasoconstriction

125
Q

DI of arni

A

nsaids, K sparing diuretics, Lithium

126
Q

ADRS of arni

A

hypotension,, hyperkalemia, cough, dizzy, renal failure

127
Q

when aer IDCs indicated?

A

when EF falls below 35

128
Q

when is biventricular pacing indicated?

A

resynchronize the heart when QRS becomes prolonged

Cardiology (inpatient) (14 decks)

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