Hemodynamic Disorder Word Documents 1, 2, and 3 Flashcards

1
Q

What is the pressure of the right atrium?
Lest atrium?
Right ventricle (systolic)?
Left ventricle (systolic)

A

right atrium: 3 mmHg
Lest atrium: 8 mmHg
Right ventricle (systolic): 25 mmHg
Left ventricle (systolic): 130 mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What 2 things represent preload

A

end diastolic pressure and volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

the resitance the ventricle must overcome to pump out all of its contents is…

A

afterload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

systolic ventricular wall tension is _____ and diastolic ventricular wall tension is _____

A

afterload

preload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the laplace relationship?

A

ventricular wall stress is proportional to the pressure and radius of the camber and inversely proportional to the thickness of the wall
S = Pv x R / 2t

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

If the thickness of the ventricular wall increases (while pressure and radius of ventricular chamber stays constant), will the stress on the ventricular wall increase or decrease?

A

stress will decrease

during diastole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are examples of endogenous “inotrophic” substances and exmaples of drugs that are “inotrophic”

A

epi and nor epi

dobutamine and milrinone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What condition is being describe below?
What can cause this condition?

When ventricular compliance decreases below the ability of the atrium to fill normally

A

restrictive cardiomyopathy

caused by fibrosis, amyloidosis, interstitial infiltration by anything that is more rigid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Impaired cardiac filling is called ____ and impaired cardiac pumping is ____

A

diastolic dysfunction and systolic dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Will diastolic dysfunction typically reduce the ejection fraction?

A

no

EF = SV / EDV (they decrease proportionally)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the 5 major categories of the factors that determine the CO?
Imp concept

A
preload
afterload
contractility 
compliance 
heart rhythm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Are there more pts with chonic or acute HF?

A

chronic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

CAD as a causes of HF by _____

A

dec contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Uncontrolled/severe HTN causes HF by _____

A

increasing afterload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Aortic stenosis causes HF by _____

A

increasing afterload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What can cause HF without changing ejection fraction?

What can causes HF by decreasing ejection fraction?

Why is there a difference?

A

No change to EF:

  • left ventricular hypertrophy
  • restrictive cardiomyopathy
  • pericardial disease

Decreasing EF:

  • aortic stenosis
  • severe HTN
  • CAD

those that decrease EF all increase the afterload (dec SV with Inc EDV), while those that have no change in EF decrease both the SV and the EDV!

EF = SV/EDV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the 2 most common symptoms of HF?
What are the 2 most specific symptoms of HF?

What 7 signs of HF?

A

common: dyspnea and fatigue
specific: paroxysmal nocturnal dyspnea and orthopnea
signs: tachycardia, tachypnea, hypotension, pulmonary crackles, wheezing, diaphoresis, and gallops

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How does HF cause dyspnea? (what is the mechanism)

A

congestion of blood causes inc pulmonary pressure which increases filtration of fluid into interstitium. this inc in ISF compresses the alveoli and increases their resistance to airflow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How does HF cause paroxysmal nocturnal dyspnea? (what is the mechanism)

A

lying down causes a redistribution of the blood volume such that venous return is increased. the heart in failure cannot pump out this inc venous BV so there is a back up of it into the lungs –> pulmonary HTN and edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How does HF cause tachycardia? (what is the mechanism)

A

CO = SV x HR

to compensate for the dec in SV, the HR will increase to try to maintain CO/Ejection fraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What happens when pulmonary venous pressure goes over 25 mmHg?

A

tansudate passes not only into interstitium but also into the airspaces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How does HF cause diaphoresis? (what is the mechanism)

A

dec in CO causes a stimulation of SNS = sweating increased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

When is an S3 gallop heard (what part of cardiac cycle)?
What is it attributed to?
low or high pitched?

A

early diastole

rapid filling of ventricle

low pitched

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

______ is a biomarker of HF and the level correlates with _____

A

BNP correlates with severity of HF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the effects of BNP? (3)
How is this counter-regulatory?
Why is that important?

A

it causes (1) an excretion of Na and water, vasodialtion

(2) inhibition of renin secretion (therefore also dec angio II and aldo),
(3) inhibits ADH

BNP compensates for/opposes the actions that low BP has on the kidney

helps to maintain homeostasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is the most common cause of HF with preserved ejection fraction?

A

HTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is an S4 gallop assc with?

What causes this sound?

What state name does this sound like (imp concept

A

HF due to HTN

the sound of left atrial contraction as it works to inject blood into a stiffened left ventricle

Tennessee

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the profiles of acute HF?

A

A: Warm and dry: perfused extremities (normal or due to vasodialtion) and no edema, no JVD, no crackles

B: Warm and Wet: perfused extremities, edema, JVD, crackles

C: Cold and dry: poor perfusion of extremities (due to dec CO or abn vasoconstriction), no edema JVD, or crackles

D: Cold and wet: poor perfusion of extremities, edema JVD, or crackles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What commonly causes warm and dry HF profile?

A

transient myocardial ischemia

HF due to lung disease (RT heart failure)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Cold and dry is most commonly caused by

A

hypovolemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Mitral regurg + left ventricular dilation + exercise would produce what acute HF profile?

A

cold and dry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Describe the action of the “respiratory pump”

A

rapid breathing promotes negative intrathorasic pressure during inspiration which promotes the movement of blood into the heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What CN does info from the carotid body travel on to get tot he CNS?

A

9 and 10

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What effect does the presence of epi have on the liver?

A

induced glycogenolysis and raises the blood glc level = causes a shift of of water into the plasma/intravasular space

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What 2 process result in “autotransfusion”

A

epi inc glycogenolysis in liver to inc blood glc to inc OPc = fluid into PV

vasopressin (arteriole contriction dec HPc and fluid moves into PV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How can cardiogenic shock be distinguished from hypovolemic shock?

A

the central venous pressure will be elevated in CS and low in HS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is the most common cause out aortic stenosis in pts younger than 65? older than 65?

A

congenital anomalous bicuspid valve

senile degeneration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

crecendo-decrecendo systolic murmur + weak or delayed pulse + atrial (S4) gallup

A

aortic stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What are the pathophysiologic consequences of mitral regurgitation?

A
  1. decreased forward SV
  2. inc left atrial volume and pressure –> dilation (if chronic)
  3. volume related stress on left ventricle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

“Flash pulmonary edema” is assc with …

What is the mechanism of developing it?

A

sudden mitral regurgitation

inc left atrial pressure which is transmitted back to the lungs = rapud pulmonary congestion and edema
**medical emergency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is the most common symptom of acute mitral regurg? chronic mitral regurg?

A

acute: dyspnea
chronic: fatigue + paroxysmal nocturnal dyspnea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

apical holosytoic (pan systolic) murmur

A

mitral regurgitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

In terms of SV, how is actue and chronic mitral regurgitation different?

A

in chronic there is more blood going backwards than acute bc the left atrium dilates and pressure falls (favoring the movement of blood backwards to the left atrium)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What drug can be given to decompensated mitral regurgitation pts?

A

ACEi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

assc with Marfan syndrome

A

mitral valve prolapse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

mitral valve prolapse heart sound

A

mid systolic click and late systolic murmur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

RHF follows what kind of infection

A

group A beta-hemolytic streptocoocal pharyngitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What are Aschoff bodies and what disease are they assc with?

A

foci of fibrinoid necrosis with histiocyes and anitschkow cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

sign of RHD

A

systolic and diastolic murmur + pericardial friction rub

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

When do symptoms of RHD appear? I.e what age group does it affect?!

A

20 years after childhood infection ~ 30s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Complications of RHD

A

mitral stenosis (fused and shortened chordae)
and/or
aortic regurgitation which lead to…

left atrial HTN
left atrial dilation
atrial fibrillation
left atrial thrombus formation
pulmonary HTN
right ventricular hypertrophy and right heart failure
***basically the compications are anything that will result from not being able to get blood into the left ventricle/overloading the left atrium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

WHat are MacCallum patches?

What are they assc with

A

RHD

maplike areas of atrial endocardial thickening and fibrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

gross pathology of RHD

A

shortened, thickened, fused chordae

MacCallum patches

54
Q

What are the 4 etiologies of aortic regurgitation?

A
  1. insufficiency due to anomalous bicuspid valve
  2. endocarditis
  3. chronic rheumatic valve deformation
  4. dilation of aortic ring by aortic aneurysm or dissection
55
Q

consequences of acute aortic regurg on heart chambers

A

inf left ventricular diastolic pressure and volume –> pulmonary congestion and edema

56
Q

consequences of chronic aortic regurg on heart chambers

A

left ventricle increases muscle mass –> inc compliance and less elevated ventricular diastolic pressure
(lancelace relationship stress = 1/2thickness)

57
Q

How does aortic regurg affect diastolic blood pressure?

A

drops bc blood is leaking back into the heart

58
Q

How does aortic regurgitation affect the blood supply of the heart itself?

A

since it causes a dec in diastolic pressure it will decrease the blood supply to the heart

** remember, the blood flows thru the coronary ostia during diastole (when diastolic BP drops, less blood is available for the CA)

59
Q

What is the heart sounds assc with decompensated aortic regurg?

A

daistolic decrescendo + hyperdyanmic bounding + rapidly collapsing pulse (corrigan pulse) + head bobbing with each pulse (de Musset sign

60
Q

What is de Musset sign? What is it assc with?

A

head bobing with each pulse

assc with aortic regurg

61
Q

Why is the pulse pressure widedned with aoritc regurg?

A

inc ventricular systolic pressure and volumes –> inc ejection fraction (inc systolic pressure)
then more blood falls backwards decreased diastolic pressure)

62
Q

Tx for aortic regurgitation

A

valve replacement

63
Q

Mecanical valves require life long treatment with _____

A

anti-coagulants

64
Q

What are the common complications of surgical valve replacement?

A
structural failure
leak
thrombosis
embolism
bleeding
endocarditis
65
Q

autoimmune inflammation of heart valves

A

libman-sacks endocarditis

66
Q

where do the vegetations form in libman sacks endocarditis?

A

mitral and tricuspid on either or both sides

67
Q

condensed naked nuclei of dead, degenerate, cells that were ingested by phagocytes

A

hematoxylin bodies

68
Q

chronic adhesive pericarditis

A

complication of libman sacks endocarditis

69
Q

In what conditions do marantic endocarditis form secondary to?

A
adenocarcinomas
DIC
chronic sepsis
Swan-Ganz right heart cateterization
**anything that will make pt hyper coagulable
70
Q

Marantic endocarditis is the deposition of ____ on valves and is important bc they ….

A

blood clots

frequently embolize and is the precursor to infective endocarditis

71
Q

friabile masses of blood clot and infecting organisms

A

vegetation

72
Q

What is the pathogenesis of infective endocarditis?

A
  1. vascular injury
  2. platelet and fibrin deposition
  3. microbial seeding
  4. microbial multiplication
73
Q

what is the difference between acute and subacute bacterial endocarditis?

A
ABE = sudden and due to virulent orgs (S. aureus) 
SBE = insidious and due to less virulent orgs (strep viridans)
74
Q

What organism typically causes PVE (prosthetic)?

A

Staph epidermis

75
Q

where does the endocarditis typically form in IV drug users?

A

tricuspid valve

76
Q

On what sided valves does 75% of infective endocarditis occur?

A

left

77
Q

70% of pts with infective endocadritis also have ______

A

a predisposing heart disease

MVP, prosthetic valve, RHD, previous occurrence, etc

78
Q

Adherence of some _____(name species) to valves is facilitated by _____

A

strep (esp strep mutans)

dextran

79
Q

elevated ESR

A

non-specific infective endocarditis lab finding but is present in 95% of cases)

80
Q

What test has >90% specificity for picking up infective endocarditis

A

transesophageal ECG

81
Q

T or F Abcensce of vegetation of transesophageal ECG rules out endocarditis.

A

F

82
Q

Duke criteria

A

infective endocarditis

83
Q

What is the most common cause of right heart failure?

A

left heart failure

84
Q

What is the most common cause of isolated right heart failure?

A

pulmonary disease (vascular or parenchymal)

85
Q

What is cor pulmonale? What causes it

A

RHF due to pulmonary disease (HTNive diseases)

  • emphysema
  • embolism
  • interstitial lung disease
86
Q

How is actue and chronic cor pulmonale distinguished?

A

acute: dilation of right heart chanmbers
chronic: hypertrophy of right heart chambers

87
Q

Acute on chronic cor pulmonale is characterized by

A

dilation superimposed on hypertrophy

88
Q

What do all the lung disease that cause cor pulmonale have in common?

A

pulmonary HTN

89
Q

What are the 4 common manifestations of RHF?

A
  1. leg edema
  2. hepatomegaly
  3. asciteis
  4. JVD
90
Q

Sildenafil (viagra)

A

drug that will work on the pulmonary arterial vessels to decrease pulmonary HTN

91
Q

What is the term for toal lack of cardiac puping

A

asystole

92
Q

What frequently causes sudden death?

A

80% attributed to CAD
cardiac electrical signaling malfunction
–> ventricuakr tachyarrythmia

93
Q

How are electrical signals to contract spread rapidly from cell to cell?

A

low resistance gap-junctions

94
Q

mutations in genes for cell adhesion

A

RT ventricular cardiomyopathy

95
Q

L-type ion channel

A

calcium channel open in phase 2

96
Q

L type ion channels are in close proximity to ____

A

ryanodine receptors on SR

97
Q

mutation in ryanodine receptor is assc with what condition?

A

familial catecholeminergic ryanodine receptors

98
Q

What is the term for a cells abilty to depolarize itself?

A

automaticiy

99
Q

How do injured myocytes develop automaticity? (healthy ones do not have this property)

A

injured myocytes have leaky membrane that causes their resting membrane potential to become less negative. this allows them to be closer to threshold for depolarization to initiate an arrhythmia

100
Q

What is the term for abnormal ion fluxes that interrupt repolarizations

A

afterdepolarizations

101
Q

afterdeoplarizations that occur in phase 2 or 3 are called _____
Afterdepolarizations that occur in phase 4 are called ____

A

early

delayed

102
Q

early afterdepolarizations that occur during the long, plateau of phase 2 are due to defective _____

A

Ca ion channels

103
Q

early afterdepolarizations that occur during phase 3 are due to defective _____

A

Na channels (Na sodium inflow)

104
Q

delyaed afterdepolarizations that occur during phase 4 are due to _____

A

high intracell Ca from chatecholamine stimulation

105
Q

During what phase does re-entry tachycardia NOT occur? WHy?

A

2

bc they myocytes are refractory to another AP until they are repolarized

106
Q

What typically causes re-entry tachycardias?

A

patchy myocardial ischemia (necrosis) or scarring

107
Q

What is a heart block?
What cuases it?
What usually causes it in young AA females?

A

electrical impulse cannot travel through bundles of purkinjie fibers

caused by myocardial scarring and amyloidosis

AA young women = cardiac sarcoidosis

108
Q

the time it takes for a signal to SA node to AV node is represented by the ___ on an EKG. and the normal time is _____

A

PR interval: 120-200 milliseconds

109
Q

What is it called when the PR interval is prolonged (>200 milliseconds)?

A

first degree AV block or first degree heart block

110
Q

The QRS interval is normally less than or = to ____

A

100 milliseconds

111
Q

wider (long) QRS intervals usually indicate …

A

impulses from an abnormal place or ones that were abnormally conducted

112
Q

prolonged QT interval usually indicates …

A

myocardial ischemia
low K, Ca, Mg
channelopathy

113
Q

What part of the heart do the following leads correspond to and is the blood supply?
V1-4
V5 and 67
II, III, aVF

A

anterior left ventricle (LAD coronary a)
lateral left ventricle (left circumflex artery)
inferior left ventricle (right CA)

114
Q

What EKG change corresponds to a major epicardial CA blockage?

A

elevated ST segment

inverted T wave

115
Q

What is sinus tachycardia?

How is is differentiated from a tachyarrythmia?

A

when person with a normal heart exercises and get their heart rate over 100 bpm with normal SA node conduction

a sinus tachycardia will not go over 220 - age bpm

116
Q

irregular rhythm
high to normal rate (60 to 220)
no p waves

A

atrial fibrillation

117
Q

2 p waves for every QRS complex with HR ~ 150 bpm

A

atrial flutter

118
Q

responds to valsalva maneuvers, carotid sinus massage and immersion of the face in a pan of ice water

A

supraventricular tachycardia

119
Q

widened QRS > 220 msec with HR less than 200 bpm

A

ventricular tachycardia

120
Q

chaotic EKG with no clear QRS complexes

A

ventricular fibrillation

121
Q

punch or baseball to sternum that precipitates a fata arrhythmia

A

commotio cordis

122
Q

A prolonged QTc over ____ miliseconds is a signal of dangerous heart disease

A

440

123
Q

mutations in I-Ks
Name?
EKG?

A

LQT1

prolonged QT allowing –> early afterdepolarizations

124
Q

Mutations in cardiac Na channel
Name?
EKG?

A

brugada syndrome
elevated ST with ventricular fibrillation @rest
–> phase 2 reentry

125
Q

mutations in cardiac ryanodine R
name?
EKG?

A

familial catecholeminergic polymorphic VT

VT or VF during emotional stress –> delayed afterpolarizations

126
Q

Which channelopathy is assc with the following:
Phase 2 renetry
early afterdepolarizations
delayed afterpolarizations

A

brugada (Na channel)
LTQ1 (I-Ks)
familial catecholeminergic polymorphic VT (ryanodine)

127
Q

Viral myocaditis is assc with what 2 virsues?

A

Parovirus B

human herpes virus 6

128
Q

What are the 2 phases of viral myocarditis?

A

direct viral infection of myocytes –> autoimmune attack on myocytes

129
Q

higher incidence in northern italy

A

RT ventricular cardiomyopathy

130
Q
mutations in (with a 2nd hit)
desmoplakin
plakoglobin
plakophillin 2
desmocollin 2
desmophillin 2
A

RT ventricular cadriomyopathy

131
Q

fatty replacement of myocytes with lymphocytic infiltration and later fibrous scarring

A

RT ventricular cardiomyopathy