Cardiology Flashcards

(98 cards)

1
Q

what layers does the pericardial sac consist of?

A

serous inner layer - visceral (inner) and parietal pericardium (fibrous outer)

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2
Q

how much clear liquid lies between the layers of the heart?

A

40-50mL

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3
Q

Which branches feed the LV?

A

PDA, Cx, LAD

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4
Q

Which branch is also known as a widowmaker?

A

Left Anterior Descending (LAD)

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5
Q

If a patient is having an inferior heart attack, which branch is this affecting?

A

PDA and leads 2&3

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6
Q

If a patient is having an ANTERIOR heart attack, which branch is this affecting?

A

LAD, v1 and v2

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7
Q

If a pt is having a LATERAL heart attack, which branch is this affecting?

A

Circumflex, L1

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8
Q

What percentage does the PDA supply blood of LV arising from RCA and Cx?

A

80%;20%

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9
Q

automaticity is another word for

A

pacemaker

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10
Q

what are the pacemakers and conductors of the heart? which have a faster velocity, why?

A

Pacemakers- SA/AV node
Conductors- His and Purkinje
conductors are faster bc the AV node has a delay in order to fill the heart

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11
Q

where is the electrical connection in the heart?

A

AV and His bundle

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12
Q

The ____ distal the pacemaker is, the ______ the heart rate

A

distal, slower

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13
Q

the p wave, QRS. and T wave measure…

A

P wave: atrial depolarization
Qrs: ventricular depolarization
T wave: atrial repolarization

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14
Q

What needs to be maintained in the heart?

A

Cardiac OUTPUT

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15
Q

What 3 parameters is the stroke volume dependent on?

A

preload, after load, contractility

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16
Q

what do catecholamines and inotropic drugs do to the heart?

A

increase calcium thus increasing contractility

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17
Q

are the nodal cells or the ventricular cells faster? Why?

A

phase 0 is faster so it spikes up in ventricular cells
-BUT depolarization is faster in phase 4 of the nodal (pacemaker) cells

“depolarization is faster but action potential is slower in nodal”

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18
Q

how do myosin and actin interact to give rise to ____?

A

CONTRACTION;

there’s calcium release that binds to troponin C

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19
Q

what two mechanisms consist of a Bradycardia

A

SA node and AV node block

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20
Q

In Sick Sinus Syndrome, what does the ekg read?

A

a Sinus pause, and Junctional rhythm where the AV node takes over to generate a beat.
a missing p wave

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21
Q

what are the 3 degrees of an AV block in Bradycardia?

A

1st- long AV conduction (lengthened PR interval > 0.22s) but still 1:1 AV conduction
2nd- not all atrial impulses are conducted to ventricles (missing QRS or random)
3rd- no association b/w atrial and ventricular activity

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22
Q

Which degree in bradycardia is pathological and in need of a pacemaker?

A

MOBITZ II- constant PR interval, but QRS is skipped (dropped randomly)

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23
Q

Which degree in bradycardia is in need of an organ donor?

A

3rd degree AV block

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24
Q

LONG PR INTERVAL

A

1st degree AV block

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25
PR interval lengthens w/ each cycle until QRS is completely skipped
2nd - degree AV block : Wekebebach
26
PR remains constant but QRS is skipped a. mobitz type 2 b. sick sinus syndrome c. wekebach d. 1st degree AV block
a.
27
reasons why AV blocks can occur?
increasing age, vagal input, side effect of drugs
28
Examples of congenital disorders
muscular dystrophy, lyme dz. Lupus, CAD, gout
29
what are 3 ways tachycardia can occur?
inc automaticity, re-entry, and late/delayed
30
a more rapid phase 4 depolarization can be due to: a. inc automaticity b. long QT syndrome c. wolf-parkinson d. reentry
a. increase automaticity = SA node firing faster, inc HR
31
a long QT syndrome: a) inc automaticity b) triggered tachycardia c) supraventricular tachy d) delay repolarization
b. AND d
32
what are some medications pts take and have polymorphic v tach (torsades de pointes) aka twisting of the points?
procainamide or quinidine and dig toxicity
33
what leads to a prolonged plateau in Long QT syndrome?
reduced fxn of K channels
34
what is the most common Reentry tachycardia and what is it indicated by on an ekg?
Wolf-Parkinson White- delta wave
35
if there is a short PR and slurred upstroke to QRS on an ekg, this would be indicative of?
Delta Wave
36
what occurs when an accessory pathway could block impulse due to refractory period
premature articular contraction (PAC) a form of reentry or Wolff-parkinson white
37
if the QRS is wide, the tachycardia arises from..?
from ventricular tissue or is an SVT w WPW
38
when p waves are occurring after QRS, this signifies
WPW reentry
39
LV failure etiology (5)
volume overload, pressure overload, restricted filling, myocyte loss, decreased myocyte contractility
40
pathophys of LV failure (3 changes)
hemodynamic changes, neuro-hormonal changes, cellular changes
41
What are the two types of hemodynamic changes
HFrEF- decreased outside REDUCED | HFpEF- decreased filling PRESERVED
42
what are the curve shifts in HFrEF and HFpEF?
HFrEF- contractility line decreases HFpEF-compliance (bottom) line increases (left up) *both decrease SV*
43
what are 3 ways the heart tries to maintain CO during HFrEF? explain in shifting of curve as well
1. Inc prelooad- shift of a' to right 2. Inc release of catecholamines- - contractility line up c' 3. Hypertrophy and inc vent volume--- compliance line to right
44
a decreased relaxation, decreased elastic recoil, or increased stiffness of the ventricle is indicative of _____. Examples include
HFpEF; | -HTN and Ischemia
45
compensatory responses during neurohormonal changes in LV failure (4)
sympathetic system activation RAAS Vasopressin Cytokine release
46
what are the two major groups in cytokine release of LV failure that help myocyte hypertrophy?
Interleukins (ILs) and tumor necrosis factor
47
elevated _____ levels cause increase cardiac contractility and an inc HR to help maintain CO
epinephrine
48
what causes the production of Angiotensin II?
low BP stimulating release of renin
49
what helps maintain GFR despite a reduced CO?
angiotensin II and sympathetic activation
50
angio II stimulates aldosterone syntethsis which leads to ____ and potassium ____ by kidneys
sodium resorption and potassium excretion
51
vasopressin helps ____ of water in renal tubules
reabsorption
52
excessive endothelia release may be responsible for _____ in pulmonary arteries
hypertension
53
what two sarcoplasmic reticulum proteins have reduced levels of mRNA from failing hearts
phospholamban and Ca2+ATPase
54
there is a downstream of B-1 receptors, uncoupling of the signal transduction pathway and up regulation of inhibitory G proteins leading to....
desensitization of B adregenic receptors as a result of chronic sympathetic activation
55
alpha1 receptors are slightly increased in heart failure for induction of....
myocardial HYPERTROPHY-- to inc HR
56
can cardiac proliferate during adult form?
no
57
what is the function of myocytes that cannot proliferate, thus is a constant turnover producing large myocytes?
they do NOT contract normally and have decreased ATPase activity
58
what causes holes in the myocardium?
myocyte loss via apoptosis (by TNF)
59
what two things cause an inc in fibrous tissue in interstitial spaces of the heart?
collagen deposition | and endothelin release
60
what sx occurs when there is a short blood supply to skeletal muscles?
fatigue
61
what sx occurs when renal perfusion normalizes only at night?
nocturia
62
what is a sx secondary to ischemia with CAD?
chest pain
63
what are the 3 clinical presentations of a pt with RV failure?
SOB, pedal edema, abdominal pain
64
What is the most common cause of RV failure?
LV failure bc of the inc afterload placed on RV
65
* in cardiomyopathy, a thicker and reduced chamber size indicates: a) cardiac dilation b) physiological hypertrophy c) Idiopathic DCM d) pathological hypertrophy
d) pathological hypertrophy | slide 92
66
*What is the most common cause of cardiomyopathy? which one requires cardiac transplants?
dilated cardiomyopathy--> idiopathic DCM`
67
alcohol is a cause in which cardiomyopathy?
dilated
68
a biventricular characteristic is seen in which cardiomyopathy?
dilated
69
*what is the number one cause of sudden death in young athletes?
HOCM
70
what area of the heart is most affected in HOCM and what does it block?
septum --> thickens up closing off the outflow of blood through the aorta
71
*cells appearing as whorls are indicative of?
HOCM
72
signs and symptoms of HOCM
dyspnea and Angina
73
what is the rarest form of cardiomyopathy?
restrictive cardiomyopathy
74
which type of cardiomyopathy has a filling problem thus heart can't relax?
restrictive cardiomyopathy
75
which cardiomyopathy looks similar to normal heart?
restrictive cardiomyopathy
76
define stenosis vs regurgitation
stenosis- narrow | regurgitation- leaky
77
systole vs diastole murmurs
systole --> Mc Ao aortic stenosis or mitral regurgitation | diastole --> Mo Ac aortic regurgitation or mitral stenosis
78
long latent period of slowly increasing obstruction before sx appear is seen in a) aortic regurgitation b) mitral stenosis c) aortic stenosis d) mitral regurgitation
c)
79
what are the 3 cardinal symptoms of AS and the life expectancies of each one if left untreated?
chest pain--> 5 years, syncope--> 3 years, heart failure --> 2 years
80
*comparison of carotid pulse and PMI in AS?
carotid pulse is decreased and delayed | pluses parvus & pulses tardus*
81
You do an en echo on a pt's (age30-70) heart and find tissue inflammation and adhesion/fusing of commissures, which type of AS is this? a) congenital b) rheumatic c) degenerative d) glue
b) rheumatic slide 120* * congenital: partially fused, Abel flow--> fibrosis and calcification-> sx before 30y degenerative: inflexible leaflets, calcium deposits at bases, pt 70y
82
if you see concentric hypertrophy and a prominent a wave, this indicative of
aortic stenosis | -causing LV hypertrophy; dependent on atrial kick
83
in order to maintain the stroke volume in AS, what increases? think of the pressure/vol graph
LVED pressure increases, (preload to allow more blood out)
84
The sound of AS is typically described as?
crescendo-decrescendo | quiet or silent S2 bc of hypertrophy
85
what is the difference between HOCM and AS and how can this be tested?
decrease in preload in HOCM- valsalva maneuver--> HOCM murmur increase similarities: hypertrophy, crescendo-decrescendo sound * *slide 128
86
What is the most common murmur sound in chronic AR?
Diastolic rumble --> Austin Flint murmur
87
What signs are found in acute AR?
none bc it happens so fast
88
Where does blood enter from in aortic regurgitation during diastole?
BOTH- the left atrium AND the aorta (leaking) thus increasing volume
89
if you see eccentric hypertrophy, this is indicative of?
aortic regurgitation
90
systemic diastolic BP inc or dec in Aortic regurgitation? | what about diastolic in the ventricle?
systemic diastolic pressure DECREASES because not squeezing enough blood out into the system*** - diastolic in ventricle increases because there is more blood in the ventricle * slide 131*
91
no relaxation/contraction exists in a) aortic stenosis b) aortic regurgitation c) mitral stenosis d) mitral regurgitation
b ***
92
pathophysiology with a mitral valve of 1 cm^2
c) mitral stenosis | * aortic stenosis AVA = < 0.8 cm
93
a main pathophysiologic abnormality is elevated pulm pressure and RIGHT sided pressure a) aortic stenosis b) aortic regurgitation c) mitral stenosis d) mitral regurgitation
c) mitral stenosis
94
**hoarseness or Ortner Syndrome during Mitral Stenosis is due to
LA enlargement impinging on recurrent laryngeal nerve
95
What is heard during mitral regurgitation?
holosystolic pitched regurgitant murmur
96
most common cause of mitral stenosis?
rheumatic
97
most common cause of mitral regurgitation?
mitral valve prolapse, followed by CAD
98
atrial v waves are present in which valvular heart disease?
mitral regurgitation | -reuptake of the blood from ventricle through mitral valve