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CPR II Exam #1 > Heart I > Flashcards

Heart I Flashcards

1
Q

Cardiac weight in female vs male

A

F: 250-320gm
M: 300-360 gm

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2
Q

Avg. size of right and left ventricles

A

Rt: 0.3-0.5 cm thick
Lt: 1.3-1.5 cm

Greater than these values is hypertrophic

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3
Q

Hypertrophy

Dilation

Cardiomegaly

A

Hypertrophy: increase in ventricular thickness

Dilation: enlarged chamber size

Cardiomegaly: increased cardiac weight

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4
Q

How do valves generally get their nourishment?

A

Diffusion

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5
Q

3 types of valve damage and common example of each:

A

Collagen damage: mitral prolapse
Nodular calcification: calcific aortic stenosis
Fibrotic thickening: Rheumatic heart disease

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6
Q

ANP function

A

Promotes arterial vasodilation and activate renal salt and water elimination (naturesis and diuresis), which is beneficial in setting of HTN and CHF.

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7
Q

What is the normal rate of spontaneous depolarization of the SA node?

A

60-100 bpm

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8
Q

Blood supply to the myocardium (3)

A

LAD (and diagonal branches)
LCX (marginal branches)
RCA

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9
Q

When does blood flow into the myocardium?

A

During ventricular diastole, once the aortic valve closes.

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10
Q

What stem cells are in the myocardium? (2)

How much is replaces yearly?

A

Bone marrow derived precursors and cardiac stem cells.

About 1% yearly. Not enough to overcome necrosis.

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11
Q

What changes occur in the myocardium and chambers in aging? (3)

A

Increased LV size
Increased epicardial fat
Lipofuscin and basophilic degeneration

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12
Q

What changes occur in the heart valves in aging? (4)

A

Aortic and mitral annular calcification
Fibrous thickening
Mitral leaflets buckle -> increase in left atrium size
Lambl excrescenses

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13
Q

What are Lambl excrescences?

A

Small filiform processes that form on the closure line of aortic and mitral valves, likely from small thrombi.

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14
Q

What changes occur in the vasculature of the heart in aging? (2)

A

Coronary atherosclerosis

Stiffening of the aorta

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15
Q

CHF occurs when…

How can the heart meet its needs?

A

The heart is unable to pump blood at a rate to meet peripheral demand.

It can only meet the demand with increased filling pressure.

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16
Q

What might CHF result from? (2)

A

Loss of myocardial contractile function

Loss of ability to fill the ventricles during diastole (diastolic dysfunction)

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17
Q

What chamber hypertrophies in CHF?

A

LV

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18
Q

Cardiac myocytes become hypertrophic when… (2)

A

Sustained pressure or vol. overload (systemic HTN or aortic stenosis)
Sustained trophic signals (beta-adrenergic stimulation)

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19
Q

What occurs in the setting of pressure overload hypertrophy? (2)

A

Myocytes become thicker

LV increases in thickness concentrically

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20
Q

What occurs in the setting of volume overload hypertrophy? (2)

A

Myocytes elongate

Ventricular dilation occurs

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21
Q

How should heart hypertropy by measured in pressure and volume overload?

A

Pressure: wall thickness

Vol.: weight

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22
Q

Left-sided HF is most commonly a result of: (4)

A

Myocardial ischemia
HTN
Left-sided valve DZ
Primary myocardial DZ

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23
Q

Clinical effects of LSHF are due to: (2)

A

Pulmonary circulation congestion

Decreased tissue perfusion

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24
Q

What are common SX of LSHF?

A 
Edema
Cyanosis
Pulmonary SX
Tachycardia
DOE
Fatigue
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25
Q

What changes occur in the chambers in LSHF?

A

(1) LV hypertrophy

LV dysfunction leads to (2) LA dilation, which can lead to AFib, stasis and thrombus

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26
Q

What effect does LSHF at the kidneys? (2)

A 
Lower EF can cause decreased glomerular perfusion -> increased renin -> increased BV.
Prerenal azotemia (increased nitrogen levels)
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27
Q

What effect does LSHF have at the brain? (1)

A

Lower cerebral perfusion -> hypoxic encephalopathy

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28
Q

What cells are found in LSHF upon histologic exam?

A

HF cells = hemosiderin-laden Mo

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29
Q

What is the most common cause of RSHF?

A

LSHF

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30
Q

Isolated RSHF is from any cause of pulmonary HTN, for example: (3)

A

Parenchymal lung diseases
Primary pulmonary HTN
Pulmonary vasoconstriction

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31
Q

In primary RSHF, what is the big problem?

A

The venous system is highly congested.

This kind is much more rare than isolated RSHF.

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32
Q

What are complications of primary RSHF? (5)

A 
Liver congestion (nutmeg liver)
Splenic congestion -> splenomegaly
Effusions involving peritoneum, pleura and pericardium
LE edema
Renal congestion
33
Q

2 key features of CHF

A

Inadequate CO

Increased congestion of venous circulation

34
Q

Most common genetic cause of congenital heart disease:

A

Trisomy 21

35
Q

What do most defects arise from embryologically?

A

Arterioventricular spetae -> endocardial cushion

36
Q

What genetic pathway is responsible for bicuspid aortic valve?

A

NOTCH1

37
Q

What genetic pathways are responsible for Tetralogy of Fallot?

A

JAG1

NOTCH2

38
Q

What heart defects are left-to-right shunts? (3)

A

ASD
VSD
PDA

*most common

39
Q

ASD presention/onset

A

Usually asympomatic until adulthood

>30 y/o

40
Q

Most common ASD is:

Where does it occur within the septum?

A

Secundum ASD (90%)

Center of atrial septum

41
Q

Which 2 ASDs are less common?

Where do they occur within the septum?

A

Primum anomalie (5%) - near AV valves and may be associated with valvular abnormalities.

Sinus venosa defects (5%) - near entrance of SCV and may be associated with anomalies in venous return to RA.

42
Q

Left-to-right shunting causes volume overload on the rigth side, which may lead to: (3)

A

Pulm HTN
RSHF
Paradoxical embolism

May be closed surgically w/ normal survival.

43
Q

PFO outlook:

What is a unique problem that can occur in a PFO?

A

80% close by 2 y/o.
Remaining 20% have flap that can open if right sided pressure is great enough (even temporary pressure hikes can cause shunting)

Paradoxical embolus

44
Q

What is the most common form of congenital heart disease?

What are the 2 subtypes?

A

VSD (50% of small VSDs close spontaneously)

Membranous VSD (90%) in membranous IV septum
Infundibular VSD: below pulmonary valve or within muscular septum
45
Q

Large VSDs can cause significant shunting which can lead to (2)

A

RV hypertrophy

Pulm HTN

46
Q

Unclosed large VSD will ultimately lead to:

A

Shunt reversal, leading to cyanosis and death.

47
Q

Why does a PDA remain open?

A

If infants are hypoxic and/or have increased pulmonary vascular pressure.

48
Q

What sort of murmur accompanies PDA?

A

Harsh, machinery-like murmur (PDA)

49
Q

Presentation of PDA

A

Usually ASX at birth

50
Q

Isolated PDA should be:

When should it stay open? How is it done?

A

Closed ASAP

Should stay open in patients w/ obstruction of pulmonary or systemic outflow. Via PGE, the PDA stays open.

51
Q

What shunt causes cyanosis?

A

R-to-L

52
Q

4 cardinal features of Tetralogy of Fallot

A

VSD
Obstruction of RV outflow
Aorta overrides the VSD
RV hypertrophy

53
Q

What malformation looks like a “boot”? Why?

A

ToF because of right ventricular hypertrophy

54
Q

What does the clinical severity of ToF depend on?

Mild vs. classic

A

Subpulmonary stenosis

Mild: L to R shunt
Classic: R to L shunting w/ cyanosis
*most infants are cyanotic from birth.

55
Q

Transposition of the great vessels results in:

Common features of the malformation (4)

A

2 separate systemic and pulmonary circulations -> incompatible w/ life.

Approx 1/3 have VSD
2/3 have PFO or PDA
RV becomes hypertrophic and LV atrophies
W/O surgery, pts. die within a few mo.

56
Q

Coarctation of the Aorta w/ PDA

A

Infantile form
Cyanosis in lower half of body
Associated w/ Turner syndrome (XO)

57
Q

Coarctation of the Aorta w/o PDA

A

Adult form
ASX
Claudication and cold LE
May eventually see LV hypertrophy

58
Q

SX of Aortic Coarctation (3)

A

Murmurs throughout systole
Vibratory thrill
Concentric LVH

59
Q

3 obstructive lesions

A

Coarctation of the Aorta
Pulmonary stenosis/atresia
Aortic stenosis/atresia

60
Q

When does Eisenmenger syndrome occur?

A

When pressure in the pulmonary arteries becomes so high that it causes oxygen-poor blood to flow from the right to left ventricle and then to the body, leading to cyanosis.

This damages the walls of the pulmonary aa. and leads to RV hypertrophy.

61
Q

Stable angina

Where is the occlusion?
SX? Relieved by?
What induces it?

A

Stenotic occlusion of coronary a.
Squeezing, burning sensation relieved by rest/vasodilators.
Induced by physical activity, stress.

62
Q

Prinzmental variant angina is…

Relieved by:

What is it unrelated to?

A

Episodic coronary a. spasm.

Relieved by vasodilators.

Unrelated to activity, HR or BP.

63
Q

Unstable (Crescendo) angina definition

What causes it?

What might be imminent/

A

Transient, often recurrent chest pain induced by myocardial ischemia insufficient to cause MI. Increases in freq., duration, and severity.

Usually rupture of atherosclerotic plaque w/ patrial thrombus.

Acute MI, as 50% have evidence of myocardial necrosis.

64
Q

Classic presentation of MI

A

Prolonged CP (>30 min)
Diaphoresis
Dyspnea
Nausea-vomiting

25% are ASX

65
Q

Times for:

Onset of ATP depletion
Loss of contractility
ATP reduced to 50%, 10%
Irreversible cell injury
Microvascular injury
A 
Onset of ATP depletion: secs.
Loss of contractility: <2 min
ATP reduced to 50%: 10 min, 10%: 40 min
Irreversible cell injury: 20-40 min
Microvascular injury: >1 hr
66
Q

Areas of infarct: LAD (40-50%) (3)

A

Apex
LV anterior wall
Anterior 2/3 of septum

67
Q

Areas of infarct: RCA (30-40%) (3)

A

RV free wall
LV posterior wall
Posterior 1/3 of septum

68
Q

Areas of infarct: LCX (15-20%) (1)

A

LV lateral wall

69
Q

Ac. MI after 24 hrs (3)

A

Coagulative necrosis
Pyknotic nuclei
Loss of cross striation

70
Q

MI after 1-3 days (2)

A

Loss of striations

Neutrophilic infiltration

71
Q

What comes into the heart 3-4 days after MI?

What comes into the heart 7-10 days after an MI?

What comes into the heart 10 days after an MI?

A

PMNs: Neutrophils, eosinophils, and basophils.

Mo.

Granulation tissue

72
Q

4 ways to treat an MI

A

Thrombolysis
Angioplasty
Stent placement
CABG

73
Q

Most sensitive and specific biomarkers of myocardial damage (2)

Why?

When do each peak?

A

cTnT: 12-48 hrs
cTnI: max at 24 hrs
*both elevate 3-12 hrs

They are specific because they are not normally in circulation.

74
Q

Where does CK exist?

Why is it less specific?

A

Brain, heart, skeletal muscle.

Because it is found elsewhere.

75
Q

What markers peak at 24 hrs? (2)

A

CK-MB

cTnI

76
Q

When does CK-MB return to normal?

cTnI?

cTnT?

A

CK-MB: 48-72 hrs

cTnI: 5-10 days

cTnT: 5-14 days

77
Q

What is the most common COD of pts. w/ MI?

A

Arrythmias

78
Q

6 major complications of MI

A
  1. Arrhythmia
  2. Contractile dysfunction
  3. Fibrinous pericarditis
  4. Myocardial rupture (2-4 days post MI)
  5. Infarct expansion
  6. Ventricular aneurysm

CPR II Exam #1 (30 decks)

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