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CPR II Exam #1 > Heart I > Flashcards

Heart I Flashcards

(78 cards)

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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
What changes occur in the chambers in LSHF?
(1) LV hypertrophy | LV dysfunction leads to (2) LA dilation, which can lead to AFib, stasis and thrombus
26
What effect does LSHF at the kidneys? (2)
``` Lower EF can cause decreased glomerular perfusion -> increased renin -> increased BV. Prerenal azotemia (increased nitrogen levels) ```
27
What effect does LSHF have at the brain? (1)
Lower cerebral perfusion -> hypoxic encephalopathy
28
What cells are found in LSHF upon histologic exam?
HF cells = hemosiderin-laden Mo
29
What is the most common cause of RSHF?
LSHF
30
Isolated RSHF is from any cause of pulmonary HTN, for example: (3)
Parenchymal lung diseases Primary pulmonary HTN Pulmonary vasoconstriction
31
In primary RSHF, what is the big problem?
The venous system is highly congested. This kind is much more rare than isolated RSHF.
32
What are complications of primary RSHF? (5)
``` Liver congestion (nutmeg liver) Splenic congestion -> splenomegaly Effusions involving peritoneum, pleura and pericardium LE edema Renal congestion ```
33
2 key features of CHF
Inadequate CO | Increased congestion of venous circulation
34
Most common genetic cause of congenital heart disease:
Trisomy 21
35
What do most defects arise from embryologically?
Arterioventricular spetae -> endocardial cushion
36
What genetic pathway is responsible for bicuspid aortic valve?
NOTCH1
37
What genetic pathways are responsible for Tetralogy of Fallot?
JAG1 | NOTCH2
38
What heart defects are left-to-right shunts? (3)
ASD VSD PDA *most common
39
ASD presention/onset
Usually asympomatic until adulthood | >30 y/o
40
Most common ASD is: Where does it occur within the septum?
Secundum ASD (90%) Center of atrial septum
41
Which 2 ASDs are less common? Where do they occur within the septum?
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
Left-to-right shunting causes volume overload on the rigth side, which may lead to: (3)
Pulm HTN RSHF Paradoxical embolism May be closed surgically w/ normal survival.
43
PFO outlook: What is a unique problem that can occur in a PFO?
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
What is the most common form of congenital heart disease? What are the 2 subtypes?
VSD (50% of small VSDs close spontaneously) ``` Membranous VSD (90%) in membranous IV septum Infundibular VSD: below pulmonary valve or within muscular septum ```
45
Large VSDs can cause significant shunting which can lead to (2)
RV hypertrophy | Pulm HTN
46
Unclosed large VSD will ultimately lead to:
Shunt reversal, leading to cyanosis and death.
47
Why does a PDA remain open?
If infants are hypoxic and/or have increased pulmonary vascular pressure.
48
What sort of murmur accompanies PDA?
Harsh, machinery-like murmur (PDA)
49
Presentation of PDA
Usually ASX at birth
50
Isolated PDA should be: When should it stay open? How is it done?
Closed ASAP Should stay open in patients w/ obstruction of pulmonary or systemic outflow. Via PGE, the PDA stays open.
51
What shunt causes cyanosis?
R-to-L
52
4 cardinal features of Tetralogy of Fallot
VSD Obstruction of RV outflow Aorta overrides the VSD RV hypertrophy
53
What malformation looks like a "boot"? Why?
ToF because of right ventricular hypertrophy
54
What does the clinical severity of ToF depend on? Mild vs. classic
Subpulmonary stenosis Mild: L to R shunt Classic: R to L shunting w/ cyanosis *most infants are cyanotic from birth.
55
Transposition of the great vessels results in: Common features of the malformation (4)
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
Coarctation of the Aorta w/ PDA
Infantile form Cyanosis in lower half of body Associated w/ Turner syndrome (XO)
57
Coarctation of the Aorta w/o PDA
Adult form ASX Claudication and cold LE May eventually see LV hypertrophy
58
SX of Aortic Coarctation (3)
Murmurs throughout systole Vibratory thrill Concentric LVH
59
3 obstructive lesions
Coarctation of the Aorta Pulmonary stenosis/atresia Aortic stenosis/atresia
60
When does Eisenmenger syndrome occur?
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
Stable angina Where is the occlusion? SX? Relieved by? What induces it?
Stenotic occlusion of coronary a. Squeezing, burning sensation relieved by rest/vasodilators. Induced by physical activity, stress.
62
Prinzmental variant angina is... Relieved by: What is it unrelated to?
Episodic coronary a. spasm. Relieved by vasodilators. Unrelated to activity, HR or BP.
63
Unstable (Crescendo) angina definition What causes it? What might be imminent/
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
Classic presentation of MI
Prolonged CP (>30 min) Diaphoresis Dyspnea Nausea-vomiting 25% are ASX
65
Times for: ``` Onset of ATP depletion Loss of contractility ATP reduced to 50%, 10% Irreversible cell injury Microvascular injury ```
``` 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
Areas of infarct: LAD (40-50%) (3)
Apex LV anterior wall Anterior 2/3 of septum
67
Areas of infarct: RCA (30-40%) (3)
RV free wall LV posterior wall Posterior 1/3 of septum
68
Areas of infarct: LCX (15-20%) (1)
LV lateral wall
69
Ac. MI after 24 hrs (3)
Coagulative necrosis Pyknotic nuclei Loss of cross striation
70
MI after 1-3 days (2)
Loss of striations | Neutrophilic infiltration
71
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?
PMNs: Neutrophils, eosinophils, and basophils. Mo. Granulation tissue
72
4 ways to treat an MI
Thrombolysis Angioplasty Stent placement CABG
73
Most sensitive and specific biomarkers of myocardial damage (2) Why? When do each peak?
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
Where does CK exist? Why is it less specific?
Brain, heart, skeletal muscle. Because it is found elsewhere.
75
What markers peak at 24 hrs? (2)
CK-MB | cTnI
76
When does CK-MB return to normal? cTnI? cTnT?
CK-MB: 48-72 hrs cTnI: 5-10 days cTnT: 5-14 days
77
What is the most common COD of pts. w/ MI?
Arrythmias
78
6 major complications of MI
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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