Cardiac Physiology Flashcards
(111 cards)
1
Q
Which disease is the # 1 cause of death?
A
Cardiovascular Disease
2
Q
Major underlying cause of ischemia I due to:
A
Atheroscerosis (plaquing)
Artery Spasm
3
Q
Causes of Inflamation
A
High blood cholesterol (dyslipidemia)
recruitment &expression of pro-inflammatory cytokines
4
Q
Inflammatory pathways promote:
A
Thrombosis
5
Q
Thrombosis is responsible for:
A
MI & most strokes
6
Q
The Nervous System can modulate
A
Inflammation
7
Q
Hemostasis is:
A
Prevention of blood loss
8
Q
Mechanisms of hemostasis:
A
Vascular Spasm
Formation of platelet plug
Blood coagulation
Fibrous tissue growth to seal
9
Q
Vascular Constriction associated with:
A
Trauma
10
Q
SNS induced constriction from pain is caused by:
A
Neural Reflexes
11
Q
Responsible for most of the constriction
A
Local myogenic spasm
12
Q
Local humoral factors include:
A
Thromboxane A2 from platelets (especially important in smaller vessels)
13
Q
Platelets contain:
A
Contractile proteins (actin & myosin) Enzymes Calcium ADP & ATP Thromboxane A2 Serotonin Growth Factors
14
Q
Platelet Cell Membrane Contains:
A
Glocoproteins (adhere to damaged area
Phospholipids containing platelet factor 3 (initiates clotting)
15
Q
Mechanism of Platelet Activation:
A
When platelets contact damaged area they:
- Swell
- Irregular form w/ irradiating processes protruding from surface
- Contractile proteins contract causing granule release
- Secrete ADP, Thromboxane A2, & Serotonin
16
Q
Thromboxane A2 is a/an:
A
Vasoconstrictor &
Potentiates the release of granule contents
17
Q
Platelets are important in:
A
Minute ruptures
18
Q
A lack of platelets is associated with:
A
Small hemorrhagic areas under the skin and throughout internal tissues
19
Q
Platelets have a half-life of:
A
8-12 days
20
Q
Platelets primarily eliminated by:
A
Macrophage action (mostly occurs in spleen)
21
Q
On average there are ______platelets per ul
A
150,000-300,000
22
Q
Role of Endothelium:
A
Prevents platelet aggregation
Produces PGI2
Produces factor VIII
23
Q
PGI2’s role in endothelium:
A
Its a vasodilator
Stim. Platelet adenyl cyclase which suppresses release of granules
limits platelet extension
24
Q
Factor VIII’s role in endothelium:
A
Clotting
25
Aspirin blocks:
Thromboxane A2 & prostacyclin production by inhibiting fatty acid cyclooxygenase which converts arachidonic acid to PGG2 & PGH2
26
Anticoagulants prevent:
Clots from forming via:
Chelators (tye up calcium)
Heparin (complexes w/ Antithrombon III)
Dicumarol (Inhibits Vit. K dependent factors; II, VII, IX, X aka Cumadin/ warfarin)
27
Dissolving clots that have already formed is called:
Lysis of Clots
28
The inactive form of plasmin which circulates in the blood
Plasminogen
29
Endogenous Activators of Plasminogen are found in:
Tissues, plasma, & urine
30
Exogenous Activators of Plasminogen:
Streptokinase
| Tissue Plasminogen Activator (tPA)
31
Most of the frank tissue damage associated w/ infarction occurs via:
Reperfusion
32
Reperfusion associated w/
Formation of highly reactive oxygen species w/ unpaired electrons (free radicals)
33
Free radicals are generated when:
pressure on tissues relieved & again perfused w/ blood
34
The ability to open up alternate routes of blood flow to compensate for a blocked vessel
Collateralization
35
The formation of new blood vessels
Angiogenesis
36
Collateralization occurs via:
Angiogenesis
Vasodilation
SNS stimulation (may impede via vasoconstriction and/ or augment via the release of NPY)
37
Extrinsic mechanism of thrombosis:
Initiated by chemical factors released by damaged tissues
38
Intrinsic mechanism of thrombosis:
requires only components in blood trauma to blood exposure to collagen (or foreign surface)
39
Clotting Factors:
```
I - fibrinogen
II - Prothrombin
III -Thromboplastin
IV - Calcium
V - Proaccelerin
VII - Serum prothrombin conversion accelerator
VIII - Antihemphilic factor (A)
```
40
Clotting Factors Cont:
```
IX - Antihemophilic factor (B)
X - Stuart factor
XI - Antihemophilic factor (C)
XII - Hageman factot
XIII - Fibrin stab. Factor
Prekallikrein
High molecular weight kininogen
Platelets
```
41
Hepatocytes (liver's) role in clotting:
```
Liver synthesizes 5 clotting factors;
I - fibrinogen
II - Prothrombin
VII - SPCA
IX - AHF B
X - Stuart factor
```
42
Hepatocytes (liver's) role in clotting Cont.:
Coumarin depresses liver formation of II, VII, IX, & by blocking action of Vit K
43
Hemphilia is sex linked on the _____chromosome
X Chromosome
| mostly men
44
85 % of Hemophilia cases occur due to a defect in:
Factor VIII
45
15 % of Hemophilia cases occur due to a defect in:
Factor IX
46
Key step to clotting is the conversion of:
Fibrinogen to fibrin which requires thrombin
47
Autoimmune disorder where the body makes antibodies against phospholipids in cell membranes
Antiphospholipid antibody syndrome
48
Antiphospholipid antibody syndrome causes ______ to form
Clots
49
Amino acid in the blood that may irritate blood vessels prompting atherosclerosis.
Homocysteine
50
Homocysteine levels can be reduced by taking
folic acid, B6 and B12
51
Produced 2-8 months after birth spontaneously
Agglutinins
52
Immediate Hemolysis in mismatched transfusions
less common
53
Delayed Hemolysis in mismatched transfusions
More common
54
Syncytium =
many acting as one
55
Intercalated discs create
low resistance pathways connecting cells end to end
56
Na+
Inc. at depol
| Dec. at repol
57
Ca++
Inc. at depol
| Dec. at Repol
58
K+
Dec. at DepolInc. at repol
59
Tetradotoxin blocks fast Na+ channels selectively changing a fast response into
a slow response
60
During resting membrane potential ______ and ____ are closed and ____ channels are open
Na+ and Ca++ closed
| K+ open
61
If the Na+/K+ pump is inhibited, what accumulated?
Ca+
62
Ca+ accumulation in the cardiac cell _____contractile strength
Increases
63
Absolute Refractory Period
Unable to re-stim cardiac cell
| Occurs during the plateau
64
Relative Refractory Period
Requires a supra-normal stimulus
| Occurs during repol
65
Normal pacemaker of the heart
SA node
66
The SA node is:
less (-) at Er, has a leaky membrane to Na+ and Ca++, and contracts feebly
67
Cells of the AV node and perkinje system are under overdrive suppression by the
SA node
68
Delays the wave of depolarization from entering the ventricle
AV node
69
Allows the atria to contract slightly ahead of the ventricles
AV node
70
Slow conduction velocity due to smaller diameter fibers
AV node
71
AV node may act as a slower pacemaker in absence of
SA nodr
72
AS Heart Rate Inc, cycle length:
decreases
73
At a resting heart rate systole is ____diastole
74
During systole perfusion of the myocardium is restricted by the
contracting cardiac muscle compressing blood vessels
75
Isovolumic contraction and ejection
Systole
76
Isovolumic relaxation, rapid inflow, diastasis, atrial systole
Diastole
77
Volume of ventricles at the end of filling
End Diastolic Volume
78
Volume in ventricles at the end of ejection
End Systolic Volume
79
Volume ejected by ventricles
Stroke Volume
80
% of EDV ejected
Ejection Fraction (SV/EDV * 100)
81
Normal Ejection Fraction
50-60%
82
Stretch on the wall prior to contraction
Preload
83
Changing aortic BP during ejection of blood from the left ventricle
Afterload
84
Associated with atrial contraction
A wave
85
Associated with ventricular contraction
C wave
86
Associated with atrial filling
V wave
87
LV pressure > Aortic pressure =
Aortic Valve open
88
Aortic pressure > LV pressure =
Aortic valve closed
89
AV valves
Mitral and tricuspid
90
Semilunar valves
Aortic and pulmonic
91
Valve not opening fully
Stenoic
92
Valve not closing fully
Insufficient/leaky
93
Valve creates vibrational noise
murmor
94
Systolic Heart Murmur =
Aortic and pulmonary stenosis + mitral & tricuspid insufficiency
95
Diastolic Murmur
Aortic and pulmonary insufficiency + mitral & tricuspid stenosis
96
Both Systolic and Diastolic Murmur =
Patent ductus arteriosis combined valvular defect
97
Law of Laplace
At a given operating pressure as ventricular radius INC, developing wall tension also INC.
98
Anything that effects the heart rate
Chronotropic
99
Anything that effects conduction velocity
Dromotropic
100
Anything that effects strength of contraction
Inotropic
101
Within physiologic limits the heart will pump all the blood that returns to it without allowing excessive damming of blood in veins
Frank-Starling Law of the Heart
102
Mechanism of Frank-Starling:
Increased venous return causes increased stretch of cardiac muscle fibers
103
Increased stretch of cardiac muscles causes:
An increase in cross-bridge formation, calcium influx, and stretch on SA node
104
When cardiac fibers are stretched and the force of contraction is increased, this is called
Heterometric autoregulation
105
3 methods of Heterometric Autoregulation:
Flow induced
Pressure induced
Rate induced
106
Flow induced means:
inc. stroke volume maintained as EDV dec.
107
Pressure induced means:
Inc. in aortic BP will Inc. force of contraction
108
Rate induced means:
Inc. HR will Inc. force "treppe"
109
Stretch on SA node will:
Increase Ca+/Na+ permeability, increases HR
110
Sympathetic innervation:
Increases HR, strength of contraction, and conduction velocity
111
Parasympathetic innervation:
Decreases HR, strength of contraction, conduction velocity
