CV Flashcards
(135 cards)
1
Q
Neural control centers for the heart are located here:
A
Medulla oblongata
2
Q
What type of innervation stimulates the heart?
A
Sympathetic
3
Q
What receptors respond to norepinephrine?
A
Beta1-adrenergic
4
Q
What innervation generally inhibits the heart?
A
Parasympathetic
5
Q
What receptors respond to acetylcholine?
A
Muscarinic
6
Q
What is the pattern of electrical transmission?
A
SA node > preferred pathways > AV node > bundle of His> R/L bundle branches > purkinje fibers
7
Q
Systole is further divided into:
A
Isovolumetric ventricular contraction and ventricular ejection
8
Q
Diastole is further divided into:
A
Isovolumetric ventricular relaxation and ventricular filling
9
Q
Stroke volume equals:
A
EDV -ESV
10
Q
Cardiac output equals:
A
HR x SV
11
Q
Ejection fraction
A
SV/ EDV
12
Q
The most important variable of resistance is
A
The radius of the blood vessel
13
Q
Structure of the blood vessel walls includes these 3 structures:
A
- Tunica intima- endothelium
- Tunica media- smooth muscle
- Tunica externa- connective tissue
14
Q
These are low-resistance vessels that serve as conduits for blood flow.
A
Arteries
15
Q
Arteries function as pressure reservoirs that maintain blood flow during
A
Diastole
16
Q
Elastic arteries are closer to this and easily distend.
A
Heart
17
Q
Muscular arteries are closer to these and have more smooth muscle.
A
Arterioles
18
Q
These regulate blood flow and distribution by changing the radius from signals that may be extrinsic/systemic or intrinsic/local.
A
Arterioles
19
Q
Mechanisms of intrinsic control of arterioles are:
A
- Active hyperemia
- Flow autoregulation
- Reactive hyperemia
- Response to injury
20
Q
Mechanisms of extrinsic control include these:
A
- ANS
2. Hormones
21
Q
The most important control signals for the arterioles include:
A
- SNS
- Epi
- Angiotensin II/ ADH
- ANP
- Prostacyclin
- EDRF
22
Q
What does epi do?
A
It vasodilator skeletal muscle vessels and vasoconstricts peripheral blood vessels.
23
Q
What does angiotensin II/ ADH do?
A
Vasodilator
24
Q
What does prostacyclin do?
A
Vasodilator
25
What does EDRF do?
Nitric oxide- vasodilation
26
These are leaky thin-walled vessels with a large cross-sectional area allowing slow passage of blood that facilitates transport and exchange.
Capillaries
27
Difference between hydrostatic and interstitial fluid pressure favors this:
Filtration
28
Difference between osmotic pressures in plasma and interstitial fluid favors this:
Absorption
29
This is the accumulation of excess fluid in the interstitial space:
Edema
30
Increased hydrostatic pressure causes:
Increased arterial or venous pressure or arterial dilation
31
Major function of this is to maintain blood volume but also important in defense and fat absorption.
Lymphatic
32
Excessive accumulation of lymph due to damaged or obstructed lymph.
Lymphedema
33
Acute inflammation of lymph vessels
Acute lymphangitis
34
These return blood to heart through low-resistance blood conduits.
Veins
35
Sympathetic stimulation of veins causes:
the Smooth muscle to contract which raises venous pressure
36
This drug inhibits Na-K- ATPase which results in an increased Na to exchange with Ca. This results in an increase in Ca intracellularly which enhances cardiac contractility.
Digitalis
37
What cardiac drugs are vasodilators?
Nitroglycerin and calcium channel blockers
38
What cardiac drugs reduce contractility and heart rate which reduces myocardial demand. Increases cardiac output by increasing ventricular filling by relaxing the obstructing muscle.
Beta-adrenergic antagonists
39
These cardiac drugs reduce afterload through vasodilation.
Ace inhibitors
40
When lipids, such as cholesterol and triglycerides, collect in the blood. Normally transported in the blood by proteins, which form lipoproteins.
Hyperlipidemia
41
This may have a genetic basis and is a defective synthesis of apoproteins, lacks appropriate or defective receptors, and there is a defect in how the cell handles cholesterol.
Primary hyperlipidemia
42
Secondary causes of hyperlipidemia include:
High caloric intake, obesity, sedentary lifestyle, diabetes mellitus and is more common.
43
These are mostly triglycerides, very little protein
Chylomicrons
44
These are triglycerides, cholesterol, and protein.
Very-low density lipoproteins
45
These are bad cholesterol and is the main carrier of cholesterol: triglycerides, half cholesterol, one quarter protein
Low-density lipoproteins LDL
46
This is good cholesterol: 20% cholesterol, half protein
High-density lipoprotein HDL
47
Chlylomicrons are synthesized here as a part of fat reabsorption.
Small intestine
48
LDL and HDL are synthesized and released by this.
Liver
49
This is the main carrier of cholesterol:
LDL
50
This is a more reverse carrier, brings cholesterol from tissues to liver, allows body to recycle cholesterol.
HDL
51
Increase of cholesterol on the blood, characterized by LDL 70-130 mg/dL.
Hypercholesteremia
52
Where do we want LDL, HDL, total cholesterol, and triglyceride levels?
LDL <100
HDL 40-60
Total <200
Triglycerides 10-150
53
When managing hypercholesteremia what primary target?
To lower LDLs.
54
Type of lipid lower med that prevents the liver from manufacturing cholesterol.
Statins
55
Type of lipid lowering med that prevents body from absorbing cholesterol.
Bile acid sequestrants
56
Type of lipid-lowering med that limits body’s absorption of cholesterol.
Cholesterol-absorption inhibitors
57
Type of lipid-lowering med that decreases synthesis of VLDL by liver, stimulates clearance of triglycerides from circulation.
Fibrates
58
Type of lipid-lowering med that blocks synthesis and release of VLDL from liver, reduces IDL and LDL level and increases HDL concentrations.
Nictonic acid
59
A condition in which an artery wall thickens as a result of the accumulation of fatty materials.
Atherosclerosis
60
This correlated with lipid changes in the tunica intima, endothelial layer of artery, and increased collagen in tunica media, middle layer of the vessels.
Atherosclerosis
61
Biggest risk factor for atherosclerosis is:
Hypercholesteremia
62
Risk factors for atherosclerosis:
Hypertension, smoking, elevated cholesterol, obesity, diabetes.
63
These are changes in dilation of blood vessel wall, which can lead to rupture and bleeding.
Aneurysms
64
Where do aneurysms typically form?
Aorta but can form in other arteries and veins
65
This is bounded by complete vessel wall and all blood remains in that vascular compartment.
True aneurysm
66
This is a localized dissection or tear in the wall of the vessel that forms a hematoma outside the vessel, enlarging it. It may be hounded only by outer layer of the vessel wall and supporting tissue.
False aneurysm
67
Type of aneurysm that is small, spherical dilation of vessel at a bifurcation point. Seen in structures like the circle of Willis in brain, where bifurcated vessels are common.
Berry aneurysm
68
Type of aneurysm that involves entire circumference of vessel, characterized by a gradual, progressive dilation.
Fusiform
69
Type of aneurysm that extends over part of circumference of a vessel and appears like a sac.
Saccular
70
A false aneurysm resulting from a tear in the tunica intima; allows blood to enter vessel wall and creates a pocket filled with blood.
Dissecting aneurysm
71
This is a group of diseases that cause inflammatory injury and possible necrosis of blood vessel walls.
Vasculitides
72
Involves endothelial lining and smooth muscle cells of vessel wall. Includes arteries, veins, and capillaries. Typically results from direct injury, infectious agent immune processes.
Vasculitis
73
Obstruction of large arteries that supply the body’s peripheral structures.
Peripheral artery disease
74
Risk factors for peripheral artery disease and typically seen in:
Smoking, diabetes and men 60-70s
75
Vasculitis that affects medium-sized arteries. Usually found in plantar or digital vessels. Primarily arterial but can involve veins and nerves.
Thromboangitis obliterans
76
An intensive vasospasm of arteries and arterioles, typically in fingers, less often in toes. No clear cause, but generally in young women exposed to cold or strong emotions.
Raynaud’s phenomenon
77
Raynaud’s phenomenon occurs in nearly all individuals with this:
Scleroderma
78
MAP is a regulated variable governed by:
Feedback inhibition
79
Baroreceptors for pressure are found :
In carotid sinus and aortic arch
80
Afferent pathways for Blood pressure regulation are in:
The carotid sinus nerve and aortic depressor nerve.
81
These pathways feed information to integrating center (medullary cv center) in the brainstem.
Afferent pathway
82
Efferent pathways for blood pressure control are:
In the vagus nerve (to heart) and sympathetic nerves (to heart, arterioles, and veins)
83
This pathway includes variables that change heart rate and contractility, as well as vessel radius
Efferent pathways
84
MAP equals:
CO x TPR
85
Short term regulators of MAP:
Baroreceptor reflex and feedback inhibition
86
Long term regulator of MAP:
Blood volume
87
Increased tension on blood vessel walls leads to:
An increase in blood pressure
88
Chronic elevation of blood pressure without evidence of other disease:
Primary or essential hypertension
89
Clear other cause of hypertension such as diabetes that increases CO or TPR, and indirectly affects MAP.
Secondary hypertension
90
A severe increase in arterial blood pressure. If untreated may result in severe damage to renal, cardiac, or cerebral function.
Hypertensive crisis
91
Enlarges tortuous veins that may lead to edema and stasis ulcers as a result of chronic venous insufficiency.
Varicose veins
92
These originate in the superficial sap genius veins caused by prolonged standing and increased intraabdominal pressure.
Primary varicose veins
93
Result from impaired blood flow in the deep venous channels.
Secondary varicose veins
94
Chronic venous disease of the lower extremities is characterized by:
Venous HTN
Varicose veins
Venous ulcers due to insufficiency
95
Stasis of blood, increased blood coagulability and vessel wall injury are components of:
Virchows triad
96
Acute inflammatory response that results in exudate accumulation around the heart.
Acute pericarditis
97
Formation of scar tissue between pericardial layers.
Restrictive or constrictive pericarditis
98
Fluid accumulation in pericardial sac.
Pericardial effusion
99
Accumulation of exudates such as blood in pericardial sac, under pressure.
Cardiac tamponade
100
Rapid, unchecked increase in pressure in pericardial sac that impairs diastolic filling, reduces CO, and compromises perfusion in the body.
Cardiac tamponade
101
A lack of blood flow to tissue.
Ischemia
102
Ischemia that can compromise or lead to cell injury.
Injury
103
Death of myocardial cells
Infarct
104
Results from narrowing of coronary arteries due atherosclerotic processes, reduced blood flow to heart.
Coronary artery disease
105
Represents a disease of the heart muscle fibers that usually affects cardiac performance.
Cardiomyopathy
106
3 main forms of CM:
Dilated
Restrictive
Hypertrophic
107
Involves dilation of the heart chambers impairing the function of the heart as a pump.
Dilated cardiomyopathy
108
DCM is heterogeneous and commonly shows:
Autosomal dominant pattern
| X-linked recessive pattern
109
Characterized by hypertrophy of muscle mass that can lead to obstruction of blood filling.
Hypertrophic cardiomyopathy
110
Familial HCM is inherited as an
Autosomal dominant trait
111
These have in the gene encoding myosin have been associated with HCM.
De nova mutations
112
Involves rigid ventricular walls that restrict blood filling but spare contractile properties of the muscle.
Restrictive cardiomyopathy
113
Primary causes of RCM include:
Endocarditis
114
Secondary causes of RCM include:
Amyloidosis
Hemachromatosis
Sarcoidosis
115
Infection of the endocardium, heart valves, or cardiac prosthesis resulting from bacterial or fungal infection.
Endocarditis
116
Most patients with endocarditis are:
IV drug users
Have prosthetic valves
Have rheumatic heart disease
117
Narrowing of the valve opening leads to greater resistance to blood flow through the valve.
Stenosis
118
Failure of valve to close completely results in backflow of blood
Insufficiency
119
Inflammatory destruction of valve in response to b-hemolytic streptococcus is a common cause
Rheumatic fever
120
Occurs when heart cannot pump sufficient blood to meet the metabolic demands.
Heart failure
121
Heart failure is often characterized by:
Intravascular and interstitial volume overload
| Poor tissue perfusion
122
Most common cause of heart failure is:
```
Coronary artery disease
Also typical:
HTN
DCM
Valvular heart disease
```
123
Systolic dysfunction results from conditions reducing contractility such as:
Ischemic heart disease
| Cardiomyopathy
124
Most common causes of left ventricular dysfunction include:
HTN
Acute myocardial infarction
Valvular defects including stenosis or regurg from aortic or mitral valve
125
Right sided heart failure results in:
Fluid backup into the systemic and hepatic systems
| Peripheral edema and ascites, external jugular veins
126
When right sided heart failure occurs in response to chronic pulmonary disease it’s referred to as:
Cor pulmonale
127
Reduced tissue and organ perfusion and eventually organ dysfunction and failure.
Shock
128
Acute life threatening condition where body tissues are inadequately perfumes or unable to use oxygen.
Shock
129
Shock leads to:
Cell death, lactic acidosis, and reperfusion injury
130
Type of shock where heart fails as a pump and can’t maintain CO.
Cardiogenic
131
Type of shock where intravascular volume is inappropriately distributed, vasodilation causes hypovolemia
Distributive
132
Examples of distributive shock:
Septic
Neurogenic
Anaphylactic
133
Type of shock with inadequate blood volume. Venous return is reduced as fluid is lost from intravascular space that results in decreased ventricular filling and a drop in SV.
Hypovolemic
134
Type of shock where blood flow is impeded by physical or mechanical obstruction.
Obstructive
135
Complications of shock:
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Acute respiratory distress syndrome
Acute renal failure
GI ulceration
DIC
Multiple organ dysfunction syndrome
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