Cardiology (Exam 2) Flashcards
(147 cards)
1
Q
Functions of CV System
A
Delivery and removal of substances
2
Q
Right Heart
A
Pulmonary circulation
Pumps blood through lungs
3
Q
Left Heart
A
Systemic circulation
Pumps blood through body
4
Q
Flow of blood
A
Artery –> arteriole –> capillary –> venule –> vein
5
Q
Major difference between veins and arteries
A
Arteries have much thicker tunica media to tolerate higher forces of pressure
6
Q
Hypertension
A
Damages blood vessels
7
Q
Hypertension is usually…?
A
Asymptomatic until organ damage occurs
8
Q
Systole
A
Heart contraction
9
Q
Diastole
A
Heart relaxation
10
Q
Normal Blood Pressure
A
<120/<80
11
Q
Blood pressure
A
Cardiac output x peripheral resistance
12
Q
Cardiac output
A
Amount of blood the heart pumps per minute
13
Q
Alpha1 Receptors
A
Vasoconstriction
14
Q
Beta1 Receptors
A
Vasodilation
15
Q
Vasodilator Hormones
A
Prostacylin
Natriuretic peptides
Nitric oxide
16
Q
Vasoconstrictor Hormones (2)
A
Angiotensin II
Vasopressin
17
Q
Blood Viscosity
A
Increase in RBCs increases viscosity
18
Q
Blood Volume
A
RAAS activation increases blood volume
19
Q
ACE
A
Converts angiotensin I to angiotensin II
found in lungs
20
Q
ADH
A
Antidiuretic Hormone
Vasopressin
21
Q
Renin
A
Converts angiotensinogen to angiotensin I
22
Q
Release of ADH
A
Leads to water reabsorption and increase in blood volume
23
Q
Release of aldosterone
A
Reabsorption of NaCl and water, excretion of K+ –> increased blood volume
24
Q
Renin release is increased by (2)
A
Activation of renal beta1 receptors
Decrease in renal perfusion
25
Primary Hypertension
no single identifiable cause
Genetic or environmental factors
26
Secondary Hypertension
Specific medical condition
27
arteries have
low volume and high pressure
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veins have
high volume and low pressure
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purpose of muscle pumps and valves in veins
to keep blood flow in the correct direction
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the most common cardiovascular disease
hypertension
31
renin release is increased by
activation of beta 1 receptors
decrease in renal perfusion
32
hypertension is associated with
an increased peripheral resistance of the arterial system
33
4 factors that may contribute to hypertension
over activation of RAAS
over activation of the sympathetic nervous system
vascular endothelial dysfunction
sodium retention
34
overactivation of the sympathetic nervous system
E/NE released from sympathetic neurons and adrenal medulla will activate beta 1 receptors in the heart, kidneys or alpha 1 in the arteries
35
vascular endothelial dysfunction
damage to blood vessels and impaired vascular relaxation
biggest factor for HTN
36
sodium retention leads to
increased blood volume
37
organs most effected from hypertension
eyes
heart
kidneys
brain
38
damage of HTN on the brain
ischemic or hemorrhagic stoke
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damage of HTN on the kidneys
chronic kidney disease
40
damage of HTN on the heart
heart failure, arrhythmia, myocardial infarction
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damage of HTN on the eyes
retinopathy
42
dyslipidemia
abnormal blood lipid levels
43
hyperlipidemia
increased blood lipid levels
44
patients with dyslipidemia are initially
asymptomatic
45
dyslipidemia can lead to
atherosclerosis
46
atherosclerosis
disease of arterial system characterized by fatty plaques within vasculature
plaques lead to stenosis then ischemia
47
what is a major contributor to atherosclerosis
elevated LDL
48
atherosclerotic cardiovascular disease (ASCVD) includes
cerebrovascular disease
peripheral artery disease
coronary artery disease
49
cerebrovascular disease
plaques in cerebral vasculature
can lead to ischemic stroke or transient ischemic attack
50
peripheral artery disease
plaques in peripheral arteries (lower limbs) reducing blood flow and oxygen supply
51
coronary artery disease (ischemic heart disease)
plaques in coronary arteries
can lead to myocardial infarction
52
familial hypercholesterolemia
most common genetic disorder leading to dyslipidemia
autosomal dominant disorder, mutations of uptake of LDL by the liver, leading to more in the blood
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which form of familial hypercholesterolemia is more severe?
homozygous
54
lipoproteins
lipid protein complexes
made up of triglycerides, cholesterol, phospholipids and proteins
55
lipoproteins are classified by
what protein they contain
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Apo-B containing lipoprotein
chylomicrons
VLDL, IDL, and LDL
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Apo-A1 containing lipoprotein
HDL (tissues to liver)
58
chylomicrons
transports dietary TH and cholesterol from intestines to tissues
59
three cholesterol pathways
exogenous
endogenous
reverse
60
exogenous cholesterol pathway
cholesterol from the diet is digested and absorbed in GI tract
61
endogenous cholesterol pathway
cholesterol synthesized in the liver
LDL transports cholesterol to tissues and excess LDL is taken up by vasculature or returned to liver for reuptake
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reverse cholesterol pathway
removal by HDL and degradation of cholesterol by bile
63
pathophysiology of atherosclerosis
in liver cells
cholesterol and triglycerides packaged into VLDL particles --> exported to blood --> converted to IDL--> LDL
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hypertriglyceridemia
dyslipidemia that is caused by a number of drugs or conditions
elevated TG associated with increased CV risk
65
extreme elevations of hypertriglycedemia can lead to
acute pancreatitis
66
patho of acute pancreatitis
excessive breakdown of TG into free fatty acids --> toxicity and inflammatory response
67
symptoms of acute pancreatitis
persistent severe epigastric abdominal pain, nausea, and vomiting
68
symptoms of peripheral artery disease
skin loses integrity, pain in the affected area
may be asymptomatic
69
intermittent claudication (PAD)
pain caused by ischemia to the limbs
usually during exercise, resolved at rest
pain at rest = severe PAD
70
main symtptom of ischemic heart disease
angina (chest pain due to inadequate supply of oxygen)
71
stable ischemic heart disease
stable angina
occurs in a predictable manner and lasts a short time
gradual stenosis over time
72
acute coronary syndrome
acte obstruction in blood flow to the heart
due to plaque rupture followed by thrombus formation
can lead to heart attack
73
types of acute coronary syndrome
unstable angina
non-ST elevation myocardial infarction
ST elevation myocardial infarction
74
infarction
death of tissue
75
unstable angina
markers not present
ST segment not elevated
76
NSTEMI
markers present
ST segment not elevated
77
STEMI
markers present
ST segment elevated
78
most severe acute coronary syndrome
STEMI = complete blockage
79
after MI, what forms and what is different about it?
scar tissue
can't contract and relax like healthy tissue
80
2 cardiac markers
creatine phosphokinase MB
Troponins (cardiac troponin 1)
81
heart failure
cardiomyopathy
heart is unable to pump enough blood to meet the metabolic demands of the body
82
heart failure =
a reduction in cardiac output
83
heart failure typically refers to
left side heart failure
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systolic heart failure
heart failure with reduced ejection fraction
85
diastolic heart failure
heart failure with preserved ejection fraction
86
CV symptoms of heart failure
tachycardia
peripheral edema and ascites (swelling in abdomen)
87
pulmonary symptoms of heart failure
pulmonary edema (fluid in lungs)
dyspnea (difficulty breathing)
cough
88
other symptoms of heart failure
sudden weight gain
fatigue
89
preload
pressure within the ventricle or stretching of the myocytes at the end of diastole
90
afterload
resistance to ejection of blood from the ventricle
91
contractility
force of contraction
92
cardiac output =
stroke volume x heart rate
93
heart rate is primarily dependent on the
autonomic nervous system
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preload is dependent on
venous return
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venous return is dependent on
fluid volume and venous tone
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after load is dependent on
arterial tone (BV diameter)
97
contractility is dependent on
ANS, Ca2+ and preload
98
HFpEF (diastolic HF)
heart is unable to fill normally
associated with stiffening myocardium
99
HFrEF (systolic HF)
heart is unable to contract normally
associated with dilation of heart chambers (ventricles)
100
what helps us classify heart failure?
ejection faction (EF) = stoke volume/ end diastolic volume
101
Hypertension pathophysiology
increase in after load --> stress on myocardium -> ventricle walls thicken/dilate --> inefficient pumping
102
ischemic heart diseases pathophysiology
reduced blood flow to myocardium over time --> ischemia/angina and weakening of myocardium (thin walls)
103
most common cause of heart failure
myocardial infarction
104
conditions that can lead to HF
abnormal heart valves or congenital heart defects
cardiotoxic medications (ex: chemotherapies)
other conditions (ex: diabetes)
105
compensatory mechanisms activated to increase cardiac output
activation of RAAS
activation of SNS
activation of RAAS and SNS --> cardiac remodeling
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activation of RAAS
increases blood volume --> increases preload --> increases stroke volume
107
problem of activation of RAAS
causes edema and increases afterload
108
activation of SNS
activation of beta1 on the heart --> increases HR and contractility
109
problem with activation of SNS
increases after load and workload of the heart
110
activation of RAAS and SNS --> cardiac remodeling
cardiac hypertrophy to increase contractility
111
problem of activation of RAAS and SNS --> cardiac remodeling
scarring and tissue damage which impairs cardiac function
112
compensatory mechanisms can help maintain cardiac output initially but
overtime lead to worsening of heart failure
113
acute decompensated HF
sudden worsening of HF, leads to need for hospitalization
114
ADHF occurs due to
1. excessive fluid overload --> severe dyspnea
2. excessive reduction in cardiac output --> hypotension
115
patients with ADHF are categorized by
tissue perfusion and fluid status
116
tissue perfusion
warm = stable
cold = hypoperfusion
117
fluid volume
dry = stable
wet = fluid overload
118
fluid status is measured by
pulmonary capillary wedge pressure
119
perfusion Status is measured by
cardiac index
120
cardiac index
cardiac output/ body surface area
121
arrythmia
disturbance of electrical signals in the heart leadings to an irregular rate or rhythm
122
arrhythmia can occur due to
damage/structural change, electrolyte alteration or drugs that alter cardiac function
123
symptoms of arrhythmia
palpitations, lightheadedness, syncope, fatigue, cardiac arrest
124
arrhythmias range from
asymptomatic to life-threatening
125
arrhythmias can be classified by
where they originate, how they affect heart rate and type of impulse abnormaility
126
cardiac conduction system
pacemaker cells generate action potential without input from the nervous system
127
sinoatrial node
primary pacemaker of the heart
128
atrioventricular node
spontaneously generates 40-60 action potentials per minute
129
If SA node fails,
AV node can take over
130
heart block
failure in the normal propagation of action potentials from atrium to ventricle
131
heart block results in
bradycardia or skipped beats
132
reentry (accessory pathway)
impulse reenters and excites areas of the heart more than once due to dysfunction of the refractory period
133
atrial fibrillation
most common type of arrhythmia
unpredictable
134
complications of chronic A-fib
stoke and heart failure
135
ventricular fibrillation
electrical signals fire from multiple locations in the ventricular leading to inability of the ventricles to pump properly
136
ventricular fibrillation is
life threatening and a form of cardiac arrest
137
shock
CV system fails to refuse the tissues adequately resulting in widespread impairment of cellular metabolism
138
shock leads to
organ failure and death
139
types of shock
hypovolemic shock
cariogenic shock
distributive shock
140
hypovolemic shock
low fluid volume
141
cardiogenic shock
damage or dysfunction of the heart
unable to pump blood forward
142
distributive shock
leaky blood vessels and excessive vasodilation
143
examples of distributive shock
septic shock, anaphylactic shock and neurogenic shock
144
pathophysiology of arryhthmias
due to damage or structural change in cardiac tissue, electrolyte alteration or drugs that alter cardiac function
145
most arrhythmias are
tachyarrythmias
146
if another tissue spontaneously depolarizes more frequently than the SA node,
it controls heart rate and rhythm
147
atypical automaticity (ectopic pacemaker)
group of cardiac cells that gain automaticity and begin spontaneously depolarizing
