Cardiovascular Disease Flashcards
(181 cards)
1
Q
two divisions of cardiovascular disease
A
peripheral vascular disease
heart disease
2
Q
two branches of peripheral vascular disease
A
atherosclerotic
vasculitis
3
Q
four divisons of heart disease
A
coronary artery disease
valvular disease
HTN heart disease
cardiomyopathy
4
Q
T/F cardiovascular illness is the most common serious disorder in the US
A
true
5
Q
what percent of the following have cardiovascular disease
people at age 20
people over 75
total population
A
5%
75%
20%
6
Q
what is the most common cause of death in the US
A
cardiovascular disease
7
Q
systolic pressure
A
pressure at which blood flow resumes in an occluded arterty
8
Q
diastolic reading
A
pressure at which flow returns to normal in an occluded artery
9
Q
most current guidelines for blood pressure
Normal
elevated
Stage 1
Stage 2
A
normal: 120/80
elevated: systolic >120, diastolic >80
stage 1 HTN: >/= 130/80
stage 2 HTN: >/= 140/90
10
Q
based on new HTN guidelines how many people are afflicted
A
103million
11
Q
of the 75% of the patients who have HTN and are aware of it, how many are getting treated?
how many are controlled?
A
50% are being treated
25% are under control
12
Q
Dr Dodges suggested take home messages regarding HTN
A
- 140/90 is still a reasonable threshold for the intiation of medical treatment of HTN
- lifestyle modification are useful for patients with elevate BP
- patients with diabetes or other comorbidities, medical treatment should be considered
13
Q
four classifications of HTN
A
primary/essential/idiopathic
renal
endocrine
pregnancy induced
14
Q
what is the most common form of HTN
A
primary/essential/idiopathic
15
Q
two conditioned associated with renal hypertension
A
narrowed renal artery
chronic renal disease
16
Q
three endocrine conditions associated with HTN
A
cushings
pheochromcytoma
congenital adrenal hyperplasia
17
Q
three conditions associated with pregnancy induced HTN
A
toxemia
pre-eclampsia
eclampsia
18
Q
pheochromocytoma
5 primary symptoms
A
a rare tumor of the adrenal medulla or sympathetic ganglion that secretes norepinephrine
- severe headaches
- diaphoresis
- palpitation
- tremor
- anxiety
19
Q
T/F HTN is generally asymptomatic
A
true
20
Q
what are three general symptoms associated with HTN
A
Headaches
malaise/fatigue
symptoms of complications
21
Q
where are BP recordings most accurate
A
at home and work, not in the office
22
Q
the hydraulic equation
define the variables
A
BP = CO x PVR
BP = cardiac output x peripheral resistance
23
Q
three ways to decrease BP by decreasing CO
A
reduce HR
reduce contractility
reduce venous return/decrease blood volume
24
Q
how to reduce BP by decreasing PVR
two methods to achieve this
A
vasodilation
- direct action on the vessels
- CNS control
25
two key elements manipulated to regulate blood pressure
sympathetic nervous system input
renal blood flow
26
two primary sympathetic receptors manipulated to control BP
Alpha 1 vascular receptors
Beta 1 cardiac receptors
27
two factors related to renal blood flow that can be manipulated to regulate BP
renin-angiotensin-aldosterone pathway
total vascular volume
28
descrive the RAA pathway (5)
* renin is released by the kidneys in response to decreasing BP
* renin converts angiotensinogen to angiotensin I
* angiotensin converting enzyme converts angiotensin I to II
* angiotensin II stimulated an increase in BP and the release of aldosterone from the kidney
* Aldosterone causes salt retension
29
two key RAA hormones
Angiotensin II
aldosterone
30
what is the function of aldosterone II
triggers vasoconstriction
aldosterone production and release from the adrenal cortex
31
three facts about aldosterone
most potent natural mineralocorticoid
helps with sodium and fluid retention
also induces cardiac growth
32
what is the sympathetic response to decreased BP
* activation of Beta adrenergic receptors in the heart
* activation of Alpha adrenergic receptors in smooth muscle
33
what is the effect of sympathetic activation of Beta receptors in response to Decreased BP
increased cardiac output through contractility
34
what is the effect of sympathetic stimulation of alpha receptors in response to decreased BP
increased peripheral resistance through vasoconstriction
35
what is the renal response to decreased blood pressure
decreased renal blood flow
36
what happens in response to decreased renal blood flow
renin is released
glomerular filtration is decreased
37
what has been the primary reason for decreasing number of cardiac death since the 1970
decreased in smoking
improved treatment
38
what two factors increase water retention in response to decreased blood pressure
decreased glomerular filtration
aldosterone production
39
what is the result of increased sodium and water retention in response to low BP
increasd blood volume, which increases cardiac output
40
what is the effect of angiotensin to released in response to renin production
aldosterone production leading to increased salt and water retention
increased peripheral resistance
41
two HTN treatment strategies
reduce cardiac output
reduce peripheral vascular resistance
42
two methods to reduce cardiac out in HTN treatment
block beta 1 sympathetic action
reduce blood volume
43
what is the result from blocking beta 1 sympathetic action
reduced cardiac rate and contractility
44
three methods to reduce peripheral resistance in HTN treatment
block alpha 1 sympathetic action
block central sympathetic action
directly dilate the blood vessels
45
four groups of drugs used to treat HTN
diuretics
sympathetic receptor blocker
direct vasodilators
RAA blockers
46
how do diuretic function to decrease blood pressure
lower blood volume
47
how do sympathetic receptors blockers function to lower HTN
block alpha and beta receptors
48
what is the function of direct vasodilators in the treatment of HTN
reduce peripheral vascular resistance
49
what is the function of blocking RAA in treating HTN
reduce blood volume and peripheral resistance
50
three common diuretics (examples)
thiazides (hydrochorthiazide)
loop diuretics (furosimide)
potassium sparring diuretics (spironolactone)
51
four common sympathetic receptor blockers (examples)
beta blocker (atenolol, propanolol)
alpha blockers (prazosin, terazosin)
alpha and beta (labetalol)
centrally acting (methyldopa, clonidine)
52
thee common vasodilators (examples)
calcium channel blockers (diltiazem, amlodipine)
arterial (hydralazine, minoxidil, diazoxide)
arterial and venous (nitroprusside)
53
four common RAA blockers (examples)
angiotensin converting enzyme (ACE) inhibitors (catopril, benazopril)
angiotensin II receptor antagonist (losartan)
aldosterone antagonist (spironolactone)
renin inhibitor (aliskiren)
54
thee factors that influence cardiac output
HR
contractility
filling pressure
55
thee factors that influence PVR
arterial diameter
arterial length
elasticity
56
distinguish between treatments for mild and severe HTN
mild to moderate HTN usually uses one drug
severe HTN uses multiple drugs
57
mitigating factors to consider in treatment of HTN
other medical conditions
RAA work less well on african americans
cost
58
why are ACE inhibitors effective
because angiotensin I is really just a precuros without much effect on blood pressure
59
what angiotensin II a potent actor on BP
it triggers the aldosterone production to increase blood volume
it acts on the blood vessels to increase peripheral resistance
60
three popular single drugs used in intial HTN treatment
ACE inhibitor
calcium channel blocker
diuretic
61
the useful conbinations of drugs used in intitial treatment of HTN
ACE inhibitor + diuretic
Beta blocker + diuretic
beta blocker + alpha blocker
62
what is the goal of HTN treatment
maintenance of 120/80 BP for high risk patients
\<135/85 for mild to moderate risk patients
63
limbo goal for high risk hypertensives
trying to go as low as is safely possible for people with severe comorbities (diabetes, CAD, CVA)
64
what is the risk of decreasing blood pressure too low
toxicity
orthostatic hypertension
65
three common side effects of HTN treatment
electrolyte imbalances
annoying dry cough
malaise, fatigue
66
why drugs used to treat HTN will cause low potassium?
high?
diuretics
ACE and aldosterone inhibitors
67
what common HTN treatment will cause annoying dry cough
ACE inhibitors
68
what common HTN treatment can cause malaise and fatigue
beta blockers
69
what constitutes a "hypertensive emergency"
200/140
70
how would treatment differ for a patient with BP \<200/140 vs \>200/140
over 200/140 needs hospitalization due to stroke or MI concerns
below 200/140 can be managed outpatient
71
does HTN mangement need to be life long
preferably not, as long as necessary but short as possible
72
step down strategy for HTN treatment
decreasing dose based on stable normal pressures attained through lifestyle changes
73
what is the main cause of cardiovascular disease
atherosclerosis
74
atherosclerosis
vessel narrowing due to fatty deposits in the arteries related to lipid metabolism and cholesterol
75
two sources of cholesterol
exogenous (diet and absorption)
endogeneous (production of cholesterol from the liver)
76
lipoproteins
macromolecule consisting of lipid and protein
77
LDL
transporter of endogeneous cholesterol
78
HDL
removes LDL cholesterol and triglycerides
79
best goal of LDL/HDL
why is this a good goal
make your lows low and highs high
decreasing LDL reduces risk of atherosclerosis
increased HDL decreases risk
80
how is HDL increased
weight loss and exercise
81
HDL paradox
drugs that decrease LDL reduce risk
drugs that increase HDL do not reduce risk
82
83
atherosclerotic process
* fatty streaks
* monocyte aggregation
* LDL oxidation
* formation of foam cells
* inflammation leading to LDL accumulation
84
fatty streaks
LDL accumulation under endothelium
85
what causes the oxidation of LDL in fatty streaks
monocytes
86
foam cells
monocytes that become macrophages and ingest oxidized LDL
87
what is considered the unifying element in the pathogenesis of atherosclerosis
how was this decided
inflammtion
inflammatory markers correlate to CV disease risk
88
C reactive protin
an inflammtion marker related to heart disease
89
risk factors for atherosclerosis
* smoking
* hypertension
* diabetes
* family HX
* age
* dyslipidemia
* lifestyle
90
age range for increased atherosclerosis risk for men and women
\>/=45 men
\>/= 55 for women
91
dyslipidemia related to atherosclerosis
high LDL
low HDL
92
three lifestyle issues that increase risk of atherosclerosis
obesity
physical inactivity
atherogenic (inflammatory) diet
93
why is the age related risk for athersclerosis different for men and women
women haver higher HDL
estrogen raises HDL
94
two chronic effects of atherosclerosis
coronary effects
peripheral vascular disease
95
two coronary effects of chronic atherosclerosis
angine pectoris
congestive or chronic heart failure
96
three peripheral vascular disease associated with the effects of chronic atherosclerosis
renal artery stenosis
femoral/popliteal stenosis
aortic aneurysm formation
97
T/F most myocardial infarctions are caused by HTN
false, caused by atherosclerotic plaque rupture
98
what happens when an atherosclerotic plaque ruptures
a blood clot forms around the rupture and blocks the artery
99
four treatments for atherosclerosis
lifestyle changes
treatment of hyperlipidemia with statins
treat HTN
treat diabetes
100
when are symtpoms of mild atherosclerosis noticed?
severe?
50% occulsion, usually on exertion
80%, effects can be felt at rest
101
5 lipid lowering agents
niacin
bile acid binding agents
HMG-CoA reductase inhibitors
fibric acid derivatives
inhibitors of sterol absorption
102
common name of HMG-CoA reducatse inhibitors
statins
103
what is the effect of statin drug treatment
reduction of endogenous cholesterol synthesis
lowers LDL
104
three common statins
atorvastatin (lipitor)
simvastatin (zocor)
lovastatin (mevacor)
105
two adverse effects of statins
liver damage
muscle damage
106
what must be monitored during statin treatment due to the liver damaging side effects
liver enzymes
107
two conditions related to muscle damage from statin drugs
myopathy
rhabdomyolysis
108
when are statins contraindicated
pregnacy
children
109
what is a lesser known issue with statin?
what is the result
muscle weakness
reduction in activities
110
PCSK9 inhibitors
new drug that stimulated production of an enzyme show to decrease LDL and decrease risk of heart disease
111
two PCSK9 drugs
alirocumab (praluent)
evolcumab (repatha)
112
what is the benefit of PCSK9 treatment
drawback?
produce better lipid reduction that statins
very expensive
113
three causes of ischemia
vessel stenosis or occulsion
vasospasm
pump failure
114
what is the key component of ischemia
O2 supply is not sufficient for demand
115
other oxygen transport issues related to heart damage that arent ischemia
hypotension
chronic anemia
increased metabolism
116
three causes of hypotension that can result ischemia
acute blood loss
anesthesia
cardiac arrhythmia
117
causes of increased metabolism related to cardiac ischemia
hyperthyroid
fever
118
symptoms of
acute
subacute
chronic
ischemia
acute: acute coronary syndrome
subacute: angina
chronic : CHF
119
acute coronary syndromes
acute MI with ST segment elevation
acute MI without St elevation
unstable angina
120
three main forms of coronary heart disease (CHD)
acute coronary syndrome
stable angina
CHF
121
acute myocardial infarction
mycardial death due to abrupt reduction in coronary blood flow almost always caused by atherosclerosis
122
what is the intitial event of an acute MI
a plaque rupture
123
how many AMIs occur yearly
what percent are fatal
1.1 million
20-40%
124
T/F more than 50% of AMI death occur suddenly
true
125
symptoms of acute MI
squeezing pressure chest pain
can be felt in the stomach or left arm, face, shoulder
anxiety
diaphoresis
GI distress
126
T/F 30% of AMIs are asymptomatic
treu
127
what percent of AMIs are precipitated by strenous events
50%
128
why are AMIs more common in the AM
BP is higher
increased blood viscosity
cortisol secretion is at its highest
129
T/F most women have atypical AMI presentation
true, more likely to be Dx as gi
130
STEMI is usually indicative of what
transmural ischemia (involves the full thickness of the cardiac wall)
131
what is more common, STEMI or NSTEMI
NSTEMI (55-60%)(
132
NSTEMI is indicative of what
ischemia that is subendocardial rather than transmural
133
NSTEMI treatment
supportive measures
anticoagulation
134
NSTEMI supportive treatments
rest
oxygen
sedation/analgesia
control of arrhytmia
135
differentiate between the vascular causes of STEMI vs NSTEMI
STEMI is more likely to be in one of the great vessels
NSTEMI usually comes from a small vessel
136
anticoagulation therapy for NSTEMI
heparin
antiplatelets
137
STEMI treatment
reperfusion
supportive measures similar to NSTEMI
138
two methods for reperfusion in response to STEMI
percutaneous coronary intervention
thrombolytic therapy
139
supportive measures for STEMI
aspirin
oxygen
decrease myocardial oxygen demand
control arrhytmia
140
PCI vs thrombolysis
preference
when would thrombolysis be used
PCI is preferred
thrombolytics are indicated with PCI isn't available and early treatment
early is key
141
PCI
stent placement
142
AMI prognosis factors
age
size of vessel
prior infarctions
nature of treatment
143
T/F the risk of death within 90 days of AMI is 75%
false, 1-22%
144
two main causes of MI mortality
cardiac arrhythmia (v fib)
pump failure (cardiogenic shock)
145
when is cardiogenic shock the more common cause of MI mortality
in the case of large infarctions
146
treatment of v fib
cardioversion (defibrilation)
147
three treatments of cardiogenic shock
vasopressors (maintain pressure)
inotropic agents to improve contractility
mechanical assist deveices
148
two types of mechanical assist devices used in cardiogenic shock
balloon pumps
LVADs
149
preventing the recurrance of MI
lifestyle changes
beta blockers
statins
ACE inhibitors
antiplatelet drugs
150
three faces of angina pectoris
stable
unstable
variant
151
stable angina
recurring episodes of chest pain brought on by exertion and relieved by rest
152
unstable angina
angina that occurs with minimal activty or at rest
153
variant (prinzmetal) angina
extreme fatigue associated with minimal exertion related to coronary vasospasm
154
pathophysiology of stable angina
unmet oxygen demand cuased by coronary atherosclerosis, anemia, fever, hyperthyroid
155
typical anginal episode
lasts 2-15 minutes
substernal pain with radiation
intiated by lifting, eating, emotions, cold weather
156
treatment of stable angina
acute treatment with vasodilation
decrease frequency of attacks
157
how to decrease stable angina attacks
HTN control
lipid management
lifestyle modification
cononary revascularization
158
three drugs used in the treatment of stable angina
nitrates
beta blockers
calcium channel blockers
159
prognonsis for stable angina
some will improve, but most will develop CHF or have progress to acute cononary syndrome within 3-5 years
160
chronic heart failure 9CHF) definition
ventricular function insufficent to meet the metabolic and blood flow demands
161
why is the indicidence of CHF increasing
people who used to die from AMIs are now living with decreased heart function
162
two types of CHF
CHF with reduced EF (systolic heart failure)
CHF with preserved heart failure (diastolic heart failure)
163
ejection fraction
fraction of ventricular volume eject by each beat of the heart, normally 50-65%
164
how is EF determined
echocardiogram
165
visious cycle of CHF
chronic ischemia damages myocardium
remodeling occurs due to stretching leads to cardiomegaly
overstretched remodeled myocardium reduces ventricular function leads to fluid overload and high BP
leads to increased ischemia
166
four factors to prevent CHF
lipid control
HTN treatment
lifestyle changes
prevent or reduce damage from AMI
167
CHF symptoms
dyspnea, orthopnea, edema
168
CHF signs
peripheral edema, JVD
169
CHF signs on CXR
cardiomegaly, pulmonary edema
170
CHF signs on echocardiogram
ventricular ejection fraction
171
CHF lab signs
elevated BNP
172
BNP
brain natriuretic peptide
173
CHF EKG signs
left ventricular hypertrophy
174
orthopnea
the inability to sleep supine without breathing issues
175
CHF treatment strategy I
reduce cardiac work load (limit activity, reduce weight, control HTN)
reduce blood volume (decrease Na, diuretics)
176
CHF treatment strategy II
reduct cardiac remodeling (aldosterone antagonists)
treat hyperlipidemia (statins, even if lipids are normal)
177
two agents that improve survival with CHF
beta blockers
ACE inhibitors
178
dyspnea as it relates to CHF
air hunger with minimal exertion
179
what is the 5 year survival rate once diagnosed with CHF
50%
180
who is usually victim of idiopathic cardiomyopathy
young and healthy people, generally with a precipitating even (viral infection, pregnancy)
181
what is the treatment for idiopathic cardiomyopathy
spontaneous remission, but LVADs or transplant can be required
