Cardiovascular Disease Flashcards
two divisions of cardiovascular disease
peripheral vascular disease
heart disease
two branches of peripheral vascular disease
atherosclerotic
vasculitis
four divisons of heart disease
coronary artery disease
valvular disease
HTN heart disease
cardiomyopathy
T/F cardiovascular illness is the most common serious disorder in the US
true
what percent of the following have cardiovascular disease
people at age 20
people over 75
total population
5%
75%
20%
what is the most common cause of death in the US
cardiovascular disease
systolic pressure
pressure at which blood flow resumes in an occluded arterty
diastolic reading
pressure at which flow returns to normal in an occluded artery
most current guidelines for blood pressure
Normal
elevated
Stage 1
Stage 2
normal: 120/80
elevated: systolic >120, diastolic >80
stage 1 HTN: >/= 130/80
stage 2 HTN: >/= 140/90
based on new HTN guidelines how many people are afflicted
103million
of the 75% of the patients who have HTN and are aware of it, how many are getting treated?
how many are controlled?
50% are being treated
25% are under control
Dr Dodges suggested take home messages regarding HTN
- 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
four classifications of HTN
primary/essential/idiopathic
renal
endocrine
pregnancy induced
what is the most common form of HTN
primary/essential/idiopathic
two conditioned associated with renal hypertension
narrowed renal artery
chronic renal disease
three endocrine conditions associated with HTN
cushings
pheochromcytoma
congenital adrenal hyperplasia
three conditions associated with pregnancy induced HTN
toxemia
pre-eclampsia
eclampsia
pheochromocytoma
5 primary symptoms
a rare tumor of the adrenal medulla or sympathetic ganglion that secretes norepinephrine
- severe headaches
- diaphoresis
- palpitation
- tremor
- anxiety
T/F HTN is generally asymptomatic
true
what are three general symptoms associated with HTN
Headaches
malaise/fatigue
symptoms of complications
where are BP recordings most accurate
at home and work, not in the office
the hydraulic equation
define the variables
BP = CO x PVR
BP = cardiac output x peripheral resistance
three ways to decrease BP by decreasing CO
reduce HR
reduce contractility
reduce venous return/decrease blood volume
how to reduce BP by decreasing PVR
two methods to achieve this
vasodilation
- direct action on the vessels
- CNS control
two key elements manipulated to regulate blood pressure
sympathetic nervous system input
renal blood flow
two primary sympathetic receptors manipulated to control BP
Alpha 1 vascular receptors
Beta 1 cardiac receptors
two factors related to renal blood flow that can be manipulated to regulate BP
renin-angiotensin-aldosterone pathway
total vascular volume
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
two key RAA hormones
Angiotensin II
aldosterone
what is the function of aldosterone II
triggers vasoconstriction
aldosterone production and release from the adrenal cortex
three facts about aldosterone
most potent natural mineralocorticoid
helps with sodium and fluid retention
also induces cardiac growth
what is the sympathetic response to decreased BP
- activation of Beta adrenergic receptors in the heart
- activation of Alpha adrenergic receptors in smooth muscle
what is the effect of sympathetic activation of Beta receptors in response to Decreased BP
increased cardiac output through contractility
what is the effect of sympathetic stimulation of alpha receptors in response to decreased BP
increased peripheral resistance through vasoconstriction
what is the renal response to decreased blood pressure
decreased renal blood flow
what happens in response to decreased renal blood flow
renin is released
glomerular filtration is decreased
what has been the primary reason for decreasing number of cardiac death since the 1970
decreased in smoking
improved treatment
what two factors increase water retention in response to decreased blood pressure
decreased glomerular filtration
aldosterone production
what is the result of increased sodium and water retention in response to low BP
increasd blood volume, which increases cardiac output
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
two HTN treatment strategies
reduce cardiac output
reduce peripheral vascular resistance
two methods to reduce cardiac out in HTN treatment
block beta 1 sympathetic action
reduce blood volume
what is the result from blocking beta 1 sympathetic action
reduced cardiac rate and contractility
three methods to reduce peripheral resistance in HTN treatment
block alpha 1 sympathetic action
block central sympathetic action
directly dilate the blood vessels
four groups of drugs used to treat HTN
diuretics
sympathetic receptor blocker
direct vasodilators
RAA blockers
how do diuretic function to decrease blood pressure
lower blood volume
how do sympathetic receptors blockers function to lower HTN
block alpha and beta receptors
what is the function of direct vasodilators in the treatment of HTN
reduce peripheral vascular resistance
what is the function of blocking RAA in treating HTN
reduce blood volume and peripheral resistance
three common diuretics (examples)
thiazides (hydrochorthiazide)
loop diuretics (furosimide)
potassium sparring diuretics (spironolactone)
four common sympathetic receptor blockers (examples)
beta blocker (atenolol, propanolol)
alpha blockers (prazosin, terazosin)
alpha and beta (labetalol)
centrally acting (methyldopa, clonidine)
thee common vasodilators (examples)
calcium channel blockers (diltiazem, amlodipine)
arterial (hydralazine, minoxidil, diazoxide)
arterial and venous (nitroprusside)
four common RAA blockers (examples)
angiotensin converting enzyme (ACE) inhibitors (catopril, benazopril)
angiotensin II receptor antagonist (losartan)
aldosterone antagonist (spironolactone)
renin inhibitor (aliskiren)
thee factors that influence cardiac output
HR
contractility
filling pressure
thee factors that influence PVR
arterial diameter
arterial length
elasticity
distinguish between treatments for mild and severe HTN
mild to moderate HTN usually uses one drug
severe HTN uses multiple drugs
mitigating factors to consider in treatment of HTN
other medical conditions
RAA work less well on african americans
cost
why are ACE inhibitors effective
because angiotensin I is really just a precuros without much effect on blood pressure
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
three popular single drugs used in intial HTN treatment
ACE inhibitor
calcium channel blocker
diuretic
the useful conbinations of drugs used in intitial treatment of HTN
ACE inhibitor + diuretic
Beta blocker + diuretic
beta blocker + alpha blocker
what is the goal of HTN treatment
maintenance of 120/80 BP for high risk patients
<135/85 for mild to moderate risk patients
limbo goal for high risk hypertensives
trying to go as low as is safely possible for people with severe comorbities (diabetes, CAD, CVA)
what is the risk of decreasing blood pressure too low
toxicity
orthostatic hypertension
three common side effects of HTN treatment
electrolyte imbalances
annoying dry cough
malaise, fatigue
why drugs used to treat HTN will cause low potassium?
high?
diuretics
ACE and aldosterone inhibitors
what common HTN treatment will cause annoying dry cough
ACE inhibitors
what common HTN treatment can cause malaise and fatigue
beta blockers
what constitutes a “hypertensive emergency”
200/140
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
does HTN mangement need to be life long
preferably not, as long as necessary but short as possible
step down strategy for HTN treatment
decreasing dose based on stable normal pressures attained through lifestyle changes
what is the main cause of cardiovascular disease
atherosclerosis
atherosclerosis
vessel narrowing due to fatty deposits in the arteries related to lipid metabolism and cholesterol
two sources of cholesterol
exogenous (diet and absorption)
endogeneous (production of cholesterol from the liver)
lipoproteins
macromolecule consisting of lipid and protein
LDL
transporter of endogeneous cholesterol
HDL
removes LDL cholesterol and triglycerides
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
how is HDL increased
weight loss and exercise
HDL paradox
drugs that decrease LDL reduce risk
drugs that increase HDL do not reduce risk
atherosclerotic process
- fatty streaks
- monocyte aggregation
- LDL oxidation
- formation of foam cells
- inflammation leading to LDL accumulation
fatty streaks
LDL accumulation under endothelium
what causes the oxidation of LDL in fatty streaks
monocytes
foam cells
monocytes that become macrophages and ingest oxidized LDL
what is considered the unifying element in the pathogenesis of atherosclerosis
how was this decided
inflammtion
inflammatory markers correlate to CV disease risk
C reactive protin
an inflammtion marker related to heart disease
risk factors for atherosclerosis
- smoking
- hypertension
- diabetes
- family HX
- age
- dyslipidemia
- lifestyle
age range for increased atherosclerosis risk for men and women
>/=45 men
>/= 55 for women
dyslipidemia related to atherosclerosis
high LDL
low HDL
three lifestyle issues that increase risk of atherosclerosis
obesity
physical inactivity
atherogenic (inflammatory) diet
why is the age related risk for athersclerosis different for men and women
women haver higher HDL
estrogen raises HDL
two chronic effects of atherosclerosis
coronary effects
peripheral vascular disease
two coronary effects of chronic atherosclerosis
angine pectoris
congestive or chronic heart failure
three peripheral vascular disease associated with the effects of chronic atherosclerosis
renal artery stenosis
femoral/popliteal stenosis
aortic aneurysm formation
T/F most myocardial infarctions are caused by HTN
false, caused by atherosclerotic plaque rupture
what happens when an atherosclerotic plaque ruptures
a blood clot forms around the rupture and blocks the artery
four treatments for atherosclerosis
lifestyle changes
treatment of hyperlipidemia with statins
treat HTN
treat diabetes
when are symtpoms of mild atherosclerosis noticed?
severe?
50% occulsion, usually on exertion
80%, effects can be felt at rest
5 lipid lowering agents
niacin
bile acid binding agents
HMG-CoA reductase inhibitors
fibric acid derivatives
inhibitors of sterol absorption
common name of HMG-CoA reducatse inhibitors
statins
what is the effect of statin drug treatment
reduction of endogenous cholesterol synthesis
lowers LDL
three common statins
atorvastatin (lipitor)
simvastatin (zocor)
lovastatin (mevacor)
two adverse effects of statins
liver damage
muscle damage
what must be monitored during statin treatment due to the liver damaging side effects
liver enzymes
two conditions related to muscle damage from statin drugs
myopathy
rhabdomyolysis
when are statins contraindicated
pregnacy
children
what is a lesser known issue with statin?
what is the result
muscle weakness
reduction in activities
PCSK9 inhibitors
new drug that stimulated production of an enzyme show to decrease LDL and decrease risk of heart disease
two PCSK9 drugs
alirocumab (praluent)
evolcumab (repatha)
what is the benefit of PCSK9 treatment
drawback?
produce better lipid reduction that statins
very expensive
three causes of ischemia
vessel stenosis or occulsion
vasospasm
pump failure
what is the key component of ischemia
O2 supply is not sufficient for demand
other oxygen transport issues related to heart damage that arent ischemia
hypotension
chronic anemia
increased metabolism
three causes of hypotension that can result ischemia
acute blood loss
anesthesia
cardiac arrhythmia
causes of increased metabolism related to cardiac ischemia
hyperthyroid
fever
symptoms of
acute
subacute
chronic
ischemia
acute: acute coronary syndrome
subacute: angina
chronic : CHF
acute coronary syndromes
acute MI with ST segment elevation
acute MI without St elevation
unstable angina
three main forms of coronary heart disease (CHD)
acute coronary syndrome
stable angina
CHF
acute myocardial infarction
mycardial death due to abrupt reduction in coronary blood flow almost always caused by atherosclerosis
what is the intitial event of an acute MI
a plaque rupture
how many AMIs occur yearly
what percent are fatal
1.1 million
20-40%
T/F more than 50% of AMI death occur suddenly
true
symptoms of acute MI
squeezing pressure chest pain
can be felt in the stomach or left arm, face, shoulder
anxiety
diaphoresis
GI distress
T/F 30% of AMIs are asymptomatic
treu
what percent of AMIs are precipitated by strenous events
50%
why are AMIs more common in the AM
BP is higher
increased blood viscosity
cortisol secretion is at its highest
T/F most women have atypical AMI presentation
true, more likely to be Dx as gi
STEMI is usually indicative of what
transmural ischemia (involves the full thickness of the cardiac wall)
what is more common, STEMI or NSTEMI
NSTEMI (55-60%)(
NSTEMI is indicative of what
ischemia that is subendocardial rather than transmural
NSTEMI treatment
supportive measures
anticoagulation
NSTEMI supportive treatments
rest
oxygen
sedation/analgesia
control of arrhytmia
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
anticoagulation therapy for NSTEMI
heparin
antiplatelets
STEMI treatment
reperfusion
supportive measures similar to NSTEMI
two methods for reperfusion in response to STEMI
percutaneous coronary intervention
thrombolytic therapy
supportive measures for STEMI
aspirin
oxygen
decrease myocardial oxygen demand
control arrhytmia
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
PCI
stent placement
AMI prognosis factors
age
size of vessel
prior infarctions
nature of treatment
T/F the risk of death within 90 days of AMI is 75%
false, 1-22%
two main causes of MI mortality
cardiac arrhythmia (v fib)
pump failure (cardiogenic shock)
when is cardiogenic shock the more common cause of MI mortality
in the case of large infarctions
treatment of v fib
cardioversion (defibrilation)
three treatments of cardiogenic shock
vasopressors (maintain pressure)
inotropic agents to improve contractility
mechanical assist deveices
two types of mechanical assist devices used in cardiogenic shock
balloon pumps
LVADs
preventing the recurrance of MI
lifestyle changes
beta blockers
statins
ACE inhibitors
antiplatelet drugs
three faces of angina pectoris
stable
unstable
variant
stable angina
recurring episodes of chest pain brought on by exertion and relieved by rest
unstable angina
angina that occurs with minimal activty or at rest
variant (prinzmetal) angina
extreme fatigue associated with minimal exertion related to coronary vasospasm
pathophysiology of stable angina
unmet oxygen demand cuased by coronary atherosclerosis, anemia, fever, hyperthyroid
typical anginal episode
lasts 2-15 minutes
substernal pain with radiation
intiated by lifting, eating, emotions, cold weather
treatment of stable angina
acute treatment with vasodilation
decrease frequency of attacks
how to decrease stable angina attacks
HTN control
lipid management
lifestyle modification
cononary revascularization
three drugs used in the treatment of stable angina
nitrates
beta blockers
calcium channel blockers
prognonsis for stable angina
some will improve, but most will develop CHF or have progress to acute cononary syndrome within 3-5 years
chronic heart failure 9CHF) definition
ventricular function insufficent to meet the metabolic and blood flow demands
why is the indicidence of CHF increasing
people who used to die from AMIs are now living with decreased heart function
two types of CHF
CHF with reduced EF (systolic heart failure)
CHF with preserved heart failure (diastolic heart failure)
ejection fraction
fraction of ventricular volume eject by each beat of the heart, normally 50-65%
how is EF determined
echocardiogram
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
four factors to prevent CHF
lipid control
HTN treatment
lifestyle changes
prevent or reduce damage from AMI
CHF symptoms
dyspnea, orthopnea, edema
CHF signs
peripheral edema, JVD
CHF signs on CXR
cardiomegaly, pulmonary edema
CHF signs on echocardiogram
ventricular ejection fraction
CHF lab signs
elevated BNP
BNP
brain natriuretic peptide
CHF EKG signs
left ventricular hypertrophy
orthopnea
the inability to sleep supine without breathing issues
CHF treatment strategy I
reduce cardiac work load (limit activity, reduce weight, control HTN)
reduce blood volume (decrease Na, diuretics)
CHF treatment strategy II
reduct cardiac remodeling (aldosterone antagonists)
treat hyperlipidemia (statins, even if lipids are normal)
two agents that improve survival with CHF
beta blockers
ACE inhibitors
dyspnea as it relates to CHF
air hunger with minimal exertion
what is the 5 year survival rate once diagnosed with CHF
50%
who is usually victim of idiopathic cardiomyopathy
young and healthy people, generally with a precipitating even (viral infection, pregnancy)
what is the treatment for idiopathic cardiomyopathy
spontaneous remission, but LVADs or transplant can be required
