Transcript NPLEX Combination Review Chapter 1

NPLEX Combination Review
Cardiovascular Part 1
Paul S. Anderson, ND
Medical Board Review Services
Copyright MBRS
• SGOT / AST “A sick heart can beat f-AST”
– Identify and monitor HEART!!! , Kidney,hepatocellular damage
– Increased in early MI (peak at 24-36 hrs.)
• SGPT / ALT “L is for Liver”
– Identify and monitor hepatocellular damage.
– ALT>AST Mainly = Liver Dz.
• GGT / GGTP
– Useful in detecting space-occupying lesions, biliary dysfunction
and ETOH abuse – Chemical toxicity.
• CPK
– Most often performed to document an acute MI; should be
performed upon admission to hospital (after 12 hours but before 24
hours).
– CPK-MB elevation also may be associated with pulmonary
embolism.
LDH (118.0 – 273IU/ml)
Principle measurement to diagnose conditions in which there
is tissue damage.
• Isoenzymes:
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LDH-1 Normally Lower than LDH-2
In MI: LDH-1>LDH-2!
Liver Dz: LDH< AST&ALT
Pernicious Anemia LDH may be 50X Normal
LDH-5 Increase in Muscle Dz’s
• LDH ELEVATIONS
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–
–
Acute MI
Myocarditis
Liver disease
Tissue necrosis
CHF
Shock
Pancreatitis
Acute renal infarction
Hemolysis
Skeletal muscle disease
Trauma
Multi-system disease
Collagen-vascular disease
MI
– Troponin-1Increase
2-4 hours post-MI
– CK / MB Increase
4-6 hours post
– Myoglobin Increase
4-8 hours post
– AST
6- 36 hours post
– LDH-1>LDH-2!
12-48 hours post
Plasma Lipid Profile
Used to determine cardiac risk and to aid in the diagnosis of
lipoprotein metabolism disorders:
• Total cholesterol (< 200mg/dL)
– HDL (< 35 mg/dL confer increased myocardial risk)
– LDL (> 100mg/dL associated with increased myocardial risk)
• Triglycerides (< 250mg/dL)
• Apolipoprotein A1 (> 140mg/dL) Lipoprotein portion of
HDL.(Higher = better) may be more useful than HDL
cholesterol to identify patients with CAD
• Apolipoprotein B (70 –110 mg/dL) major apoprotein of LDL and
VLDL; elevated levels indicate increased myocardial risk
• Lipoprotein (a) (< 30mg / dL)
– Correlates CAD risk; concentrations > 30mg/dL correlate 2X greater risk
of developing CAD. (<20 desirable range). Used in predicting stent
closure post-surgery.
Plasma Lipid Profile
• Genotyping Hyperlipidemia
Fredrickson’s Types:
– Sub Types I, II, III, IV (Definitive dx with lipid
electrophoresis)
– IV Most Common
• Chol. = / > 200
• HDL = Low / LDL = High
• TG > Chol.
– II Second Most Common
• Chol. > 200
• TG Normal
• Homocysteine
– Increased levels in serum may confer increased myocardial risk.
• Ammonia (NH3) (5-50mmol/l)
– Severe liver disease is the most common cause of elevated levels.
• Vitamin B12 (> 200pg/ml)
– Decreased values in pernicious anemia and alcoholism.
• Folate (200 – 640ng/ml)
– DECREASED in megaloblastic anemia and alcoholism.
– INCREASED in acute renal failure and liver disease.
• TIBC (% Transferrin saturation) 255 –450mcg/dL
– Usually performed in conjunction with serum iron in the evaluation and
diagnosis of iron-deficiency anemia, chronic disease anemia and
thalassemias.
– INCREASED: Fe deficiency anemia, PG and OBC.
– DECREASED: Anemia chronic disease, sideroblastic anemia and
hemochromatosis.
Calculating % Fe. Saturation
• Serum Iron:
Serum Iron (mcg/dL) / TIBC
– VERY labile! Changes quickly.
(mcg/dL)
• Ferritin (20 – 300ng/ml)
– Detection of iron deficiency and anemia by reflecting storage of iron.
Vascular Studies
• ARTERIAL
– AORTA: Performed when working-up probable aneurysms
– CAROTID: Performed to ensure normal vascular anatomy of common carotid
artery, internal and external carotids; ruling out stenos is or occlusion
– LEA: Examining extremity arterial anatomy, normal triphasic blood flow, plaques
or other pathological lesions and normal segmental blood pressure.
• VENOUS
– LEV: Normal venous anatomy with spontaneous, phasic blood flow pattern,
normal venous augmentation with no pathological valves present.
• Advantages
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Noninvasive without radiation risk.
May obviate need for costly hospitalization.
Structural image therefore useful for patients with organ function dysfunction.
Does not require ingestion of contrast dyes.
• Disadvantages
– Requires skilled technician to operate transducer.
– Air-filled structures cannot be studied with this procedure.
– Obese & restless patients cannot be adequately studied.
• Interfering factors
– Bowel gas (air) complicates procedure.
– No open wound or dressing can be used to visualize deep structures.
Electrocardiogram
• Resting ECG
– Performed to establish baseline ECG.
• Stress / exercise ECG
– Graded exercise tolerance test. Systolic values usually
increase. Diastolic usually remains unchanged.
– Test measures the efficiency of the heart during a dynamic
exercise stress period.
– Valuable for diagnosing IHD, underlying pathophysiological
functioning.
• Holter monitor
– Method of continuously recording the ECG; often for 24
hours.
– Provides documentation of suspected cardiac rhythm
disturbances.
• Infarction
ECG Findings
– Pathologic Q-Waves
• .04 sec or > & 1/3 as deep as R-Wave is high (all but AVR)
– S-T Segment changes
• Tall T’s, (S-T elevations)
– Age of infarct
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•
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Hyperacute: Normal Q, ST Elevation, upright T
Acute: Q MB Pathologic, ST Less Elevated, T inverted
Recent: Q-Change, Isoelectric S-T, Symmetrical T inv.
Old: Significant Q- changes, Isoelectric T waves
• Drug / Electrolyte changes
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Digitalis: Scooped S-T’s
Hyperkalemia: Wide P & QRS, Peaked T
Hypokalemia: Flat T wave, U wave present
Hypercalcemia: Short Q-T
Hypocalcemia: Long Q-T
• Pericarditis: P-R Depression, S-T elevation
Clinical Considerations: ECG
• Interfering factors:
– Race: ST elevation with T-wave inversion more
common in people of African decent.
– Food Intake: High CHO may shift electrolytes and
induce ST depression and T-wave inversion.
– Anxiety: May induce ST depression and/ or T-wave
inversion.
– Pre-testing activity may alter results.
• Procedural preparation and aftercare
– Proper lead placement
– Instruct patient regarding procedure
– Recognize limitations of ECG
Stress EKG
• Indications
– Definite indications
• Atypical symptoms in men or menopausal women
• Assess prognosis in patient with known CAD
• Assess patient with Exercise-induced
dysrhythmia
– Possible indications:
• Typical or atypical symptoms in menopausal
women
• Assess response to therapies
• Evaluate variant Angina
• Serial testing in patient with known CAD
Family Practice Notebook
Stress EKG
• Contraindications
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Aortic Dissection
Critical Aortic Stenosis
Critical Left Ventricular outflow-tract obstruction
Idiopathic Hypertrophic Subaortic Stenosis (IHSS)
Inability to Exercise to adequate level of exertion
Uninterpretable Electrocardiogram
• Left Bundle Branch Block (Adenosine Nuclear needed)
• Electronically paced rhythm (Pacemaker)
• WPW Syndrome
• Abnormal ST segments (>1 mm ST abnormality)
Recent or active cerebral ischemia
Severe uncontrolled Hypertension
Uncompensated Congestive Heart Failure
Unstable Angina
Digoxin Use (Class IIB Recommendation)
Cardiac revascularization within last 5 years
Family Practice Notebook
Ankle Brachial Index
•
Technique
–
Measure highest systolic reading in both arms
•
•
•
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Record first doppler sound as cuff is deflated
Record at the radial pulse
Use highest of the two arm pressures
Measure systolic readings in both legs
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Cuff applied to calf
Record first doppler sound as cuff is deflated
Use doppler ultrasound device
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•
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Record dorsalis pedis pressure
Record posterior tibial pressure
Use highest ankle pressure (DP or PT) for each leg
Calculate ratio of each ankle to brachial pressure
•
Divide each ankle by highest brachial pressure
Family Practice Notebook
Ankle Brachial Index
• Interpretation
– Ankle-Brachial ratio >0.95: Normal
– Ankle-Brachial ratio <0.95: Peripheral Vascular
Disease
– Ankle-Brachial ratio <0.6: Intermittent
Claudication
– Ankle-Brachial ratio <0.5: Multi-level disease
– Ankle-Brachial ratio <0.26: Resting ischemic pain
• Ankle-Brachial ratio <0.2: Gangrenous
extremity
Family Practice Notebook
Carotid Evaluation / Ultrasound
• Interpretation of carotid bruit
– Degree of stenosis by atherosclerotic Plaque
• Minimum stenosis causing bruit: 50% (<3 mm lumen)
• Prolonged, high-pitched bruit: >75% (1.5 mm lumen)
– Location
• Plaque involves posterior wall of common carotid
• Affects bifurcation and flow into internal carotid
• Risk of distal thrombus formation in internal carotid
– Carotid bruit associated risk of stroke at 1 year
• Asymptomatic carotid bruit: 1% risk at 1 year
• Transient Ischemic Attack history: 1.7% risk
• Other studies question bruit significance
Family Practice Notebook
Carotid Evaluation / Ultrasound
• Evaluation
– Carotid Artery Duplex Ultrasonography
• Standard diagnostic tool for carotid stenosis
• Less expensive than MRA
• Accuracy for diagnosing severe carotid stenosis
– Test Sensitivity: 86%
– Test Specificity: 87%
– Carotid Magnetic Resonance Angiography (MRA)
• Better than ultrasound at defining carotid anatomy
• Accuracy for diagnosing severe carotid stenosis
– Test Sensitivity: 95%
– Test Specificity: 90%
Family Practice Notebook
Echocardiogram
• Indication
– Every patient with Congestive Heart Failure!
– Distinguishes
• Systolic Dysfunction
• Diastolic Dysfunction
– Identify underlying valve disease
– Identify underlying ischemic heart damage
– Quantify Congestive Heart Failure severity
Echocardiogram
• Assessment
– Chamber size (diastolic and end-systolic dimensions)
• Left Ventricular Hypertrophy
• Left Atrial Enlargement
– Ejection Fraction (EF)
• Systolic Dysfunction: EF < 45%
• Diastolic Dysfunction (isolated): EF > 50%
• Echocardiogram accuracy is +/- 5% at best
– Heart Valve Function and dysfunction
– Wall thickness and wall motion abnormalities
Family Practice Notebook
Thrombolysis
• Needed when the intrinsic clotting
mechanisms are activated
– Arrhythmias
– Fibrillation
– Prosthetic valves
– Hyper-coaguable (thick) blood
• High Fibrinogen
• Dehydration
• Multiple sites in the clotting cascade can
be affected
Antithrombotics
MOA
Uses
Adverse
Effects
Other
Vitamin K
antagonist
Thrombosis,
rheumatic heart
disease,
embolism,
ischemic heart
disease
Prolonged
bleeding,
hemorrhage,
diarrhea,
fever,
rash
Monitor
prothrombin
time
Outpatient
Warfarin
[Coumadin]
(Extrinsic)
Factors
2,7,9,10
Antithrombotics
MOA
Uses
Adverse
Effects
Other
Inhibits
clotting factors
by binding to
antithrombin
III (AT3) and
ENHANCING
the thrombin
blockade of
AT3.
Prevention
of deep
vein
thrombosis,
embolism,
DIC
Hemorrhage,
cutaneous
necrosis,
chills,
pruritus,
fever
Administer
cautiously
in menstruating
women,
patients
with liver
disease or
blood
disease
Mainly IV /
inpatient
Heparin
CLOTTING PATHWAYS
Intrinsic Pathway:
Blood trauma (turbulence and viscosity) or
collagen and blood contact.
Drugs: Warfarin, ASA,
Vitamin-E, EFA’s
Extrinsic Pathway: Damage
outside of blood vessels.
Measured by:
PTT
Drugs: Heparin
Measured by
PT/INR
Factors
2-7-9-10
Antithrombin III keeps
Thrombin INACTIVE
PROTHROMBIN ACTIVATOR
made up of V&X: Started by X alone and V
becomes active with + feedback
Antithrombotics
MOA
Uses
Clopidogrel
[Plavix]
Prevent formation of
platelet aggregating
substance: thromboxane
A2 (TxA2) – The proinflammatory cytokine
produced by COX activity
along with PG2 in the
arachadonate cascade.
Reduce risk of Salicylism
MI, Stroke
(ASA),
GI distress,
bleeding,
tinnitus, rash,
occult blood
Aspirin (ASA)
Adverse
Effects
TTP(Plavix)
ASA for Prevention
• Most patients use 75-162mg / day “low dose ASA”
– Average is one 81mg ASA (baby aspirin)
• Am J Cardiol 2008;102:396-400 compared the effects of
aspirin 300 mg/day and combined therapy with aspirin 100
mg/day and clopidogrel 75 mg/day on platelet function
– Both strategies significantly decreased ADP- and collagen-induced
platelet aggregation, the authors report:
• 18 of 30 patients treated with aspirin 300 mg/day and
• 25 of 30 treated with aspirin 100 mg/day and clopidogrel 75 mg/day had
adequate platelet inhibition.
• "Increasing the aspirin dose to 300 mg/day or adding
clopidogrel to aspirin can provide adequate platelet inhibition
in a significant number of those patients with impaired
responses to low-dose aspirin," the investigators conclude.
Clopidogrel (Plavix) Rx:
• 75 mg Tablets
• Preventive: 75mg qd
• Acute (STMI): 300mg loading dose then
75mg qd
• Literature lists continuing ASA Rx as well
Clopidogrel and aspirin versus aspirin alone for the
prevention of atherothrombotic events.
N Engl J Med. 2006; 354(16):1706-17 (ISSN: 15334406)
• CONCLUSIONS: In this trial, there was a
suggestion of benefit with clopidogrel treatment
in patients with symptomatic atherothrombosis
and a suggestion of harm in patients with
multiple risk factors. Overall, clopidogrel plus
aspirin was not significantly more effective
than aspirin alone in reducing the rate of
myocardial infarction, stroke, or death from
cardiovascular causes.
Cardiac Function - Basics
Cardiac Function
• Electrical function
– Creates the rhythmic pumping of blood via muscular
contraction
– When irregular creates
• Arrhythmias
• Extra beats
• Hydraulic function
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Mass movement of blood through the chambers
Pushed by muscle contraction
Controlled by valves in the system
When irregular creates
• Murmurs
• Aberrant blood flow
Cardiac Muscle Physiology
EPI
Beta blockers
B-1
EPI
Adenylate cyclase
cAMP
Adrenergic
receptor
Cyclase-a
ATP
CA++ Channels
++
CA
Prot.Kinase-a
Influx
Ca++
CA++
Channel Blockers
Prot. Kinase
Cross Bridge
Formation
“Phosphorylation”
Tension
Generation
Cardiac AP and Ca++ Channel
Ca++ Channel Open
Carnitine at the Mitochondrial Membrane
Drugs to correct rhythm
disturbances:
• These drugs are used to “calm” the
electrical impulses in the heart.
• This “calming” creates less aberrant heart
beating
• These drugs come in four classes
– Two classes are also anti-hypertensive drugs
– Two classes are specifically rhythm agents
Class I Antiarrhythmics
MOA
Uses
Adverse Effects Other
Digoxin
Inhibits the
sodium/potassium
pump to increase
intracellular calcium.
CHF,
Fatigue
paroxysmal
atrial
tachycardia,
arrhythmias
Cardiac
Glycoside
Calcium drives the
cardiac AP plateau.
muscular
weakness
Monitor blood
levels.
Toxicity may
be life
threatening.
atrial fibrillation,
agitation
atrial flutter,
blurred vision
Yellow halo
around vision
may develop.
anorexia
nausea
(also)
Lidocaine
Quinidine
**NOT Quinine!
Decreases
automaticity,
conduction velocity
and prolongs
refractory period
Has anticholinergic
effects
Atrial flutter
atrial fibrillation
premature atrial
and ventricular
depolarization
Arrhythmia,
nausea
vomiting
diarrhea
cinchonism
fever
vertigo
headache
Prolongs QRS
and QT
intervals on
EKG
Cinchonism!
•
•
•
•
•
Quinine AND Quinidine:
Tinnitus / Hearing Loss
Headache / Nausea
Dizziness / Vertigo
Visual changes
Digitalis / Quinidine Rx:
• Digitalis:
–
–
–
–
(Capsules 0.05, 0.1, 0.2mg::Tabs 0.125, 0.25 mg)
Dose 0.05 to 0.35mg bid
Therapeutic dose levels in 7-21 days
Measure trough level; Effective level 0.8-2 ng/mL
• Quinidine:
–
–
–
–
(Sulfate; 200, 300mg:: Gluconate; 324mg ER)
Dose 300-400mg sulfate q-6hrs
Dose 324 ER q-8-12hrs
Measure trough level 30-35 hours after starting or
changing therapy; Effective level 2-6 mcg/mL
Antiarrhythmics
MOA
Adverse Effects
Class II
Beta Blockers
Class III
Amiodarone
•delay in repolarization
•prolongation in AP
•slowing of electrical
conduction
•reduction in SA node fct.
•decreased conduction
through accessory
pathways
Class IV
Calcium
Channel
Blockers
•About 7 out of every 10 patients
will experience some type of
reaction, and between 1 in 20
and 1 in 5 will experience side
effects that are severe enough to
stop the medication.
•The most severe side effect
related to the lungs. These
reactions can be fatal. (One in 10
of those that develop lung toxicity
will die.)
•rare, fatal liver toxicity has
occurred
Other
Diuretics
Na+ HANDLING ALONG THE NEPHRON
•
•
•
•
•
Numbers = % Na
Arrows = Direction of flow
PROXIMAL TUBULE
– Reabsorbs 67% (2/3) Na & H2O
– Reabsorbs all Glucose, HCO3, &
Amino Acids
– Reabsorbs Na via Cotransport with
Glucose, AA’s, PO4; And via
Countertransport in the
Na+ / H+
Exchange.
– Site of Carbonic Anhydrase
Inhibitor activity (Blocks HCO3
reabsorption)
THICK ASC. LOOP of HENLE
– Reabsorbs 25% of Na
– Na-K-Cl cotransporter
– Site of Loop Diuretic action
DISTAL TUBULE / COLL. DUCT
– Reabsorbs 8% Na via. Na-Cl
cotransporter
– Site of thiazide diuretic action
Na+ HANDLING ALONG THE NEPHRON
• PROXIMAL TUBULE
– Reabsorbs 67% (2/3) Na &
H2O
– Site of Carbonic Anhydrase
Inhibitor activity (Blocks
HCO3 reabsorption)
• THICK ASC. LOOP of HENLE
– Reabsorbs 25% of Na
– Site of Loop Diuretic action
• DISTAL TUBULE / COLL. DUCT
– Reabsorbs 8% Na via.
Na-Cl cotransporter
– Site of thiazide diuretic
action
Antihypertensive/ MOA
Diuretics
Chlorothiazide
(Hydrochlorothiazide –
HCTZ)
Furosemide
[Lasix]
Uses
Adverse Effects Other
Inhibits sodium and
chloride reabsorption in distal
tubule resulting in
a decrease in the
glomerular filtration
rate
HTN
Hypokalemia,
oliguria, anuria,
GI disturbance,
hypercalcemia,
hyperglycemia,
hyperuricemia,
renal failure
Loop diuretic,
inhibits sodium and
chloride reabsorption in the
Loop of Henle
Edema,
HTN
Edema
Hypokalemia,
oliguria, anuria,
GI disturbance,
hypercalcemia,
hyperglycemia,
hyperuricemia,
ototoxic,
hypovolemia
C.I. in
patients with
hypersensitiv
-ity to
thiazide or
sulfonamide
drugs
Antihypertensive/ MOA
Diuretics
Uses
Adverse Effects Other
Triamterene
Potassium
sparing diuretic
acts on distal
tubules
Edema,
HTN
**Hyperkalemia,
Aldosterone
antagonist
Edema
HTN
Same,
plus breast
deformity and
tenderness
nausea,
vomiting,
diarrhea
May turn
urine blue
Folic Acid
Base
(Often in
combination with
HCTZ as “Maxzide”
Spironolactone
Some
endocrine
uses
(PCOS…)
Multiple
toxicities
ALDOSTERONE
Spironolactone
BLOCKS!
Leads to Na
EXCRETION (in
urine) and K
retention (in blood)
Diuretics
• HCTZ
– 12.5mg capsules; 25, 50, and 100mg tablets
• Edema: 50-100mg qd until edema resolved
– Short term only
– Max Dose 200 mg acutely
• HTN:
– 12.5 – 50mg qd
• HCTZ / Triamterene
– 25mg / 37.5mg - Maxzide; 50mg / 75mg – Maxzide-25
• Furosemide
– 20, 40, and 80mg Tablets
• Edema: 80 mg qd (may increase as required up to 600mg total
daily)
• HTN: 40mg bid
Antihypertensive Drugs:
• Beta Blockers
–END IN “-OLOL”
• ACE Inhibitors
–END IN “-PRIL”
• ARB’s (Angiotensin Receptor Blockers)
–END IN -SARTAN
• Catecholamine Agent
– ONLY ONE: Reserpine
• Calcium Channel Blockers
– All the rest!
Beta-Blockers
Cardiac Muscle Physiology
EPI
Beta blockers
B-1
EPI
Adenylate cyclase
cAMP
Adrenergic
receptor
Cyclase-a
ATP
CA++ Channels
++
CA
Prot.Kinase-a
Influx
Ca++
CA++
Channel Blockers
Prot. Kinase
Cross Bridge
Formation
“Phosphorylation”
Tension
Generation
Antihypertensives
Beta Blockers
MOA
Uses
Adverse Effects Other
Atenolol
Acebutolol
Betaxolol
Bisoprolol
Esmolol
Metoprolol
1
adrenergic
receptor
Hypertension,
angina
Fatigue,
drowsiness,
vertigo,
dizziness,
bradycardia,
hypotension,
bronchospasm,
CHF
Enhance
effects of
digitalis
Propranolol
Carteolol
Nadolol
Pindolol
Sotalol
Timolol
Blocks both
Hypertension,
angina,
arrhythmias,
migraines,
essential
tremors
Fatigue,
bradycardia,
hypotension,
lethargy, nausea,
vomiting,
diarrhea, CHF
Abrupt
discontinuati
on may
cause
tachycardia
and rebound
hypertension
blocker,
decreases
cardiac output
and renin
release
1 and 2
adrenergic
receptors
Beta Blockers
• Atenolol (Tenormin)
– 25, 50 or 100mg tablets
– HTN:
• 50 mg qd
• Increases to 100 mg qd maximun
– Migraine Prophylaxis
• 100mg qd
Calcium Channel Blockers
Cardiac Muscle Physiology
EPI
Beta blockers
B-1
EPI
Adenylate cyclase
cAMP
Adrenergic
receptor
Cyclase-a
ATP
CA++ Channels
++
CA
Prot.Kinase-a
Influx
Ca++
CA++
Channel Blockers
Prot. Kinase
Cross Bridge
Formation
“Phosphorylation”
Tension
Generation
Cardiac AP and Ca++ Channel
Ca++ Channel Open
Antihypertensives
Ca++ Channel
Blockers
MOA
Uses
Adverse Effects Other
Bepridil
Mibefradil
Calcium channel
blocker
Angina,
hypertension
Constipation,
hypotension,
dizziness,
edema, nausea,
CHF
Increased
levels with
cimetidine
Diltiazem
[Cardizem]
Calcium channel
blocker
Angina,
hypertension,
atrial
fibrillation or
flutter
Headache,
edema,
dizziness,
arrhythmias,
CHF, nausea,
constipation,
rash
Increased
levels with
cimetidine
Amlodipine
Felodipine
Nicardepine
Nefidipine
Nifedipine
[Procardia]
Calcium channel
blocker
Angina,
hypertension
Dizziness, CHF,
MI edema,
headache,
weakness,
nausea,
Capsule
passed in
stool,
medicine
released in
gut
Verapamil
[Isopten]
Calcium Channel Blockers
• Amlodipine (Norvasc)
– 2.5, 5 and 10mg tablets
– Angina
• 5 to 10 mg qd
– HTN
• 2.5 to 5 mg qd
• Maximum dose is 10 mg qd
Angiotensin Agents
ALDOSTERONE – RENIN – ANGIOTENSIN SYSTEM
ACE-I - BLOCK
ARB BLOCK
Antihypertensives
MOA
Uses
Adverse Effects Other
ACE
Inhibitors
Inhibits
ACE
[angiotensin
converting
enzyme] in
the lungs.
Hypertension,
heart
failure
Dry
persistent
cough
Tachycardia,
hypotension,
urticaria,
rash, Renal
dysfunction
headache
Hyperkalem
ia
Captopril
Benazepril
Enalapril
Lisinopril
Fosinapril
Contraindicated
in pregnancy
Antihypertensives
MOA
Uses
Adverse Effects
ARB’s
Candi-/ IrbeEpro- / LoTelme- / Val(sartan)
Blockade of
ANG-2
Receptors
Hypertension in
those with
ACE
intolerance
due to
Cough
Hypotension
Renal Dysfunction
Hyperkalemia
Angiotensin Agents
• ACE Inhibitors
– Quinapril (Accupril)
• 5, 10, 20 and 40mg tablets
• Dose for HTN 10-20 mg to start
• Maximum dose 80 mg qd
• ARB’s
– Candesartan (Atacand)
• 4, 8, 16 and 32 mg tablets
• 16 mg qd starting dose
• Often used 8 – 16 mg bid
No "clinically meaningful difference" in
hypertension
• "With the exception of rates of cough, the available
evidence does not strongly support the hypothesis
that ACE inhibitors and ARBs have clinically
meaningful differences in benefits or harms for
individuals with essential hypertension," according to
the report's authors, led by Dr David B Matchar
(Duke Center for Clinical Health Policy Research,
Durham, NC).
• He and his colleagues analyzed 69 reports based on
61 randomized and observational studies that lasted
at least three months and directly compared an ACE
inhibitor and an ARB in adults with essential
hypertension and evaluated meaningful end points
like blood pressure control, treatment compliance,
and adverse events.
Peripheral Anti-Adrenergic
Peripheral antiadrenergic
MOA
Uses
Adverse Effects Other
Reserpine
Depletes
catecholamine
stores in PNS
[and maybe
CNS]
Essential
hypertension
Drowsiness, sedation,
nervousness,
depression, Decr. HR,
nasal congestion,
nausea / diarrhea
Parasympathetic
Predominance
Do NOT
administer MAO
inhibitors and
Reserpine within
two weeks of
each other
Rx of Reserpine:
Available in 0.1 and 0.25mg tablets
Common Rx’s:
- 0.1 qd to bid
- 0.25 qd to bid
Do not use in catecholamine responsive depressives.
Overdose symptoms include hyper-parasympathetic activity.
But doesn’t Rauwolfia and
Reserpine use make people
kill themselves?
Lets go through this now:
Peripheral antiadrenergic
MOA
Uses
Adverse Effects Other
Reserpine
Depletes
catecholamine
stores in PNS
[and maybe
CNS]
Essential
hypertension
These are
RARE in hypercatecholamine
patients.
Drowsiness,
sedation,
nervousness,
depression,
Decr. HR, nasal
congestion,
nausea /
diarrhea
Parasympathetic
Predominance
Do NOT
administer
MAO
inhibitors
and
Reserpine
within two
weeks of
each other
Rauwolfia and Reserpine
• Reserpine Tablets:
– 0.1 and 0.25mg available
– Dose is 0.1 – 0.25 qd – bid
• Rauwolfia:
– Watch tincture concentration
– Average dose 1-3 mL qd - bid
Anti-Anginal Drugs
Anti-anginal
drugs
MOA
Nitroglycerin
Increases blood supply Angina
to heart; decreases
preload and afterload
Headache,
dizziness,
hypotension,
tachycardia,
bradycardia, rash
Amyl Nitrate
Unknown, thought to
be dilation of arterial
and venous system
Angina
Throbbing
headache,
dizziness,
hypotension,
tachycardia,
bradycardia,
Antidote for
cyanide
poisoning
Papaverine
HCl
“Cardiac vessel
dilation”
Angina
Similar to Nitro.
No longer used
Calcium
Channel
Blockers
See above
Angina
Uses
Adverse Effects
Other
Nitrate Rx:
• NTG
– SL-Tablets 0.3, 0.4 or 0.6mg
– Acute angina:
• Dose 1 SL tablet up to 1 tablet every 5 minutes for
3 doses
• Other dose forms available:
– Spray, Cream, Long Acting Capsules
Angina Rx:
• L-Arginine PO dose
– 1000 – 2000mg bid
• Magnesium Glycinate PO dose
– 100-300mg bid
• Zinc PO dose
– 20-50mg bid (taken in the middle of a meal to
decrease nausea!)
Lipid Management
Basics:
• HDL:
– “Good” although there are better and worse forms.
• Acts more like a hormone than a lipid molecule
• LDL:
– “Bad” although there are better (larger) and worse
(smaller) forms.
– Carry OXIDANTS!
– Generally LOWERING these makes one less
inflammatory
• Triglycerides:
– Stimulated in production by CHO intake
– Elevations often indicate Pro-Inflammatory status and
disorders of Insulin – Sugar biochemistry
LDL Oxidation: The LDL has the potential to carry
an incredible load of free radical.
Anti-Oxidant effects of Vitamins E, C, GSH and the RBC - Lipid –
Plasma Interaction
RBC
Plasma
LDL
Reduced Glutathione
ASC
Toco R
Oxidized
Glutathione
ASC R
DHA
LDL + R = “oxidized LDL”
Toco
Cholesterol Transport
Cellular Cholesterol Balance
High Cholesterol Types
• Lipoprotein Electrophoresis
– 5 Sub categories of hyperlipidemia
• Fredrickson’s Genotypes
– Types 2 & 4 are most common
• Type 4 is 1-2 X more common than Type 2
– Generally High TC, TG’s (higher than TC), and LDL
– Responds to carbohydrate restriction
– Poor response to low fat diets
• Type 2
– generally High TC, LDL, and NORMAL TG’s
– Responds better to reduced fat diets
Sugar / Insulin and TG Synthesis
TG’s
to
Blood
BLOOD
Acyl Units
CHO  AcetylCoA
CYTOSOL
[AcetylCoA Carboxylase] Insulin(+)
Esterify to TG’s
Malonyl CoA
Palmitate
(-)
CPT-1
MITOCHONDRIA
Acyl Units
Beta Oxidation
Energy
Lipid Lowering
Agents
MOA
Uses
Adverse
Effects
Lovastatin
[Mevacor]
HMG CoA
reductase
inhibitor
Hyperlipidemia
GI distress,
Monitor
headache,
liver
dizziness,
function
abdominal
cramps, rash,
liver toxic,
rhabdomyaloysis
Simvastatin
[Zocor]
Atorvastatin
[Lipitor]
Other
Fulvistatin
[Lescol]
Pravistatin
[Pravacol]
Check AST and ALT prior to Rx, and at 6 weeks post-Rx.
Rx along with 75-100 mg Co-Q10 minimum.
Discontinue if patient has muscle pain concomitant to Rx – EVEN if
LFT’s are normal.
Statin Rx:
• Atorvastatin (Lipitor)
– 10, 20, 40 and 80mg tablets
• Dose 10 to 20mg qd
• Start at 40mg qd if LDL reduction need is greater
than 45%
• Maximum dose 80mg qd
• Draw Lipids and LFT’s 4 weeks after
therapy initiation or does adjustment
A Multicenter Placebo Controlled Dose Ranging Study of
Atorvastatin
Journal of Cardiovascular Pharmacology and Therapeutics, Vol.
3, No. 2, 119-123 (1998)
• Patients received placebo or atorvastatin 10, 20,
40, 60, or 80 mg once daily.
• Adjusted mean decreases in LDL cholesterol for
patients receiving atorvastatin 10, 20, 40, 60,
and 80 mg were 37%, 42%, 50%, 52%, and
59%, respectively, compared with a mean
increase of 0.3% for patients receiving placebo
Lipid Lowering
Agents
Cholestyramine
[Questran]
MOA
Uses
Adverse
Effects
Other
Combines with
bile acid to form
an insoluble
compound that is
excreted
Hyperlipidemia
Constipation,
fecal
impaction,
abdominal
pain, nausea
Reduces
absorption of fat
soluble
vitamins
Lipid Lowering
Agents
MOA
Uses
Niacin
Stimulates
hepatic lipid
metabolism
Hyper- Niacin flush,
lipidrash, GI
emia
distress
Adverse
Effects
Other
Give with B-Complex
and Vitamin C to
avoid Hepatic Effect.
May be Rx’d alone or in a combination of Niacin and a low dose
statin.
Rx a high potency B-Complex AND Vitamin C (gram per gram of
Niacin).
Rx takes at least 1500 – 2000 mg daily to have any significant effect
on lipids.
SLOW release is generally better tolerated.
Slow release is NOT more dangerous than immediate release if
Rx’d properly.
LOWERS: TC, LDL AND TG
RAISES: HDL
Niacin Rx:
• Niacin Extended Release (Niaspan)
– 250, 500, 750 or 1000mg tablets
• Start with 1000 mg hs, work up to 1500 –
2000mg hs
– Avoid spices, tannins etc with medication
– 81mg ASA taken with the Niacin reduces
flushing
Advicor Rx:
• Lovastatin / Niacin combination:
– 20/500, 20/750, 20/1000 or 40/1000mg
– Dose is 1 po qhs
Fibrates
• Fenofibrate (TriCor…)
– Multiple dose formats
• To lower Triglycerides
– 48 – 145 mg qd
– Maximum dose 145mg
Lovaza
• Omega-3-acid ethyl esters (1 gram
capsules)
– Normal Sig is 2 capsules bid
• Indicated alone or with Statins in patients
with high (200-499) or very high (>500)
triglycerides.
– Alone in very high TG
– With 40 mg Statin in high TG
Cardiovascular (CV) causes
of chest pain
• Angina: Covered later
PERICARDITIS
• Usually more localized, sternal or over cardiac
apex
• sharp, stabbing, knife-like pain
• lasts hours to days
• aggravated by deep breathing or lying supine
and relieved by sitting up and leaning forward
• may auscultate friction rub
DISSECTING AORTIC ANEURYSM
• anterior chest pain, may radiate to back
• excruciating, tearing pain; sudden onset,
lasts hours to days
• pain unrelated to anything
• BP lower in left arm
Noncardiac causes of chest
pain
• GI disorders: peptic ulcer, esophageal
reflux, hiatal hernia, cholecystitis; pain usu
burning, cramping, aching; worse supine;
may be meal related
• Musculoskeletal disorders: variable
location; aching pain, made worse with
movement or palpation; touching surface of
chest aggravates the pain.
• Spontaneous Pneumothorax: unilateral
location; sharp, localized; sudden onset
lasting many hrs; dyspnea, SOB, painful
breathing
Noncardiac causes of chest
pain
• Pulmonary Embolism: pleurisy type pain,
dyspnea, pleural rub, pain over area of
infarction; hemoptysis with lg infarction
• Pulmonary Hypertension: substernal pain,
pressure, dyspnea, accentuated pulmonary
second heart sound
• Anxiety States: localized pain, sharp, burning;
moves from place to place, brief duration,  with
emotional situations; frequent sighing
EKG
Wave Propagation
P-wave means Atria!
No p-wave! Ventricles!
Axis!
Deviation!
EXTREME
RAD
LAD
HAPPY!!
RAD
Infarction causes
deflection of the
Axis! (RAD)
Hypertrophy
Accentuates the Axis
(LAD)
Angina Pectoris
Clinical syndrome caused by
Myocardial ischemia
(usually from CAD)
Angina Pectoris
• Transient precordial pain, brought on by exertion and
relieved by rest
• Pain may be vague or crushing; may radiate to left
shoulder, jaw, throat, teeth, arms
• Pain may be worse after meal or in cold weather; may
change as collateral circulation builds up
• Usually relieved with sublingual nitroglycerin (NTG)
within 2-3 min.
• EKG often normal with attacks
– exercise test may show ST abnormalities that help
with diagnosis (ST depression = ischemia)
Unstable Angina
• More severe form of angina
• Same etiology as exertional angina
• Variant angina (Prinzmetal’s angina) =
angina at rest with ST segment elevation
during attack
• May occur at same time of day
• Felt to be from coronary artery spasm
Acute Myocardial Infarction
• When insufficient coronary blood supply persists
after myocardial energy reserves have been
depleted, the myocardial cells become
irreversibly ischemic and the process of necrosis
termed “myocardial infarction”
• Pain not relieved with NTG
• Apprehension and sense of “doom”
• Most MI’s occur at 9 a.m. on Mondays
Five major signs and symptoms of MI
• pain or discomfort in the jaw, neck, or
back
• feeling weak, lightheaded, or faint
• chest pain or discomfort
• pain or discomfort in the arms or
shoulder
• and shortness of breath
MI
• All symptoms typically come and go on a
3-5 minute cycle.
• In women the signs may be:
– More significant nausea
– Back pain (above the kidney area)
– No neck or arm pain, often little chest pain
– These signs and symptoms cycle on a 3-5
minute rate as well
Acute Myocardial Infarction
• Abnormal EKG with Q waves
• CPK MB fraction elevated
• ECHO shows abnormal left ventricular wall
motion
Heart Failure
Congestive Heart Failure
• Clinical syndrome in which the heart fails
to pump enough blood to meet the body’s
need
• Leads to
– Dyspnea On Exertion
– Paroxysmal Nocturnal Dyspnea
– Orthopnea
Diastolic Heart Failure
• Classically, heart failure has been almost
synonymous with left ventricular systolic failure
(pump failure)
• Diastolic dysfunction of the left ventricle occurs
when there is impairment of relaxation of the
ventricle resulting in delayed filling and
increased pulmonary venous pressure
• This combined with secondary compensatory
tachycardia results in  left ventricular volume
Adaptive Mechanisms in CHF
• Ventricular dilation—will eventually lead to 
diastolic pressure and pul edema (left failure)
and/or systemic edema (right failure)
• Reduced blood flow to the kidneys salt
and water retention and  blood volume with
2º HBP ( afterload)
• Sympathetic stimulation increases venous
tone, thus shunting blood from the peripheral
tissues to the heart causing  BP
• Tachycardia and increased contractility may
precipitate ischemia in pts with CAD
Left CHF
• Cardinal clinical symptoms are DOE, chronic dry
cough and fatigue
• Tachycardia, cardiac asthma, productive rust
colored sputum, rales, displaced apical impulse,
S-3, S-4 gallop rhythms, right sided pleural
effusions, reduced carotid pulse
• Nocturia due to  renal perfusion lying down and
exercise intolerance due to  blood flow to
muscles.
• Pallor, tachypnea, restlessness, low BP
Right CHF
• Fatigue, distended neck veins, pedal edema,
ascites, pitting edema, large liver, tricuspid
regurgitation murmur and cyanosis; orthopnea
and PND.
• Diseases that produce these sx include lung
disease, pul embolus, volume overload, mitral
stenosis.
Pulmonary Heart Disease (Cor
Pulmonale)
• Right ventricular hypertrophy and eventual
failure from pulmonary diseases
• Causes include:
– COPD
– Pulmonary fibrosis or emboli
– Scleroderma
– Primary pulmonary hypertension
– Alveolar hypoxia from any cause
Cor Pulmonale
• Chronic cough, exertional dyspnea, wheezing,
fatigue, weakness, cyanosis, clubbing epigastric
pulsations, distended neck veins, hepatomegaly,
polycythemia
• CXR shows RVH
• PFTs show underlying lung disease
• ECHO shows right ventricular disease
Disturbances of Rate and
Rhythm
Normal Sinus Rhythm
• Impulses originate in SA node
• Regular rate of 60-100/min in adults
• Each P followed by QRS
Normal Sinus Rhythm
Sinus Arrhythmia
• Similar to normal sinus rhythm
• Effect of respiration changes the
frequency the SA node discharges.
Sinus Bradycardia
• Similar to NSR except the rate is < 60/min in
adults
• Physiological bradycardia occurs in healthy
individuals (usually athletes) with  vagal tone
Sinus Bradycardia
Sinus Tachycardia
• Impulses originate in SA node at rate of
100-160/min in adults
• QRS follows each P wave
Atrial Premature Beat (APB)
• Impulse is discharged prematurely by an
irritable focus in the atria
• The further from the SA node the ectopic
focus is, the more abnormal will be the P
configuration
• PR is variable, but QRS is normal
Atrial Premature Beat (APB)
Atrial Tachycardia aka Supraventricular
Tachycardia SVT
• Impulses originate in an atrial pacemaker at
rate of 140-250/min
• QRS is usually narrow
• At very rapid rates, only every 2nd P may be
followed by QRS (2:1 block)
• Vagal stimulation can terminate the AT
• Common, occurs in young people with no
known heart disease
Atrial Tachycardia
Atrial Flutter
• Impulses originate in an atrial pacemaker at rate
of 240-340/min, but some are blocked at the AV
node
• Atrial activity is represented by saw tooth-like
deflections (Flutter waves)
• Symptoms of palpitations, sweating weakness,
dizziness, syncope
• Vagal stimulation has no effect
Atrial Fibrillation
• Impulses originate in multifocal atrial pacemaker
at rate of 300-600/min, but only some are
conducted to the ventricles
• Many patients are asymptomatic
• Since there is a deficit in radial and precordial
pulse, apical pulse should be taken in patients
• Pulse is irregular, irregular
• Vagal stimulation has no effect on ventricular
rate
Atrial Fibrillation
Premature Ventricular Contractions
(PVC)
• QRS is wide (> 0.12 sec), not preceded
by P wave
• Etiology is an irritable focus in the left or
right ventricle that fires prematurely and
the impulse is spread to the opposite
ventricle with delay producing a bizarre
QRS complex
• PVCs are forerunners of ventricular
tachycardia if they are frequent (> 5/min)
• May feel palpitations or be asymptomatic
Premature Ventricular Contractions
Ventricular Tachycardia
• By definition, VT consists of at least three
consecutive QRS complexes originating
from the ventricles and recurring at a rapid
rate (over 120 beats/min).
Ventricular Tachycardia
• Ventricular tachycardia (VT) is a
tachydysrhythmia originating from a ventricular
ectopic focus, characterized by a rate typically
greater than 120 beats per minute and wide
QRS complexes
• P waves are frequently hidden or may appear as
notches at various points on the QRS-T
complexes, but at a slower rate
• Vagal stimulation has no effect
Ventricular Tachycardia
Ventricular Fibrillation
• Multiple sites in the ventricle fire impulses
in an uncoordinated fashion
• Ventricular fibrillation is a terminal
arrhythmia, uniformly requiring rapid
initiation of emergency measures
Sick Sinus Syndrome
• Sick-sinus syndrome is a general term used to indicate
abnormalities of cardiac impulse formation and intraatrial
and AV conduction that may be manifested by various
combinations of brady- and tachyarrhythmias
• CAD is the most common cause
• Symptoms include none, light headedness, fatigue,
syncope, confusion, CHF or angina
Heart Block
• Often the presenting sign of heart block is
SYNCOPE.
First Degree AV Block
• Impulses originate in SA node
• First-degree AV block is defined as a PR
interval in excess of 0.2 s at normal heart
rates
• QRS follows each P wave
Second Degree AV Block
• Second-degree AV block is characterized by
intermittent failure of conduction from atria to
ventricles and is further subdivided into type I
(Wenckebach phenomenon) and Möbitz type II
second-degree block
Second Degree AV Block Type I (Wenckebach)
• Impulses originating in SA node are conducted
through AV node at progressively slower speed.
• A blocked P wave occurs after 2-5 conducted P
waves and then repeats itself (PR interval
becomes progressively longer until the QRS is
dropped)
Second Degree AV Block Type II (Mobitz)
• In type II second-degree AV block, appropriately
timed P waves fail to conduct, but there is not a
pattern of progressive PR lengthening.
• Prognosis is not good
Third Degree (Complete) AV Block
• Impulses originate in SA node, but none are
conducted through the AV jct.
• In third-degree (complete) AV block, the atrial
and ventricular rates are regular but dissociated
• Maneuvers by the patient, such as arm
movement, standing up, or marching in place,
may increase the sinus rate (P waves) without
corresponding changes in the ventricular escape
rate, confirming loss of AV conduction.
Bundle Branch Block (BBB)
• Impulses originate in SA node, spread
through atria, but are blocked through the
right or left branches of the bundle of His
• Wide QRS
• LBBB is more ominous than RBBB
Wolff-Parkinson-White Syndrome (WPW)
• Impulses originate in SA node, spread
over atria, but bypass the AV jct. through
an accessory bundle with premature
activation of the ventricles
Vasculitis
• Large-Vessel Vasculitis
– Giant Cell Arteritis
– Takayasu's Disease
• Medium-Vessel Vasculitis
– Polyarteritis Nodosa
– Kawasaki's Disease
• Small-Vessel Vasculitis
– ANCA Associated Small Vessel Vasculitis
– Non-ANCA Small Vessel Vasculitis
Small Vessel Vasculitis
•
Symptoms
–
–
–
–
–
–
–
–
–
•
Fever
Weight loss
Malaise
Myalgias and arthralgias
Dyspnea
Cough (Hemoptysis may be present)
Diarrhea
Nausea or Vomiting
Abdominal Pain
Signs
–
Dermatologic findings
•
•
–
Palpable Purpura (duration longer than 24
hours)
Urticaria
Pulmonary findings
•
•
Interstitial Lung Disease
Pulmonary hemorrhage
–
Neurologic findings
–
Gastrointestinal findings
•
•
–
Fecal blood positive
Differential Diagnosis
•
•
•
•
•
•
Peripheral Neuropathy
Embolic disease
Sepsis
Lymphoma
Leukemia
Myelodysplastic condition
Labs
–
–
–
–
–
–
–
–
–
–
–
–
Antineutrophil Cytoplasmic Antibodies
(ANCA)
Complete Blood Count (CBC)
Normocytic Anemia
Thrombocytosis
Chemistry profile (e.g. Chem8)
Renal Function tests may show renal
insufficiency
Liver Function Tests
Increased liver enzymes
Fecal Occult Blood
Urinalysis (Glomerulonephritis)
Hematuria
Proteinuria
Murmurs:
• S-1 (T/M) ---Systole--- S-2 (A/P)---Diastole---S-1
• Systolic Murmurs: “Big Deal”
– May be normal variants
– May indicate pathology
• (Midsystolic) Aortic / Pulmonic Stenosis
• (Pansystolic - Holosystolic) Mitral/Tricuspid Regurgitation,
Ventricular Septal Defect
• Diastolic Murmurs: BIG DEAL
– (Almost) Always indicate heart disease!
• (Diastolic Rumble)Mitral Stenosis
• (Decrescendo – Immediate Diastolic Murmur)Aortic
Regurgitation
Cardiac Murmurs
• The types of valvular heart disease can be
distinguished by the type of murmur heard
on auscultation
• Stenotic lesions of the aortic and
pulmonary valve have an ejection murmur;
they are systolic in timing, have a
crescendo component and do not
completely fill systole until late ( 12
12 )
Aortic Stenosis (AS)
• Most frequent etiology for AS is senile
calcific stenosis; second is calcification of
a congenital (bicuspid) valve; third is
rheumatic heart dis.
• Sx include syncope, angina, SOB, CHF
• Signs include ejection murmur at right 2nd
ICS, weak and delayed peripheral pulses
• Diagnosis is by ECHO
Aortic Insufficiency
• SOB, palpitations, angina
• Signs include a diastolic murmur that is
“blowing” and soft, elevated systolic BP
and low diastolic BP
• CXR shows signs of CHF and/or
cardiomegaly
Mitral Stenosis (MS)
• Usual etiology for pathology is postrheumatic heart disease
• SOB, DOE, PND, which are all part of
CHF
• Murmur is diastolic with an opening snap
(due to stiff, thickened valves) followed by
a low pitched rumbling sound best heard
at the apex or left sternal border. (  2-3 )
Mitral Stenosis (MS)
• EKG may show notched P waves
indicating left atrial enlargement
• Diagnosis is by ECHO and cardiac cath
• Indications for surgery include sx,
presence of transvalvular gradient,
measured by catheter, of > 4 mm Hg.
Mitral Regurgitation
• Symptoms of dyspnea, fatigue, left
ventricular failure
• Left ventricle eventually becomes
compromised leading to cardiac dilatation
• Murmur is pansystoloic, max at apex and
radiating to axilla, blowing in quality with
prominent 3rd heart sound
• Echo
Tricuspid Stenosis (TS)
• Most frequent etiology is congenital,
RHD, neoplasms
• Right atrium is  , atrial fib is frequent
• EKG shows atrial fib and right atrial 
• Dx can be made by Echo
Tricuspid Regurgitation (TR)
• Most frequent etiology for TR is
physiologic, as a reflection from left sided
heart disease; endocarditis, especially in
drug addicts (60% are due to Staph
aureus)
• Murmur low pitched, blowing, pansystolic,
worse with inspiration and heard along left
sternal border
Endocarditis
• Infective endocarditis is a microbial infection of the
endocardium, usually a subacute bacterial endocarditis
(SBE)
• Most pts have underlying organic heart dis (abnormal
valves, septal defects);High incidence seen in IV drug
users
• Nonspecific symptoms of cough, dyspnea, arthralgia,
diarrhea, pallor, splenomegaly, abd./flank pain from emboli
• Petechiae on palate or conjunctiva or in nail beds, splinter
hemorrhages
• 90% have heart murmurs and a changing murmur with
leukocytosis is common
Endocarditis
• Blood cultures are the definitive diagnostic
procedure; may be falsely negative in 5%
• Echo confirms the vegetations
Myocarditis: Inflammation of the
myocardium
• Etiology usually caused by infection (viral, most
common); toxins, drugs, radiation, immunologic
reactions. Often follows a URI
• Typically present with heart failure following a
febrile illness or with heart failure alone
• Symptoms:
– fatigue, dyspnea, palpitation, precordial pain through
the first few weeks of the infection
Hypertension
Essential Hypertension
• No known cause
• There is a natural progression of the disease
suggesting early  in blood volume and cardiac
output might cause  resistance
• This could be mediated by enhanced
sympathetic activity or by  circulating levels of
angiotensin II
Secondary Hypertension
•
•
•
•
•
•
•
•
Renal artery stenosis
Chronic renal disease
Primary hyper-aldosteronism
Hyper or hypo thyroidism
Pheochromocytoma
Pre-eclampsia
Aortic coarctation
BCP use
Disease of the Aorta
Aneurysms
• Local dilation of the aorta resulting from
weakness of the wall with distention
• Most common etiology is atheroma; more
recently evidence of Chlamydia
pneumoniae has been found
• 90% of aortic aneurysms are abdominal
• Best noninvasive method is ultrasound
(98% accurate on determining size)
Rupture rate of aneurysm at 5
yrs
Size of aneurysm
% rupture rate
7 cm or greater
75%
6-7 cm
35%
5-6 cm
(less than 5 cm)
25%
(insufficient data)
Signs and Symptoms of AAA
• Aneurysms < 5 cm are usu asymptomatic
• Pain in abdomen or low back
• Pulsatile mass (many thin patients will
have a pulsatile mass that is normal)
• Tenderness over the pulsatile mass
• Bruit over the mass (also can be heard in
normals)
Aortic Dissection
• Occurs in ascending aorta; caused by a break
in the intima allowing blood to flow in a plane
between the media and adventitia
• Pain is severe, chest or neck; may radiate to
back and later to abdomen
• Peripheral pulses and BP may be unequal
• Syncope, hemiplegia or paralysis of the lower
extremities may occur
• CT and transesophageal echocardiography
Inflammatory Pericarditis
• Most cases are idiopathic or have a viral
etiology
• Patients typically complain of sharp central
chest pain that worsens with recumbency and
is relieved by leaning forward
• Pain may be pleuritic in nature and may radiate
to the trapezius muscle
• Patients may reveal the pathognomonic finding
for pericarditis: the pericardial friction rub
• ECHO is a more accurate test
Cardiac Tamponade
• Results from accumulation of fluid in the
pericardial sac; the heart has an inability to
contract due to space restriction
• Chest pain, dyspnea, cough, tachycardia,
tachypnea, pulsus paradoxus (fall in BP > 10
mmHg with inspiration), edema and ascites may
be seen