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492 Cards in this Set

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What is an atrial septal defect?
congenital heart defect characterized by persistence of foramen ovale or atrial-septal defect resulting in abnormal blood flow between atria
What is the cause of an ejection systolic murmur in anemia?
anemia -> O2 carrying capacity of blood reduced -> CO increases to meet metabolic demands -> heart pumps harder and faster -> creating ejection systolic murmur

constricted garden hose analogy:
-slow water speed -> no sound
-fast water speed -> sound
What is the clinical presentation and diagnostic workup of patent ductus arteriosus?
CLINICAL PRESENTATION:
dependent on size of shunt and degree of pulmonary HTN
diaphoresis with feeding
failure to thrive
tachypnea
S2 narrowly split or paradoxically split (narrows on inspiration and widens on expiration)
continuous machinery murmur
begins shortly after S1, peaks at S2, passes through S2 into diastole, becomes a decrescendo murmur and fades before S1
maximal at 2nd left intercostal space
radiates into anterior lung fields
diastolic flow murmur at apex
bounding peripheral pulses
widened pulse pressure

DIAGNOSTIC WORKUP:
CXR
EKG
ECHO
What is the ddx for ejection systolic murmur?
anemia
pregnancy
excessive exercise
What is patent ductus arteriosus?
congenital heart defect characterized by persistence of ductus arteriosus resulting in abnormal blood flow between pulmonary artery and aorta

ductus arteriosus normally closes spontaneously at 3-5 days of age
What is dextrocardia?
congenital defect where heart is situated on RT side of body
What is tetralogy of fellot?
congenital heart defect characterized by:
1. narrowing of pulmonary valve
2. thickening of RT ventricular wall
3. displacement of aorta over ventricular-septal defect
4. ventricular-septal defect
What is the clinical presentation and diagnostic workup of tetralogy of fellot?
CLINICAL PRESENTATION:
easy fatigability
exertional dyspnea
cyanotic spells characterized by:
1. sudden onset of cyanosis or deepening of cyanosis
2. dyspnea
3. altered consciousness ranging from irritability to syncope
4. decrease or disappearance of systolic ejection murmur d/t complete obstruction of right ventricular outflow tract
squatting (though rare since often diagnosed at birth)
cyanosis
clubbing
palpable RV lift
rough systolic ejection murmur at left sternal border in 3rd ICS, radiates to back

DIAGNOSTIC WORKUP:
CBC → polycythemia 2° to chronic arterial desaturation
CXR
EKG
ECHO
What is rheumatic fever?
complication of strep throat or scarlet fever
What is the etiology of rheumatic fever?
strep throat
scarlet fever

uncommon in United States
What is the clinical presentation of rheumatic fever?
recent infection
fatigue
fever
erythema marginatum → erythematous rings mostly on trunk that disappear and reappear over weeks to months
subcutaneous nodules → small painless nodules on extensor surfaces
chorea → abrupt nonrhythmic involuntary movements and muscular weakness
carditis
polyarthritis
What is the diagnostic workup of rheumatic fever?
↑ ESR
↑ CRP
↑ ASO → repeat in 10-14 days if normal
↑ PR interval on EKG → repeat in 2 weeks and 2 months if abnormal

also order:
CBC
BC if febrile
throat culture
CXR
echocardiogram → repeat in 1 month if negative
Current
Harrisons
What is the diagnostic (Jones) criteria of rheumatic fever?
recent strep throat + 2 major criteria or 1 major and 2 minor criteria

Major:
erythema marginatum
subcutaneous nodules
pericarditis, myocarditis, or endocarditis
polyarthritis
chorea

Minor:
hx of rheumatic fever or rheumatic heart disease
fever
arthralgias
↑ ESR
↑ CRP
↑ ASO
↑ PR interval on EKG
Current EMED ch19
What is the most common symptom of rheumatic fever?
arthritis
What is the management of rheumatic fever?
1. for strep throat → benzathine penicillin G 1.2 million units IM single dose
2. if penicillin allegy → erythromycin 40mg/kg daily
3. for fever and arthritis → aspirin
4. if refractory to aspirin → corticosteroids
4. bed rest until afebrile and resting HR, ESR, and EKG normal
5. to prevent recurrence → benzanthine penicillin G 1.2 million units IM every 4 weeks
-if no carditis → continue until 21 y/p
-if carditis + no valvular damage → continue for 10 years
-if carditis + valvular damge → continue for 10 years or until 40y/o if high risk for reexsposure of strep throat (parent, teacher, medical professional, military personnel)

If chorea:
1. provide calming environment
2. medications only control symptoms but do not alter duration or outcome
3. carbamazepine → may not see effect for 2 weeks, continue for 2 weeks after symptoms subside

If HF:
see HF management
Current ch10
Who is most commonly affected by rheumatic fever?
children 5-15y/o
Current ch10
What are the complications of rheumatic fever?
1. CHF
2. rheumatic heart disease
3. myocardial involvement
4. arrhythmia
5. pericardial effusion
6. rheumatic pneumonitis
Current ch10
True or false, increasing HR decreases cardiac output?
true
What are causes of increased HR?
stress, anxiety, body temperature, hormones (thyroxine, epinephrine, norepinephrine), medications
What is pulsus alternans?
pulse with alternating strong and weak beats
What is the ddx of pulsus alternans?
LT-sided HF
LT ventricular failure
low ejection fraction
pericardial effusion
asthma
*What is the etiology of endocarditis?
1. community acquired:

2. hospital acquired:
UTI, catheter infection, or nosocomial wound → bacteremia → endocarditis

3. prosthetic valve infection

4. IV drug use
*What is the clinical presentation of endocarditis?
fever
murmur
osler's nodes
subungual hemorrhages
What is the diagnostic workup of endocarditis?
BC x 3
echocardiography
Current ch118
*What is the management of endocarditis?
1. antibiotic therapy → dependent on BC results
What is the general ddx for chest pain?
cardiac
pulmonary
musculoskeletal
esophageal/GI
anxiety
What is another name for thromboangiitis obliterans?
Buerger's disease
Current ch12
What is thromboangiitis obliterans?
disease characterized by blood vessel inflammation and thrombosis
often resulting in blood vessel obstruction of the hands or feet
Who is most commonly affected by thromboangiitis obliterans?
20-40 y/o male smokers
Current ch12
What is the etiology of thromboangiitis obliterans?
cause unknown

associated with smoking
Current ch12
What are the complications of thromboangiitis obliterans?
necrosis → amputation
What is the management of thromboangiitis obliterans?
1. stop smoking to prevent amputation
2. avoid cold temperatures to prevent reduced circulation
Define dyspnea.
SOB; subjective difficulty in breathing
Define orthopnea.
SOB lying down that is relieved when upright
Define paroxysmal nocturnal dyspnea.
sudden SOB upon waking
Define rubor.
red discoloration of skin
Define pallor.
pale skin
Define cyanosis.
bluish discoloration of skin
Define diaphoresis.
sweating
Define syncope.
fainting
What is the etiology of secondary HTN?
KIDNEY:
chronic kidney disease
renal vascular HTN/disease

ENDOCRINOPATHIES:
thyroid disease
parathyroid disease
Cushing syndrome
primary hyperaldosteronism
pheochromocytoma

DRUGS:
alcohol
NSAIDs
decongestants
corticosteroids
cocaine
methamphetamines

sleep apnea
aortic coarctation
*What is the diagnostic workup of HTN?
Hct
BMP
-glucose - diabetes screening
-BUN/CREAT - kidney disease?
-calcium - parathyroid disease
LIPID -
UA - glucose, protein?
EKG - LVH?
What is the etiology of occlusive disease of the lower extremeties?
atherosclerosis

associated with:
smoking
DM
Current ch12
What is the clinical presentation of occlusive disease of the lower extremeties?
intermittent claudication of calf → exacerbated by exercise, relieved by rest

dependent rubor of foot with blanching upon elevation

reduced skin temp
atrophic changes → hair loss, thinning of skin, muscle atrophy, ulcerations (think toes!)
decreased pulses
Current ch12
Define natriuresis.
excretion of sodium in urine
Describe the renin-angiotensin-aldosterone system.
What is the etiology of an aortic aneurysm?
result from abnormal production or degradation of structural components (elastin and collagen) of aorta

associated with:
genetic or developmental diseases
trauma → penetrating or non-penetrating chest trauma
infection → syphilis, TB
vasculitis → giant cell arteritis, Takayasu arteritis
spondyloarthrapathies
degenerative diseases → associated with atherosclerosis
What is the clinical presentation of an aortic aneurysm?
Thoracic:
often asymptomatic
chest pain
SOB
cough
dysphagia
hoarseness → due to stretching of recurrent laryngeal nerve

Abdominal:
often asymptomatic
palpable, pulsatile, nontender mass
if painful → impending rupture → surgical emergency!!!
pain may refer to chest, back, or scrotum
Harrisons ch242
What is the diagnostic workup of an aortic aneurysm?
Thoracic:
CXR → widening of mediatinal shadow, displacement or compression of trachea or left mainstem bronchus
CT

Abdominal:
CT or abdominal ultrasound
Hairrons ch242
What is the initial management of an aortic aneurysm?
Thoracic:
1. long-term B-blocker
2. if symptomatic, >5.5cm, or growing >1cm per year → surgery
3. if Marfan syndrome + >5cm → surgery
4. if asymptomatic → monitor with CT every 6-12 months

Abdominal:
1. if symptomatic, expanding, or >5.5.cm → surgery
Harrisons ch242
What is an aortic aneurysm?
pathological dilation of the aorta
90% of abdominal aortic aneurysms are related to?
atherosclerosis
Harrisons ch242
widening of aortic shadow → thoracic aortic aneurysm
What is aortic dissection?
spontaneous tear in intima (inner) layer of aorta
Current ch12
What is the etiology of aortic dissection?
spontaneous

associated with:
HTN (most common)
pregnancy
bicuspid aortic valve
coarcation
abnormalities of smooth muscle, collagen, and elastin
Current ch12
What is the clinical presentation of aortic dissection?
sudden severe persistent chest pain
radiation to back, neck, or abdomen
HTN
peripheral pulses diminished or unequal
possible diastolic murmur due to aortic regurgitation
Current ch12
What is the diagnostic workup of aortic dissection?
EKG → LVH from long-standing HTN common
CXR → widened superior mediastinum
*CT → chest and abdomen
Current ch12
What is the intial treatment of aortic dissection?
EMERGENCY!!!

1. if suspected aortic dissection → aggressively lower BP via B-blocker (start even before diagnostic complete)
2. if type A or complicated type B → emergency surgery
Current ch12
What are 3 things you need to determine when talking about arrhythmias?
1. narrow or wide QRS complex
2. regular or irregular
3. normal, bradycardia, or tachycardia
What is the etiology of sinus arrhythmia?
normal in children and young adults
enhancement of vagal tone → digoxin, morphine
early sick sinus syndrome
Current Cardiology ch20
What is the management of sinus arrhythmia?
benign → no treatment necessary
Current Cardiology ch20
What is the etiology of pulmonary HTN?
primary → idiopathic; associated with genetic factors
secondary →

most common in younger women
What is the clinical presentation of pulmonary HTN?
cyanosis
dyspnea
right ventricle heave
elevated JVP
What is the diagnostic workup of pulmonary HTN?
CXR → enlarged pulmonary arteries
echocardiography → often diagnostic
What is normal pulmonary arterial pressure?
~25/9 mmHg
http://tiny.cc/merckBP
*What is the etiology of cor pulmonale?
pulmonary disease → most commonly COPD
pulmonary HTN
What is unstable angina?
angina pectoris with at least one of the following features:
1. occurs at rest or with minimal exertion, usually lasting >10 min
2. severe and of new onset (within last 4-6 weeks)
3. increasingly becomes more severe, prolonged, or frequent
What is stable angina pectoris?
1. chest or arm discomfort
2. associated with physical exertion or stress
3. relieved by 5-10 min rest or sublingual nitroglycerin
What is NSTEMI?
presentation of unstable angina + elevated cardiac biomarkers indicating myocardial necrosis
What are 3 sources of BP measurement error?
clinician
equipment
technique

http://tiny.cc/bp124
What are Korotkoff sounds?
sounds heard when measuring BP
Describe how to accurately measure BP.
ensure patient hasn't recently ingested caffeine, eaten food, or smoked cigarettes
ensure patient doesn't have full bladder
explain procedure to reduce anxiety
allow patient to quietly rest for 5 minutes
position patient correctly: have patient sit with back supported, midpoint of arm at heart level, legs uncrossed, feet on floor
use proper cuff size: bladder length should encircle 80% of adult's arm or 100% of child's arm; width should encircle 40% of adult’s arm
position cuff correctly: do not measure over clothing, snug fit, 1in above antecubital space, middle of bladder over brachial artery
take BP in warm, quiet room
do not measure when patient talking
palpate radial pulse and pump cuff to estimate systolic BP, pulse will disappear at systolic BP
place bell of stethoscope over brachial artery
rapidly inflate cuff 30mmHg above estimated systolic BP
deflate cuff 2-3 mm/sec
when sounds audible, deflate cuff 2 mmHg/pulse beat
continue slow deflation for 10 mmHg after last Korotkoff sounds heard to detect auscultory gap
rapidly and completely deflate cuff
do not inflate/deflate too slowly or quickly
record phase I (systolic BP) and phase V sounds (diastolic BP), do not round
in children or when sounds are heard nearly to 0 in adults, record phase IV sounds (ex: 136/64/10)
wait ≥30 sec to repeat or measure opposite arm
average measurements if >1 BP taken

http://tiny.cc/bp124
What are the phases of Korotkoff sounds?
phase I: when sounds appear = systolic BP
phase II: clinically insignificant
phase III: clinically insignificant
phase IV: muffled sounds
phase V: when sounds disappear = diastolic BP

http://tiny.cc/bp124
Is the stethoscope diaphragm more effective at transmitting low or high frequency sounds?
high frequency
What are examples of high frequency sounds?
splitting of sounds
opening snaps
aortic diastolic murmurs
Do you press lightly or firmly when using the stethoscope diaphragm?
firmly
Do you press lightly or firmly when using the stethoscope bell?
lightly
Is the stethoscope bell more effective at transmitting low or high frequency sounds?
low frequency
What are examples of low frequency sounds?
bruits
diastolic murmur of mitral stenosis
3rd and 4th heart sounds
Define precordium.
chest area overlying heart
Mosbys p414
Define dextrocardia.
heart located on RT side of body in mirror image of normal LT-sided heart
Mosbys p414
Define situs inversus.
heart and stomach found on LT side of body and liver on RT side
Mosbys p414
List the layers of the heart and their functions.
pericardium → outermost layer; fibrous double-walled sac encasing and protecting heart
myocardium → middle layer; muscular layer providing pumping action
epicardium → innermost layer; lines heart chambers and valves
Mosbys p414
What is the function of the atria?
collecting of blood
What is the function of the ventricles?
pumping of blood
List the pathway of blood starting from the body.
veins returning CO2 → superior/inferior vena cava → RT atrium → tricuspid valve → RT ventricle → pulmonic valve → pulmonary trunk → LT/RT pulmonary arteries → lungs → exchanges CO2 for O2 → LT/RT pulmonary veins → RT atrium → mitral valve → RT ventricle → aortic valve → ascending aorta → aortic arch → descending aorta → arteries supplying O2
Where is PMI normally seen?
LT mid-clavicular line in 5th ICS while sitting

*if in more than 1 ICP or seen while supine → suggest problem
Define systole.
phase of cardiac cycle characterized by ventricular contraction and atrial filling
Define diastole.
phase of cardiac cycle characterized by atrial contraction and ventricular relaxation
What equipment is needed for the cardiac exam?
marking pen
cm ruler
stethoscope
Describe the cardiac exam.
1. inspect precordium
2. inspect PMI → use tangential light at level of chest
3. palpate PMI → assess for heaves/lifts
4. measure PMI to midsternal line
5. palpate for thrills
6. auscultate with diaphragm
7. auscultate with bell
8. ask patient to lean forward and exhale → auscultate with diaphragm over aortic valve
9. auscultate with bell over
List signs of HF.
crackles
hepatomegaly
peripheral edema
Mosbys p428
Absent apical impulse + faint heart sounds may indicate?
pleural effusion
pericardial effusion
Mosbys p429
Apical impulse that is more forceful and widely distributed, fills systole, or inferolaterally displaced may indicate?
increased cardiac output
LT ventricular hypertrophy
Mosbys p430
A lift along the LT sternal border may indicate?
RT ventricular hypertrophy
Mosbys p430
Loss of apical impulse may indicate?
overlying air or fluid → pneumothorax, pleural effusion, pericardial effusion
displacement of heart beneath sternum
Mosbys p430
Displacement of apical impulse to right + no loss of thrust may indicate?
dextrocardia
diaphragmatic hernia
distended stomach
pulmonary abnormality
Mosbys p430
Define thrill.
palpable murmur
Mosbys p431
Thrill + systole + suprasternal notch and/or RT 2nd-3rd ICS suggests?
aortic stenosis
Mosbys p431
Thrill + systole + suprasternal notch and/or LT 2nd-3rd ICS suggests?
pulmonic stenosis
Mosbys p431
Janeway lesions indicate?
bacterial endocarditis
Define S1.
first heart sound characterized by "lubb" sound caused by closing of tricuspid and mitral valves
Mosbys p419
Which is normally silent, opening or closing of heart valves?
opening
Mosbys p419
Define S2.
second heart sound characterized by "dubb" sound caused by closing of pulmonic and aortic valves
Mosbys p419
What are the 2 parts of S2?
A2 → closing of aortic valve
P2 → closing of pulmonic valve
Mosbys p419
Define S3.
occasional third heart sound caused by filling of ventricles during diastole
Mosbys p419
Define S4.
occasional fourth heart sound caused by atrial kick
Mosbys p419
What grade murmur is a thrill?
grade IV
Mosbys p431
Thrill + systole + LT 4th ICS may indicate?
ventricular septal defect
Mosbys p431
Thrill + systole + apex may indicate?
mitral regurgitation
Mosbys p431
Thrill + systole + LT lower sternal border may indicate?
tetralogy of fallot
Mosbys p431
Thrill + systole + LT upper sternal border +/- radiation may indicate?
patent ductus arteriosus
Mosbys p431
List the 5 locations for auscultating the heart.
RT 2nd ICS at sternal border → aortic valve
LT 2nd ICS at sternal border → pulmonic valve
LT 3rd ICS at sternal border → Erb's point
LT 4th ICS at sternal border → tricuspid valve
LT 5th ICS at midclavicular line → mitral valve (PMI)
Mosbys p433
What can you do to figure out if thrill corresponds with systole or diastole?
palpate carotid pulse which coincides with S1
What is the etiology of a thrill based on timing and location?
How can you differentiate S1 from S2?
period between S1 and S2 is twice as quick as period between S2 and S1
Define thrombosis.
formation of a blood clot
Define infarction.
vascular obstruction → tissue hypoxia → tissue necrosis
Define hypoxia.
inadequate O2 supply to body or tissue
Define anoxia.
complete O2 deprivation
Define hypoxemia.
abnormally low [blood O2]
Define stroke volume.
volume of blood pumped from one ventricle of the heart with each beat
How do you calculate cardiac output?
SV X HR = CO
The jugular veins help you evaluate?
RT side of heart
List risk factors of varicose veins.
women 4x > men
genetic predisposition → Irish or German descent, mother with varicosities
age → veins become less elastic as age
race → whites > blacks
sedentary lifestyle → allows blood to pool and veins to be compromised
Mosbys p467
Describe the peripheral vascular exam.
1. inspect for JVD
2. inspect upper extremity
-skin color
-hair distribution
-varicosities
-ulcerations
-cyanosis
-clubbing
3. palpate upper extremity
-temperature
-skin texture
-edema
-capillary refill
4. assess pulses bilaterally
-carotid
-brachial
-radial
-ulnar

5. assess pulses
-abdominal aorta
-femoral

6. inspect lower extremity
-skin color
-hair distribution
-varicosities
-ulcerations
-cyanosis
-clubbing
7. palpate lower extremity
-temperature
-skin texture
-edema
-capillary refill
8. assess pulses bilaterally
-popliteal
-dorsalis pedis
-posterior tibialis
What are you assessing when palpating pulses for the peripheral vascular exam?
rhythm
amplitude
symmetry
How is the amplitude of pulses documented?
on scale of 0 to 4:
0 = absent, not palpable
1 = diminished, barely palpable
2 = expected
3 = full, increased
4 = bounding
Mosbys p470
Define tachycardia.
HR > 100
Mosbys p470
Define bradycardia.
HR < 60
Mosbys p470
Define pulsus paradoxus.
arterial pulse amplitude decreases on inspiration
Mosbys p470
What is the ddx for pulsus paradoxus?
COPD
pericardial effusion
constrictive pericarditis
Mosbys p470
Define pulsus alternans.
arterial pulse amplitude that alternates from beat to beat with weak and strong beats
Mosbys p470
Pulsus alternans is associated with?
LT ventricular HF
Mosbys p470
What is the ddx for bounding pulse?
exercise
atherosclerosis
aortic rigidity
patent ductus arteriosus
anemia
hyperthyroidism
fever
anxiety
Mosbys p470
An irregular regular HR may indicate?
sinus arrhythmia → increased HR on inspiration and decreased rate on expiration
Mosbys p470
Asymmetrical pulses suggests?
impaired circulation
Mosbys p470
Diminished femoral pulse may indicate?
aortic coarctation
Mosbys p470
What is aortic coarctation?
congenital condition characterized by narrowing of aorta where ductus arteriosus inserts
When auscultating for bruits, what should you ask the patient to do?
hold breath
Mosbys p472
What are the 5 Ps of arterial occlusion?
pain
paresthesias → if major artery occluded
pallor
pulselessness
paralysis → rarely
Mosbys p473
Compartment syndrome is characterized by?
pain
paresthesias
pallor
pulselessness
paralysis
Mosbys p473
What is the ddx for carotid bruit?
obstructive disease in carotid artery → athersclerosis, arteritis, fibromuscular hyperplasia
transmitted murmurs → aortic stenosis, severe aortic regurgitation, ruptured chordae tendinae of mitral valve
vigorous LT ventricular ejection → more common in children
Mosbys p472
Define claudication.
pain caused by muscle ischemia
How do you differentiate pain due to vascular insufficiency and pain due to musculoskeletal disorders?
Arterial:
onset during exercise
quickly relieved by rest
intensity increases with intensity and duration of exercise

Venous and Musculoskeletal:
onset during or several hours after exercise
relieved by rest but sometimes only after hours or days
greater variability than arterial pain in response to intensity and duration of exercise
Mosbys p473
What is the range for normal BP?
<120/80 mmHg
http://tiny.cc/jncvii
What is the management for normal BP?
encourage lifestyle modification:

1. ↑ fruit, vegetables, and low-fat dairy
2. ↓ sodium, fat, and alcohol → <2 drinks/day for men and <1 drink/day for women
3. get 30 minutes of aerobic exercise daily → brisk walking
4. obtain normal BMI → 18.5-24.9
http://tiny.cc/jncvii
What is the BP range for pre-HTN?
120/80-139/89 mmHg
http://tiny.cc/jncvii
What is the managment for pre-HTN?
1. encourage lifestyle modification
2. no drug therapy unless compelling indication → DM,
increased risk of coronary disease, post-MI, HF, chronic kidney disease
http://tiny.cc/jncvii
What is the BP range for stage I HTN?
140/90-159/99 mmHg
http://tiny.cc/jncvii
What is the management for stage I HTN?
1. encourage lifestyle modification
2. prescribe thiazide diuretic
http://tiny.cc/jncvii
What is the BP range for stage II HTN?
>160/100 mmHg
http://tiny.cc/jncvii
What is the management for stage II HTN?
1. encourage lifestyle modification
2. prescribe thiazide diuretic + either B-blocker, ACE inhibitor, ARB or CCB
http://tiny.cc/jncvii
For BP management, what does "lifestyle modification" consist of?
1. ↑ fruit, vegetables, and low-fat dairy
2. ↓ sodium, fat, and alcohol → <2 drinks/day for men and <1 drink/day for women
3. get 30 minutes of aerobic exercise daily → brisk walking
4. obtain normal BMI → 18.5-24.9
http://tiny.cc/jncvii
For pre-HTN management, what qualifies as a "compelling indication" for drug therapy?
DM
increased risk of coronary disease
post-MI
HF
chronic kidney disease
http://tiny.cc/jncvii
Which is more common, essential HTN or secondary HTN?
essential (95%)
Current
What patient population is most commonly affected by isolated systolic HTN?
elderly
Primary Care Medicine p130
What is hypertensive urgency?
severely elevated BP with NO signs of end-organ damage
EMED Current
What is hypertensive emergency?
severely elevated BP with signs of end-organ damage → mental status changes, cardiac ischemia, CHF, or acute renal failure
EMED Current
What are the most important complications of HTN?
coronary heart disease
stroke
HF
end-stage kidney disease
Current ch11
What is the etiology of essential HTN?
complex combination of genetic and environmental factors:

-sympathetic nervous system hyperactivity → young?
-abnormal cardiac or renal development → low birth weight?
-abnormal renin-angiotensin-aldosterone system
-abnormal natriuresis
-increased intracellular sodium and calcium
-polycythemia

-high salt intake
-low potassium intake
-high alcohol intake
-cigarette smoking
-obesity
-sleep apnea
-NSAIDs
Current ch11
When should secondary HTN be suspected?
1. presents at early age
2. presents >50y/o
3. HTN previously controlled but now refractory to treatment
Current ch11
When does essential HTN usually present?
25-55 y/o
Current ch11
What are the risk factors of essential HTN?
1. poor diet → low potassium, high sodium
2. sedentary lifestyle
3. alcohol
4. smoking
5. drugs → NSAIDs, decongestants, corticosteroids, oral contraceptives, cocaine, methamphetamines
6. obesity
Current ch11
What is the full name for B-blockers?
beta-adrenergic blocking agents
List types of B-blockers.
propranolol
atenolol
metoprolol
What is the MOA of B-blockers?
decrease activation of B1-adrenergic receptors on heart → decreasing cardiac output → decreasing BP

decrease renin → decreasing angiotensin II → decreasing aldosterone → decreasing Na+ and water retention → decreasing blood volume → decreasing cardiac output → decreasing BP
Pharmacology p220
What B-receptors do propranolol, atenolol, and metoprolol effect?
propranolol → decrease activation of B1 and B2
atenolol → decrease activation of B1
metoprolol → decrease activation of B1
Pharmacology p220
What are the contraindications for propranolol?
asthma → due to blockade of B2-mediated brochodilation
Pharmacology p220
What are the indications for B-blockers?
HTN in young white patients
HTN + concomitant diseases such as migraine HA, angina pectoris, previous MI, chronic HF, supraventricular tachyarrhythmia
Pharmacology p221
What does ACE inhibitors stand for?
angiotensin converting ezyme inhibitors
List types of ACE inhibitors.
lisinopril
captopril
benazepril
enalapril
quinapril
What class of drugs end in -olol?
B-blockers
What class of drugs end in -pril?
ACE inhibitors
What is the MOA of ACE inhibitors?
inhibit ACE → leading to decreased angiotenin II (and subsequent decreased vasoconstriciton) and increased bradykinin (and subsequent vasodilation)

ACE normally converts angiotensin I into angiotensin II leading to vasoconstriction
ACE also normally breaksdown bradykinin
bradykinin is a vasodilator
Pharmacology p222
What are the indications for ACE inhibitors?
HTN in young white patients
if used with diuretic → effect in black patients similar to white patients
post-MI
HF
diabetic neuropathy
albuminuria
Pharmacology p222
What are the adverse effects of ACE inhibitors?
dry cough
fever
rash
hyperkalemia
hypotension
angioedema or first-dose syncope → administer first dose under close observation of patient
Pharmacology p222
What are the contraindications of ACE inhibitors?
pregnancy
K supplementation
K-sparing diuretics
Pharmacology p222
What class of drug ends in -artan?
ARBs
What does ARB stand for?
angiotensin II receptor blockers
List types of ARBs.
losartan
valsartan
What are the adverse effects of ARBs?
similar to ACE inhibitors → fever, hypotension, skin rash, hyperkalemia
but compared to ACE inhibitors, risk of cough and angioedema significantly decreased
Pharmacology p223
What are the indications for ARBs?
alternative to ACE inhibitors
(i.e. if chronic cough)
HTN + diabetes → reduce nephrotoxicity of diabetes
Pharmacology p223
What are the contraindications for ARBs?
pregnancy
Pharmacology p223
What is the treatment for ischemic heart disease?
B-blocker
anti-platelet
smoking cessation
exercise
weight loss
treatment of diabetes and hyperlipidemias

if not well-controlled by B-blocker alone or B-blocker contraindicated → add or substitute CCB

if still not-well controlled → add nitrates
JNCVII
What should be prescribed for HTN + HF?
ACE inhibitor, B-blocker, and diuretic

if intolerant to ACE inhibitor → substitute ARB

if severe LT ventricular dysfunction → aldosterone anatagonist → spironolactone
JNCVII
What is the BP goal for hypertensive diabetics?
130/80 mmHg
JNCVII
What should be prescribed for HTN + DM?
thiazide diuretic, ACE inhibitor

B-blockers useful in combination
CCB useful in combination
JNCVII
What is the BP goal for patients with HTN and chronic kidney disease?
130/80 mmHg
JNCVII
What should be prescribed for HTN + chronic kidney disease?
ACE inhibitor or ARB + loop diuretic
JNCVII
How do the effectiveness of B-blockers, ACE inhibitors, and ARBs compare in blacks and whites?
monotherapy of B-blocker, ACE inhibitor or ARB less effective in blacks than whites

if combined with diuretic, these differences are abolished

ACE inhibitor less effective than either thiazide diuretic or CCB in blacks
How do the adverse effects of ACE inhibitors compare in blacks and whites?
risk of angioedema 3-4 times higher in blacks than whites

risk of cough higher in blacks than whites
What are the adverse effects of B-blockers?
CNS → fatigue, lethargy, insomnia, hallucinations
hypotension
bradycardia
sexual dysfunction → decreased libido or impotence
Pharmacology p221
Discuss the approach to modifying treatment when antihypertensive agents adversely affect sexual function?
to decrease risk of erectile dysfunction → encourage smoking cessasation, exercise, and weight loss

if erectile dysfunction occurs as a result of therapy → discontinue offending agent and prescribe a different one
JNCVII
List types of CCBs.
verapamil
diltiazem
nifedipine
amlodipine
What are the indications for CCBs?
verapamil → migraine HA, HTN, angina, supraventricular tachyarrhythmias

diltiazem → HTN, angina, supraventricular tachyarrhythmia

nifedipine and amlodipine → HTN, angina

overall useful in HTN with asthma, diabetes, angina or PVD

blacks respond well
Pharmacology p223
What is the MOA of CCBs?
block calcium channels → vasodilation of coronary vessels
Pharmacology p223
What are the adverse effects of CCBs?
verapamil → constipation

nifedipine and amlodipine → fatigue, dizziness, HA, hypotension
Pharmacology p223
What are the contraindications for verapamil?
CHF
AV block
Pharmacology p223
What class of drugs ends in -zosin?
alpha-blockers
Lists types of alpha blockers.
doxazosin
prazosin
terazosin
What is the MOA of alpha blockers?
block alpha 1 adrenergic receptors → decreasing peripheral vascular resistance and lowering BP by relaxation of arterial and venous smooth muscle
What are the indications for prazosin?
mild-to-moderate HTN
prescribed in combination with propranolol or a diuretic
Pharmacology p225
What are the adverse effects of prazosin?
reflex tachycardia
first-dose syncope
Pharmacology p225
What are the indications for alpha-blockers?
seldom used to treat HTN
Pharmacology p225
List central alpha agonists.
clonidine
guanabenz
methyldopa
What are the indications for clonidine?
HTN refractory to treatment with 2 or more drugs

useful in HTN + renal disease → does not decrease renal blood flow or glomerular filtration
Pharmacology p225
What are the adverse effects of clonidine?
sedation
drying of nasal mucosa

rebound HTN if withdrawn → so withdraw slowly
Pharmacology p226
What are the indications for methyldopa?
HTN + renal insufficiency
Pharmacology p226
What type of drug is hydralazine?
vasodilator → acting primarily on arteries and arterioles → decreasing peripheral resistance → reflex increase in HR and cardiac output
Pharmacology p226
What are the indications for hydralazine?
moderately severe HTN → prescribe with B-blocker (to balance reflex tachycardia) and loop diuretic (to decrease sodium retention)

pregnancy-induced HTN
Pharmacology p226
What are the adverse effects of hydralazine?
HA, nausea, sweating, tachycarida, arrhythmia, angina
Pharmacology p226
What are the indications for minoxidil?
severe to malignant HTN refractory to other drugs → prescribe with B-blocker (to balance reflex tachycardia) and loop diuretic (to decrease sodium retention)
Pharmacology p226
What are the adverse effects of minoxidil?
sodium and water retention volume overload, edema, and CHF
Pharmacology p226
What does NCEP stand for?
National Cholesterol Education Program
http://tiny.cc/ncep
What is the goal of NCEP?
"The goal of the NCEP is to contribute to reducing illness and death from coronary heart disease (CHD) in the United States by reducing the percent of Americans with high blood cholesterol."
http://tiny.cc/ncep
What are the NCEP guidelines for 1° prevention screening in adults?
fasting lipid profile (total cholesterol, LDL, HDL, triglycerides) for all adults >20 y/o every 5 years
http://tiny.cc/ncep1
What are the ranges for optimal, borderline, and high total cholesterol?
National Heart, Lung & Blood Institute - http://tiny.cc/ncep
NCEP Guidelines - http://tiny.cc/ncep1
Lab Tests Online - http://tiny.cc/lipid

What are the ranges for optimal, near optimal, borderline high, high, and very high LDL cholesterol?
National Heart, Lung & Blood Institute - http://tiny.cc/ncep
NCEP Guidelines - http://tiny.cc/ncep1
Lab Tests Online - http://tiny.cc/lipid

If a patient does not fast for a lipid profile, which tests are valid and what are the indications for ordering a follow-up lipid profile?
only total cholesterol and HDL are valid
order a follow-up lipid profile if total cholesterol >200 mg/dL or HDL <40 mg/dL
http://tiny.cc/ncep1
List risk factors for atherosclerosis.
1. >45y/o for men and >55y/o for women
2. FH of early heart disease
3. poor diet → high in saturated fat, trans fat, sodium, and sugar
4. lack of exercise
5. smoking
6. overweight or obesity
7. HTN
8. hyperlipidemia
9. DM
http://tiny.cc/nhlbi-atherosclerosis
What is familial hypercholesterolemia?
lipid disorder characterized by defective or absent cell-surface receptors for LDL resulting in unregulated synthesis of LDL

if heterozygous for this disorder → LDL concentrations are 2x normal; presents in 3rd-4th decade

if homozygous for this disorder → LDL concentrations 8x normal; presents in childhood

HMG CoA reductase inhibitors and bile-acid sequestrants not effective in treating this disorder
Current p1123
What is familial hyperchylomicronemia?
lipid disorder characterized by an abnormality in lipoprotein lipase

lipoprotein lipase normally enables peripheral tissues to take up triglyceride from VLDL particles and chylomicrons
Current p1123
What is the clinical presentation and diagnostic workup of familial hyperchylomicronemia?
presents in childhood with recurrent hepatosplenomegaly and pancreatitis

LIPID panel → hypertriglyceridemia
Current p1123
Do modest amounts of alcohol (1-2 ounces) increase or decrease HDL cholesterol?
increase
Current p1130
What is the normal range for triglycerides?
<150 mg/dL
Current p1133
High triglycerides increases the risk for what condition?
pancreatitis
Current p1133
What is the management of hypertriglyceridemia?
1. goal → TRIG <150 mg/dL; reduce risk of cardiovascular disease and pancreatitis
2. secondary causes → ask about alcohol, oral contraceptives, diuretics; BMP for chronic kidney disease; A1C for DM; obesity
2. dietary modification → restrict total calories; avoid alcohol, simple sugars, refined starches, and saturated/trans fats
3. exercise
4. if TRIG >500 mg/dL + refractory to dietary modification → prescribe triglyceride-lowering drug → fibric acid derivative, niacin, or HMG CoA reductase inhibitor
Current p1133
What are the ranges for borderline high, high, and very high triglycerides?
borderline high: 150-199 mg/dL
high: 200-499 mg/dL
very high: ≥500 mg/dL
http://tiny.cc/lipid
True or false, in a LIPID profile, if TRIG is too high, LDL cannot be calculated?
true
LDL cannot be calculated if TRIG >400
What should you order to determine LDL, if LDL cannot be calculated because TRIG is >400?
LDL direct
What is the management for elevated LDL?
1. goal → LDL <100; reduce risk of cardiovascular disease
2. secondary causes of total cholesterol → ask about alcohol/meds; order CMP, A1C, TSH
obstructive liver disease
chronic liver disease
nephrotic syndrome
DM
hypothyroidism
Cushing's syndrome
alcohol
oral contraceptives
corticosteroids
diuretics (short-term effects)
B-blockers (short-term effects)
2. diet therapy → reduce total fat to 25-30% of calories, reduce saturated fat to <7% of calories, reduce cholestrol to <200mg/d, eat more fruits, vegetables, and fiber, could try mediterranean diet

3. prevention/risk factor modification
-exercise 30 minutes per day
-lose weight
-reduce alcohol
-stop smoking
-control HTN
-control DM
List 2° causes of hypercholesterolemia.
obstructive liver disease
chronic liver disease
nephrotic syndrome
DM
hypothyroidism
Cushing's syndrome
alcohol
oral contraceptives
corticosteroids
diuretics (short-term effects)
B-blockers (short-term effects)
Current ch28
List 2° causes of decreased HDL.
sedentary lifestyle
obesity
B-blockers (short-term effects)
Current ch28
List 2° causes of hypertriglyceridemia.
obesity
chronic kidney disease
DM
alcohol
oral contraceptives
diuretics (short-term effects)
Current ch28
List possible systolic murmurs.
aortic or pulmonic stenosis
mitral or tricuspid regurgitation
Describe systole and diastole.
mitral and tricuspid valves close (S1)
aortic and pulmonic valves open
ventricles eject blood
aortic and pulmonic valves close (S2)
mitral and triscuspid valves open
ventricles fill with flood
List possible diastolic murmurs.
mitral or tricuspid stenosis
aortic or pulmonic regurgitation
What is another name for aortic stenosis?
systolic ejection murmur
Describe the murmur of aortic stenosis.
occurs between S1 and S2 → crescendo-decrescendo
S2 → paradoxically split, soft, or absent (since only pulmonic valve slamming shut)
What is the clinical presentation of aortic stenosis?
syncope, angina, LT ventricular HF → all present on exertion

harsh murmur between S1 and S2
crescendo-decrescendo
S2 paradoxically split, soft, or absent
best heard at RT 2nd ICS
radiation to carotid arteries

parvus et tardus → weakened and delayed carotid pulse
What is the etiology of aortic stenosis?
congenital biscuspid aortic valve → presents in middle/old age
degenerative aortic stenosis
What are the HDL CHOLESTEROL ranges for increased risk, average risk, and less than average risk for coronary heart disease?
increased: <40 mg/dL for men or <50 mg/dL for women
average: 40-50 mg/dL for men and 50-59 mg/dL for women
less than average: ≥60 for both men and women
http://tiny.cc/lipid
What is the management of aortic stenosis?
surgery for all symptomatic patients with aortic stenosis
When is a lipid profile ordered?
to determine risk of coronary artery disease
http://tiny.cc/lipid
What is the prevention of aortic stenosis?
risk factors same as atherosclerosis
When is HS-CRP ordered?
cardiac risk assessment
http://tiny.cc/hscrp
What is the etiology of aortic regurgitation?
congential biscupsid valve
HTN
endocarditis
aortic root dilation → syphilis, Marfan's syndrome, aortic dissection
ankylosing spondylitis
reactive arthritis
Where is CRP synthesized and then secreted?
liver then secreted into bloodstream
http://tiny.cc/hscrp
What is the clinical presentation of aortic regurgitation?
fatigue, exertional dyspnea, chest pain or LT ventricular HF

diastolic murmur
occurs between S2 and S1
best heard along LT sternal border

wide pulse pressure (i.e. distance between systolic and diastolic pressure widened since diastolic pressure cannot be maintained)

bounding pulse
-Corrigan's pulse → carotids
-Musset sign → head bobs with pulse
-Quinke pulse → nailbed capillary pulsations
Which is more sensitive, CRP or HS-CRP?
HS-CRP
more accurately detects lower concentrations of CRP
http://tiny.cc/hscrp
Describe the murmur of aortic regurgitation.
occurs between S2 and S1 during diastole
descrescendo
best heard along left sternal border
What does an elevated CRP indicate?
non-specific inflammation
http://tiny.cc/hscrp
What is the management of aortic regurgitation?
surgery
What is the difference b/w CRP and HS-CRP?
CRP detects elevated levels of CRP in patients w/ inflammation or infection

HS-CRP distinguishes b/w low normal and high normal levels of CRP in patients who are otherwise healthy
http://tiny.cc/hscrp
What is the prevention of aortic regurgitation?
reduce risk factors for HTN
Should HS-CRP be ordered to determine cardiac risk in a patient w/ chronic inflammation?
no
HS-CRP only meaningful in patients who are otherwise healthy
http://tiny.cc/hscrp1
What is the etiology of mitral stenosis?
pregnancy
congenital
rheumatic fever
endocarditis
What is the clinical presentation of mitral stenosis?
exertional dyspnea, orthpnea, and PND
pulmonary HTN
RT HF
Afib
Describe the murmur of mitral stenosis.
diastolic murmur
occurs between S2 and S1
opening snap (more severe the earlier the snap)
apical rumble
best heard at apex in LT lateral ducubitus position
What is the management of mitral stenosis?
if Afib → warfarin
if mild-to-moderate + planning on pregnancy → surgery
othewise surgery depends on symptoms and severity
When do initial elevation, peak elevation, and normalization occur for MYGB, CK, CKMB, and TROP?
What is the etiology of mitral regurgitation?
ventricular dilation
mitral valve prolapse
rheumatic fever
endocarditis
ischemic heart disease
List procedures used in diagnosis of cardiac disorders.
CXR
CT of heart
MRI with gadolinium contrast
resting EKG
stress EKG
ambulatory EKG (Holter/event monitoring
transthoracic ECHO
transesophageal ECHO
stress ECHO
doppler US of extremities
MUGA scan
scintigraphy with thallium scan
angiography
cardiac catheterization
What is the clinical presentation of mitral regurgitation?
if acute → no LT atrial dilation, but pulmonary congestion
if chronic → LT atrial dilation, fatigue, dyspnea

systolic murmur
occurs between S1 and S2
pansystolic
possible S3
best heard at apex radiating into axilla

can lead to Afib
Describe the murmur of mitral regurgitation.
systolic murmur
occurs between S1 and S2
pansystolic
associated with S3 if large regurgant volume
best heard at apex radiating into axilla
What is the management of mitral regurgitation?
surgery
Describe the murmur of mitral valve prolapse.
systolic murmur
pansystolic or late-systolic
single or multiple mid-systolic clicks
What is the clinical presentation of mitral valve prolapse?
usually asymptomatic
fatigue, dyspnea, palpitations, chest pain
systolic murmur
pansystolic or late-systolic
single or multiple mid-systolic clicks

skeletal changes → straight back, pectus, scoliosis
hyperreflexes
What is the etiology of mitral valve prolaspe?
common in thin females

dilated aortic root
Marfan's syndrome
What is the management of mitral vavle prolapse?
mitral valve repair
B-blocker if arrhythmia
Describe the murmur of tricuspid stenosis.
diastolic murmur
rumble mimicking mitral stenosis
louder with inspiration
best heard at LT lower sternal border
Current ch10
What is the etiology of tricuspid stenosis?
rheumatic fever (less common in U.S.)
carcinoid disease
iatrogenic → tricuspid valve repair or replacement

more common in women
Current ch10
What is the clinical presentation of tricuspid stenosis?
diastolic murmur
rumble mimicking mitral stenosis
louder with inspiration
best heard at LT lower sternal border

may lead to RT HF → elevated JVP (giant a wave), hepatomegaly, ascities, dependent edema
Current ch10
What is the management of tricuspid stenosis?
1. diuretic for edema → torsemide if gut edema → better abosorbed than furosemide
2. aldosterone inhibitor if hepatomegaly or ascites
3. surgery → bioprosthetic valve replacement
Current ch10
Describe the murmur of tricuspid regurgitation.
systolic murmur
pansystolic
increases with inspiration
possible S3
best heard at LT parasternal border
What is the etiology of tricuspid regurgitation?
pulmonary or cardiac disease, especially if pulmonary HTN present
What is the clinical presentation of tricuspid regurgitation?
systolic murmur
pansystolic
increases with inspiration
possible S3
best heard at LT parasternal border

systolic c-v wave in JVP
symptoms of RT HF → hepatomegaly, ascites, peripheral edema
cyanosis
What is the management of tricuspid regurgitation?
1. treat edema → torsemide, aldosterone inhibitor
2. treat underlying problem → LT heart disease, pulmonary HTN etc.
3. surgery → bioprosthetic valve replacement if also need to replace mitral valve
What is dilated cardiomyopathy?
condition characterized by LV dilation + systolic dysfunction (EF <50%)
Current ch10
What is the etiology of dilated cardiomyopathy?
often idiopathic
genetic diseases
postpartum
myocarditis
endocrinopathies
alcoholism
doxirubicin
major catecholamine discharge

most common in black men
Current ch10
What is the clinical presentation of dilated cardiomyopathy?
gradual signs of left ventricular HF or bi-ventricular HF: dyspnea
crackles
cardiomegaly
S3 gallop rhythm
↑ JVP
peripheral edema
ascites
Current ch10
What is the diagnostic workup of dilated cardiomyopathy?
EKG → ST-T changes, conduction abnormalities, ventricular ectopy
CXR → cardiomegaly, pulmonary edema
echocardiogram → LV dilation and dysfunction
Current ch10
What is the initial management of dilated cardiomyopathy?
1. refer to cardiologist
2. standard CHF therapy
2. restrict sodium
3. no alcohol
Current ch10
What is the most common cardiomyopathy?
dilated cardiomyopathy (25%)
Current ch10
List 4 common types of cardiomyopathy.
dilated
hypertrophic
restrictive
Tako-Tsubo
Current ch10
What is hypertrophic cardiomyopathy?
condition characterized by LVH + diastolic dysfunction
What is the etiology of hypertrophic cardiomyopathy?
hereditary
Current ch10
What is the clinical presentation of hypertrophic cardiomyopathy?
dyspnea
chest pain
postexertional syncope
↑ diastolic pressure
pulsus bisferiens
sustained PMI
S4
Current ch10
What is the diagnostic workup of hypertrophic cardiomyopathy?
EKG → LVH, exaggerated Q waves
CXR → mild cardiomegaly
echocardiogram → LVH, diastolic dysfunction
Current ch10
What is the initial management of hypertrophic cardiomyopathy?
1. B-blockers → slows HR → assisting in diastolic filling of stiff LV
2. refer to cardiologist if syncope, difficulty controlling symptoms, or high risk (FH of sudden death, marked hypertrophy, BP fails to increase with exercise)
Current ch10
Compare dilated, hypertrophic, and restrictive cardiomyopathies.
dilated → ventricles dilated
hypertrophic → ventricles thickened
restrictive → ventricles stiffened
Current ch10
Define pulsus bisferiens.
when palpating pulse, double peak can be appreciated (striking twice)
What is the ddx for pulsus bisferiens?
aortic stenosis + aortic insufficiency
aortic insufficiency
hypertrophic cardiomyopathy
What are the complications of hypertrophic cardiomyopathy?
sudden death
often due to post-exertional arrhythmia
often in young athletes
What is the etiology of angina pectoris?
usually atherosclerotic heart disease
congenital anomolies
arteritis
dissection
emboli
severe myocardial hypertrophy
severe aortic stenosis or regurgitation
hyperthyroidism
anemia
paroxysmal tachycardias
What is the clinical presentation of angina pectoris?
precordial chest pain
precipitated by exertion or stress
relieved by rest or nitrates
usually <3 minutes; possibly 15-20 minutes if caused by meal or anger
if >30 min → think ustable angina, MI, etc!!
What is the diagnostic workup of angina pectoris?
CPP
EKG
scintigraphy
What is the most common cause of angina pectoris?
atherosclerotic heart disease
Symptomatic aortic stenosis is a contraindication for EKG stress testing, true or false?
true
Which is more common, left HF or right HF?
left HF
What is the Functional Classification of Heart Disease?
classification system used for patients with heart disease to quantify and monitor symptoms associated with rest/activity
Describe the components of the Functional Classification of Heart Disease.
What is class I of the Functional Classification of Heart Disease?
no limitation of physical activity → ordinary physical activity does not cause undue fatigue, dyspnea, or anginal pain
Current
What is class II of the Functional Classification of Heart Disease?
slight limitation of physical activity → ordinary physical activity causes symptoms
Current
What is class III of the Functional Classification of Heart Disease?
marked limitation of physical activity → ordinary physical activity causes symptoms
Current
What is class IV of the Functional Classification of Heart Disease?
unable to engage in physical activity w/out discomfort → symptoms may be present at rest
Current
When monitoring patients with heart disease, it is best to document SPECIFIC activities that cause symptoms, true or false?
true → grocery shopping, vacuuming, climbing stairs, etc.
Current
What is the clinical presentation of left HF vs. right HF?
Left HF: think lungs!!!
fatigue
exertional dyspnea
orthopnea
PND
cough
crackles
pulmonary edema
gallop
cardiomegaly


Right HF: think body!!!
elevated JVD and JVP
dependent peripheral edema
hepatomegaly
ascites
Current ch10
Why do orthopnea and PND occur in heart failure?
when lying down, blood reaches the heart more easily than when standing which increases the heart's workload → if heart failure present, the heart can't compensate appropriately → blood backs up into lungs → SOB
Clinical Pathology p3
Define preload.
pressure that fills ventricles during diastole
Clinical Pathology p3
Define afterload.
resistance that heart faces during systole
Clinical Pathology p3
What are the 2 goals for treatment of HF?
HF causes ↓ forward flow and ↑ backup of flow, so goals are:

1. ↑ forward flow by increasing cardiac output
↑ force of ventricular contraction → inotropes
↓ rate of ventricular contraction → B-blockers
2. ↓ backup of flow by decreasing heart's workload
↓ intravascular volume → decrease preload → diuretics
dilate arteries → decrease afterload → vasodilators
Clinical Pathology p3
What is the clinical use of inotropes in HF?
↑ force of ventricular contraction → increasing cardiac output → increasing foward flow and decreasing backup of flow
Clinical Pathology p4
What is the clinical use of beta-blockers in HF?
↓ rate of ventricular contraction → allowing for more filling time → increasing cardiac output → increasing foward flow and decreasing backup of flow
Clinical Pathology p4
What is the clinical use of diuretics in HF?
↓ intravascular volume → decrease preload → decrease heart's workload → decrease backup of flow
Clinical Pathology p4
What is the clinical use of vasodilators in HF?
dilate arteries → decrease afterload → decrease heart's workload → decrease backup of flow
Clinical Pathology p4
Describe the renin-angiotensin-aldosterone system in relation to HF.
HF → decreased blood flow to kidneys → kidney releases renin → renin converts angiotensinogen to angiotensin I → ACE converts angiotensin I to angiotensin II → angiotensin II causes vasoconstriction + release of aldosterone from adrenals → aldosterone causes ↑ sodium (and water) reabsorption → increased BP
Clinical Pathology p5
What is the MOA of ACE inhibitors?
decrease conversion of angiotensin I to angiotensin II → preventing vasoconstriction and aldosterone release → preventing sodium/water retention → preventing ↑ BP → preventing back up of fluid
Clinical Pathology p5
What is the MOA of ARBs?
block angiotensin II receptors → preventing vasoconstriction and aldosterone release → preventing sodium/water retention → preventing ↑ BP → preventing back up of fluid
Clinical Pathology p5
What does the ACE in ACE inhibitors stand for?
angiotensin converting enzyme inhibitors
What drugs should be avoided in HF?
alcohol, NSAIDs, CCB, some anti-arrhythmic drugs
Pharmacology 187
List 5 ACE inhibitors.
lisinopril
captopril
benazepril
enalapril
quinapril
What are the indications for ACE inhibitors?
all stages of left HF
post-MI
Pharmacology p189
What is the patient education for ACE inhibitors?
1. take on empty stomach → otherwise food may decrease absorption
Pharmacology p189
What are the adverse effects of ACE inhibitors?
postural hypotension, renal insufficiency, hyperkalemia, angioedema, peristent dry COUGH
Pharmacology p189
What type of medication may cause an adverse effect of a persistent dry cough?
ACE inhibitors
Pharmacology p189
What is the MOA of digoxin?
1. inhibits Na+/K+ exchange by Na+/K+ ATPase
2. intracellular [Na+] increases
3. Na+ concentration gradient decreases disrupting the Na+/Ca2+ exchanger
4. less Ca2+ is pumped into the extracellular space
5. more Ca2+ remains intracellularly causing ↑ force of ventricular contraction
Pharmacology p191
What are the indications for digoxin?
severe LT ventricular systolic dysfunction after initiation of ACE inhibitor and diuretic therapy

HF with atrial fibrillation

*not indicated for diastolic dysfunction or RT venticular HF
Pharmacology p192
What are the adverse effects of digoxin?
digoxin toxicity
→ digoxin has narrow therapeutic window and long half-life (36 hours)
→ mainly eliminated by kidneys so renal failure can lead to toxicity
→ hypokalemia enhances toxicity so give K+ supplementation or K-sparing diuretic
→ arrhythmia → usually due to hypokalemia
→ nausea and vomiting
→ fatigue, HA, confusion, vision changes
Pharmacology p193
What are the drug interactions for digoxin?
quinidine
verapamil
amiodarone

cause digoxin intoxication by displacing digoxin from protein-binding sites and by competing with digoxin for renal excretion
Pharmacology p193
What is the patient education for digoxin?
requires periodic blood draw to monitor digoxin and potassium levels
What are the contraindications for digoxin?
hypersensitivity to digoxin
history of toxicity
ventricular tachycardia
ventricular fibrillation
constrictive pericarditis
amyloid disease
Wolff-Parkinson-White syndrome + Afib
Drug Handbook p444
List 4 inotropes.
digoxin
dobutamine
dopamine
epinephrine
What are the indications for dobutamine?
acute HF
What are the contraindications for dobutamine?
hypersensitivity to dobutamine
idiopathic hypertrophic subarotic stenosis
Drug Handbook p470
What is the MOA for dobutamine?
stimulates B1 adrenergic receptors → increase intracellular [cAMP] → activation of protein kinase → phosphorylation of slow Ca2+ channels → increase in intracellular [Ca2+] → increase in force of ventricular contraction
Pharmacology p194
What are the adverse effects of doputamine?
↑ HR and BP (but occasionally hypotension)
increased ventricular ectopy
premature ventricular beats
What is class of drug is spironolactone?
potassium-sparing diuretic
What is the MOA of spironolactone?
anatgonist of aldosterone → preventing sodium (and water retention), myocardial hypertrophy, and hypokalemia
Pharmacology p195
What is the patient education for spironolactone?
do not take K+ supplements
Pharmacology p195
What are the adverse effects of spironolactone?
GI → gastritis, peptic ulcer
endocrine → gynecomastia, menstrual irregularities, ↓ lidibo
CNS → fatigue, confusion
Pharmacology p195
S3 heard in context of HF suggests?
dilated heart/systolic dysfunction
Pathophysiology p8
S4 heard in context of HF suggests?
hypertrophic heart/diastolic dysfuction
Pathophysiology p8
What are the MOA, indications, contraindications, adverse effects, and drug interactions of dopamine?
MOA → stimulate dopaminergic and beta-adrenergic receptors

indications → adjunctive therapy in treatment of shock (including cardiac decompensation) that persists after adequate fluid replacement

contraindications → hypersensitivity, pheochromocytoma, ventricular fibrillation

adverse effects → palpitations, angina, hypotension, tachycardia, vasoconstriction, ectopic beats, dyspnea, nausea, vomiting, HA

drug interactions →
Drug Handbook p480
What are the MOA, indications, contraindications, adverse effects, and drug interactions of epinephrine?
think EPI PEN!!!

MOA → stimulates alpha and beta receptors → vasoconstriction → increase in force of ventricular contraction

indications → cardiac arrest, bronchospasm (asthma, anaphylaxis), nasal congestion, viral croup, decrease superficial hemorrhage

contraindications → none to epi pen in life threatening situation

adverse effects →

drug interactions →
Drug Handbook p526
What is the clinical presentation of rheumatic fever?
recent infection
fatigue
fever
erythema marginatum → erythematous rings mostly on trunk that disappear and reappear over weeks to months
subcutaneous nodules → small painless nodules on extensor surfaces
chorea → abrupt nonrhythmic involuntary movements and muscular weakness
carditis
polyarthritis
What is the most common symptom of rheumatic fever?
arthritis
What is pericarditis?
inflammation of the pericardium
What is the etiology of pericarditis?
infection → cocksackieviruses, echoviruses
inflammation in lung or myocardium
post MI
post cardiac surgery
hemopericardium
uremia
autoimmune disease → RA, SLE
neoplasm → lung, breast, renal cell carcinoma, Hodgkin disease, lymphoma
drug toxicity → penicillins, clozapine, minoxidil
radiation
Current ch10
What is the diagnostic workup of pericarditis?
↑ elevated ESR
EKG → diffuse ST segment elevation, often PR depression, sometimes T wave inversion
CXR → often normal, possible cardiac enlargement if fluid present, R/O extracardiac disease
Current ch10
What is the most common cause of pericarditis?
viral infection

usually cocksackieviruses and echoviruses

sometimes influenza, varicella, mumps, EBV, hepatitis, or HIV

rarely TB or bacterial → pneumococci from lung infection or borrelia burgdorferi from lyme disease
Current ch10
Describe the EKG often found in pericarditis.
diffuse ST segment elevation
possible PR segment depression
Current ch10
pericardial effusion
Current ch10
What are the characteristics of a pericardial friction rub?
high frequency → use diaphragm
scratching, grating, squeaking sound
3 components → 1 systolic sound between S1 and S2 + 1 diastolic sound during early diastole + 1 diastolic sound during late diastole
loudest at lower left sternal border, during inspiration
sometimes better detected during forced expiration while leaning forward
pericardial friction rub
What is the management for pericarditis?
1. if viral → symptomatic treatment
-aspirin 650mg every 3-4 hours or indomethacin
-if unresponsive → corticosteroids x 2 weeks
-may recur or be complicated by cardiac tamponade
2. if post-MI or cardiac surgery → symptomatic treatment
-aspirin 650mg every 3-4 hours x 2-4 weeks
-if severe → corticosteroids
-to prevent recurrences → colchicine x few months
Current ch10
What is rheumatic heart disease?
condition characterized by damaged heart valves due to rheumatic fever
What is the management of rheumatic fever?
1. for strep throat → benzathine penicillin G 1.2 million units IM single dose
2. if penicillin allegy → erythromycin 40mg/kg daily
3. for fever and arthritis → aspirin
4. if refractory to aspirin → corticosteroids
4. bed rest until afebrile and resting HR, ESR, and EKG normal
5. to prevent recurrence → benzanthine penicillin G 1.2 million units IM every 4 weeks
-if no carditis → continue until 21 y/p
-if carditis + no valvular damage → continue for 10 years
-if carditis + valvular damge → continue for 10 years or until 40y/o if high risk for reexsposure of strep throat (parent, teacher, medical professional, military personnel)

If chorea:
1. provide calming environment
2. medications only control symptoms but do not alter duration or outcome
3. carbamazepine → may not see effect for 2 weeks, continue for 2 weeks after symptoms subside

If HF:
see HF management
Current ch10
Who is most commonly affected by rheumatic fever?
children 5-15y/o
Current ch10
What is the clinical presentation of rheumatic heart disease?
history of rheumatic fever → may be single attack or repeated attacks

damage to valve cusps, commissures, and chordae tendineae → stenosis and/or insufficiency

50-60% → mitral valve
20% → mitral and aortic valves
10% → mitral and/or aortic + tricupsid valves
Current ch10
What valve is most commonly affected in rheumatic heart disease?
mitral valve
Current ch10
What are the complications of rheumatic heart disease?
endocarditis
What is the clinical presentation of pericarditis?
fever
dyspnea
anterior pleuritic chest pain → worse when supine, relieved when upright
may radiate to neck, shoulders, back, or epigastrium
pericardial friction rub
What is superficial thrombophlebitis?
inflammation of a superficial vein due to a blood clot
Current ch12
What is the etiology of superficial thrombophlebitis?
spontaneous → pregnancy, postpartum, varicose veins, thromboangitis obliterans
trauma → blow, irritating solution from IV
hypercoaguable states → factor V leiden, protein S deficiency, protein C deficiency, antithrombin III deficiency
abdominal cancer → pancreatic carcinoma → systemic hypercoaguability
oral contraceptives
iatrogenic → IV, PICC

20% associated with occult DVT
Current ch12
What is the most common cause of superficial thrombophlebitis?
IV or PICC lines
Current ch12
What is the clinical presentation of superficial thrombophlebitis?
localized dull pain
redness, warmth, induration, and tenderness along a superficial vein (usually great saphenous vein) or at recent IV site

inflammation clears in 1-2 weeks but firm cord may persist
Current ch12
What is the most common site of superficial thrombophlebitis?
great saphenous vein
Current ch12
superficial thrombophlebitis
What is the management of superficial thrombophlebitis?
1. if localized → NSAIDs, local heat
2. if extensive or near superficial-deep vein junction → ligation and division of vein
3. broad-spectrum antibiotics to prevent septic phlebitis

If septic phlebitis develops:
1. may be indicated by fever/chills or positive culture
2. continue antibiotics x 7-10 days
3. heparin
4. possible excision of vein
Current ch12
What is the patient education for superficial thrombophlebitis caused by varicose veins?
often recurrent
Current ch12
What is the prognosis of superficial thrombophlebitis and septic phlebitis?
superficial thrombophlebitis → generally benign and brief

septic phlebitis → 20% mortality rate
Current ch12
What are the complications of superficial thrombophlebitis?
cellulitis
gangrene
septic phlebitis
DVT
PE
What is the prevention of superficial thrombophlebitis?
1. monitor IV lines daily
2. remove IV if inflammation develops to prevent septic phlebitis and thrombotic complications
3. avoid remaining still for long periods of time
Current ch12
What does PICC line stand for?
peripherally inserted central catheter
Current ch12
What is chronic venous insufficiency?
disorder characterized by limited venous return to heart caused by malfunctioning valves → scarred valves or dilated vein prevents valve closure → blood pools → pressure increases → causing edema and skin changes
Current ch12
What is the etiology of chronic venous insufficiency?
leg trauma
DVT
varicose veins
arteriovenous fistula
neoplastic obstruction
Current ch12
What is the clinical presentation of chronic venous insufficiency?
lower extremities:
dull aching
itching
pitting edema
liposclerosis
brown skin discoloration around ankles
ulcers around ankles
secondary varicosities
Current ch12
What causes the brown skin discoloration seen in chronic venous insufficiency?
blood leaks out of blood vessels → hemoglobin broken down into hemosiderin → hemosiderin permanently deposited in dermal macrophages
Current ch12
chronic venous insufficiency
chronic venous insufficiency
What is the management of chronic venous insufficiency?
1. compression stockings worn from mid foot to just below knee
2. elevate legs intermittently during day
3. elevate legs above heart with pillows at night
4. avoid long periods of sitting/standing
5. if refractory to above → pneumatic compression of leg

If ulceration:
1. control edema
2. apply compression or semi-rigid gauze boot and change every 2-3 days
Current ch12
What is the prevention of chronic venous insufficiency?
aggressive management of DVT
compressive stockings for varicose veins
Current ch12
What is the etiology of varicose veins?
usually hereditary
pregnancy
prolonged standing
heavy lifting
superficial thrombophlebitis with deep vein complications
arteriovenous fistula → diagnose by presence of bruit
obstruction due to neoplasm

vein dilation causes malfunctioning of valves → blood pools
Current ch12
What is the clinical presentation of varicose veins?
asymptomatic or aching pain exacerbated by standing
dilated tortuous superficial veins in lower extremities
often great saphenous vein, sometimes small saphenous vein
secondary varicosities
Current ch12
What is the management of varicose veins?
1. compression stockings
2. intermittent elevation of legs
3. sclerotherapy
4. surgery
Current ch12
Who is most commonly affected by varicose veins?
women following pregnancy
Current ch12
What is the prevention of varicose veins?
wear compression stockings during pregnancy
Current ch12
varicose veins
Why is surgical removal of varicose veins often not helpful?
removal of one vein just puts more pressure on adjacent veins creating more varicose veins
What are diuretics?
medications that increase urine flow
Pharmacology p261
What are the classes of diuretics?
carbonic anhydrase inhibitors
osmotic diuretics
loop diuretics
thiazide diuretics
potassium-sparing diuretics
List classes of diuretics in order of most effective to least effective.
loop diuretics < thiazide diuretics < potassium sparing diuretics
Pharmacology p261
List types of carbonic anhydrase inhibitors.
acetazolamide
What is the MOA for carbonic anhydrase inhibitors (acetazolamide)?
inhibition of HCO3- reabsorption in proximal convoluted tubule
Pharmacology p261
What are the indications for acetazolamide?
prophylaxis for mountain sickness
↓ intraocular pressure of open-angle glaucoma
Pharmacology p272
What are the contraindications for acetazolamide?
hepatic cirrhosis
Pharmacology p272
What are the adverse effects of acetazolamide?
hypokalemia
metabolic acidosis
renal stone formation
drowsiness
paresthesia
Pharmacology p272
List types of osmotic diuretics.
mannitol
What is the MOA for osmotic diuretics?
cause increased water secretion (not increased Na+ excretion like other diuretics)
Pharmacology p272
What are the indications for mannitol?
maintain urine flow following:
increased ICP due to shock
acute renal failure due to shock
drug toxicity
trauma

prevents kidneys from failing
Pharmacology p272
What are the adverse effects of mannitol?
extracellular water expansion and dehydration
hypo and hypernatremia
Pharmacology p272
List types of loop diuretics.
furosemide
torsemide
bumetanide
ethacrynic acid
What is the MOA for loop diuretics?
inhibition of Na+/K+/2Cl- cotransport in ascending loop of Henle → retention of Na+, Cl-, and water in tubule
Pharmacology p261
What are the indications for loop diuretics?
acute pulmonary edema due to HF
hypercalcemia
hyperkalemia
Pharmacology p269
What are the adverse effects of loop diuretics?
ototoxicity → especially ethacrynic acid
hypokalemia
hypomagnesemia
hyperuricemia → furosemide and ethacrynic acid
hypotension
Pharmacology p269
List types of thiazide diuretics.
hydrochlorathiazide
chlorothiazide
metolazone
Describe chlorothiazide.
thiazide diuretic
MOA → inhibits Na+/Cl cotransporter in ascending loop of Henle
indications → mild-to-moderate HTN; adjunctive therapy for edema
contraindications → renal failure
Drug Handbook p308
What is the MOA for thiazide diuretics?
inhibition of Na+/Cl- cotransporter in distal convoluted tubule → retention of water in tubule
Pharmacology p261
What are the indications for thiazide diuretics?
HTN
mild-to-moderate HF (if thiazide fails → prescribe loop diuretic)
hypercalciuria
diabetes insipidus
Pharmacology p267
What are the adverse effects of thiazide diuretics?
hypokalemia
hyperuricemia

hyponatremia
hypomagnesemia
hypercalcemia
hyperglycemia
volume depletion → hypotension
hyperlipidemia
hypersensitivity
Pharmacology p267
List the thiazide diuretics from most effective to least effective?
metolazone < hydrochlorothiazide < chlorothiazide
Pharmacology p265
How does the strength of metolazone compare to the other thiazide diuretics?
more potent
causes Na+ excretion even in advanced renal failure
Pharmacology p268
List types of potassium sparing diuretics.
spironolactone
triamterene
amiloride hydrochloride
What is the MOA for potassium-sparing diuretics?
occurs in collecting duct and tubule

spironolactone → aldosterone agonist → inhibits aldosterone-mediated Na+ resorption/K+ secretion
triamterene and amiloride → block Na+ channels
Pharmacology p261
What are the indications for spironolactone?
adjunctive therapy to prevent hypokalemia
severe HF
hepatic cirrhosis
secondary hyperaldosteronism
Pharmacology p270
What are the adverse effects of spironolactone?
GI upset → nausea, peptic ulcer
gynecomastia
menstrual irregularities
hyperkalemia → lethargy, mental confusion
Pharmacology p270
What are the indications for triamterene and amiloride hydrochloride?
adjunctive therapy to prevent hypokalemia
Pharmacology p271
What are the adverse effects of triamterene?
leg cramps
hyperkalemia
hyperuricemia
↑ BUN
Pharmacology p271
What is the effect of adrenergic stimulation on heart, lungs, and blood vessels?
heart → increase HR, contractility, and conduction velocity
lungs → bronchiole dilation (relaxing smooth muscle)
blood vessels → vasoconstriction in skin and mucous membranes; dilation to liver and skeletal muscle
What is the effect of cholinergic stimulation on heart, lungs, and blood vessels?
heart → decreases HR, contractility, and conduction velocity
lungs → bronchiolar constriction, increase in mucus secretion
blood vessels → vasodilation
What class of drug is epinephrine?
catecholamine → adrenergic receptor agonist
Pharmacology p71
What are the indications for epinephrine?
1. cardiac arrest
2. brochoconstriction → acute asthma, anaphylactic shock
3. glaucoma
4. anesthetics
3.
Pharmacology p71
*What are the adverse effects of epinephrine, norepinephrine, and isoproterenol?
adverse effects → CNS disturbances (HA, tremor, tension, anxiety, fear), cardiac arrhythmia, pulmonary edema, cerebral hemorrhage

NE also causes blanching and skin sloughing at site of injection due to extreme vasoconstriction
Pharmacology p71
What are the clinical uses of norepinephrine?
shock → NE causes vasoconstriction → increase in vascular resistance → increase BP

*though metaraminol preferred b/c it does not reduce blood flow to kidneys
Pharmacology p74
What class of drug is norepinephrine?
catecholamine → adrenergic agonist
What are the adverse effects, contraindications, and toxicities of norepinephrine?
same as epinephrine + blanching and skin sloughing along injected vein (due to extreme vasoconstriction)
Pharmacology p75
What class of drug is isoproterenol?
synthetic catecholamine → B1- and B2-adrenergic receptor agonist
Pharmacology p75
What are the clinical use of isoproterenol?
1. stimulation of heart in emergency situations
2. rarely used as brochodilator in asthma
Pharmacology p75
What class of drug is phenylephrine?
synthetic noncatecholamine → primarily binds alpha1 receptors
causes vasoconstriciton → raising BP
no effect on heart
Pharmacology p77
What is the clinical use of phenylephrine?
nasal decogestant
increase BP
terminate supraventricular tachycardia
Pharmacology p77
What are the adverse effects of phenylephrine?
hypertensive HA
cardiac irregularities
Pharmacology p77
What class of drug is ephedrine?
noncatecholamine → mixed action adrenergic agonist
Pharmacology p79
What are the clinical uses of ephedrine?
raise BP
treat asthma via bronchodilation
nasal decongestant
Pharmacology p79
What class of drug is ephedrine?
noncatecholamine → mixed action adrenergic agonist
Pharmacology p79
What are the clinical uses of ephedrine?
raise BP
treat asthma via bronchodilation
nasal decongestant
Pharmacology p79
What is the MOA and clinical use of B-blockers?
MOA → B-adrenergic agonists → diminsh phase 4 depolarization → depressing automaticity, prolonging AV conduction, and decreasing HR and contractility
clinical use → atrial flutter, atrial fibrillation, AV-nodal reentrant tachycardia, prevention of ventricular arrhythmia following MI
What is the MOA and clinical use of digoxin?
MOA → cardiac glycoside → shortens refractory period in atrial and ventricular myocardial cells while prolonging refractory period and decreasing conduction velocity in AV node

clinical use → atrial flutter, atrial fibrillation, paroxysmal supraventricular tachycardia, HF

*digoxin toxicity → can lead to ventricular fibrillation
What is the MOA and clinical use of CCBs?
MOA →
clinical use → atrial flutter, atrial fibrillation, supraventricular tachycardia, HTN, angina
What is the MOA and clinical use of quinidine?
MOA → Na+ channel blocker → binds to Na+ channels → prevents Na+ influx → slows phase 0 depolarization in ventricular muscle fibers

clinical use → atrial, junctional, and ventricular tachyarrhythmias; maintain sinus rhythm following cardioversion of atrial flutter or a-fib; prevent frequent ventricular tachycardia
What is the MOA and clinical use of lidocaine?
MOA → Na+ channel blocker → shortens phase 3 repolarization and decreases duration of AP
clinical use → ventricular arrhythmias arising during myocardial ischemia
What should be prescribed for atrial fibrillation?
first line → B-blocker
second line → CCBs, digoxin

if ≥1 risk factor for stroke → long-term warfarin with INR 2.0-3.0
List 2 Na+ channel blockers.
lidocaine
quinidine
What is lidocaine?
Na+ channel blocker used to treat ventricular arrhythmias often associated with MI
What is quinidine?
Na+ channel blocker used to treat atrial, junctional, or ventricular arrhythmias
List arrhytmias treated by B-blockers, CCBs, digoxin, quinidine, and lidocaine.
BBs:
-atrial flutter
-atrial fibrillation
-supraventricular tachycardia
-ventricular tachycardia

CCBs:
-atrial flutter
-atrial fibrillation
-paroxysmal supraventricular tachycardia

DIGOXIN:
-atrial flutter
-atrial fibrillation
-paroxysmal supraventricular tachycardia

QUINIDINE:
prevention of atrial, junctional, and ventricular arrhythmias
-atrial fibrillation
-paroxysmal supraventricular tachycardia
-premature atrial contraction
-ventricular tachycardia
-premature ventricular contraction
-following cardioversion for atrial flutter or fibrillation

LIDOCAINE:
-ventricular arrhythmias (often due to MI)
What is the clinical use of nitroglycerin and isosorbide dinitrate for angina and how does it effect myocardial O2 demand?
clinical use → stable angina, prinzmetals

MOA → vasodilator
1. dilation of large veins → decreased venous return → decreased preload → decreased work of heart → decreased myocaridal O2 demand
2. dilation of coronary arteries → increased blood supply to myocardium
What is nitroglycerin?
vasodilator
List nitrates.
nitroglycerin
isosorbide dinitrate
What is isosorbide dinitrate?
vasodilator
What is the clinical use of ranozaline and how does it effect myocardial O2 demand?
clinical use → chronic angina
*does not relieve acute angina

MOA →
What type of nitrate should be given for prompt relief of ongoing stable angina attack?
sublingual nitroglycerin
Pharmacology p210
What are the routes of administration, onset, and duration of nitroglycerine and isosorbide dinitrate?
NITROGLYCERIN:
1. sublingual tablet or spray
-onset → 2 min
-duration → 25 min

2. transdermal patch
-onset → 30 min
-duration → 8-14 hrs

3. oral sustained release tablet
-onset → 35 min
-duration → 4-8 hrs

ISOSORBIDE DINITRATE:
1. sublingual
-onset → 5 min
-duration → 1 hr

2. oral slow-release tablet
-onset → 30 min
-duration → 8 hrs
Pharmacology p211
What should you prescribe for newly diagnosed stable angina?
nitroglycerin or isosorbide dinitrate sublingual tablet or spray

take if angina attack
can also take before activities that may precipitate angina attack
Current ch10
What are the adverse effects of nitrates?
HA!!!
facial flushing
postural hypotension
tachycardia
Pharmacology p211
Discuss tolerance to nitrates.
tolerance develops rapidly where blood vessels become desensitized to vasodilation

TO AVOID TOLERANCE:
-schedule daily 8-12 hr nitrate-free interval to restore sensitivity
-remove transdermal patch at night
-if prinzmetal's angina → remove transdermal patch in afternoon since angina worsens early in morning
Pharmacology p211
Nitrates are contraindicated if taking what drug?
sildenafil (Viagra) → potentiates action of nitrates → may cause extreme hypotension

*can prescribe ranolazine instead
Pharmacology p211
List drugs for treatment of angina.
acute → nitrates

chronic →
-first line → B-blockers, ranozaline
-third line → CCBs
What is the clinical use of pentoxifylline (Trental)?
MOA → reduces blood viscosity
clinical use → symptomatic treatment of intermittent claudication due to chronic occlusive arterial disease of limbs
Drug Handbook p1173
What is the pharmological treatment following MI?
1. immediate chewable aspirin → 162mg or 325mg
2. if aspirin allergy → clopridogrel 300mg or 600mg
3. if STEMI → aspirin + clopridogrel
4. if STEMI (not NSTEMI) → thrombolytic therapy or coronary angioplasty
5. thrombolytic therapy → streptokinase or tissue plasminogen activator
6. continued aspirin 81mg and heparin
7. long term → aspirin 81mg, clopridogrel or both
What does HMG COA reductase inhibitors stand for?
3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors
Pharmacology p253
What is the common name for HMG COA reductase inhibitors?
statins
Pharmacology p253
What are the indications for prescribing HMG COA reductase inhibitors?
1. elevated LDL
2. hyperlipidemias
*not familial hypercholesterolemia
Pharmacology p253
What are the first-line agents for elevated LDL?
HMG COA reductase inhibitors
Pharmacology p253
HMG COA reductase inhibitors are effective in patients who are homozygous for familial hypercholesterolemia, true or false?
false → since these patients lack LDL receptors
Pharmacology p253
What is the MOA for HMG COA reductase inhibitors?
inhibition of HMG COA reductase → decreased cholesterol synthesis → decreased [intracellular cholesterol] →
1. increased LDL receptor synthesis→ increased number of LDL receptors → increased internalization of LDL → decreased plasma cholesterol
2. decreased VLDL secretion → decreased plasma cholesterol
Pharmacology p253
What are the contraindications of HMG COA reducatse inhibitors?
adolescents
pregnancy
breast-feeding
renal insufficiency
Pharmacology p255
What are the adverse effects of HMG COA reductase inhibitors?
1. liver failure → monitor LFTs
2. myopathy and rhabdomyolysis → usually associated with renal insufficiency or drug interaction → monitor CK
Pharmacology p255
What is rhabdomyolysis?
disintegration of muscle
Pharmacology p255
What are the drug interactions for HMG COA reductase inhibitors?
increase in warfarin → monitor INR
Pharmacology p255
What is the patient education for HMG COA reductase inhibitors?
1. do not take if pregnant or breast-feeding
2. must periodically get blood drawn to monitor LFTs and CK
3. if taking warfarin → must periodically get blood drawn to monitor INR
Pharmacology p255
What are other names for niacin?
nicotinic acid
vitamin B3
Pharmacology p255
What are the indications for niacin?
1. decreased HDL
2. increased LDL
3. hypercholesterolemias
4. familial hyperlipidemias
Pharmacology p255
What is the most effective agent for increasing HDL levels?
niacin
Pharmacology p255
What is the MOA of niacin?
inhibition of lipolysis in adipose tissue → decreased plasma levels of cholesterol and triglycerides
Pharmacology p255
What are the adverse effects of niacin?
*cutaneous flush
*pruritus
nausea and abdominal pain
hyperuricemia and gout → niacin inhibits uric acid secretion
impaired glucose tolerance
hepatotoxicity
Pharmacology p255
What are the drug interactions of niacin?
alcohol → may increase cutaneous flushing
gout meds → allopurinol, probenecid, sulfinpyrazone
DM meds
What is the patient education for niacin?
if experience cutaneous flushing:
1. usually lasts 15-30min
2. may be accompanied by pruritus, especially in clothing-covered areas
3. take 300mg aspirin 30min before niacin to reduce flushing
4. flushing is usually self-limited after several weeks of a consistent dose
Pharmacology p256
Which HMG COA reductase inhibitors are most effective at decreasing LDL, increasing HDL, and decreasing triglycerides?
decreasing LDL → atorvastatin, rosuvastatin
increasing HDL → pravastatin, simvastatin
decreasing triglycerides → atorvastatin
Pharmacology p255
List HMG COA reductase inhibitors in order of most effective to least effective at reducing LDL.
atorvastatin = rosuvastatin > pravastatin = simvastatin > lovastatin = fluvastatin
Pharmacology p255
Name 5 HMG COA reductase inhibitors.
atorvastatin
simvastatin
pravastatin
lovastatin
fluvastatin
Name 2 bile-acid sequestering agents
cholestyramine
colestipol
What are the indications for prescribing bile-acid sequestering agents?
1. elevated LDL
*though not as effective as statins
Pharmacology p257
What is the MOA of bile-acid sequestering agents?
bind negatively charged bile acids and bile salts in small intestine → complex secreted in feces → preventing bile acids from returning to liver → lowering [bile acid] → causing hepatocytes to increase conversion of cholesterol to bile acids → decreasing[intracellular cholesterol] → increasing LDL uptake into cell → decreasing plasma LDL
Pharmacology p257
List the categories of drugs used to treat elevated LDL, decreased HDL, and elevated TRIG in order of most effective to least effective.
elevated LDL → HMG CoA reductase inhibitors > bile acid sequestrants > niacin > fibrates
decreased HDL → niacin > fibrates > HMG CoA reductase inhibitors > bile acid sequestrants
elevated TRIG → fibrates > niacin > HMG CoA reductase inhibitors > bile acid sequestrants
Pharmacology p259
List statins and how they effect LDL, HDL, and TRIG.
lovastatin → decreases LDL, increases HDL
pravastatin → decreases LDL and TRIG
fluvastatin, simvastatin, and atorvastatin → decreases LDL and TRIG, increases HDL
Which is the cheapest statin?
lovastatin (but also least potent)
MI:
-sudden prolonged (>30 min) anterior chest discomfort; often describe as “gas” or pressure
-worsening
-occurs at rest or with minimal exertion
-diaphoresis
-anxiety
-SOB
-soft heart sounds may indicate LV dysfunction
-S4 is common
-S3 is less common and indicates significant LV dysfunction
-mitral regurgitation murmur may indicate papillary muscle dysfunction or rupture
-cyanosis, cold temp, weak peripheral pulses, abnormal cap refill indicate low cardiac output
-ST segment elevation with MI, Q waves, mean axis deviation, poor R wave progression
-ST segment depression with angina or subendocardial MI
-inverted T waves with ischemia
-give aspirin 162 or 325mg
-if present <12 hours with STEMI, reperfusion therapy either via percutaneous coronary intervention or via thrombolytic therapy
AORTIC DISSECTION:
-sudden searing chest pain
-radiation to neck, back, or abdomen
-HTN
-diminished or unequal pulse in extremities
-LVH common
-mediastinal widening on CXR
-lower BP to 100-120 with B-blocker
-CT
-surgical intervention if involving arch of aorta