Cardiology

Causes of chest pain (cardiac and non)
Disease/condition Pathophysiology/ Causes Signs and Symptoms Diagnostics Treatments/Management
Typical angina Precordial chest pain
Associated w/myocardial ischemia
but w/o necrosis
Precipitated by stress, exercise, or
exertion
Caused by significant coronary
stenosis
NO CELL DEATH
Discomfort in chest; sub
sternal or retrosternal
Burning, heavy or squeezing
sensation
Resting ECG: May show
transient ST depression
during chest pain; changes
resolve with relief of pain,
25% will have normal ECG
Cath: definitive dx
procedure
Stress test: most useful non-
invasive procedure
Promptly relieved by rest or
Nitroglycerine
Attain acceptable exercise
tolerance, prevent frequent
ischemia and infarction
Lifestyle changes: smoking,
weight, HTN, cholesterol
Aspirin, NTG, BB, CCB
PCI, CABG
Atypical Angina Unrelated to exercise
Most common in DM, females and
elderly
Palpitations w/o chest pain
May see pain in r/l chest,
abdomen, back, arm or jaw in
absence of sub sternal pain
Antacids
Acute Myocardial
Infarction
Result of prolonged myocardial
ischemia
Cell death caused by occlusion (from
plaque)
Sudden onset by lasts 30 minutes or
longer.
Pain is more severe than angina and
typically in crescendo pattern

Substernal pain that may
radiate.
Heaviness, pressure, burning,
tightness
Arrhythmias, hypotension,
CHF, diaphoresis, wakness,
SOB, cough, N/V
Some pt. may have painless
MI
Cardiac enzymes: CK, CK-
MB, troponin I and II
CKMB/CK total >5% = MI
ECG: most important dx test
ST elevation of 1mm or
more in at least 2 leads
Oxygen
Morphine
Anti-platelet: Plavix, UFH or
LMWH
STEMI: BB, statins, cath
Pericarditis Lasts many hours to days
Pain worse with deep inspiration,
movement or supine.
More localized than angina
Over sternum or apex; may
radiate to neck/left shoulder
Sharp, stabbing, knifelike
Pericardial friction rub
Improved with sitting up/leaning
forward
Aortic Dissection Sudden onset, relenting
Occurs in setting of HTN
Pain in anterior chest that may
radiate to the back
Excruciating, tearing, knifelike
Murmur of AI, pulse, or BP
asymmetry, cold extremity

Pulmonary Embolism Substernal or over area of
pulmonary infarction
Sudden onset, lasts minutes to
hours.
Pleuritic or angina-like pain
Dypnea, tachycardia,
hypotension, hypoxia,
hemoptysis, signs of Rt. HF


Disease/condition Pathophysiology/ Causes Signs and Symptoms Diagnostics Treatments/Management
Hypertension Primary: 90-95% of cases: there is
no identifiable or treatable cause
Secondary: identifiable/treatable
cause (renal, endocrine, drug, etc)
Causes include: renal HTN, sleep
apnea, Cushing syndrome, coarction
of aorta
Symptoms not often present
In long standing HTN:
ventricular hypertrophy, aortic
insufficiency murmurs, S4
heart sounds, S# gallop.
Compare upper and lower
extremity BPs
BP elevated on at least 3
separate days or if >160/100

Normal BP <120/<80
Prehypertension: 120-
139/80-89
Stage 1: 140-159/90-99
Stage 2: >160/>100

Serum chemistries, CBC,
lipids
Home BP monitoring
Eliminate treatable causes of
secondary HTN
Lifestyle modification
Goal BP: <140/90 in most adults,
<130/80 in DM and renal disease
Diuretics, BB, ACEI, ARBS, CCB,
etc…
ACEI contraindicated in
pregnancy
Congestive Heart
Failure
Systolic: Decrease in myocardial
contractility which leads to reduced
SV and CO; inadequate ventricular
filling and subsequent chamber
dilation.
Diastolic: abnormal filling,
secondary to impaired relaxation of
the ventricle (may be due to a stiff
non-compliant chamber of excessive
hypertrophy.
Acute: sudden reduction in CO and
hypoperfusion without peripheral
edema
Chronic: Develops and progresses
slowly. Seen in pts with dilated
cardiomyopathy or multivalvular
disease.
Left-sided: hemodynamic overload
secondary to AR, increased
peripheral resistance from HTN,
weakened muscle from MI, or
valvular disease
Right-sided: caused by left
ventricular dysfunction, PHT, PE,
COPD, congenital or valvular disease
Left-sided: dyspnea on
exertion, orthopnea,
weakness and fatigue, weight
gain, paroxysmal nocturnal
dyspnea, oliguria, rales, S3
gallop, S4 gallop.
Right sided: dyspnea on
exertion, peripheral edema,
JVD, hepatomegaly,
hepatojugular reflux, ascites,
weight gain, weakness and
fatigue, nocturia
Staging:
ACC/AHA
A: at risk for developing heart
failure w/o evidence of
cardiac dysfunction
B: evidence of cardiac
dysfunction w/o sx
C:evidence of cardiac
dysfunction w/sx
D:symptoms of heart failure
despite maximal therapy
NYHA
I: no sx at any level of exertion
II: sx with heavy exertion
III: sx with light exertion
IV: sx with no exertion

Lab studies:
CBC, CMP, thyroid function,
BNP, LFTs, cardiac enzymes

ECG: may identify
underlying dysrhythmia,
evolving MI, LVH, or
repolarization changes of
myocardial ischemia

CXR, echo, radionucleotide
angiography, cath


Pharm:
Diuretics (HCTZ, Lasix)
ACEI: Enalapril, Lisnopril
ARB
BB: Atenolol, Metoprolol,
Propanolol, etc…
Digoxin
Vasodilating agents: nitrates,
Isosorbide, Hydralazine, NTG tabs
Warfarin or Dabigatron

Surgical: revascularization, CABG,
transplantation, ICD,
biventricular pacing.

Non-pharmacological: aimed at
correcting reversible casues such
as valvular lesions, myocardial
ischemia, uncontrolled HTN,
arrhythmias, or diet (low in salt
etc…)
Valvular Heart Diseases
Disease/condition Pathophysiology/ Causes Signs and Symptoms Diagnostics Treatments/Management
Acute Rheumatic
Fever (ARF)
Group A-hemolytic strep (follow
epidemics of streptococcal
pharyngitis)
Has become rare with abx
(especially PCN)

Acute onset, febrile illness,
along with variable
combinations of:
Arthritis: polyarthritis,
migration of pain, large joints
Arthralgia
Carditis:”pancarditis”, chest
pain, friction rub, murmurs
Chorea: neurological disorder,
muscle weakness (milking sn)
skin manifestations: erythema
marginatum, rheumatic nodules.
Jones criteria Want to suppress inflammatory
response, provide symptomatic
relief and minimize cardiac insult.
Benzathine PCN
Pen V-K
Erythromycin (PCN allergy)
NSAIDs
Aortic Stenosis (AS) Outflow tract obstruction of blood
from the LV that can occur at the
valve (valvular), above the valve
(supravalvular) or below the valve
(subvalvular)
AS happens as a result of adhesions
and fusion of the commissures and
cusps. Leaflets and ring become
vascularized, resulting in retraction
and stiffening of the cusps.
Calcification occurs and the AV
orifice is reduced to a smaller
opening.
Major compensatory mechanism of
LV outflow tract obstruction is LVH










Most pts are asymptomatic, but
some may get: angina, syncope,
dizziness, dyspnea, dysonea on
exertion (orthopnea, PND,
pulmonary edema)
Physical findings: palpable
systolic thrill in the carotids or at
the base, harsh, midsystolic
ejection murmur, S4 gallop,
single S2 sound, faint diastolic
murmur, systolic ejection click
in younger pts
ECG: severe AS shows
LVH, with or without ST-T
changes. Possible LBBB or
RBBB
Echocardiogram: LV wall
motion, outflow, mass and
cavity size. AV thickening
and area
narrowing/gradient.

Prophylaxis abx for invasive
procedures which prevents
against endocarditis
Mild AS pts can live a normal life
Moderate AS pts should avoid
severe physical activity.
A-fib should be converted to a
NSR
Severe AS: if symptomatic
despite meds, surgery for
valvular replacement, biprostetic
or mechanical valve
Disease/condition Pathophysiology/ Causes Signs and Symptoms Diagnostics Treatments/Management
Aortic Regurgitation
(AR)
Abnormal regurgitant flow from the
aorta back into the left ventricle,
through a non-compliant aortic
valve. Also referred to as aortic
insufficiency.

In acute AR, the LV is of normal size
and non-compliant.

In chronic AR there is LV
compensation, increasing LV dilation
to accommodate the increased LV
volume. AR subjects the LV to
volume overload primarily but also
to excessive pressure load.
Compensation results in LV
dilatation (eccentric hypertrophy)
with some increased LV muscle wall
thickness.
Symptoms:
DOE, fatigue, reduction in
exercise tolerance,
uncomfortable palpitations,
dizziness/light headedness.
Physical Findings:
bounding pulses, blowing, early-
diastolic murmur heard best
along the LSB, with the patient
leaning forward after exhaling,
low-frequency, mid-diastolic
rumbling at the apex in severe
AR (diastolic murmurs are soft),
Quinke’s sign (pulsatile
blanching and reddening of the
nail bed with pressure).
Asymptomatic patients are
monitored with echo to asses LVF

Afterload reduction vasodilators
(CCB or ACEI) for asymptomatic
pt with associated HTN

Symptomatic pts and even
asymptomatic pt with severe AR
and impaired LVF (EF<0.50)
should be considered for surgical
correction.

Mitral Regurgitation
(MR)
regurgitant blood flow from the LV
back into the LA usually a result of
an incompetent MV. Occurs during
systole.
The severity of MR and the ratio of
forward CO to backflow are dictated
by 5 factors:
1.) Size of the mitral orifice during
regurge
2.)Systolic pressure gradient
between LV and LA
3.)Systolic vascular resistance
4.) Compliance of the LA
5.)Duration of regurge with each
contraction

Acute MR may present with
flash pulmonary edema, it is a
result of sudden rupture of the
chordae tendineae (THIS IS A
MEDICAL EMERGENCY!)
Symptoms of chronic MR are
usually from low cardiac output,
especially during exertion:
fatigue, weakness, dyspnea,
orthopnea, PND, Peripheral
edema
Chronic MR as a result of
rheumatic fever: holosystolic
murmur heard best at the apex,
radiating into the left axila.
Acute MR: murmur may have a
decrescendo quality, an S3 may
also be heard indicating an
increase in volume return to LV

CXR: may show pulmonary
edema in acute and
enlarged LA and LV in
chronic
ECG: in chronic MR may
show LAE and LVH
Echo: evaluates the mitral
valve for gradient flow; LA
and LV size and function
Cath: identifies coronary
ischemic etiology
(papillary muscle
dysfunction)

Acute: IV diuretics, vasodilators

Chronic: repair or replace and
continual monitoring by echo

Disease/condition Pathophysiology/ Causes Signs and Symptoms Diagnostics Treatments/Management
Mitral Stenosis (MS) Stiffening of the mitral apparatus
resulting in decreased forward flow
from the LA into the LV
Most common cause of MS is
rheumatic fever
A stenotic MV obstructs the outflow
of blood into the LV resulting in an
increase in pressure in the LA. This
increase in pressure is then sent
back into the pulmonary system
(increases venous and capillary
pressure)
Dyspnea on exertion, dyspnea at
rest, reduced exercise tolerance,
orthopnea, PND
Symptoms with advanced MS:
pulmonary hypertension (PHT),
JVD, hepatomegaly, ascites,
edema.
Physical findings: Ventricular
“tap” in patients, loud S1, high
pitched opening snap, diastolic
rumble
diuretics to reduce vascular
congestion
in AF beta blockers
CCB
valvuloplasty is the treatment of
choice.
Mitral Valve Prolapse Asymptomatic “billowing” of the
mitral valve leaflets retrograde into
the LA during systole; it can be
accompanied with MR.
Enlargement of the valve leaflets
(posterior leaflet); normal collagen
and elastin matric on the valve
fibrosa is fragmented and replaced
with myxomatous connective tissue.
usually asymptomatic but may
have chest pain or palpitations
from associated arrhythmias.
Midsystolic click: tensing of
leaflet or chordae
Late systolic murmur best heard
at the apex: from regurgitant
flow back into LA
Made by Echo which
reveals posterior
displacement of one or
both of the leaflets.
ECG is usually normal
unless there is an
underlying LAE or LVH.

Tricuspid Stenosis (ST) rare and usually the result of long
term RF
OS, JVD
diastolic murmur heard best at
the sternum and increased with
inspiration
Surgery

Tricuspid Regurge (TR) Most commonly from RV
enlargement and usually functional
and not structural
pulsatile liver
systolic murmur louder on
inspiration in the left sternal
border
Treat underlying conditions
responsible for RV size and/or
pressure.
Also treat with diuretics or
surgical repair.
Pulmonic Stenosis
(PS)
Rare and almost always caused by a
congenital deformity of the valve.
carcinoid syndrome
(encasement and immobilization
of the leaflets)
a systolic murmur
balloon valvuloplasty
Pulmonic Regurge
(PR)
Primarily in the setting of severe
pulmonary hypertension, dilation of
the annulus and enlarged
pulmonary artery
Causes a high-pitched,
decrescendo murmur along the
LSB.
Treat underlying conditions to
help alleviate regurgitation.
Myocardial and Pericardial Diseases
Disease/condition Pathophysiology/ Causes Signs and Symptoms Diagnostics Treatments/Management
Myocarditis Inflammatory disease of the
myocardium
Causes:
Viral: direct invasion of the
monocytes by virus: Coxsackie B,
echovirus, HIV
Bacterial

Pleuritic chest pain: worsens
with inspiration especially if
pericardial involvement
Nonspecific: fever, malaise,
myalgia
tachycardia, pericardial friction
rub, mitral and tricuspid
murmurs
ECG: ST segment and T
wave abnormalities
Endomyocardial biopsy:
evidence of myocardial
inflammation and necrosis
needed (but not finding it
does not exclude
diagnosis)

Most cases resolve w/o
treatment so supportive
treatment of symptoms
Avoid exercise

Cocaine Use Rapid onset of action; increased
myocardial oxygen demand
increases the HR, systemic arterial
pressure, and LV contractility,
marked vasoconstriction and
enhance platelet aggregation and
thrombus.
Most damage with repeated
use.
It can cause angina, MI, LVH,
dysrhythmias, cardiomyopathy,
SCD

urine drug screen Oxygen, Benzodiazepines,
thrombolytics, PCI
NTG and Verapamil: NO BBs
(cocaine affects both alpha and
beta receptors and a BB may
cause the alpha to work
unopposed on the heart)
Pericarditis Inflammation of the visceral and
parietal membrane that covers the
entire heart
Causes: Idiopathic, Viral: coxsackie
B, echovirus, adenovirus, mono, Hep
B, Bacterial: purulent, TB, Fungal:
histoplasmosis; Dressler’s syndrome,
connective tissue disorders,
neoplastic disease, drugs, trauma,
parasites, uremia.
Chest pain: abrupt onset, sharp,
stabbing pain, pleuritic, worse
when supine, relieved/reduced
by sitting
Dyspnea, anxiety, myalgia
pericardial friction rub
(CLASSIC), tachypnea, fever,
dysrhythmias (SVT), restricted
breathing (aka splitting)
ECG: diffuse ST elevation
with concavity and no
reciprocal depression, also
PR elevation
CXR, echo, lab studies
(CBC, TB, ESR, ANA, renal
and thyroid, RF)

Usually self-limiting; rest;
treatment of underlying causes
Pain meds, non-
steroidal/steroidal, NO
anticoagulants due to risk of
developing hemopericardium
Pericardial resection (rare)

Cardiac Tamponade Emergent condition in which fluid
accumulates in the pericardium. The
blood significantly elevates the
pressure on the heart, preventing
the heart’s ventricles from filling
properly.
End result is ineffective pumping of
blood, shock, and often death
Beck’s triad: hypotension,
jugular venous distension and
muffled heart sounds
Constant chest pain, fatigue,
dyspnea, tachycardia,
hypotension, signs of
compression of adjacent
structures.



Decreased/muffled heart
sounds
CXR, ECG, Echo, Pulsus
Paradoxus (fall of
10mmHg with inspiration)



IV fluids and O2 (for shock)
drainage (pericardiocentesis)
surgery(pericardiotomy)




Disease/condition Pathophysiology/ Causes Signs and Symptoms Diagnostics Treatments/Management
Constrictive
Pericarditis
Secondary to progressive scarring of
the pericardium
Filling of the heart chambers is
restricted; elevation and
equalization of diastolic pressures in
all four cardiac chambers.
right-sided heart failure,
exertional dyspnea, cough,
orthopnea, fatigue, muscle
weakness, chest pain is rare.
salt restriction, avoid drugs that
reduce HR, surgical removal or
the pericardium

Hypertrophic
Cardiomyopathy
Most common genetic CV disease
Most common cause of sudden
death in young people, including
athletes
Sudden cardiac death is most visible
and devastating consequence
Symptoms can occur late
Suspected by heart murmur,
positive family history, abnormal
EKG, or onset of symptoms
SCD: Most common before age
25-30. Most pts who die
suddenly have mild or no
symptoms. Risk of SCD declines
with age but does not
disappear.
2-D echo is principal
diagnostic tool: LVH varies
from massive and diffuse
to mild segmental wall
thickening.
Intervention to reduce SCD:
Pharmacology
AICD: primary prevention
Implant at age 20: 4:1 excess of
ICD implants to lives saved.

Atrial Fibrillation Most common sustained arrhythmia
in adults
Fibrillation in which the normal
rhythmic contractions of the cardiac
atria are replaced by rapid, irregular
twitching of the muscular wall.
Biggest concern for those with AF is
a CVA (stroke)
Often associated with other CV
disorders such as: HTN, CHF, DM,
ischemia, valvular, congenital
Chaotic rhythm with an atria rate in
excess of 350 to 600 bpm; quivering
atria; no concerted contractile
effort. This results in an irregular
rhythm
P-waves on the ECG are not present.
4 kinds: paroxysmal, recurrent,
persistent, or permanent
Rarely life-threatening
May be asymptomatic if the rate
is controlled.
Fatigue, dizziness, dyspnea,
palpitations
Syncope, TIA, CVA

Thyroid function study
Echocardiogram
Other cardiac studies to
assess for occult disease
CHADS score:
0-1: aspirin
2 or more: oral
coagulation therapy
In rapid a-fib, rate control is key,
but be cautious of BP
diltiazem IV
Cardioversion (within first 48
hours)
Anticoagulation: Warfarin is the
DOC
Target INR for AF is 2.0 to 3.0
An exception to anticoagulation
treatment is “lone atrial
fibrillation”