CARDIO-COMPREHENSIVE

ANATOMY
SA and AV nodes are supplied by
RCA..infarction of which will cause
BRADYCARDIA or HEART BLOCK
LAD is where the CORONARY ARTERY
OCCLUSION TAKES PLACE
Posterior part of heart is LA
(enlargement causes dysphagia or
hoarseness due to Recurrent Laryngeal
Nerve compression)

PHYSIOLOGY

PHYSIOLOGY
CO = SV * HR
FICKS PRINICIPLE
CO = rate of oxygen consumption/
(arterial oxygen content venous
oxygen content)

PHYSIOLOGY
MAP = 2/3 DIASTOLIC + 1/3 SYSTOLIC
PULSE PRESSURE = SYSTOLIC DIASTOLIC
(INVERSLY PROPORTIONAL TO COMPLIANCE)
Pathology: PP INCREASED in hyperthyroidism,
aortic regurgitation, arteriosclerosis, sleep
apnea, exercise
PP DECREASED in aortic stenosis, cardiogenic
shock, cardiac tamponade, advanced heart
failure

SV = EDV - ESV

Physio
STROKE VOLUME
SV-CAP SV is affected by
Contractility, Afterload, and Preload
SV increases C increases, P
increases, A decreases
Contractility increased with
Catecholamines (adrenaline),
Digitalis (blocks Na/K pump)

Physio
ACE inhibitors and ARBs decrease both
PRELOAD and AFTERLOAD
PRELOAD
Approximated by EDV
vEnodilators decrease prEload
(NITROGLYCERIN)

AFTERLOAD
Approximated by MAP (increase in MAP leads to LV
hypertrophy)
vAsodilators decreases Afterload
(HYDRALAZINE)

RESISTANCE
Depends on pressure, viscosity, and
length of vessels
Viscosity is increased in:
Polycythemia, Hyperprotinemic
states (Multiple Myeloma),
Spherocytosis
Viscosity is decreased in: Anemia

HEART SOUNDS
S1 mitral closure (QRS) and
tricuspid closure
S2 aortic and pulmonary valve
closure
S3 early diastole during rapid
ventri phase (CHF, mitral regurg)
S4 late diastole (LV Hypertrophy)

 A wave Atrial
contraction
C wave RV
Contraction
X descent
Atrial relaXation
V wave
increased RA
pressure going
against tricuspid
Valve
Y descent
blood flow
descending from
RA to RV

ECG abnormalities
Atrial fib X-descent is lost
Tricuspid regurg V-wave is very
elevated (pressure of blood in veins
is elevated)
Tricuspid stenosis X-descent will
decrease (cant lose pressure in
veins)

MURMURS
Mitral Regurg Holosystolic, high-pitched, blowing murmur. Loudest at
apex. Enhanced by increased TPR (squatting, hand grip)
Tricuspid Regurg Caused by RV dilation. Enhanced during
inspiration.
Aortic stenosis Crescendo-Decrescendo systolic ejection murmur.
Loudest at base, radiates to carotids. Pulsus parvus et tardus (weak and
delayed pulses). Due to age related calcific aortic stenosis.
VSD Harsh, holosystolic murmur. Loudest at tricuspid area. Increased
afterload
Mitral valve Prolapse Crescendo late systolic murmur with
midsystolic click. Enhanced by decreased venous return (standing,
valsalva)
Aortic Regurg High pitched blowing early diastolic decrescendo
murmur. Wide pulse pressure, head bobbing. Due to aortic root dilation,
bicuspid aortic valve
Mitral stenosis Follows Opening Snap (half leaflet in motion
during diastole). Delayed rumbling late diastolic murmur. Enhanced
during expiration.
PDA Machine-like murmur. Loudest at S2. Due to Cogenital rubella
or prematurity. Heard in infraclavicular area.

ECG
P-wave ATRIAL
DEPOLARIZATION
PR-interval conduction
delay through AV
QRS-complex
VENTRICULAR
DEPOLARIZATION
QT-interval contraction
of ventricles
T-wave VENTRICULAR
REPOLARIZATION
U-wave caused by
Hypokalemia, Bradycardia

Abnormalities
Torsades de pointes
Ventricular tachycardia, shifting sinusoidal
waveforms on ECG, can progress to Ventricular
Fibrillation.

Congenital long QT interval

Inherited disorder of myocardial repolarization due
to ion channel defects. Sudden cardiac death risk.

Wolff-Parkinson-White Syndrome
Abnormal fast accessory conduction pathway from
atria to ventricle bypassing the rate slowing AVnode.

PATHOLOGY

Congenital Heart Diseases

RIGHT LEFT shunts
Early cyanosis (Blue Babies)
5 Ts

Truncus arteriosus (1 vessel)

Transposition (2 switched vessels)
Tricuspid atresia (3 sided valve closed)
Tetralogy of Fallot (4= tetra)
TAPVR (5 letters)

Persistent Truncus
arteriosus
Failure of truncus arteriosus to divide
into pulmonary trunk and aorta
Patients can have accompanying
VSD

Transposition of Great
Vessels
Aorta leaves RV, and Pulmonary
trunk leaves LV
Separation of systemic and
pulmonary circulations
Not compatible with life unless a
shunt is placed
Failure of Aorticopulmonary septum
to spiral

Tricuspid atresia
Absence of tricuspid valve and
hypoplastic RV

Tetralogy of Fallot
Caused by anterosuperior
displacement of the infundibular
septum
Squatting helps increasing SVR,
decreasing R-L shunt, improving
cyanosis
Pulmonary infundibular stenosis
RVH Boot shaped heart
Overriding aorta
VSD

Congenital Heart Diseases

LEFT RIGHT shunts
Late cyanosis (Blue kids)
VSD > ASD > PDA

VSD
Most common congenital heart
defect
Asymptomatic at birth, symptoms
manifest weeks later
Most self resolve
Larger lesions LV overload Heart
failure

ASD

Defect in the interatrial septum

Loud S1, wide fixed split S2
Occurs in septum secundum
Symptoms range from none to heart
failure
Septa have missing tissue rather
than unfused (like in patent foramen
ovale)

Patent ductus arteriosus

In fetal period, shunt is RL (normal)
Neonatal period there is decreased
lung resistance, making the shunt
LR, leading to RVH, and LVH,
leading to heart failure
Machine like murmur
Patency maintained by PGe
Patency ended by Indomethacin

Coarctation of Aorta
Preductal (Infantile)
Aorta narrowing proximal to the insertion of
ductus arteriosus
Associated with Turner syndrome

Postductal (Adult)
Aorta narrowing distal to the insertion of
ductus arteriosus
Associated with Notching of ribs (collateral
circulation), hypertension in upper
extremities, and radiofemoral delay

Arteriosclerosis
Common sites: Abdominal Aorta > Coronary
artery > popliteal artery > carotid artery
Monckeberg
Calcification of media of arteries especially radial
and ulnar
Intima not involved
pipestem arteries on x-ray

Arteriosclerosis
Hyaline: thickening of small arteries in essential HTN
or DM
Hyperplastic: onion skinning as seen in severe HTN

Aneurysms
Abdominal aneurysm
Associated with arteriosclerosis, most commonly in hypertensive
male smokers > 50 y/o age

Thoracic aneurysm
Cystic medial degeneration due to HTN (older patients) or Marfan
syndrome.
Associated with tertiary syphilis (obliterative endarteritis of the
vasa vasorum)

Aortic dissection
Longitudinal intraluminal tear forming a
false lumen
Associated with hypertension, bicuspid
aortic valve, inherited connective tissue
disorders (Marfans)
Tearing chest pain radiating to the back
Mediastinal widening
Can result in pericardial tamponade,
aortic rupture, and death

Ischemic heart disease

manifestations
Angina
Stable Secondary to atherosclerosis. Pain on exertion. Relieved
by rest. ST depression.
Unstable Thrombosis with incomplete coronary artery occlusion.
Pain at rest. ST depression.
Prinzmetal Secondary to coronary artery spasm. Due to tobacco,
cocaine, triptans. Relieved by CCBs, nitrates, smoking cessation. ST
elevation.

Coronary steel syndrome

Distal to coronary stenosis, vessels are maximally dilated at
baseline.

Sudden Cardiac death

Death from cardiac causes within 1 hour of onset of symptoms,
most commonly due to a lethal arrhythmia (ventricular fibrillation).
Associated with cardiomyopathy.

Diagnosis
Cardiac troponin 1 Rises after 4 hours and
is increasing for 7-10 days
CK-MB Found in myocardium. Useful for
diagnosing reinfarction following acute MI
because levels return to normal after 48
hours
ECG changes Include ST elevation (STEMI,
acute transmural infarct). ST depression
(subendocardial infarct). Pathologic Q waves
(evolving or old transmural infarct).

LEADS

Cardiomyopathies
Dilated
Idiopathic or congenital
Alcohol, Beriberi, Coxsackie B virus, Cocaine, Chagas, Doxorubicin
(ABCCCD)
Heart failure, S3, dilated heart on ECG, balloon appearance on CXR
Tx: Na restriction, ACE inhibitors, Beta-blockers, Diuretics, digoxin

Hypertrophic
Familial, autosomal dominant
Can be associated with Friedreich ataxia
Cause of sudden death in young athletes
S4, systolic murmur

Restrictive
Causes include: sarcoidosis, amyloidosis, postradiation fibrosis,
endocardial fibroelastosis, Loffler syndrome (endomyocardial fibrosis
with a prominent eosinophilic infiltrate), and hemochromatosis

CHF
Clinical syndrome of cardiac pump dysfunction
Symptoms include: dyspnea, orthopnea, and
fatigue
Rales, JVD, and pitting edema
Systolic dysfunction low EF, poor contractility,
often secondary to ischemic heart disease
Diastolic dysfunction normal EF and
contractility, impaired relaxation, decreased
compliance.
Right sided heart failure is due to cor pulmonale

Bacterial endocarditis
Fever, Roth spots (retina), Osler nodes,
Murmur, Janeway lesions, Anemia, Nail
Splinter hemorrhages, Emboli. (FROM
JANE)
Acute S. aureus (high virulence), large
vegetations on previously normal valves,
rapid onset.
Subacute Strep. Viridans (low virulence),
smaller vegetations, sequela of dental
procedures.

Rheumatic fever
A consequence of pharyngeal infection with
Group A Beta Hemolytic Streptococci
Early death due to myocarditis
Affects heart valves mitral > aortic
>>>tricuspid
Early lesion is mitral valve regurgitation, late
lesion is mitral stenosis
Aschoff bodies (granuloma with giant cells), ASO
titer increase, M protein
Chorea, Arthritis, Nodules, Carditis, Erythema,
Rheumatic anemia (CANCER)

Acute pericarditis

Sharp pain, aggravated by inspiration

Relieved by sitting up and leaning forward
Presents with friction rub
Widespread ST-segment elevation and/or PR
dpression
Fibrinous caused by Dressler syndrome, uremia,
radiation. Presents with friction rub.
Serous viral pericarditis (resolves
spontaneously)
Suppurative/purulent usually cased by bacterial
infections (Pneumococcus, Strepto)

Vasculitis
Large-vessel
Temporal (giant cell) arteritis
Elderly females
Unilateral headache (temporal artery), jaw claudication
Could lead to irreversible blindness due to opthalmic
artery occlusion
Focal granulomatous inflammation

Takayasu arteritis
Asian females <40 y/o
pulseless disease (weak upper extremity pulses,
night sweats, arthritis, myalgias, skin nodules, ocular
disturbances)
Granulomatous thickening and narrowing of aortic arch

Medium-vessel
Polyarteritis nodosa
Young adults
Hepatitis B serospositivity
Involves renal vessels, not pulmonary arteries, microaneurysms
Fever, weight loss, malaise, headache, abdominal pain, hypertension,
neurologic dysfunction, renal damage

Kawasaki disease
Asian children < 4 y/o
Fever, cervical lymphadenitis, conjunctival injection, changes in
lips/oral mucosa (strawberry tongue), hand-foot erythema,
desquamating rash

Buerger disease
Heavy smokers, males < 40 y/o
Intermittent claudiation leading to gangrene
Raynaud phenomenon is often present

Small-vessel
Wegners polyangiitis
Upper respiratory tract (perforation of nasal septum,
chronic sinusitis, otitis media)
Lower respiratory tract (hemoptysis, cough, dyspnea)
Renal (hematuria, red cell casts)

Churg-strauss
Ashtma, sinusitis, palpable purpura, peripheral
neuropathy
Pauci-immune glomerulonephritis
Necrotizing vasculitis with eosinophilia
MPO-ANCA/p-ANCA, increased IgE level

PHARMACOLOGY

Calcium Channel Blockers

(CCBs)
Amoldipine, nimodipine, nifedipine
(dihydropyridine), diltiazem,
verapamil (non-dihydropyridine)
Block voltage dependent L-type calcium channels reduce
muscle contractility
Vascular muscle: amoldipine = nifedipine > diltiazem >
verapamil
Heart: veramapil (veramapil = ventricle) > diltiazem >
amoldipine = nifedipine
Dihydropyridines (except nimodipine): HTN, angina, Raynauds
Nondihydropyridines: HTN, angina, atrial fibrillation/flutter
Nimodipine: Subarachnoid hemorrhage (prevents cerebral
vasospasm)

Hydralazine
Increase cGMP smooth muscle relaxation
Vasodilation of arterioles > veins, afterload
reduction
Severe HTN, CHF. First line therapy for HTN in
pregnancy, with methyldopa
Given with Beta-Blockers to prevent reflex
tachycardia
Contraindicated in angina/CAD (reflex
tachycardia)
Can cause Lupus-like Syndrome

Hypertensive Emergency
Nitroprusside:
Short acting
Increase cGMP (direct release of NO)
Can cause cyanide toxicity (releases cyanide)

Fenoldopam:
Dopamine D1 receptor agonist
Coronary, peripheralm renal, and splanchnic
vasodilation
Decreases BP and increases natriuresis

Antianginal therapy
Goal is to reduce myocardial Oxygen
consumption
Decrease end-diastolic volume, BP, HR,
contractility

Lipid lowering agents

Cardiac glycosides
Digoxin
Direct inhibition of Na/K ATPase
indirect inhibition of Na/Ca
exhanger/antiport
Increases Ca positive inotropy
Stimulates vagal nerve decreasing HR
(initiating parasympathetic response)
Cholinergic toxicity is a side effect