Clinical Aspects and Pathology of Hypertension.

1. Select the cause of hypertension from a list. 2. Recognize associated organ pathology. 3. Predict complications that
may be associated with the lesions that develop from hypertension.
CAUSE of ORGAN PATHOLOGY COMPLICATIONS
Hypertension
Renal Causes of Secondary Hypertension: renal artery stenosis, renal vasculitis, glomerulonephritis, polycystic kidney
disease, renin-producing tumors, chronic renal disease.
Renal Artery The affected kidney senses decreased blood flow and auto-regulates The UNAFFECTED kidney is
Stenosis to increase blood pressure. exposed to high blood
= ‘Goldblatt kidney’. pressure (through auto-
~ renal artery stenosis can be caused by: regulation by affected kidney)
(1) Atherosclerosis  nephrosclerosis (hardening
(2) Fibromuscular dysplasia – more common in middle-aged women; of vessel walls).
several forms, differentiated by the involved arterial wall layers.

Endocrine Causes of Secondary Hypertension: hyperaldosteronism, exogenous hormones, pheochromocytoma,

hypothyroidism, hyperthyroidism, pregnancy-induced.
Primary The adrenal gland secretes aldosterone, which increases blood Conn Syndrome (aldosterone-
Hyper- pressure by causing Na+ reabsorption in the kidneys; pathologies: producing adenoma) 
aldosteronism (1) adrenal cortical hyperplasia, (2) adrenal cortical adenoma. uncontrolled blood pressure
 increased risk of stroke,
heart disease, kidney failure.

Effects of Hypertension:
I. CARDIAC DAMAGE:
~ Chronic left ventricular hypertrophy (> 1.5 cm concentric left ventricle thickness) due to chronic systemic vascular
resistance (“cardiomegaly with left ventricular hypertrophy”). * cardiomegaly = > 400g in men, > 350g in women.

Other complications: Aortic dissection (in conjunction w/

atherosclerosis), MI (from increased oxygen demand of hypertrophic
myocardium), cardiac arrhythmia (abnormal electrical conduction
through thickened myocardium).

II. BLOOD VESSEL DAMAGE:

~ Arteriosclerosis – damage to arterioles from chronic exposure to elevated blood pressure.
Hyaline Arteriosclerosis Hyperplastic Arteriosclerosis

~ amorphous eosinophilic material. ~ onion skin appearance.

~ seen in benign hypertension. ~ seen in malignant hypertension.

Arteriosclerosis  chronic ischemia  glomerular sclerosis } NEPHROSCLEROSIS – hyalinization of glomeruli.

Hypertensive kidney damage can take one of two forms:
BENIGN chronic nephrosclerosis. MALIGNANT acute nephrosclerosis.

Shrunken, contracted Necrotizing

and granular kidney. arteriolitis.

III. BRAIN DAMAGE:

~ Stroke (hemorrhagic infarction) – most commonly located in basal ganglia, thalamus, cerebellum, subcortical white
matter.
~ Ruptured berry aneurysm – commonly located in Circle of Willis, anterior communicating artery, posterior
communicating artery.

Pathology of Atherosclerosis.

1. Define the three conditions associated with arteriosclerosis in terms of the cause, pathogenesis, vessels involved, and
clinical complications. Arteriosclerosis is the hardening and thickening of arterial walls:
I. ARTERIOLAR SCLEROSIS.
Hyperplastic (intimal thickening; “onion skin” appearance – malignant hypertension) or hyaline (acellular thickening;
“amorphous eosinophilic” – benign hypertension).
II. MEDIAL CALCIFICATION .

Aka Monckeberg medial

sclerosis.

III. ATHEROSCLEROSIS. (Often interchangeable with arteriosclerosis); characterized by intimal atheromas (fibrofatty
plaques).
Common sites: aorta, coronary artery, popliteal artery, internal carotid artery. Pathogenesis:
intimal (endothelial) injury  inflammation.
~ endothelial cells are crucial to vessel integrity and response to injury; endothelial dysfunction
leads to monocyte adhesion and emigration, smooth muscle recruitment, and macrophage
activation  macrophages engulf lipid (foam cells) - “fatty streak” formation  smooth muscle
proliferation, ECM deposition  fibrofatty atheroma formation.

Complications: calcification, thrombosis (typically in

“vulnerable plaque”: thin fibrous cap, moderate
luminal narrowing, lipid rich center), embolism (mostly
from aorta to organs or lower limbs  gangrene; if
from carotid, carotid bruit is present & may cause
stroke), hemorrhage, ulceration, rupture, aneurysm.

* arterial embolus stroke, heart attack, gangrene. * venous embolus  pulmonary embolism.
* aneurysm – weakening, dilatation and rupture of vessel wall; saccular / fusiform / dissecting / false aneurysm
(extravasation of blood  hematoma).
~ common aneurysms include:
ABDOMINAL AORTIC DISSECTION CEREBRAL BERRY SYPHILITIC MYCOTIC
AORTIC ANEURYSM ANEURYSM ANEURYSM
ANEURYSM
Usually in Two types: Congenital (NOT Caused by Caused by
abdominal aorta (1) hypertensive / atherosclerotic, (2) atherosclerotic) tertiary syphilis infection
below renal genetic (Marfan syndrome). weakening of vessel (NOT (bacterial or
arteries (can Both types are characterized by cystic wall, typically at atherosclerosis). fungal) of
extend to iliac medial degeneration (myxomatous branch points in Circle ~ Treponema blood
arteries); occurs degeneration of aortic media  of Willis. infects vasa vessel.
more commonly in fragmented elastic fibers, intimal tear); vasorum 
men over 60 and is dissection usually starts in arch of aorta linear
due to or aortic root. calcification of
atherosclerosis. elastic lamina 
AAA is clinically dilatation of
significant when > RUPTURE  aortic valve ring
5 cm in diameter. subarachnoid & ascending
~ can be detected hemorrhage, aorta, aortic
as “pulsatile intraparenchymal insufficiency.
abdominal mass”; hematoma.
rupture may cause Classic symptoms: sudden onset of Clinical signs of
sudden death; Tx: excruciating chest pain (may radiate to rupture: sudden onset
aortic graft; middle of back); x-ray: widening of of excruciating
“endoluminal mediastinum (due to hemorrhage). headache, sudden
graft”. loss of consciousness.

2. Recognize the gross and microscopic appearance of atherosclerosis, arteriolar sclerosis, Monckeberg medial sclerosis.
See above.
3. Define and recognize the cause, pathogenesis, and clinical complications of thrombophlebitis / phlebothrombosis and
superior and inferior vena cava syndromes. Atherosclerosis  venous diseases:
I. VARICOSE VEINS: tortuous dilations of lower extremity veins secondary to ↑ venous pressure (i.e. standing for long
periods of time, pregnancy, etc) – venous valves become incompetent; risk for venous thrombosis is low.
II. THROMBOPHLEBITIS (inflammation) / PHLEBOTHROMBOSIS (no inflammation): deep vein thrombosis of lower
extremities (other sites: pelvic veins, prostatic veins, dural sinuses); major complication = pulmonary embolus.
III. SUPERIOR / INFERIOR VENA CAVA SYNDROME: obstruction of vena cava due to neoplasm (i.e. lung cancer, liver
cancer); symptoms relate to area of obstruction.

Pathology of Acute MI and Risk Factors.

1. List causes of ischemic heart disease.

Ischemia = compromised blood supply or increased oxygen demand (supply-demand mismatch); infarction = cell death due to
ischemia; ischemic heart disease = chronic ischemia w/ or w/o infarction.
Ischemic heart disease can result from: coronary atherosclerosis, hypertension, heart failure, obesity, chronic
pulmonary disease, and any other condition that decreases oxygen delivery or increases oxygen demand.
 The right coronary artery supplies the RV, posterior LV and septum,
posteromedial papillary muscle, and AV & SA nodes  30-40% involvement in
MI; the left anterior descending artery supplies the anterior LV and septum 
40-50% involvement; the left circumflex artery supplies the lateral LV and
posterior LV and septum  15-20% involvement.

The degree of cardiac ischemia depends on degree of arterial occlusion,

collateral circulation, overall health of the heart, and arrhythmia.

2. Recognize the most common site of coronary vessel compromise and the area of the heart most commonly affected.
3. List local factors that enhance or diminish ischemia. See above.
4. Recognize or describe the microscopic changes of an infarct over time.

Consequences of acute myocardial infarction include: (1) acute change in

coronary artery plaque – rupture of vulnerable plaque, hemorrhage, thrombosis,
(2) ischemic damage to myocardium, (3) myocyte necrosis, (4) other
complications. *Infarct histology undergoes a series of progressive changes; cells
involved: neutrophils, macrophages, fibroblasts.

EARLY changes (<24 hrs)
Initially, no visible
histological change 
coagulative necrosis
(“contraction band
necrosis”)  neutrophil
response.
MIDDLE changes (1-3 days)
Neutrophils  cellular
debris  macrophages.
LATER changes (3-7 days)
Macrophages 
phagocytosis  fibroblasts.
*** greatest risk of
myocardial rupture at 4-7
days!
HEALING (>7 days)
Fibroblasts 
neovascularization 
collagen / fibrin.
~ myocardial scar.

5. Predict post-infarct clinical complications.

Arrhythmia “Myocardial irritability.” Heart block (depending on location of infarct) can lead to bradycardia,
ventricular tachycardia, premature ventricular contractions.

Myocardial (1) free wall  hemopericardium, (2) septum  acute VSD with left-to-right shunt, (3) papillary muscle
Rupture  acute mitral valve insufficiency.

Pericarditis * Dressler’s Syndrome (fibrinous pericarditis) can occur 1-7 days after acute MI (acute inflammatory
exudate), 6-8 weeks after acute MI (“autoimmune”), and after bypass graft surgery (post-pericardotomy
syndrome). Triad: fever + pleuritic pain + pericardial effusion.
 “chest pain, friction rub”.

Mural Akinesis / hypokinesis of infarcted myocardium  blood pooling on endocardial surface, thrombus
Thrombus formation  EMBOLIZATION can lead to stroke or gangrene.
Ventricular
Aneurysm Infarcted myocardium is thinned and balloons outward w/
forceful contractions of adjacent myocardium 
thrombus can form in aneurysm.

Aneurysm can begin to form only a few days after infarct.

Ventricular Infarcted myocardium dies (scar tissue formation) and surrounding myocardium hypertrophies  zones
Remodeling of fibrosis with surrounding hypertrophy; myocardium can become thick & stiffened.

* OTHER COMPLICATIONS:
~ Chronic ischemic heart disease – typically progresses to congestive heart failure (non-contractility of scarred
myocardium).
~ Sudden cardiac death – patient may have severe coronary artery atherosclerosis, but NO occlusive thrombus and/or
NO myocardial infarction; death is due to ARRHYTHMIA (typically ventricular fibrillation).

* Associated CLINICAL CONCEPTS:

~ Angina pectoris is chest pain due to ischemia of the heart muscle. Two types:
Stable Angina Unstable Angina
Chronic atherosclerosis; imbalance in coronary perfusion Thrombosis of coronary artery from plaque pathology 
and oxygen demand. “preinfarction angina”.
~ symptoms precipitated by activity (i.e. exercise) and are ~ Occurs at rest or with minimal exertion, is of new onset
minimal/non-existent at rest. / severe and/or occurs with a “crescendo” pattern – more
severe, prolonged or frequent than before.

* Prinzmetal angina occurs at rest and is due to episodic ischemia from coronary vasospasm.
~ Reperfusion injury – after blood is restored to ischemic heart muscle via PTCA (percutaneous transluminal coronary
angioplasty) and/or thrombolysis (usually within 30 min to 3-4 hrs), the damaged myocardium is susceptible to
hemorrhage, arrhythmia, and further ischemia (caused by inflammation, oxidative stress).
~ Myocardial stunning – myocytes are not lethally damaged and can recover in a few days with reperfusion.
~ Myocardial hibernation – myocytes with chronic sub-lethal ischemia may “hibernate” for days – weeks and recover
function at a later time.

Serum biomarkers of myocardial infarction: Mb, CK-MB, Troponin I and T. Troponins T

and I are both sensitive (proportions of positives correctly identified) and specific
(proportion of negatives correctly identified). CK-MB is sensitive but not as specific.
Combination of the two  best diagnosis.
ASCVD Risk Factors (Dr. Charyk).

CVD = cardiovascular disease; ASCVD = atherosclerotic

cardiovascular disease.
~ coronary artery disease: responsible for angina, MI, and
ischemic cardiomyopathy.  1 in 6 deaths in US per yr.
~ cerebrovascular disease: causes stroke and TIA.
~ peripheral vascular disease: causes lower extremity
claudication (impairment in walking), arterial insufficiency.
~ carotid artery disease: source of embolic stroke. 
someone has a stroke every 40 seconds in the US!
~ aortic atherosclerosis: can result in abdominal or thoracic
aneurysm.
RISK FACTORS: age (> 55 for men, >65 for women), male sex, family history of premature CVD, hypertension, smoking,
dyslipidemia (↑ TG, LDL, ↓ HDL), sedentary lifestyle, diabetes, obesity (BMI > 30).
* LDL goals and LDL levels at which therapy should be initiated depends on the number of risk factors present in a patient – e.g.
patients with more than 2 risk factors should aim for an LDL of <130 while patients with 0-1 risk factors should aim for LDL < 160.

Framingham Study: Epidemiological study (1948 – ongoing) to collect data including family history, lifestyle details,
exams & lab tests, and health of participants followed over time  used to investigate genetic patterns of common
diseases such as DM, osteoporosis, dementia, etc.
~ identifies common factors/characteristics contributing to CVD.
~ allows for risk calculation, i.e. 60 yr old male  12% risk, 60 yr old male PLUS smoker  22% risk, etc.

Patient w/ Chest Pain.

1. Discuss the multiple etiologies of chest pain.

* Cardiac causes of chest pain include: (1) coronary syndromes – angina, acute coronary syndromes, coronary spasms,
acute MI (non-ST elevation MI  subendocardial infarction, ST elevation MI  transmural infarction), (2) non-coronary
causes – pericarditis, aortic dissection, mitral valve prolapse, pulmonary hypertension, chest trauma, radiation therapy,
aortic valve disease.
* NON-cardiac causes of chest pain include: pulmonary embolism, GERD, neurological conditions (i.e. herpes zoster),
musculoskeletal trauma, psychiatric conditions (i.e. acute anxiety).
2. Discuss the pathophysiology of myocardial ischemia.
The heart has an absolute requirement for aerobic production of ATP (e.g. exercise can ↑ myocardial oxygen needs 6x).
Normal coronary circulation balances oxygen supply and demand; myocardial ischemia develops when supply < demand.
~ Coronary blood flow is determined mainly by:
Decreased O2 supply to myocardium can be caused by:
severe anemia (low Hb; patient w/ angina will have more
frequent symptoms if anemia develops), hypoxia (low
pO2; patient w/ angina will have more symptoms if moved
to higher altitude), poisoning ( methemoglobin),
inadequate coronary blood flow (occlusion, spasm, artery
disease), left ventricular hypertrophy (↑ demand),
decreased cardiac output.

* O2 consumption can be estimated by: (SYSTOLIC BLOOD PRESSURE) X (HEART RATE).

Consequences of myocardial ischemia: transient reduction in ventricular compliance (S4), elevated left ventricular end
systolic pressure, electrophysiological abnormalities (↓ in resting membrane potential, post-repolarization
refractoriness, ↓ conduction velocity, loss of intracellular K+ and increase in extracellular K+.

3. Discuss the pathophysiology and clinical presentations of myocardial ischemia, myocardial infarction.
STABLE ANGINA classically manifests as constrictive left precordial pain radiating to the left arm and fingers. Atypical
presentation: pain w/o radiation, toothache, epigastric pain, cervical pain, jaw pain, dizziness, diaphoresis, nausea,
dyspnea. Typical angina is more common in males and atypical more common in females.
~ Angina is graded as follows:
CLASS I – only strenuous exercise causes angina.
CLASS II – slight limitations to ordinary activities such as walking uphill or climbing stairs (> 1 flight).
CLASS III – marked limitations; angina develops when walking less than 2 blocks or climbing 1 flight of stairs.
CLASS IV – inability to conduct activities of daily life.
UNSTABLE ANGINA presents with ↓ exercise tolerance, nocturnal pain, and pain at rest.
~ Pathogenesis: atherosclerotic plaque develops  lipid-laden macrophages (foam cells) accumulate – oxidized LDL in
foam cells is cytotoxic  production of macrophage proteases and neutrophil elastases causes thinning of the plaque
fibromuscular cap  increased plaque instability, wall stress and blood flow shear  rupture of plaque 
vasoconstriction of coronary vessel at rupture site.
ACUTE MI typically presents with constrictive left precordial pain, radiating to the left arm and fingers. Atypical
presentations include pain w/o radiation, toothache, jaw pain, epigastric or cervical pain, or NO pain (seen in 50% of
patients over 75). CNS effects include diaphoresis, nausea/vomiting, cool/clammy skin. Inflammatory response  mild
fever.
~ acute ischemia can lead to stunning (segmental dysfunction) – myocardial blood flow is normal, but function is
depressed.
~ left ventricular remodeling occurs after large MI and is characterized by cardiomyocyte lengthening, ventricular wall
thinning, infarct expansion, inflammation, scar formation, dilation and reshaping of LV, accumulation of collagen.
 increased systolic & diastolic wall tension and MVO2 (mixed venous oxygen saturation), reduced myocyte shortening
and subendochondrial perfusion, dysynchronous depolarization, mitral regurgitation, ventricular arrhythmias,
ventricular fibrillation.
4. Review the therapeutic options for the management of myocardial ischemia.
Management of angina: (1) reduction of myocardial work by BP control, HR control, and afterload (LV wall tension
during ejection) reduction, (2) increase of coronary flow by PTCA, coronary bypass surgery, (3) improvement of skeletal
muscle conditioning.
Management of acute MI: (1) pain management, (2) restoration of coronary flow (PTCA, thrombolytic therapy), (3)
prevention of recurring coronary thrombosis (anticoagulant therapy, reduction of platelet aggregation), (4) reduction of
afterload, (5) management of electrical disorders, (6) management of hemodynamic consequences (see above).
ECG.
Basics of ECG I.

ECG is used for diagnosis of ischemic heart disease (IHD), arrhythmias, ECG abnormalities (i.e. bundle branch block),
electrolyte abnormalities, etc.
P-wave = atrial depolarization, QRS complex = ventricular depolarization, T wave =
ventricular repolarization.
The P-R interval (from start of P-wave to start of QRS complex) represents the delay
between the start of atrial depolarization and the start of ventricular depolarization. An
extended P-R interval signifies delayed conduction through the AV node; a shortened P-R
interval signifies pre-excitation syndrome (partial premature contraction).

The Q-T interval (from the start of QRS to the end of T-wave) represents
the total time for ventricular depolarization and repolarization.
The PR segment (from end of P to beginning of QRS) may change in
pericarditis but is rarely clinically significant. The ST segment (from end of
QRS to start of T-wave) is when the ventricles are completely depolarized
– if there is damage in the ventricle, the ST segment shifts. Ischemia
usually shifts the ST segment DOWN, while infarction shifts it UP.

The R-wave is always (+) – it is never inverted! Q- and S-waves are (-). Q-wave may be absent.
ECG measurement: standard & augmented leads are placed on the arms and legs, with one leg as the ‘reference’.
Precordial leads are placed on the chest, starting at the 4th intercostal space.

LEAD I is the voltage difference between the two arms; LEAD II is

the voltage difference between the R arm and L leg; LEAD III is the
voltage difference between the L arm and the L leg.
 Einthoven’s Triangle.
* Averaged L arm and L leg compared w/ R arm  aVR (augmented
voltage of the right arm); averaged R arm and L leg compared w/ L
arm  aVL; averaged two arms compared with L leg  aVF.

Result: 12 STANDARD LEADS – 6 limb leads (I, II, III, aVR, aVL, aVF) + 6 chest leads (V1 – V6). The P-wave is usually seen
more clearly in Leads I & II.
~ The calibration signal (rectangular) is equivalent to 1mV (each ECG box is 1mm = 1/10 mV). The paper speed allows to
measure the duration of each wave, etc.

Normal paper speed = 25 mm/sec, 5 mm (one

“big square”) = 0.2 sec and 1 mm (one “little
square”) = 0.04 sec.
Amplitude is usually expressed in mm; 10 mm
= 1 mV.

Rate: 300 “big squares” = 1 minute, so to get an estimate of heart rate, add up the amount of “big squares” between
each QRS complex (e.g. 4 “big squares”  300 / 4 = 75 bpm).
* Automatic rate calculation by machine MAY BE wrong (arrhythmias, artifacts, etc)!
NORMAL VALUES:
~ Normal P-wave is < 0.12 sec and < 3 mm (not wider than 3 “little squares”).
~ Normal PR interval < 0.24 sec (<6 mm) and > 0.12 sec (> 3mm).
~ Normal QRS complex < 0.12 sec (< 3mm).
~ Normal ST segment is elevated / depressed no more than 1 mm at rest and no more than 2 mm on exertion.
~ Normal QT interval 0.38 – 0.43 s (~ 2 “big squares”).
NORMAL VARIANTS:
~ Early repolarization – no discernible ST segment (most prominent toward V2 and V3); commonly found in young
adults (particularly males), athletes. a.k.a. “J point elevation”.
~ ST depression – visible in V4 – V6, BUT looks ELEVATED in V1, V2  “reciprocal change”.
~ Artifacts – AC interference, somatic muscle tremor (muscle movement, i.e. in tense patient), movement artifact.

Basics of ECG II.

Electrical heart axis – average of all depolarizations in the heart. Depolarization wave begins in R atrium  R & L
ventricles; because the L ventricle is thicker, the depolarization wave is directed to the left.

Lead I is at 0°; Lead II is at 60° toward left foot and Lead III is at
120° toward right foot.
The axis normally lies between 0° and aVF (90°). “Left axis” is aVR and aVL are
between 0° and -30° (may still be NORMAL). “backwards”.
Anything less than -30° is definitely a left axis deviation. Greater
than 90° (toward or beyond Lead III) is right axis deviation.
* Anything between -90° and 180° is extreme deviation or a
possible error in lead placement.

Mean electrical axis CALCULATION:

~ look for LARGEST deflection (tallest R-wave) – this is close to where the true QRS axis is.
~ alternatively, look for the SMALLEST net deflection (not most negative!) – this is close to 90° to the axis.
~ quick “rule-of-thumb”:

Net deflection at RIGHT ANGLES to the mean electrical axis should

be 0! (i.e. if axis = +60, aVL lead should have no deflection).

In a patient with pericardial effusion, the axis changes with

each heartbeat (heart moves in pericardial sac).
Clinical Use of ECG.

CONDITION CAUSES ECG

Left Aortic stenosis, - characterized by a tall R-wave (usually V6 or V5).
ventricular hypertension, Standard criteria:
hypertrophy athletic heart. ~ R-wave (in V5 or V6) ≥ 27mm.
(LVH) ~ S-wave (in V1) + R-wave (V5/V6) ≥ 35mm  more sensitive, less
specific criteria.
~ R-wave in aVL ≥ 11mm.
 in this image, the T-wave is inverted and the ST segment is
depressed; this “strain pattern” is commonly seen in ischemia (due
to small vessel disease as consequence of prolonged hypertension)
AND coronary artery disease (no way to distinguish the two).

* Criteria are not specific or sensitive, so someone with LVH may not
fulfill the criteria, and someone w/o LVH may. E.g. young people with thin chest walls
often appear to have LVH; obese people with LVH, however, may give a false
negative.
Right COPD, pulmonary - characterized by V1 R-wave > V1 S-wave (which is normally larger in V1).
ventricular hypertension, ASD
(atrial septal RV1 > SV1 and ≥ 5 mm
hypertrophy
defect) or VSD PLUS right axial deviation. Left axis deviation,
(RVH)
(ventricular septal however, is not a strong predictor for LVH!
defect 
increased work in * The T-wave is inverted (as in LVH), indicating strain
right heart, PS on the right ventricle due to ischemia.
(pulmonary
stenosis).
* Also seen in
children *Biventricular hypertrophy is difficult to observe on ECG because
< 5yrs – LVH and RVH cancel each other out – LVH gives a large S-wave in V1
dominant right while RVH gives a large R-wave.
ventricle.
Left atrial Anything that Widening of the P-wave due to prolonged atrial depolarization (P > 0.12 sec).
hypertrophy increases the
size / workload ~ “notched” or “M-
of the left shaped” P-wave.
atrium – mitral ~ P is biphasic in V1;
stenosis (“P negative wave ≥ 1
mitrale”). mm.
Text

Right atrial Pulmonary The duration of the P-wave remains the same, but the HEIGHT is increased.
hypertrophy hypertension (“P
pulmonale” –
feature of cor
pulmonale).

ASD —> Left - Right shunt

~ Tall P-wave in Lead II; P ≥ 2.4 mm (or 3 mm).

Ischemic ↓supply or
heart ↑demand of Characterized by T-wave inversion (seen
disease oxygen – constantly in LVH, RVH, but often only upon
(IHD) observed on
exercise in ischemia) and ST segment depression
stress test or
some form of (heart is depolarized during this interval; ischemic
controlled segment of heart is not maintaining membrane
physical activity. potential ).

Infarction Necrosis caused

by ischemia due (1) ST elevation – “injury current” (reversible).
to obstruction, (2) Loss of R-wave – partial thickness infarct.
compression, (3) Q-wave development - (transmural
trauma, infarction – across entire wall)negative
vasoconstriction, deflection before R-wave; Q-wave is > 0.04(S), >
etc.
1/3(R).
(4) T-wave inversion – defects in repolarization.

Age of infarct:
ACUTE RECENT / INDETERMINATE OLD
~ ST elevation. ~ Inverted T-wave. ~ Pathological
~ 3-4 days. ~ Months. Q-wave.
~ Up to years!

Pericarditis Infection, MI,

trauma, side Diffuse, non-specific, concave ST
effect, etc. segment elevations in all leads
except aVR and V1.

Spectrum of acute coronary syndrome (reflects degrees of damage to myocardium):

stable angina  unstable angina  non-STEMI (ST elevation MI)  STEMI.

Arrhythmias.

Normal ventricular conduction consists of the SA node, AV node,

Bundle of His, and three fascicles leading to the ventricles: right
bundle and anterior & posterior fascicles (on the left).
Because the left ventricle is much bigger than the right, we see a
negative deflection in V1 (right) and a positive deflection in V6
(left).
Abnormal ventricular conduction:
CONDITION MECHANISM ECG
Right bundle ~ common abnormality that tends  widening of QRS (> 0.12 s), “R-S-R pattern” in V1.
branch block to occur w/ age or as a normal
(RBBB) variant.
~ the septum depolarizes,
followed by left ventricular
depolarization, but the right
ventricle depolarizes a fraction of
a second later (it needs to wait for
wave of depolarization to spread
from LV).
~ type of intra-ventricular block.
Left bundle ~ anterior and posterior left  widening of QRS, “R-S-R pattern” (more wedge-shaped than
branch block fascicles blocked  septum RBBB) in V6 and LEFT-sided leads.
(LBBB) depolarization REVERSES (now
right to left); septum is followed
by right ventricles depolarization,
then the left.
~ can be intermittent (i.e. induced
by carotid sinus massage).
Hemi-block ~ ONE of the two left fascicles is QRS is NOT widened because there is still connection to the AV
blocked  change in vectors of LV node via one of the fascicles.
depolarization. ~ shape is normal; electrical axis altered, making it impossible to
(1) L anterior HB: ventricle diagnose other conditions from the ECG.
depolarizes from postero-inferior
side, coming antero-superiorly 
LEFT AXIS DEVIATION.
(2) L posterior HB: ventricle
depolarizes from antero-superior
side, going in reverse direction 
RIGHT AXIS DEVIATION.

* Bifascicular blocks (i.e. RBBB + LAHB or RBBB + LPHB) can also occur; loss of the third fascicle  ventricular block.
* ECGs can also be used to monitor drug & electrolyte abnormalities:
HYPERKALEMIA HYPOKALEMIA
Tall T-wave (T-wave > QRS), smaller Prominent U-wave (seen
P-wave and wider QRS – the waves in hypomagnesemia also);
eventually fuse, resembling flattening of T-wave to
ventricular tachycardia  cardiac mimic long QT syndrome.
arrest.

1. Premature contractions – how origin affects appearance. Premature contractions (“heart beats sooner than it ought
to”) are also known as PVCs, extrasystoles, or ectopic beats; defined in terms of where they come from (i.e. atrial,
supraventricular, ventricular).

Premature Contraction ECG

atrial PVC – normal QRS complexes, but a premature
atrial contraction (P-wave) is seen, followed by a
premature ventricular contraction.  “premature
ventricular contraction of atrial origin”.
ventricular PVC – QRS is abnormally shaped (wide), NO
P-wave preceding QRS (no atrial contraction; premature
contraction began in ventricle), T-wave is inverted (if
QRS is +).
* Multifocal PVCs (different shapes) – dangerous!
junctional PVC – originates in AV node; characterized by
narrow QRS complexes (normal conduction through
ventricles and fascicles, normal T-wave); NO P-wave – no
atrial contraction; AV node depolarization triggers
ventricular contraction. * Because ventricular
depolarization can depolarize the atria, a notch may
sometimes be seen in the QRS complex.

Bigeminy – abnormal heart beats occur every other concurrent beat (i.e. PVC  pause  normal beat  PVC).
~ benign and stable; patient may feel the ‘normal heart beat’ following the compensatory pause because the heart has
overfilled. RULE: the longer the RR interval, the more likely the next beat is to be a PVC. Trigeminy – every 3rd beat is
abnormal. Quadrigeminy – every 4th beat is abnormal.

2. Re-entry.
Arrhythmias originate from (1) abnormal focus, (2) re-entry – if one segment is slow, the electrical
current can travel down a different segment and re-enter the first segment after it has finished
repolarizing.
* Can happen in AV node, where conduction is deliberately slowed to allow ventricular filling.
* Changes in QT interval promote re-entry; QT intervals > 0.43 and < 0.35 increase risk.
* Re-entry can also arise from accessory pathways (i.e. Wolff-Parkinson-White syndrome).

3. Supra-ventricular arrhythmias – SVT, A fib and A flutter. 4. Ventricular arrhythmias – VT, V flutter, VF.
ARRHYTHMIA MECHANISM ECG
Atrial ~ Random electrical activity in the atria, bombarding Results in irregular QRS complex; pulse is
Fibrillation the AV node. irregularly irregular.
~ Can be classified as first / single episode, paroxysmal ~ A fib can be fast or slow; goal is to keep
(recurrent episodes < 7 days; MORE DANGEROUS ventricular response rate relatively slow.
because clots can form going in and out of A fib),
persistent (episodes > 7 days), or permanent.
* Trigger zones found in myocardial sleeves of
pulmonary veins (ablation possible, but not always best
outcome) – rate control & anti-coagulation usually best
Tx.
Consequences of A fib: 10% ↓ in CO from loss of atrial
contraction (may be significant in CHF, mitral stenosis),
thrombi / emboli.
Atrial Flutter ~ Slow rate of atrial depolarization (about 300/min), w/ ~ in 2:1 conduction, atrial depolarization rate
regular bombardment of AV node  regular is about 300, ventricular depolarization is
conduction (not random). 150; in 1:1 conduction, the patient is most
~ Regular QRS waves, but w/ “saw-tooth” appearance likely dead, as the ventricles cannot contract
– each tooth represents atrial depolarization.  at 300 bpm!
Tx similar to A fib (rate control + anti-coagulation),
cardioversion, ablation of “cavo-tricuspid isthmus”,
right between the vena cava and tricuspid valve.
Atrial Paroxysmal atrial tachycardia (PAT) = run of 4 or more Multifocal AT  variable PRs and P-waves;
Tachycardia APCs (atrial premature contractions), 140-220 / min. narrow complexes (suggestive of
* Can be a complication of excessive Digoxin therapy. supraventricular arrhythmia).

Junctional Focus at or near AV node leads to abnormal rhythm;

Arrhythmia normal narrow complexes, but inverted P-wave and PR
interval is very short. 

Ventricular - abnormally shaped QRS waves (vs. narrowed QRS in

Arrhythmia supraventricular / atrial arrhythmias)  decreased
cardiac output.
- ventricular tachycardia: > 100 / min, 4+ PVC
(premature ventricular contractions), no P-waves.
- sustained if lasts more than 30 sec.
* PVCs are DANGEROUS (esp. when multifocal and
occurring > 6/min) because if the QRS complex occurs
on top of the T-wave (“R on T”), coordination of
depolarization / repolarization breaks down  may
cause cardiac arrest.
~ monomorphic less dangerous than polymorphic.
~ Torsade de Pointes: “twisting of the points”;
complication of overuse of anti-arrhythmic drugs.
5. AV conduction block – first, second, third degree and SA block.
1st DEGREE 2nd DEGREE 3rd DEGREE
Relatively (1) Type I (Wenckebach) at AV node – progressive COMPLETE dissociation of atrial and
insignificant; lengthening of PR interval ; RR intervals actually shorten. ventricular rhythm  ventricle
characterized by assumes its inherent rhythm
PR > 0.20. (idioventricular rhythm).
~ HR drops to about 40, resulting in
heart failure / death.
~ pacemaker required.
 benign!
(2) Type II (Mobitz) at bundle of His – can lead to profound
bradycardia; normal PR interval, followed suddenly by no
conduction.

 dizziness, lack of perfusion, etc. Pacemaker usually

required.
6. Pre-excitation – WPW.