Transcript NPLEX Combination Review Cardiovascular Part 2

NPLEX Combination Review
Cardiovascular Part 3
Paul S. Anderson, ND
Medical Board Review Services
Copyright MBRS
Angina Pectoris
Clinical syndrome caused by
Myocardial ischemia
(usually from CAD)
Angina Pectoris
• Transient precordial pain, brought on by exertion and
relieved by rest
• Pain may be vague or crushing; may radiate to left
shoulder, jaw, throat, teeth, arms
• Pain may be worse after meal or in cold weather; may
change as collateral circulation builds up
• Usually relieved with sublingual nitroglycerin (NTG)
within 2-3 min.
• EKG often normal with attacks
– exercise test may show ST abnormalities that help
with diagnosis (ST depression = ischemia)
Unstable Angina
• More severe form of angina
• Same etiology as exertional angina
• Variant angina (Prinzmetal’s angina) =
angina at rest with ST segment elevation
during attack
• May occur at same time of day
• Felt to be from coronary artery spasm
Acute Myocardial Infarction
• When insufficient coronary blood supply persists
after myocardial energy reserves have been
depleted, the myocardial cells become
irreversibly ischemic and the process of necrosis
termed “myocardial infarction”
• Pain not relieved with NTG
• Apprehension and sense of “doom”
• Most MI’s occur at 9 a.m. on Mondays
Five major signs and symptoms of MI
• pain or discomfort in the jaw, neck, or
back
• feeling weak, lightheaded, or faint
• chest pain or discomfort
• pain or discomfort in the arms or
shoulder
• and shortness of breath
MI
• All symptoms typically come and go on a
3-5 minute cycle.
• In women the signs may be:
– More significant nausea
– Back pain (above the kidney area)
– No neck or arm pain, often little chest pain
– These signs and symptoms cycle on a 3-5
minute rate as well
Acute Myocardial Infarction
• Abnormal EKG with Q waves
• CPK MB fraction elevated
• ECHO shows abnormal left ventricular wall
motion
Heart Failure
Congestive Heart Failure
• Clinical syndrome in which the heart fails
to pump enough blood to meet the body’s
need
• Leads to
– Dyspnea On Exertion
– Paroxysmal Nocturnal Dyspnea
– Orthopnea
Diastolic Heart Failure
• Classically, heart failure has been almost
synonymous with left ventricular systolic failure
(pump failure)
• Diastolic dysfunction of the left ventricle occurs
when there is impairment of relaxation of the
ventricle resulting in delayed filling and
increased pulmonary venous pressure
• This combined with secondary compensatory
tachycardia results in  left ventricular volume
Adaptive Mechanisms in CHF
• Ventricular dilation—will eventually lead to 
diastolic pressure and pul edema (left failure)
and/or systemic edema (right failure)
• Reduced blood flow to the kidneys salt
and water retention and  blood volume with
2º HBP ( afterload)
• Sympathetic stimulation increases venous
tone, thus shunting blood from the peripheral
tissues to the heart causing  BP
• Tachycardia and increased contractility may
precipitate ischemia in pts with CAD
Left CHF
• Cardinal clinical symptoms are DOE, chronic dry
cough and fatigue
• Tachycardia, cardiac asthma, productive rust
colored sputum, rales, displaced apical impulse,
S-3, S-4 gallop rhythms, right sided pleural
effusions, reduced carotid pulse
• Nocturia due to  renal perfusion lying down and
exercise intolerance due to  blood flow to
muscles.
• Pallor, tachypnea, restlessness, low BP
Right CHF
• Fatigue, distended neck veins, pedal edema,
ascites, pitting edema, large liver, tricuspid
regurgitation murmur and cyanosis; orthopnea
and PND.
• Diseases that produce these sx include lung
disease, pul embolus, volume overload, mitral
stenosis.
Pulmonary Heart Disease (Cor
Pulmonale)
• Right ventricular hypertrophy and eventual
failure from pulmonary diseases
• Causes include:
– COPD
– Pulmonary fibrosis or emboli
– Scleroderma
– Primary pulmonary hypertension
– Alveolar hypoxia from any cause
Cor Pulmonale
• Chronic cough, exertional dyspnea, wheezing,
fatigue, weakness, cyanosis, clubbing epigastric
pulsations, distended neck veins, hepatomegaly,
polycythemia
• CXR shows RVH
• PFTs show underlying lung disease
• ECHO shows right ventricular disease
Disturbances of Rate and
Rhythm
Normal Sinus Rhythm
• Impulses originate in SA node
• Regular rate of 60-100/min in adults
• Each P followed by QRS
Normal Sinus Rhythm
Sinus Arrhythmia
• Similar to normal sinus rhythm
• Effect of respiration changes the
frequency the SA node discharges.
Sinus Bradycardia
• Similar to NSR except the rate is < 60/min in
adults
• Physiological bradycardia occurs in healthy
individuals (usually athletes) with  vagal tone
Sinus Bradycardia
Sinus Tachycardia
• Impulses originate in SA node at rate of
100-160/min in adults
• QRS follows each P wave
Atrial Premature Beat (APB)
• Impulse is discharged prematurely by an
irritable focus in the atria
• The further from the SA node the ectopic
focus is, the more abnormal will be the P
configuration
• PR is variable, but QRS is normal
Atrial Premature Beat (APB)
Atrial Tachycardia aka Supraventricular
Tachycardia SVT
• Impulses originate in an atrial pacemaker at
rate of 140-250/min
• QRS is usually narrow
• At very rapid rates, only every 2nd P may be
followed by QRS (2:1 block)
• Vagal stimulation can terminate the AT
• Common, occurs in young people with no
known heart disease
Atrial Tachycardia
Atrial Flutter
• Impulses originate in an atrial pacemaker at rate
of 240-340/min, but some are blocked at the AV
node
• Atrial activity is represented by saw tooth-like
deflections (Flutter waves)
• Symptoms of palpitations, sweating weakness,
dizziness, syncope
• Vagal stimulation has no effect
Atrial Fibrillation
• Impulses originate in multifocal atrial pacemaker
at rate of 300-600/min, but only some are
conducted to the ventricles
• Many patients are asymptomatic
• Since there is a deficit in radial and precordial
pulse, apical pulse should be taken in patients
• Pulse is irregular, irregular
• Vagal stimulation has no effect on ventricular
rate
Atrial Fibrillation
Premature Ventricular Contractions
(PVC)
• QRS is wide (> 0.12 sec), not preceded
by P wave
• Etiology is an irritable focus in the left or
right ventricle that fires prematurely and
the impulse is spread to the opposite
ventricle with delay producing a bizarre
QRS complex
• PVCs are forerunners of ventricular
tachycardia if they are frequent (> 5/min)
• May feel palpitations or be asymptomatic
Premature Ventricular Contractions
Ventricular Tachycardia
• By definition, VT consists of at least three
consecutive QRS complexes originating
from the ventricles and recurring at a rapid
rate (over 120 beats/min).
Ventricular Tachycardia
• Ventricular tachycardia (VT) is a
tachydysrhythmia originating from a ventricular
ectopic focus, characterized by a rate typically
greater than 120 beats per minute and wide
QRS complexes
• P waves are frequently hidden or may appear as
notches at various points on the QRS-T
complexes, but at a slower rate
• Vagal stimulation has no effect
Ventricular Tachycardia
Ventricular Fibrillation
• Multiple sites in the ventricle fire impulses
in an uncoordinated fashion
• Ventricular fibrillation is a terminal
arrhythmia, uniformly requiring rapid
initiation of emergency measures
Sick Sinus Syndrome
• Sick-sinus syndrome is a general term used to indicate
abnormalities of cardiac impulse formation and intraatrial
and AV conduction that may be manifested by various
combinations of brady- and tachyarrhythmias
• CAD is the most common cause
• Symptoms include none, light headedness, fatigue,
syncope, confusion, CHF or angina
Heart Block
• Often the presenting sign of heart block is
SYNCOPE.
First Degree AV Block
• Impulses originate in SA node
• First-degree AV block is defined as a PR
interval in excess of 0.2 s at normal heart
rates
• QRS follows each P wave
Second Degree AV Block
• Second-degree AV block is characterized by
intermittent failure of conduction from atria to
ventricles and is further subdivided into type I
(Wenckebach phenomenon) and Möbitz type II
second-degree block
Second Degree AV Block Type I (Wenckebach)
• Impulses originating in SA node are conducted
through AV node at progressively slower speed.
• A blocked P wave occurs after 2-5 conducted P
waves and then repeats itself (PR interval
becomes progressively longer until the QRS is
dropped)
Second Degree AV Block Type II (Mobitz)
• In type II second-degree AV block, appropriately
timed P waves fail to conduct, but there is not a
pattern of progressive PR lengthening.
• Prognosis is not good
Third Degree (Complete) AV Block
• Impulses originate in SA node, but none are
conducted through the AV jct.
• In third-degree (complete) AV block, the atrial
and ventricular rates are regular but dissociated
• Maneuvers by the patient, such as arm
movement, standing up, or marching in place,
may increase the sinus rate (P waves) without
corresponding changes in the ventricular escape
rate, confirming loss of AV conduction.
Bundle Branch Block (BBB)
• Impulses originate in SA node, spread
through atria, but are blocked through the
right or left branches of the bundle of His
• Wide QRS
• LBBB is more ominous than RBBB
Wolff-Parkinson-White Syndrome (WPW)
• Impulses originate in SA node, spread
over atria, but bypass the AV jct. through
an accessory bundle with premature
activation of the ventricles
Vasculitis
• Large-Vessel Vasculitis
– Giant Cell Arteritis
– Takayasu's Disease
• Medium-Vessel Vasculitis
– Polyarteritis Nodosa
– Kawasaki's Disease
• Small-Vessel Vasculitis
– ANCA Associated Small Vessel Vasculitis
– Non-ANCA Small Vessel Vasculitis
Small Vessel Vasculitis
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Symptoms
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Fever
Weight loss
Malaise
Myalgias and arthralgias
Dyspnea
Cough (Hemoptysis may be present)
Diarrhea
Nausea or Vomiting
Abdominal Pain
Signs
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Dermatologic findings
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Palpable Purpura (duration longer than 24
hours)
Urticaria
Pulmonary findings
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Interstitial Lung Disease
Pulmonary hemorrhage
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Neurologic findings
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Gastrointestinal findings
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Fecal blood positive
Differential Diagnosis
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Peripheral Neuropathy
Embolic disease
Sepsis
Lymphoma
Leukemia
Myelodysplastic condition
Labs
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Antineutrophil Cytoplasmic Antibodies
(ANCA)
Complete Blood Count (CBC)
Normocytic Anemia
Thrombocytosis
Chemistry profile (e.g. Chem8)
Renal Function tests may show renal
insufficiency
Liver Function Tests
Increased liver enzymes
Fecal Occult Blood
Urinalysis (Glomerulonephritis)
Hematuria
Proteinuria
Murmurs:
• S-1 (T/M) ---Systole--- S-2 (A/P)---Diastole---S-1
• Systolic Murmurs: “Big Deal”
– May be normal variants
– May indicate pathology
• (Midsystolic) Aortic / Pulmonic Stenosis
• (Pansystolic - Holosystolic) Mitral/Tricuspid Regurgitation,
Ventricular Septal Defect
• Diastolic Murmurs: BIG DEAL
– (Almost) Always indicate heart disease!
• (Diastolic Rumble)Mitral Stenosis
• (Decrescendo – Immediate Diastolic Murmur)Aortic
Regurgitation
Cardiac Murmurs
• The types of valvular heart disease can be
distinguished by the type of murmur heard
on auscultation
• Stenotic lesions of the aortic and
pulmonary valve have an ejection murmur;
they are systolic in timing, have a
crescendo component and do not
completely fill systole until late ( 12
12 )
Aortic Stenosis (AS)
• Most frequent etiology for AS is senile
calcific stenosis; second is calcification of
a congenital (bicuspid) valve; third is
rheumatic heart dis.
• Sx include syncope, angina, SOB, CHF
• Signs include ejection murmur at right 2nd
ICS, weak and delayed peripheral pulses
• Diagnosis is by ECHO
Aortic Insufficiency
• SOB, palpitations, angina
• Signs include a diastolic murmur that is
“blowing” and soft, elevated systolic BP
and low diastolic BP
• CXR shows signs of CHF and/or
cardiomegaly
Mitral Stenosis (MS)
• Usual etiology for pathology is postrheumatic heart disease
• SOB, DOE, PND, which are all part of
CHF
• Murmur is diastolic with an opening snap
(due to stiff, thickened valves) followed by
a low pitched rumbling sound best heard
at the apex or left sternal border. (  2-3 )
Mitral Stenosis (MS)
• EKG may show notched P waves
indicating left atrial enlargement
• Diagnosis is by ECHO and cardiac cath
• Indications for surgery include sx,
presence of transvalvular gradient,
measured by catheter, of > 4 mm Hg.
Mitral Regurgitation
• Symptoms of dyspnea, fatigue, left
ventricular failure
• Left ventricle eventually becomes
compromised leading to cardiac dilatation
• Murmur is pansystoloic, max at apex and
radiating to axilla, blowing in quality with
prominent 3rd heart sound
• Echo
Tricuspid Stenosis (TS)
• Most frequent etiology is congenital,
RHD, neoplasms
• Right atrium is  , atrial fib is frequent
• EKG shows atrial fib and right atrial 
• Dx can be made by Echo
Tricuspid Regurgitation (TR)
• Most frequent etiology for TR is
physiologic, as a reflection from left sided
heart disease; endocarditis, especially in
drug addicts (60% are due to Staph
aureus)
• Murmur low pitched, blowing, pansystolic,
worse with inspiration and heard along left
sternal border
Endocarditis
• Infective endocarditis is a microbial infection of the
endocardium, usually a subacute bacterial endocarditis
(SBE)
• Most pts have underlying organic heart dis (abnormal
valves, septal defects);High incidence seen in IV drug
users
• Nonspecific symptoms of cough, dyspnea, arthralgia,
diarrhea, pallor, splenomegaly, abd./flank pain from emboli
• Petechiae on palate or conjunctiva or in nail beds, splinter
hemorrhages
• 90% have heart murmurs and a changing murmur with
leukocytosis is common
Endocarditis
• Blood cultures are the definitive diagnostic
procedure; may be falsely negative in 5%
• Echo confirms the vegetations
Myocarditis: Inflammation of the
myocardium
• Etiology usually caused by infection (viral, most
common); toxins, drugs, radiation, immunologic
reactions. Often follows a URI
• Typically present with heart failure following a
febrile illness or with heart failure alone
• Symptoms:
– fatigue, dyspnea, palpitation, precordial pain through
the first few weeks of the infection
Hypertension
Essential Hypertension
• No known cause
• There is a natural progression of the disease
suggesting early  in blood volume and cardiac
output might cause  resistance
• This could be mediated by enhanced
sympathetic activity or by  circulating levels of
angiotensin II
Secondary Hypertension
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Renal artery stenosis
Chronic renal disease
Primary hyper-aldosteronism
Hyper or hypo thyroidism
Pheochromocytoma
Pre-eclampsia
Aortic coarctation
BCP use
Disease of the Aorta
Aneurysms
• Local dilation of the aorta resulting from
weakness of the wall with distention
• Most common etiology is atheroma; more
recently evidence of Chlamydia
pneumoniae has been found
• 90% of aortic aneurysms are abdominal
• Best noninvasive method is ultrasound
(98% accurate on determining size)
Rupture rate of aneurysm at 5
yrs
Size of aneurysm
% rupture rate
7 cm or greater
75%
6-7 cm
35%
5-6 cm
(less than 5 cm)
25%
(insufficient data)
Signs and Symptoms of AAA
• Aneurysms < 5 cm are usu asymptomatic
• Pain in abdomen or low back
• Pulsatile mass (many thin patients will
have a pulsatile mass that is normal)
• Tenderness over the pulsatile mass
• Bruit over the mass (also can be heard in
normals)
Aortic Dissection
• Occurs in ascending aorta; caused by a break
in the intima allowing blood to flow in a plane
between the media and adventitia
• Pain is severe, chest or neck; may radiate to
back and later to abdomen
• Peripheral pulses and BP may be unequal
• Syncope, hemiplegia or paralysis of the lower
extremities may occur
• CT and transesophageal echocardiography
Inflammatory Pericarditis
• Most cases are idiopathic or have a viral
etiology
• Patients typically complain of sharp central
chest pain that worsens with recumbency and
is relieved by leaning forward
• Pain may be pleuritic in nature and may radiate
to the trapezius muscle
• Patients may reveal the pathognomonic finding
for pericarditis: the pericardial friction rub
• ECHO is a more accurate test
Cardiac Tamponade
• Results from accumulation of fluid in the
pericardial sac; the heart has an inability to
contract due to space restriction
• Chest pain, dyspnea, cough, tachycardia,
tachypnea, pulsus paradoxus (fall in BP > 10
mmHg with inspiration), edema and ascites may
be seen