Download Anterior wall myocardial infarctions are associated with an

Anterior wall myocardial infarctions are associated with an increased risk of arterial
thromboembolism. Therefore, these patients require full doses of heparin when they are
hospitalized, followed by 3 months of warfarin therapy. Other indications for chronic
anticoagulation in the setting of acute MI are the presence of a mural thrombus, atrial
fibrillation, history of systemic embolization, congestive heart failure, and severe LV dysfunction.
This thrombus can occasionally embolize to the extremities. The onset is usually sudden and
associated with a cold leg without any pulses. The lesion is
usually identified by angiogram. The best treatment for this patient is an
embolectomy, which can be performed under local anesthesia.
Anticoagulation must be continued with heparin. Distal pulses must
routinely be checked in all patients who suffer an MI
The role of fibrinolytic therapy for embolic disease has
been disappointing. This therapy can be associated with significant
bleeding and has to be administered over a period of several hours. The
therapy does not always work and may delay resolution of symptoms.
Embolectomy is a quick procedure and has immediate results.
Recently, intra-arterial thrombolysis has become an alternative to surgical
embolectomy. The choice depends on several factors. If the patient has a
clot in the proximal arteries, such as bifurcation of the common femoral
artery, embolectomy is better, whereas, for embolus in distal arteries such
as the tibial artery, intra-arterial thrombolysis may be a good alternative.
(Choice B)
In general, intravenous heparin should be started immediately
in all patients with a high index of suspicion for embolism. However, it is not
the definitive therapy.
Patients who
have arterial occlusive disease generally hang their legs over the side of
the bed.
Patients who suffer an MI and develop a cold leg need an
echocardiogram. The thrombus is generally found on the left ventricular
wall. Patients with an MI can also develop a left ventricular aneurysm,
mitral regurgitation or ventricular septal perforation. Echocardiography is
diagnostic for these complications. It also determines the left ventricular
ejection fraction and the presence of pericardial effusions, if any. However,
in a patient with a cold leg, with a confirmed angiogram, an embolectomy
carries a higher priority. The majority of left ventricular thrombus after an MI
will resolve with anticoagulation therapy. Echocardiography is required to
follow these patients.
Age-dependant idiopathic sclerocalcific changes are the most frequent
cause of isolated aortic stenosis in elderly patients. These changes are
common and usually have minimal hemodynamic significance, but
sometimes may be severe.
In patients who present with stable angina and hypertension, a betablocker is the drug of choice.
Question ---------------------------------------------------------------------A 65-year-old white female, with chronic congestive heart failure, was
admitted for community-acquired pneumonia. She is receiving aspirin,
digoxin, furosemide, levofloxacin, and oral simvastatin. She is feeling better
and her pneumonia is resolving. While planning for discharge she
developed recurrent sustained ventricular tachycardia with stable vital
signs during the nighttime. The patient has recieved amiodarone and now
is stable in sinus rhythm. A recent echocardiogram showed an ejection
fraction (EF) of 35%. What is the most important next step in the
management at this stage?
A.Add beta blocker
B.Add spiranolactone
C.Measure serum electrolytes
D.Stop simvastatin
E.Discharge the patient
Normal Labs
Explanation:
When someone is having recurrent VT, first thing to do after stabilizing the patient is to search
for underlying cause. This patient, most likely, has an electrolyte imbalance due to diuretics.
Furosemide commonly causes hypokalemia, which may lead to digoxin toxicity. Therefore,
ordering serum electrolytes and serum digoxin level is the most reasonable approach.
Adding a beta-blocker is a good thing for chronic heart failure but not the next step in this
case.
Spironolactone is a potassium sparing diuretic that is not indicated at this
stage.
The most probable diagnosis in this patient is situational syncope related to
micturition. The scenario described (middle age or older male with prostatic
hypertrophy, who lost his consciousness after awakening and voiding at
night) is typical for this type of syncope. The pathophysiologic mechanism
underlying the situational syncope includes autonomic dysregulation, which
can be partially explained by straining and rapid bladder emptying.
Cardioinhibitory and/or vasodepressor mechanisms may be involved.
Cardiovascular causes like arrhythmia (Choice A) are less likely because
there are no signs of a structural heart disease on the physical examination
and the ECG.
Situational syncope should be considered in the differential diagnosis of syncopal episodes.
The typical scenario would include a middle age or older male, who loses his consciousness
immediately after urination, or a man who loses his consciousness during coughing fits.
Always suspect malignant hypertension in patients with very high blood
pressure (>/= 200/140 mmHg). Presence of papilledema on
ophthalmoscopy confirms the diagnosis. The pathologic change
responsible for end-organ damage in malignant hypertension is
fibrinoid
necrosis
of small arterioles.
papilledema should be present in order to make a diagnosis of
malignant hypertension. Renal failure with elevated creatinine level
(Choice B)
and oliguria
(Choice D)
can develop rapidly in this case without
treatment, but its presence is not required to diagnose malignant
hypertension. Left ventricular hypertrophy on ECG
(Choice A)
is not a
diagnostic criterion for malignant hypertension.
The presence of a left to right shunt, with an oxygen step up at the level of
the right ventricle, will confirm the diagnosis of ventricular septal rupture.
Presence of a left to right shunt differentiates ventricular septal rupture
from other mechanical complications of acute MI particularly acute MR,
which can also produce a pansystolic murmur.
‘V’ waves in the pulmonary capillary wedge pressure tracing may be
present in MR but not in ventricular septal rupture.
The diagnosis of ventricular septal rupture can be made if there is evidence
of left to right shunting on Swan-Ganz catheter readings, when a 2D-echo
is not available.
Viral or idiopathic
myocarditis is most commonly seen following Coxsackie B infection. Viral
myocarditis is seen in about 3.5-5 % of patients infected with Coxsackie B
virus. Other viruses implicated are adenovirus, cytomegalovirus, echovirus,
hepatitis C, influenza virus, parvovirus B-19, and Epstein-Barr virus. The
diagnosis is made by echocardiogram, which typically shows dilated
ventricles with diffuse hypokinesia resulting in low ejection fraction (systolic
dysfunction). Viral myocarditis can cause dilated cardiomyopathy by direct
viral damage, as well as sequel of humoral or cellular immune responses to
persistent viral infection.
Eccentric hypertrophy of the heart is seen following chronic
volume overload, as seen in valvular regurgitation
Hypokinesia of the inferior wall would be seen in case of
inferior wall myocardial infarction
Procainamide is a class I A drug used to treat atrial and ventricular arrhythmias. it has few side
effects including:
nausea, lupus like syndrome, agranulocytosis and prolonged QT. It does not cause lung fibrosis.
Quinidine is a class I A anti arrhythmic agent used in the treatment of atrial arrhythmias. It
does have a few well-known side effects including:
diarrhea, tinnitus, prolonged QT, torsades, hemolytic anemia and thrombocytopenia. It does not
cause lung fibrosis.
Lidocaine is a Class I B anti arrhythmic agent used in the treatment of ventricular arrhythmias.
High doses can cause: confusion, seizures, and respiratory depression. It does not cause lung
fibrosis.
Please remember the 5 common side effects of the amiodarone class III: It is an excellent drug
for both atrial and ventricular arrhythmias but the multiple side effects limits its long-term use.
1- Pulmonary toxicity: Pulmonary toxicity is associated with total cumulative dose rather
than the serum drug levels. Longer the use of amiodarone, the higher the chance that
patient develops pulmonary fibrosis.
“Three months later he returns with dyspnea on exertion, and chest-x ray reveals
bilateral lung fibrosis. All cultures are negative and a lung biopsy reveals lipoid
pneumonitis”.
2- Thyroid dysfunction: It can also cause thyroid dysfunction including both
hypothyroidism (most common, 85%) and hyperthyroidism (15%). Since, the thyroid
dysfunction is so common with the amiodarone, patients should have TSH level checked
before starting treatment and every 3-4 month intervals.
3- Hepatotoxicity: Transient elevation of aminotransferases occurs in upto 25% of
patients. These patients are usually asymptomatic; however, the drug should be
stopped if there is more than 2 fold elevation of aminotransferases.
4- Corneal deposits: Corneal deposits occur in most patient’s receiving amiodarone
because the drug is secreted by lacrimal gland. Most patients do well without problems
with visual acuity. Presence of corneal deposits is not a contraindication.
5- Skin reactions: Skin reactions, specifically a bluish-slate gray discoloration of the skin
(usually most prominent on the face) is also seen.
In cases of restrictive cardiomyopathy:
chest x-ray shows only mild or no enlargement of the cardiac silhouette.
Echocardiography shows a symmetrically thickened ventricular wall, a normal or slightly reduced
ventricular cavity size, and a normal or near normal systolic function.
Regarding the cause of restrictive cardiomyopathy in this patient,
the appearance of ‘speckled pattern’ suggests the diagnosis of cardiac amyloidosis.
This patient is most likely suffering from a combination of primary amyloidosis and myeloma
suggested by the combination of bone pain, hypercalcemia, and renal failure.
Isolated systolic hypertension (ISH) is an important cause of hypertension
in elderly patients. The pathophysiologic mechanism leading to ISH is
believed to be decreased elasticity of the arterial wall, which leads to
an increased systolic blood pressure, without concurrent increase (and
even decrease) in diastolic blood pressure. Normally during systole, the
heart ejects the blood under a certain pressure that is dumped by elastic
properties of the aorta and major arteries. Then, this elastic recoil of the
arterial wall contributes the diastolic flow of the blood and diastolic
pressure. When elastic properties of the arterial wall diminish and arteries
become more rigid, this ‘dumping’ of pressure changes during the cardiac
cycle also decreases. As a result of increased arterial rigidity, patients with
ISH have a widened pulse pressure (the difference between systolic and
diastolic pressure). Widened pulse pressure was recently recognized as an
important cardiovascular risk factor. Therefore, ISH should be treated
appropriately, in spite of the fact that diastolic pressure is not elevated.
The initial drug of choice, for these patients, is a low-dose thiazide diuretic.
Long acting dihydropyridine calcium channel blockers are an
acceptable alternative, but they are more expensive.
An increased cardiac output can be a cause of systolic
hypertension in hyperdynamic states, such as in hyperthyroidism. There is
no sign of hyperdynamic circulation in this case.
Whenever a patient of chronic aortic regurgitation develops symptoms of
LV dysfunction, he should undergo aortic valve replacement after his
congestive symptoms are relieved by intense medical treatment with
digoxin, diuretics, and vasodilators (ACE inhibitors).
Acute aortic regurgitation is an emergency and requires emergent surgery.
Sodium nitroprusside or inotropes like dopamine or dobutamine are used to
stabilize this condition before emergent surgery can take place.
Jervell-Lange-Nielson syndrome:
is one of the congenital ‘QT’ prolongation syndromes caused by molecular defects in ion
channels.
It is an autosomal recessive disease characterized by congenital deafness and QT interval
prolongation on EKG (torsades de pointes= polymorphic ventricular tachycardia, is often selfterminating but may degenerate into frank ventricular tachycardia and cause syncopal episodes
and sudden death.
The clues to the correct diagnosis in this patient are a syncopal episode without following
disorientation (post-episode confusion is more characteristic for a seizure), hearing impairment
and family history.
The most commonly used treatment modality for these patients is a beta-blocker like
propranolol.
* If the patinet is asymptomatic, or does not have a clearly documented syncope, beta blocker
alone is sufficient.
* If the patient is symptomatic, or has a documented episode of syncope, the treatment will be
beta-blocker plus a DDD pacemaker.
NOTE; Quinidine is an anti-arrhythmic agent that prolongs QT interval; therefore it is
contraindicated in this case.
Hypertrophic cardiomyopathy is the most common cause of sudden cardiac death (SCD) in
young athletes.
Congenital anomalies of coronary arteries, arrhythmogenic right ventricular dysplasia, atrial
septal defect, and Ebstein’s anomaly are all important causes of SCD in young athletes but they
are far less frequent than hypertrophic cardiomyopathy.
Patients with artificial pacemakers and defibrillators do not require prophylaxis for infective
endocarditis.
The presence of hyponatremia indicates that the heart failure is severe:
Water retention and the associated reduction in the plasma sodium concentration parallel the
severity of the heart disease; they reflect the degree of neurohumoral activation in patients with
heart failure. Low serum sodium level is associated with high levels of renin, aldosterone,
vasopressin, and norepinephrine.
As a result, a patient's survival is significantly reduced if the serum sodium level is below 137
mg/dL. Decreasing the intake of water, not increasing sodium intake , can help to control the
electrolyte abnormalities.
The American Heart Association recommends that all
school and collegiate athletes be offered pre-participation screening, by a
skilled healthcare worker.
Noninvasive investigations like 12 lead EKG, echocardiography, and
exercise testing have a low sensitivity (many false positives) in this low risk
population and are not cost effective. Therefore, they are not
recommended for routine screening of such a large population. A detailed medical history and
physical examination is the most effective
way to screen a low risk population for the presence of underlying cardiac
disease.
A 52-year-old white male presents to emergency room for palpitations and light-headedness.
His vitals are, BP: 110/76 mm of Hg; HR: 170/min; RR: 28/min=> determisn: supra or ven? Look
at the narrow complex QRS morphology =>
This patient has classic supraventricular tachycardia. SVT is usually recognized by a HR of
>140/min, regular, loss of ‘P’ waves and narrow QRS complex.
* if the patient is stable=> 1) vagal maneuvers should be attempted initially. If these fail to
convert him to normal sinus rhythm=>
2) IV adenosine push is the drug of choice. Verapamil is no longer the drug of choice for this
purpose but can be used as a second line drug.
Clinical features of right ventricular infarction include jugular venous distension, Kussmaul’s
sign, hepatomegaly, and hypotension in the presence of clear lung fields. Sometimes tricuspid
regurgitation is also present. Along with inferior or inferoposterior MI (ST elevation), EKG shows
ST segment elevation in right-sided leads (V4R, V6R), especially in V4R, which is indicative of
acute right ventricular injury. Greater elevation of ST in lead III than lead II also suggests the
diagnosis of right ventricular infarct.
The underlying mechanism for the clinical findings of a right ventricular infarct lies in the fact
that the right ventricle becomes less compliant resulting in: decreased filling and stroke
volumes of the right ventricle with a resulting elevated central venous pressure. Right ventricle
also becomes
dilated and tricuspid regurgitation may develop. As a result of the
decreased right-sided stroke volume, there is decreased filling of the left
ventricle and hence decreased contraction and cardiac output. Left sided
filling pressures are low, as well, and pressures in the right atrium are high,
thus the lungs are clear.
The right ventricle is normally thinner than the left, as its workload is much
less. Therefore loss of its diastolic, not systolic, function gives rise to the
symptoms of right ventricular infarction.
Prinzmetal's angina. She
presented with a classic picture of this disease, with absence of risk factors
of coronary artery disease, night pain waking her up from sleep, transient
ST elevation on the EKG, absence of Q waves and negative cardiac
enzymes.
The study of choice for diagnosis and follow-up of abdominal aortic aneurysms is an abdominal
ultrasound. It allows for the measurement of the size of the aneurysm, as well as it can show
the presence of an associated thrombus.
In patients with hyperthyroidism-related tachysystolic atrial fibrillation, a
beta-blocker is the drug of choice.
Dipyridamole can be used during myocardial perfusion scanning to reveal
the areas of restricted myocardial perfusion. The redistribution of the
coronary blood flow to ‘non-diseased’ segments induced by this drug is
called coronary steal phenomenon.
Mitral valve prolapse is the most common cause of mitral regurgitation in USA.
acute cardiac tamponade secondary to a rupture of the free left ventricular wall. The presence
of
pulsus paradoxus and pulseless electrical activity are important diagnostic clues.” neck veins are
distended and measurement of blood pressure shows an 18 mm drop of systolic blood pressure
with inspiration, The EKG monitor shows sinus tachycardia”
Sometimes heart sounds become inaudible due to the accumulation
of blood within the pericardial cavity. Free wall rupture usually occurs in the
first week after MI. Risk factors include advanced age, large Q wave
infarct, a history of HTN, and no prior history of angina pectoris.
In HCM (AD on 14):
Valsalva maneuver and standing after squatting are two maneuvers that intensifying the
associated systolic murmur. On handgrip increases the systemic arterial resistance and thus
decreases the gradient and associated systolic murmur. Phenylephrine also decreases the
murmur by increasing systemic arterial pressure.
Leg elevation increases the left ventricular volume and thus decreases the gradient and the
associated murmur.
in HOCM it is the systolic anterior motion of mitral valve leaflet that causes mitral regurgitation.
First-degree heart block is a completely benign arrhythmia and requires no treatment.
If the edema is significant, the drug should be
discontinued. The clues to the correct diagnosis in this case are the
therapy with a dihydropyridine Ca-channel antagonist, amlodipine initiated
recently, and normal physical examination with normal laboratory findings.
Thus any patient who has atrial fibrillation and heart failure will benefit from
digoxin; it should be considered over before beta-blockers or calcium
channel blockers.
IV dobutamine is used when a patient is in cardiogenic shock.
Norepinephrine is a powerful vasoconstrictor and can lead
to decreased blood supply to both the lower and upper extremity.
Norepinephrine is a powerful pressor drug and frequently used to revive
patients in shock. In addition to decreasing blood supply to the digits, other
organs like the kidneys can also be affected. For this reason, the use of
this vasoconstrictor is limited in the ICU.
Thrombosis of the forearm vessels may
be seen in Buerger’s disease. Buerger’s disease is seen in young males
who are heavy smokers. Digital ischemia and gangrene are common
features.
MVP:
Auscultation of the precordium reveals mid
systolic click with late systolic crescendo-decrescendo murmur. Click and
murmur occurs earlier with Valsalva maneuver and it disappears with
squatting
Beta blockers are used to treat chest pain, palpitations, and autonomic
symptoms of MVP.
Thiazide diuretics are the initial antihypertensive of choice in patients with
Osteoporosis
LV aneurysm can cause CHF in a patient who sustained an anterior wall MI in the past.
A double apical beat and persistent elevation of the ST segment are important
diagnostic clues.
Complete heart block is a dangerous condition These patients are at very high risk for
sudden cardiac death and they should be admitted in ICU and permanent pacemaker
should be placed as soon as possible. Atropine should always be made available at the
bedside.
Chaga’s disease is a condition caused by insect-borne protozoan called Trypanosoma
cruzi, which is a common form of myocarditis in Central and South America. Major
clinical manifestations may appear after a latent period of more than a decade. At this
stage, patients usually present with cardiomyopathy, conduction abnormalities, and
certain death. This patient has classic features of cardiomyopathy. Almost all these
patients will have a have a history megacolon or mega-esophagus.
In both constrictive pericarditis and pericardial tamponade, right and left sided diastolic
pressures are equal and elevated (external compression)
Dressler’s syndrome, an autoimmune pericarditis, is a late complication of acute MI that
usually develops between the second and tenth weeks post MI.
AR:
LVH, LVF: dyspnea, breathlessness at rest. She also had episodes of paroxysmal
nocturnal dyspnea. Auscultation of lungs shows bilateral crepitations.
RVF; She noticed bilateral ankle swelling a week ago that became progressively worse.
Examination shows jugular venous distension,
- BP is 140/66 mmHg, rapidly rising carotid pulse with a sudden collapse and bilateral
ankle edema. Her apical impulse is heaving and displaced inferolaterally. Cardiac
auscultation shows an S3 gallop as well as a high-pitched, blowing, early diastolic
decrescendo murmur heard best in the left third intercostal space. Leaning forward
and holding the breath in expiration intensifies the murmur.
dilated cardiomyopathy secondary to alcoholism. Findings of thrombocytopenia,
macrocytosis, and elevated transaminases are all suggestive of alcoholism in this patient
Tapping apex beat and malar flush are important physical findings of mitral stenosis.
Pulsus paradoxus and hypotension point toward the diagnosis of pericardial tamponade.
Pulsus paradoxus is uncommon in constrictive pericarditis unless an effusion is
present. It may also be present in severe airway obstruction and superior vena cava
obstruction
The treatment of ventricular fibrillation is STAT defibrillation with 200-360 joules. If
defibrillation fails, lidocaine or amiodarone (drug of choice) can be loaded and the
patient shocked again. Epinephrine can sensitize the heart and lower the threshold for
conversion.
It has been found that prevention of recurrent attacks of rheumatic fever may slow down
the progression of mitral stenosis. Therefore, penicillin prophylaxis with monthly IM
injection of benzathine penicillin is recommended in adolescent patients in whom
the recurrence risk is high. Patients with, or without, carditis need penicillin
prophylaxis, although the recommended duration of prophylaxis is 10 years in the
former and 5 years in the latter. Patients with mitral stenosis are also at high risk for
thromboembolism. Anticoagulation is indicated if they have a history of an embolic event
or they have intermittent or chronic atrial fibrillation.
Antihypertensive management should be the first step in patients with aortic dissection
with hypertension. (Don’t measure enzymes if it is ST Depression).
only ACE inhibitors, aspirin, and beta-blockers have been shown to reduce mortality
after acute MI
ST segment depression, T wave inversion and first degree AV block can occur at
therapeutic levels of digoxin and they do not represent digitalis toxicity and therefore
there is no need for discontinuation of the drug.
Atrial tachycardia along with variable degree of AV block is the most important
EKG finding of digitalis toxicity and it has a high specificity for digitalis toxicity
Severe diastolic dysfunction is present in restrictive cardiomyopathy due to rigid
and stiff ventricle wall. Systolic function is preserved in this condition.
Severe systolic dysfunction and increased left ventricle size are features of dilated
cardiomyopathy.
Supernormal ejection fraction is present in hypertrophic cardiomyopathy as is dynamic
outflow obstruction. Diastolic dysfunction is present in HCM, due to the stiff,
hypertrophied ventricle wall.
T6 + T20-31
--------------T7
In patients presenting with significant peripheral vascular disease, calcium channel blockers are
preferred as anti-hypertensive Doxazosin is an alpha-blocker with a favorable metabolic profile.
It is not considered as a first-line drug in the treatment of hypertension, because the long-term
effects of alpha-blocker therapy are not clear. Moreover, some side effects of the alpha-blocker
therapy may be disturbing (e.g., orthostatic hypotension).
A 65-year-old American male is brought to the emergency room
for the sudden onset of severe substernal chest pain associated
with severe shortness of breath that started 40 minutes ago. He
says that the pain radiates to his left arm. He had 2 episodes of
vomiting at home and is diaphoretic. His pain is not relieved with 4
baby aspirins and 5-sublingual nitroglycerine tablets. His initial
EKG has shown diffuse ST elevation in the inferior and lateral
leads. He is started on IV Morphine and oxygen 4L/minute. His
exam shows muffled S 1, S2 and the presence of S3. Bilateral
crackles are heard halfway up to the lungs. There is obvious
jugular venous distension and 2+ pedal edema bilaterally. Stool
hem test is (FOBT) is negative. His vitals are BP: 110/70 mm Hg;
PR: 56/min; RR: 32/min; Temperature: 36.9(98.4F). His oxygen
saturation is 91% on 4L oxygen. The patient receives t-PA and IV
heparin. Which of the following is the most beneficial next step in
the management of this patient?
A.IV metoprolol
B.IV digoxin
C.IV furosemide
D.Low dose enalapril
E.IV normal saline
Normal Labs
Explanation:
This patient has acute heart failure resulting in pulmonary edema
in the setting of an acute infero-lateral MI. Even though IV betablockers improve mortality in acute MI, they are contraindicated in
the presence of pulmonary edema. Furthermore, the patient's
pulse rate is only 56/minute, which is not uncommon in inferior
infarctions. Other absolute contraindications to their use include
asthma, hypotension, severe bradycardia and heart block greater
than first degree.
Diuretics are the drugs of choice in this patient. The most
commonly used agent is furosemide. They rapidly relieve the
pulmonary edema by decreasing the preload and pulmonary
capillary pressure. Furosemide causes venodilation that occurs
earlier than the diuresis and this helps to decrease preload rapidly.
Digoxin is useful in the setting of chronic congestive heart failure
and it is not useful for the treatment of acute cardiogenic
pulmonary edema. Therapy with digoxin, in the setting of chronic
congestive heart failure, does not improve survival but it provides a
symptomatic benefit for patients with systolic dysfunction and
sinus rhythm. It is also used to control ventricular rate in patients
with heart failure who have atrial fibrillation.
IV fluids should not be used in this patient, as they will worsen the
heart failure by increasing the preload. IV fluids are used in the
setting of a right ventricular infarct that can be associated with an
inferior wall MI.
ACE inhibitors have been shown to improve survival in patients
with MI and therefore, are used routinely. They produce their
beneficial effect by decreasing the ventricular remodeling and thus
prevent the worsening of the left ventricular dysfunction.
Contraindications to their use include allergy to ACE inhibitors,
renal failure (Cr of>2.5-3.0), bilateral renal artery stenosis,
hypotension, and previous failure of ACE inhibitors. The above
patient has hypotension and therefore ACE inhibitors are
contraindicated. They improve survival in patients with congestive
heart failure but they are not useful in the acute setting of
pulmonary edema.
Educational Objective:
Know how to treat acute pulmonary edema in the setting of an
acute MI. Loop diuretics should be given to treat pulmonary
edema.
left ventricular aneurysm is a late complication of an acute MI. It usually occurs after an anterior
wall MI and may be: either asymptomatic, or it may present with congestive heart failure, an
arterial embolism, or sustained ventricular arrhythmias. Precordial examination may show a
double apical beat. Auscultation of the heart may reveal an additional S3 or S4 and sometimes
a murmur of mitral regurgitation is present due to papillary muscle dysfunction, annular
dilatation, or abnormal left ventricular geometry. Chest x-ray usually shows a characteristic
prominence of the left border of the heart. The EKG shows persistent ST segment elevation.
Thrombolytic therapy is indicated when the chest pain is suggestive of MI and there is ‘ST’
segment elevation greater than 1 mm in two contiguous leads after sublingual nitroglycerin
administration to rule out coronary vasospasm
If the PVC complexes
have the same morphology, they are referred to as "unifocal"; if of
different morphologies, "multifocal". When they are frequent, as
shown in this strip, they may alternate with a sinus beat and the
rhythm is then called bigeminy
The presence of a tapping apex beat, a loud first heart sound, and a mid-diastolic rumble at the
apex suggest the diagnosis of mitral stenosis in this patient
Non Pharmacologic Tx for HTN:
cessation of cigarette smoking is strongly encouraged in patients suffering from HTN but only to
reduce the risk of cardiovascular disease and not to reduce high blood pressure. Weight
reduction in obese patients leads to a significant fall in blood pressure. A clear association has
been found between excessive alcohol intake and development of hypertension. If average
alcohol intake is greater than 2 drinks/day, risk of development of hypertension increases by
1.5-2 times compared to the general population and the risk increases substantially if the
average alcohol intake is greater than 5 drinks/day. On the other hand moderation of alcohol
intake to 1-2 drinks per days also has been shown to have a cardioprotective effect.
Nitrates are contraindicated when a patient is continuously or
intermittently taking sildenafil (Viagra). In such settings nitrates
may cause syncope, MI, or sudden death when a patient has an
acute coronary syndrome. It is recommended not to use nitrates
within 24 hours of the last dose of sildenafil. The reason for the
dangerous interaction between nitrates and sildenafil is that both
induce nitric oxide mediated vasodilatation.
Atrial myxoma: presents with systemic symptoms, exertional dyspnea and auscultatory findings
similar to MS, but there is no opening snap. The murmur of atrial myxoma changes with
position. These patients are at high risk for systemic embolization.
clinical syndrome in
which sinus node dysfunction produces symptomatic
bradyarrhythmias, including sinus bradycardia, sinoatrial block and
sinus arrest either singly or in combination. Symptoms may range
from syncope, dizziness, confusion, and congestive heart failure.
Management of sick sinus syndrome involves elimination of significant bradycardia as well as
suppression of any associated atrial tachycardias. This is easily done by utilizing a single lead
ventricular pacemaker. Once the ventricle rate is under control, the atrial tachyarrhythmias can
be controlled with type 1 anti arrhythmic drugs (When a patient with sick sinus syndrome
develops symptoms, treatment is necessary. There is little place for vagolytic therapy (atropine)
or isoproterenol in the management of this condition. These agents are transient and are not
the solution in long-term management of symptomatic patients. )Provocative stress testing
plays a role in the diagnosis of sick sinus syndrome, but once the diagnosis is established, stress
testing is redundant. Treadmill testing can be used to delineate the range of sinus node
responses to exercise. The failure of sinus rate to increase with exercise is abnormal, however
this lack of response does not establish the sick sinus syndrome as the cause of symptoms.
Aortic dissection is a
medical emergency and should be diagnosed and treated. If
hypertension is present it should be treated aggressively before
any diagnostic studies are done.
A 65-year-old Caucasian male presents with a chief complaint of
exertional substernal chest pain radiating to the let arm. Pain is
usually relieved within 5 minutes of rest or within 5 minutes of
single sublingual nitroglycerine. His other medical problems
include type II DM and hypertension. He is a non-smoker and
drinks alcohol occasionally. His medications include metoprolol,
lisinopril, glyburide, and sublingual nitrates as needed. He is doing
well on his anti-ischemic medications. Which of the following
investigations is the most appropriate next step in the
management of this patient?
A.Exercise stress testing
B.Pharmacological stress testing
C.Coronary angiography
D.2D-echocardiography
E.Resting electrocardiogram
F.No testing required
unstable angina (USA) is defined as angina of recent onset, angina at rest, accelerated angina,
post-infarct angina, and post-revascularization angina. A change in the character, severity,
duration of previous stable angina, or failure to resolve with increasing doses of sublingual
nitroglycerin also represents unstable angina.
In unstable angina, EKG may show either ‘ST’ depression, ‘T’ wave inversion, or many times no
changes.
All patients with unstable angina should be hospitalized and treated with aspirin, IV heparin, and
IV nitroglycerin. Once the patient is free of chest pain, an angiography can be performed nonemergently.
constrictive pericarditis are idiopathic (42% in USA), post radiotherapy (31% in USA), post
surgical (11%), connective tissue disorders, neoplasm, uremia, sarcoidosis, etc. Sharp 'x' and 'y'
descent on central venous tracing is characteristic of constrictive pericarditis as is the presence
of pericardial knock (early heart sound heard after S2).
Benzodiazepines are the first-line medication, along with aspirin, and nitrates in the treatment
of cocaine-related cardiac ischemia.
The first line medication for HTN in the general population is either a thiazide diuretic or betablocker.
spontaneous mediastinal hemorrhage due to coagulation abnormality caused by warfarin. The
blood accumulated in the mediastinum causes compression of the surrounding structures
leading to cardio-vascular compromise i.e. mediastinal tamponade. It can also spread towards
the neck causing ecchymoses. Equalization of right and left cardiac filling pressures may be
present in severe cases. Pericardial tamponade can give the same clinical picture and pressure
equalization but it is excluded by the ultrasound.
Nitroglycerine is not used in AS, because it will reduce cardiac output by decreasing LV filling
pressures and it may result in hemodynamic collapse.
All patients have no BP at the onset of ventricular fibrillation and the most immediate step is to
defibrillate as soon as possible. The energy required may be 200-360 joules. More than a few
minutes of delay can lead to permanent brain injury and death. Lidocaine is an excellent agent
for ventricular arrhythmias. In the presence of ventricular fibrillation, cardioversion is the first
modality of therapy. If cardioversion does not initially work, patients may require a lidocaine
bolus followed by a second shock.
C.Amoxicillin (dental, can take the drug orally)
A.Ampicillin(dental, can’t take the drug orally)
E.Clindamycin, or mactrolide(dental, sens to PCN)
B.Ampicillin and gentamicin(lower GI/GU, not sens to PCN)
D.Vancomycin and gentamicin (lower GI/GU, sens to PCN)
The EKG findings that may be present in pericardial tamponade include sinus tachycardia, low
voltage QRS complexes, and electrical alternans. Electrical alternans is characterized by
alternating amplitudes of QRS complexes. It occurs in pericardial tamponade due to swinging of
heart within the pericardium and beat-to-beat change of the QRS axis. Presence of this finding
with the associated hypotension, distended neck veins, and muffled heart sounds represent the
diagnostic criteria for cardiac tamponade. Electrical alternans may also be present in cases of
severe cardiomegaly.
Pulmonary thromboembolism doesn’t present with pulmonary edema. Overhydration is one of
the most common causes of perioperative pulmonary edema.
Diastolic and continuous murmurs as well as loud systolic murmurs revealed on cardiac
auscultation should always be investigated using transthoracic Doppler echocardiography.
Midsystolic soft murmurs (grade I-II/IV)-MVP- in an asymptomatic young patient are usually
benign and need no further work-up.
ischemic symptoms are most likely due his anemia and a blood transfusion is most likely to be
helpful in this patient.
I.V atropine is the drug of first choice in patients with symptomatic bradycardia. Transcutaneous
pacing is the next step after atropine. If the patient has severe bradycardia with hypotension
then epinephrine is the drug of choice; however, it should not be administered if the patient is
hemodynamically stable.
Statin intolerance should be suspected if the patient develops myalgias and elevated serum
transaminases(within few weeks to few months of starting statin therapy). CPK elevation
greater than 10 times normal in the presence of myalgias defines statin induced muscle injury.
Rhabdomyolysis resulting in acute renal failure is an extremely rare side effect of statins and
occurs only when other risk factors are present. Concomitant use of drugs like gemfibrozil,
niacin and cyclosporine increases the risk for the development of myopathy. Other risk factors
include hypothyroidism and hepatobiliary disease. A possible explanation of statin induced
muscle damage is reduction of CoQ10 production by statins and CoQ10 is required for energy
production by muscle cells. Statin intolerance is treated by discontinuation of the drug and
symptoms resolve with return of CPK to baseline within a few days to a few weeks after
discontinuation. Supportive care for rhabdomyolysis is the only treatment needed. When a
patient who is taking a statin develops clinical significant myopathy, statins should be stopped
otherwise his condition may worsen.
Clinical trials demonstrated that prophylactic lidocaine decreases the frequency of VPBs and
diminishes the risk of ventricular fibrillation, but the overall prognosis is unaffected (Choice B).
The problem is that lidocaine can increase the risk of asystole in these patients
In VFib Epinephrine can sensitize the heart and lower the threshold for conversion.
New onset of RBBB indicates PE.
The primary mechanism responsible for the effect of nitroglycerin in patients with anginal pain
is dilation of veins (capacitance vessels). Increased venous capacitance and venous pooling of
the blood lead to significant decrease in ventricular preload and decrease in heart size.
Decreased tolerance to glucose is a well-known side effect of thiazide diuretic therapy. Thiazide
diuretics can also unfavorably affect lipid metabolism by increased LDL cholesterol and plasma
triglycerides
IN Diabetics, SBP<130
Acute atrial flutter with stable hemodynamics can be treated with cardioversion or can be
managed with rate control. Chronic stable atrial flutter is best treated with rate control, which is
best achieved with either calcium channel blockers or beta-blockers.
vasovagal syncope (common faint). This is also known as neurally mediated or neurocardiogenic
syncope. The clinical scenario described is very typical for this condition including prodrome
(lightheadedness, weakness, and blurred vision), provocation by an emotional situation, and
rapid recovery of consciousness. Vasovagal syncope is frequently recurrent. In this case, upright
tilt table testing with or without pharmacologic provocation (isoproterenol) may be indicated to
confirm the diagnosis (although there is no orthostatic hypotension).
Out of all the above medications, only beta-blockers have been shown to decrease
perioperative mortality, probably by decreasing intraoperative myocardial ischemia. This has
been proven in several clinical trials. Their routine use perioperatively in patients with CAD or at
risk of CAD is under consideration. Calcium channel blockers are associated with a slightly
increased risk. They may cause postoperative bleeding due to platelet inhibition. ACE inhibitors
may cause prolonged hypotension postoperatively. Patients on chronic diuretic therapy may
have hypokalemia and hypovolemia intraoperatively. Abrupt withdrawal from centrally acting
sympatholytics may cause severe rebound HTN. These are not first line drugs for treating
hypertension in any setting.
In a young male who presents with an aneurysm of the descending aorta, the most likely cause
is a history of prior blunt chest trauma.
elderly patients very poorly tolerate even what seems to be an insignificant loss of fluid. The
second point is that mild hypovolemia may predispose an individual (especially elderly) to
orthostatic syncope after bed rest (like nighttime sleep) because it takes time for the body to
adjust to the sudden change in the body position. This is caused by getting up from the bed.
Increased BUN/creatinine ratio is a sensitive indicator of the patient’s hydration status, although
it is not very specific
discontinue OCP in HTN (they cause it).
High dose nicotine is giving to increase HDL => it may cause pruritis+flushing (PGlandines dilate
vessels) <= ASA