What 3 positions must be checked in a patient when assessing their blood pressure?

What can be seen morphologically with severe heart disease (no stethiscope or tools required).

Standing, sitting, and lying down.

A "heave" in the chest.

In a supine position, what angle should the patient's head be to aid in veinous return?

What is the clinical advantage of this?

What can be seen in a patient who has heart failure (or kidney or lung disease)?

30 degrees.

Helps with ascultation/palpation of the jugular veinous pulse

When viewed from lateral, the filling level of the jugular will be greater than 3cm of vertical height above the sternal angle.

What sounds are best heard with the diaphragm?

Which are best heard with the bell?

High frequency sounds such as S1, S2, Systolic clicks and high pitched murmors)

Low frequency sounds (3rd and 4th heart sounds)

Where is it best to hear S1 on a patient's chest?

WHEN is S1 possible to be heard?

lower left sternal boarder for tricuspid, PMI for mitral

Before the carrotid upstroke

What occurs during S1?

During each of these events, where should the sound of S1 be MAXIMAL?

What part of the heart cycle does S1 signify?

Mitral valve closure-best heard at the apex of the heart (PMI).

Tricuspid valve closure-best heard at the 4th LEFT intercostal space.

Aortic and pulmonic valve opening-not usually heard.

Systole

On ascultation, you discern that a patient has a "wooshing" noise during S1.  What is this MOST LIKELY to be?

What part of the stethiscope is best used to hear this sound?

A systolic murmor indicating mitral regurgitation.

Diaphragm

What is occurring during S2?

What is best heard during S2?

Start of diastolie, Aortic and pulmonic valve closure.

Aortic valve closure is mainly heard, and thus problems heard are typically aortic in nature.

During deep inspiration, a new heart sound can be heard.  What causes this sound?

When might this sound NOT be heard?

S2 splitting due to the late closure of the pulmonic valve as a result of the increased time of ventricular ejection from the extended filling during diastole (due to the decreased intrathoracic pressure during inspiration).

In a patient with lung problems, the increased lung pressures and right ventricle pressures make it harder to fill the ventricles during diastole.  Because of this, less blood fills the ventricle than would normally, and the pulmonic and aortic valves will close at about the same time.

Which location on the chest is best to hear the:

Mitral valve

Aortic valve

pulmonary valve

tricuspid valve

PMI (left 4-5 intercostals on midclavicular line)

Right between second and 3rd intercostals on sternal boarder

Left between second and 3rd intercostals on sternal boarder

1. Ventricles are empty and have just started expanding; very low pressure (less than 5mmHg).

2. A "blip" of pressure can be seen during atrial ejection.

3. Ventricles are beginning to slow expansion, causing a rise in pressure with continued filling. This is isovolemic contraction.

4. Pressure passes 80mmHg and the aortic valve is opened, starting the ejection phase.  A peak pressure of 120 is reached about midway through ejection, and it continues until pressure drops to about 80 again.

5. ventricles relax and expand as pressure is lowered and the next filling cycle begins.

S1: start of systole just at the point of isovolemic contraction (tricuspid and mitral "slam" shut here)

S2: Start of diastolie just at the end of the ejection phase (aortic and pulmonary valves "slam" shut).

S3: "active relaxation" sound heard in individuals with heart failure due to the heart's attempt to expand its volume actively.  Hypertrophy may decrease ventricular volume, and this is one consequence.

S4: Occurs just after atrial contraction, usually just prior to S1.  Again, a thin structure such as an atria is being asked to contract forcefully against a non-compliant ventricle.

What should the diastolic ventricular pressure be around in a healthy individual?

What about in the aorta?

What does this indicate if higher than normal?

Around 10mmHg

Around 80mmHg

Can indicate heart failure in that the ventricles are not adequately emptying.

When an EKG is lined up to a ventricular pressure curve, when do the Q, R, S and T waves occur in respect to the volume curve?

What does each signal?

P wave occurs just prior to atrial contraction. signals atrial contraction

QRS complex occurs with the start of isovolemic contraction. Signals ventricular contraction.

T wave occurs mid rapid ejection, signals ventricular repolarization.

Where is the best place to hear S3?

S4?

Using the bell, best to hear along sternal boarder.

S4 can be heard everywhere.

What drug class is very helpful in the treatment of patients with heart failure? Why?

Which drug is contraindicated? Why?

Beta Blockers; avoid catacholamine surges which may cause a heart attack by overworking the heart.

Calcium channel blockers (dihydropyradines) because they decrease contractility (negative ionotrope) which is the only thing keeping the heart nourshed enough to work at all!

What is the normal cross sectional area of the mitral valve?

At what diameter is a diagnosis of mitral stenosis appropriate?

During what heart sound would mitral valve stenosis be audible? How would it sound?

4-6cm²

2cm²

S1, sounds like a "whoosh" as blood escapes through the mitral valve during systole. http://www.youtube.com/watch?v=L5DEqvgS_xs

In mitral valve stenosis, what is the most common area to be stenosed?

What about second most common?

The commissure of the valve (30%)

Cuspal region (15%)

What is the pathophysioloy of pulmonary hypertension?

How do these patients present?

1. Passive backward transmission of increased left atrial pressure.

2. Pulmonary arteriolar constriction due to decreased oxygenation.

3. Organic obliterative changes in the pulmonary vascular bed.

4. Increased overall pressure builds over time, eventually leading to right ventricular failure.

What would the effect of mitral valve regurgitation be on the physiology of the heart?

What is the mesurement and the value of this mesurement which prompts surgical intervention?

What is the logic behind this?

Contractility increases due to a decrease in effective afterload pressure, eventually leading to left ventricular hypertrophy.  Ejection fraction starts to decline with these changes.

An ejection fraction around 60%

Surgery mortality is low, and preserving ventricular function by acting sooner will benifit the patient more.

What are the clinical signs seen in a patient with mitral regurgitation?

What usually occurs just BEFORE the onset of these symptoms?

What is an important therapy to institute in these patients? How does this work?

An asymoptomatic patient with Marfan's syndrome is ascultated for cardiac problems.  You hear a mid systolic click (http://www.youtube.com/watch?v=PsmGx2XMxF8).  This is most likely what?

What is the etiology of this condition?

What would be a good therapy (if any) to put this patient on?

Mitral valve prolapse

Myxomatous proliferation and degeneration of valve leaflets brought on because of his genetic condition.

Low dose asprin.

What is the most common cause of aortic stenosis in a patient that is less than 65 years old?

What about in patients older than 65?

A bicuspid (congential) aortic valve (congenital aortic stenosis)

Degenerative (senile) acquired aortic stenosis

What is the critical valve cross sectional area regarding the aortic valve?

At what diameter should these patients undergo surgery to have the BEST prognosis?

0.7-0.8cm²

Best done when the valve area is at 1cm²

A 54 year old male presents in the ER with angina and a blood pressure reading of 165/85.  He was brought in after he fainted when getting out of bed.  You note that he is sitting straight upright and has a quickened respiration rate.  This is most likely:

What therapy should NOT be used?

Aortic stenosis

(Angina, Syncopy and/or CHF)

Should NOT use beta-blockers; the heart NEEDS to work!

Korotkoff sounds

Aortic Stenosis

A patient presents with hypertensive heart disease (167/90) and has an S4 gallop.  There is a normal EKG.  What would be the next things to order?

What kind of heart dysfunction is this primarily?

Echo

Lipid panel

electrolytes

seconary causes of hypertension screening

Diastolic dysfunction

 72 year old male with chronic atrial fibrillation of greater than 10 years’ duration is admitted following a syncopal episode. A 2D echo shows markedly dilated left atrium and LVEF 60%. Telemetry  reveals atrial fibrillation with slow ventricular response and pauses of 4 to 8 seconds associated with near syncope.

          How would you proceed?

A patient presents with a head injury after an episode of syncope.  After her recovery, she is asked about the episode and it is found that she has no history of syncope.

What would be an appropriate next step to find out what is wrong?

Depending on this result, what should be done next?

Test for structural heart disease via an echo or other methods.

If no structural heart disease is found, perform a tilt table test.

If found, do an electrophysiologic study of the heart.

A patient with a single chamber pacemaker has severe hypotension. A blood test shows an increase in ANP levels. What is this patient most likely suffering from?

What should be done?

pacemaker syndrome

Institute a dual chamber pacemaker to allow opening of the mitral and tricuspid valves.

Secondary prevention: Prevention of SCD in patients with prior VF or sustained VT.

Primary prevention: Prevention of SCD in individuals without a h/o VF or sustained VT.

VF/sustained unstable VT not in the setting of a completely reversible cause.

LVEF ≤ 35%, CHF NYHA class II, III.

Ischemic dilated cardiomyopathy, LVEF ≤ 40%, NSVT and inducible sustained VT.

Syncope, LV dysfunction, inducible sustained VT.

High risk patients with: hypertrophic cardiomyopathy, LQT syndrome, RV dysplasia, Brugada syndrome

LVEF ≤ 35%

QRS ≥ 120 msec

NYHA functional Class III or ambulatory Class IV

Optimal medical therapy

58 year old male, CAD, prior MI 1 year ago, LVEF 28%, CHF  NYHA class II, treated with a betablocker, ACE inhibitor and statin; ECG: Sinus rhythm, old anteroseptal MI, QRS 98 msec

Question :  For prevention of sudden cardiac death, you would suggest:

A bi-ventricular ICD

if it was narrow, use a normal ICD

Grade 1Very Faint

Grade 2Quiet, but Heard Immediately

Grade 3Moderately Loud, Not Associated witha Thrill

Grade 4Loud, May Be Associated with aThrill

Grade 5Very Loud

Grade 6May be Heard w/stethoscopeoff chest

RBBB

PVC from Left Ventricle

Normal

LBBB

PVC from Right Ventricle

Paced Beats

On ascultation, you notice a very pronounced and loud S1.  What could this be indictive of?

What if the sound was decreased?

Short PR

Rapid HR

Atrial Fibrillation

Mitral Stenosis

Mitral Stenosis (Immobile Leaflets)

Opposite of Causes of Increased Intensity

RBBB

Pure MR

Healthy Adolescents when in Supine Position

What are the reasons for hearing paradoxial splitting of S2?

What about for S2 increased intensity?

Paradoxical Splitting- P2 before A2

LBBB

Paced Beats

Increased Intensity

A2Systemic HTN

Dilated Aortic Root

P2Pulmonary HTN

Dilated Pulmonary Trunk

Ejection Sound- Usually High Frequency

Aortic Valve- Aortic Stenosis, Bicuspid Aortic Valve

Pulmonary Valve-Pulmonic Stenosis Vary with Respirations

Prosthetic Valves- Mechanical, Not Bioprosthetic

Opening Snap of Mitral Stenosis (MS)

High Frequency-Left Lateral Decubitus Position, Apex

Occurs after S2, before S3

MS More Severe with Short A2-OS Interval

Precordial Knock

Chronic Constrictive Pericarditis

Mitral Regurgitation

Atrial Myxoma

Older Model Prosthetic Mitral Valve

What sound can be heard that is almost pathognomonic for CHF?

Is the bell or diaphragm better to use for this?

S3 (mid diastolic sound)

Bell (low frequency)

During Atrial Phase of LV Filling

Consequence of Ventricular Stiffness

Absent in Atrial Fibrillation or Ventricular Pacing

Low Frequency Sound Best Heart 

At the Apex

Pt in Left Lateral Decubitus Position

HTN, Aortic Stenosis, Ischemic Heart Disease

aortic stenosis-creshendo-decreshendo.

Mitral valve prolapse=creshendo only

What are the characteristic sounds of mitral stenosis?

What is the best way to hear these sounds?

Follows Opening Snap

Low Pitch Rumble

Best Heard 

Apex over LV 

Using Bell of Stethoscope

Pt in Left Lateral Decubitus Position

Arrhythmias

Endocarditis

Left-sided heart failure

Left ventricular hypertrophy (enlargement) caused by the extra work of pushing blood through the narrowed valve

In mitral regurgitation, what percentage of ejection fraction is a SERIOUS risk?

What is the relationship between EF and post operative mortality?

35% or less.

As EF decreases, post surgery mortality increases.

Systolic Murmur

Diamond-Shaped, harsh, left sternal boarder to right intercostal spaces, neck and apex

Late peak, obliteration of S2, consistent with bedside Dx of Critical AS

Pulses Parvus

Delayed and Prolonged Carotid Impulse

How are patients with aortic insufficiency followed?

What are the criteria for surgery?

Follow by Echo Yearly

Endocarditis Prophalaxis for all AR

May not require medical treatment

Symptomatic Patients -valve area 0.7-0.8cm2 or less

Asymptomatic Patients-progressive LV disfunction (EF <35%) or hypotensive response to mild exercise

Delaying surgery in asymptomatic patients with good exercise tolerance is contraversial

What clinical symptoms/diseases are collected under the term Acute Coronary Syndrome (ACS)?

What do they have in common?

Unstable angina

Non-ST-segment-elevation MI

ST-segment-elevation MI

Each condition shares common pathophysiologic origins related to the instability and rupture of artherosclerotic vulnerable plaques

Intense arterial spasm

Progressive, severe, flow-limiting atherosclerosis due to intimal hyperplasia or to lipid, calcium, and thrombus deposition, or to fibrointimal hyperplasia after PCI

Coronary artery dissection

Conditions that alter myocardial oxygen demand or supply, such as intense emotion, tachycardia, or uncontrolled systemic hypertension (secondary MI)

If ischemia is neither severe nor prolonged (usually <20min) and oftern occurs at rest, patients are given a diagnosis of UA

If ischemia lasts longer than 30 minutes and is associated with elevated cardiac markers, the diagnosis of MI is made

Further classification as STEMI or NSTEMI is made on the basis of electrocardiographic findings.

EKG

Most sensitive for STEMI

Age ≥ 65 years?Yes +1

≥ 3 Risk Factors for CAD?Yes +1

Known CAD (stenosis ≥ 50%)?Yes +1

Asprin use in Past 7d?Yes +1

Severe angina (≥ 2 episodes w/in 24 hrs)?Yes +1

ST changes ≥ 0.5mm?Yes +1

+ Cardiac Marker?Yes +1

Clinical history

Physical examination

12 lead ECG

Biochemical marker measurement

Noninvasive risk stratification

Patients who have taken sildenafil, tadalafil, or vardenafil in the previous 24 hours

Systemic hypotension

Marked tachycardia

Severe aortic stenosis

Right ventricular infarct

Bradycardia

Heart block

Asthema

Diabetes patients prone to hypoglycemia

Calcium channel blockers

Dihydropyridines

Nifedipine, amlodipine

Nondihydropyridines

Verapamil, diltiazem

Describe the early invasive strategy and the early conservative strategies for patients with ACS?

When is each best to use?

In the early-invasive strategy, all patients without contraindications undergo coronary angiography with the intent to perform revascularization within 4 to 24 hours of hospital admission.

The early-conservative strategy consists of aggressive medical therapy for patients

An early-invasive treatment strategy is of most benefit to high-risk patients

An early-conservative strategy is recommended for low-risk patients

What are the characteristics of cardiogenic shock?

when does this usually occur?

What is often found on autopsy with this syndrome?

What treatments are possible for this syndrome?

Low output state characterized by elevated ventricular filling pressures, low cardiac output, systemic hypotension, and evidence of vital organ hypoperfusion

Occurs usually after an AMI

At autopsy, more than 2/3 of patients with cardiogenic shock demonstrate stenosis of 75 percent or more of the luminal diameter of all 3 major coronary vessels and loss of about 40 percent of LV mass

Same as tx for LV failure

Intraaortic balloon counterpulsation

Revascularization

What other compilcations can be found in people who develop an intraventricular septal rupture after an acute MI?

What are the characteristic physical findings in patients who have such a rupture?

How can it be treated?

Associated with complete heart block, right bundle branch block, and atrial fibrillation in 20-30 percent of cases

Characterized by the appearance of a new harsh, loud holosystolic murmur

Best heard at the lower left sternal border

Usually accompanied by a thrill

Can be recognized by 2-D echocardiography

Catheter placement of an umbrella-shaped device within the ruptured septum

What are the features that characterize a free wall rupture?

When do these occur?

Elderly

HTN

More frequently occurs in left ventricle

Seldom occurs in atria

Usually involves the anterior or lateral walls

Usually associated with a relatively large transmural infarction involving atleast 20% of the left ventricle

It occurs between 1 day and 3 weeks, but most commonly 1 to 4 days after infarction

Most often occurs in patients without previous infarction

A diabetic, obese woman dies in her living room in a matter of seconds.  Her husband states that she clutched her chest, fell over, and ceased moving and breathing almost immediately.  What did she die of?  What is the pathology of this?

What are the factors that affect the survival in a patient that has this condition?

A free wall rupture-Usually leads to hemopericardium and death from cardiac tamponade

Occasionally, rupture of the free wall of the ventricle occurs as the first clinical manifestation in patients with undetected or silent MI, and then it may be considered a form of “sudden cardiac death”

Survival depends on the recognition of this complication, on hemodynamic stabilization of the patient, and most importantly, on prompt surgical repair

True aneurysm: wide base, walls composed of myocardium and low risk of rupture.

Psuedoaneurysm: narrow base, wall composed of thrombus and pericardium, and high risk of rupture.

Due to partial or total rupture of a papillary muscle

Rare but often fatal complication of transmural MI

Complete transection of a left ventricular papillary muscle is incompatible with life because the sudden massive mitral regurgitation that develops cannot be tolerated

Rupture of a portion of a papillary muscle resulting in severe mitral regurgitation is much more frequent and is not immediately fatal

Frequently accompanies inferior LV infarction or rarely occurs in isolated form

Right-sided filling pressures are elevated, whereas left ventricular filling pressure is normal or only slighty raised

Cardiac output is often markedly depressed

Common among patients with inferior LV infarction

Unexplained systemic arterial hypotension or diminished cardiac output or marked hypotension in response to small doses of nitroglycerine in patients with inferior infarction should lead to the prompt consideration of this diagnosis

Common among patients with inferior LV infarction

Unexplained systemic arterial hypotension or diminished cardiac output or marked hypotension in response to small doses of nitroglycerine in patients with inferior infarction should lead to the prompt consideration of this diagnosis

What are two ways to detect a right ventricular infarction?

Why is this important?

What treatment should be instituted?

Most patients with RV infarction have ST segment elevation in lead V4R (right precordial lead in V4 position)

2-D echocardiography : abnormal wall motion of the right ventricle as well as right ventricular dilitation and depressed RV ejection fraction

In patients with an inferior MI, it is important to know this when thinking about treatment with nitrates which is a large contraindication with a right ventricular MI (decreases preload).

Volume expansion.

Common arrhythmia occuring during the early phases of AMI

Particularly frequent in patients with inferior and posterior infarction

Isolated sinus bradycardia, unaccompanied by hypotension or ventricular ectopy, should be observed rather than treated initially

Atropine should be utilized if hypotension accompanies any degree of sinus bradycardia

What are the characteristics of a 2nd degree heart block? (Mobitz type II)

How is this treated?

Rare conduction defect after AMI

Often progresses suddenly to complete AV block (3rd degree heart block.  This is unlike a 1st degree heart block which doesn't usually progress.)

Treated with a temporary external or transvenous demand pacemaker

What is a common situation to see a pericardial effusion?

Does this cause any sort of hemodynamic compromise such as cardiac tamponade?

More common in patients with anterior MI and with larger infarcts and when congestive heart failure is present

Majority do not cause hemodynamic compromise; when tamponade occurs, it is usually due to ventricular rupture or hemorrhagic pericarditis

What are the characteristics of Dressler syndrome?

When does it usually occur?

What is an effective treatment of this condition?

Post-myocardial infarction syndrome

Usually occurs 1 to 8 weeks after infarction

Patients present with malaise, fever, pericardial discomfort, leukocytosis, elevated ESR,and a pericardial effusion

Cause of this syndrome not clearly established (? Immunopathological process)

Treatment : ASA 650mg Q4hrs

1. A heart rate between 60-100 beats per minute.
2.  The SA node pacing the heart.
3.  Regularity- Regular
4.  A "P" wave must be present for every "QRS" complex in a ratio of 1:1.
5.  PR interval is between .12 second and .20 second.
6.  QRS complex width should be less than .12 second.

The left anterior descending coronary artery (LAD) and it's branches usually supply the anterior and anterolateral walls of the left ventricle and the anterior two-thirds of the septum.

The left circumflex coronary artery (LCX) and its branches usually supply the posterolateral wall of the left ventricle.

The right coronary artery (RCA) supplies the right ventricle, the inferior (diaphragmatic) and true posterior walls of the left ventricle, and the posterior third of the septum.

The RCA also gives off the AV nodal coronary artery in 85-90% of individuals; in the remaining 10-15%, this artery is a branch of the LCX.

[image] ECG changes are seen in anterior precordial leads V1-3, but are the mirror image of an anteroseptal MI:

[image] Increased R wave amplitude and duration (i.e., a "pathologic R wave" is a mirror image of a pathologic Q) 

[image] R/S ratio in V1 or V2 >1 (i.e., prominent anterior forces)

[image] Hyperacute ST-T wave changes: i.e., ST depression and large, inverted T waves in V1-3

[image] Late normalization of ST-T with symmetrical upright T waves in V1-3

[image] Often seen with inferior MI (i.e., "inferoposterior MI") 

[image] Q, QS, or qrS complexes in leads V1-V3 (V4)

[image] Evolving ST-T changes

 Q, QS, or qrS complexes in leads V1-V3 (V4)

 Evolving ST-T changes

but usually V1 is spared; if V4-6 involved call it "anterolateral"

What are the findings on EKG that are characteristic of left ventricular hypertrophy?

When a patient has these characteristics, what other findings on EKG are important regarding other pathology?

R wave in lead 1 greater than 11cm

On any 2 chest leads, combine an R and S wave (one on each) and have a sum of >35mm

None, left ventricular hypertrophy obscures and skews other findings

What usually sets off an episode of AVNRT? (AV Nodal Re-entry tachycardia)?

What is a very useful long term treatment for such patients?

How does this present on EKG?

A PAC (premature atrial contraction)

Beta blockers, Calcium channel blockers.  Slow down heart rate enough for the retrograde signals to be halted.

normal but narrow QRS complex without P waves.

QRS complex longer than 120ms

Prominant R waves in Leads I, aVL, V5 and V6

Hallmark=HUGE negative deflecting S waves

What leads should be used to detect a right bundle branch block?  

What would be seen?

How can this be differentiated from a left bundle branch block

V1 V2 and V3

Positive deflections

V1 is positive in RBBB, not in LBBB

Inferior limb leads (II, III, aVF) should be normal in LBBB

What can be seen in cardiac ischemia that is DIFFERENT from the appearance of an acute MI?

Using leads, how can you tell where the ischemia is?

ST depression

V4,5, and 6=Lateral

II, III, and aVF=inferior

An anomalous pulmonary vein can develop, delivering unoxygenated blood to pulmonary return. (sinus venosus)

Mitral valve defect, particularly mitral regurg. "endocardial cushion" today known as an AV valve (cleft mitral valve).

Dilated right atrium, ventricle and pulmonary artery.

A constant split of S2.

How can you distinguish an ASD from a VSD?

What can happen with a sizable VSD?

How can one distinguish from a patient foramen ovale?

No dilation of right atrium in VSD, but dilation of right ventricle and pulmonary artery.

Kids with VSD typically go into heart failure. "Size is everything".  Also, age of occurance determines how worrisome this complication is.

No dilation of the right heart, only in pulmonary vasculature.

What is Eisenmenger's complex?

What causes the main complication in this disease, and what often kills these patients?

Change from left to right shunt, to a right to left shunt.  Occurs after a long ASD or VSD. Cyanotic lesion.

Pulmonary hypertension

In which gender is a coarctation more common?

What can be seen on X-ray?

What is this associated with?

What is one typical clinical presentation especially seen in kids?

MORE COMMON IN MALES

RIB NOTCHING OCCURS DUE TO PHYSICAL ERROSION OF THE UNDERSURFACE OF THE RIBS AS A RESULT OF INTERCOSTAL COLLATERAL CIRCULATION

ASSOCIATED WITH  BICUSPID AORTIC VALVE

Systolic ejection murmur (aortic stenosis) as well as pain in the legs after running.

What are the 4 clinical findings of Tetrology of Fallot?

What do children tend to do with this disorder?

1)  INFUNDIBULAR STENOSIS

2) VENTRICULAR SEPTAL DEFECT

3) RIGHT VENTRICULAR HYPERTROPHY

4) OVERRIDING OF THE AORTA 

High incidence of ASD as well.

Children tend to "squat" as they get short of breath to aid in veinous return.

TUMOR

Trauma

Uremia

MI

Other infections

Rheumatic disease

A syndrome consisting of fever, pericarditis and pleuritis often occurring after an MI or cardiac surgery.

Treat with high dose asprin

What is the standard for diagnosing a pericardial effusion?

What can be seen on EKG and on physical exam that is not diagnostic, but is highly suggestive?

What is a test that is NOT helpful in this diagnosis?

Echo

Can see electrical alternans on EKG (heart "swinging in a liquid sack") Diminished heart sounds, including a decreased friction rub if present.

X-ray (cannot distinguish a large heart from a pleural effusion via x-ray)

Decreased arterial pressure

decreased heart sounds

distended neck veins

Indictive of a cardiac tamponade

Introduced in 1986 for dx of pericardits

Based on endomyocardial biopsy specimens

1. Active Myocarditis: if light microscopy revealed 

       infiltrating lymphocytes and myocytolysis

2. Borderline or on going Myocardits if lymphocyte

      infiltration and NO myocytolysis

3. Negative for Myocarditis if no lymphocytic infiltrate

      and no myocytolysis

In a de-acceleration injury, what usually ruptures in the ABDOMEN?

What about in the CHEST?

Duodenum

Aorta (due to the ligamentum arteriosum)

A teenager presents with severe hypertension, but normal blood pressures in their lower limbs.  On x-ray, what is one very probable finding?

What is this most likely to be?

Rib knotching

coarctation of the aorta

LESION LESS THEN 50% blockage, NEGATIVE flow across the lesion.

NO SURGICAL BACKUP (not really a problem anymore today)

SEVERE SYSTEMIC DISEASE WITH A LIMITED LIFESPAN

POSITIVE STRESS TEST

SUDDEN CARDIAC DEATH

INDIVIDUALS IN HIGH RISK PROFFESIONS

PRIOR TO SURGERY WITH BORDERLINE POSITIVE NONINVASIVE STRESS TESTS AND RISK FACTORS 

Patients unable to exercise

Preoperative risk stratification

Early postinfarct risk stratification

Left bundle branch block-EKG is abnormal anyway! Don't want to stress test.

Fixed-rate pacemakers

When would a dobutamine stress test be preferred over a persantine/adenosine stress test?

What is a major drawback to this type of stress test?

In a patient with asthema

Takes a very long time!

What can be deduced from a thallium-201 nuclear scan that cannot be gained from a technetium-99 scan?

What is the advantage of a technetium scan?

Myocardial viability (parts of the heart can be inactive due to "cardiac shock", and can only be picked up with this type of scan)

Allows for more accurate imaging, allowing better pictures to be taken and even ejection fraction to be calculated.

Class I:No symptoms with ordinary activity

Class II:Slight limitation of physical activity.

Comfortable at rest, but ordinary physical activity results in fatigue, palpitation, dyspnea, or angina

Class III:Marked limitation of physical activity. Comfortable at rest, but less than ordinary physical activity results in fatigue, palpitation, dyspnea, or anginal pain

Class IV:Unable to carry out any physical activity without discomfort. Symptoms of cardiac insufficiency may be present even at rest

Classes II and III are most treatable (usually don't see class I in the doctor's office)

Stage A:  Patient at high risk for developing HF with no structural disorder of the heart

Stage B:  Patient with structural disorder without symptoms of HF

Stage C:  Patient with past or current symptoms of HF associated with underlying structural heart disease

Stage D:  Patient with end-stage disease who requires specialized treatment strategies

Frank-Starling Mechanism

 Neurohormonal Activation (Sympathetic nervous system (SNS), Renin-angiotensin-aldosterone system (RAAS), and Vasopressin (a.k.a. antidiuretic hormone, ADH)).

 Ventricular Remodeling