Cardiology Flashcards Preview

Medicine > Cardiology > Flashcards

Flashcards in Cardiology Deck (55):
1

Tx unstable angina

Continuous cardiac monitoring

ASA and Clopidogrel acutely and for 9-12 mo

LMWH (Enoxaparin) for 2 days minimum

Beta blocker

O2

Nitrates for pain

Decide between medical mgmt and PCI. 90% resolve with above tx in 2 days. If not - cath, but if so - stress test.

Use TIMI score to decide on conservative vs aggressive tx.

2

Indications for PCI in unstable angina

1) Symptoms not resolving after 48 hours of medical therapy

2) Hemodynamic instability

3) Vent arrhythmia

4) New MR

5) New septal defect

3

Variant Angina

1) Alternative name
2) Cause
3) Dx
4) Tx

1) Printzmetal

2) Transient coronary artery vasospasm +/- fixed plaque

3) ST elevation during pain. Indicates transmural ischemia.

Angiogram showing vasospasm when given ACh (provokes vasoconstriction)

4) CCBs and Nitrates (vasodilators).

Lifestyle modification

4

MI

1) Mechanism
2) Presentation
3) Associated symptoms
4) Expect painless or atypical presentation in...
5) ECG changes
6) STEMI vs. NSTEMI vs. Unstable Angina
7) See below for Cardiac Enzymes

1) Previous plaque ruptures. Thrombus forms. Vessel occludes.

2) CP (pressure). Radiation. Same pain as angina but more severe and lasts longer. No relief with nitro.

3) Dyspnea. Diaphoresis. Weakness/fatigue. N+V. Syncope. Sense of doom.

4) Post-op pts. DM. Elderly. Women.

5) Peaked Ts (early). ST elevation (acute). Q waves (late). T wave inversion may occur, as may ST depression (if subendocardial injury).

6) STEMI is transmural (full thickness). NSTEMI is subendocardial (involves inner 1/3). Unstable angina presents in same way as NSTEMI but NO TROPONIN ELEVATION.

5

RV Infarct

1) Presentation
2) ECG changes
3) What not to do...

1) Hypotension. Elevated JVP. Hepatomegaly. Clear lungs.

2) Inferior lead changes (2, 3, AVF).

3) Do NOT give Nitrates or Diuretics. Will cause CV collapse.

6

ECG Leads for a given Infarct Location

1) Anterior
2) Posterior
3) Lateral
5) Inferior

1) V1 - V4

2) Reciprocal changes in V1 and V2 (IE ST depression and large R waves)

3) I and AVL

4) II, III, AVF

7

Cardiac Enzymes

1) Which ones are useful in detecting MI?
2) How long after event will they start to be elevated?
3) How long before they return to normal?
4) When do they reach their peak?
5) How often do you measure them?
6) Falsely elevated in?
7) If concerned with recurrent infarction, what do you measure?

1) Troponins T and I

2) 3-5 hours post event

3) Return to normal in 5 - 14 days

4) Peak at 24-48 hours

5) Measure at admission, then q8h

6) Renal failure

7) CK-MB, because it will return to baseline much faster than Troponin (within 72 hours)

8

Tx for Acute

1) Admit to cardiac-monitored floor

2) O2 and analgesics (see below)

3) ASA - Reduces re-occlusion

4) Beta blocker - Reduce O2 demand and remodelling

5) ACE inhibitor - Reduce mortality somehow

6) Statins - Stabilize plaques + lower cholesterol

7) Nitrates - Dilate coronary arteries (increase supply). Vasodilation (reduce preload)

8) Morphine Sulphate - Analgesia. Vasodilation (reduce preload)

9) LMWH (Enoxaparin)

10) Revascularization - Best within 90 minutes of arrival. Thrombolysis vs. PCI vs. CABG.

9

Indications for emergent CABG

Patient is having MI and has any of the following:

1) Hemodynamically unstable

2) Ventricular arrhythmia

3) Cardiogenic shock

Almost never done if patient is stable

10

Post - MI medications

1) Beta blocker

2) Statin

3) ASA and Clopidogrel

4) ACE inhibitor

11

Thrombolytic Therapy for Acute MI

1) Indications
2) Window of usefulness
3) Absolute contraindications
4) Drug of choice

1) PCI not an option. ST elevation in 2 contiguous leads. Pt refractory to nitro.

2) Best if within 6 hours. Can't give if > 24 hrs since onset of CP.

3) Recent trauma/active bleed risk (including TRAUMATIC CPR). Pts with stroke risk. Recent Sx. Bleeding disorders.

4) Alteplase. Alternatives = Streptokinase, Tenecteplase.

12

Complications of Acute MI

1) CHF

2) Arrhythmia (Tx given after ":")
- PVCs
- A Fib
- VTach: Cardiovert if unstable. IV Amiodarone if stable.
- V Fib: Immediate unsynchronized cardioversion + CPR.
- PSVT
- Sinus Tach: Tx underlying issue.
- Sinus Brady: Observation
- Asystole: Defibrillate b/c it might be subtle V Fib. Transcutaneous pacing.
- AV Block: No Tx for 1st degree and 2nd degree type I (Wenkebach). Tx for 2nd degree type II (fixed PR but random dropped beat) and 3rd degree (AV dissociation) require emergent pacemaker

3) Recurrent Infarction
- Look for ST elevation and recurrent spike in CK-MB. If levels elevated 36 hours after initial event, suspect re-infarction.

4) Mechanical Complications
- Free wall rupture: 90% mortality. Usually within 4 days of event, but 90% will happen within 2 weeks. Stabilize + pericardiocentesis + Sx.
- Septum rupture: Occurs within 10 days. Emergent Sx.
- Papillary muscle rupture: Pw new onset MR. Echo + emergent Sx + afterload reduction with Na-Nitroprusside or ballon pump (encourages blood to flow into aorta instead of atria).
- Ventricular pseudoaneurysm: Rupture contained by pericardium. Echo + emergent Sx b/c they tend to become free wall ruptures.
- Ventricular aneurysm: Medical mgmt b/c often don't rupture.

5) Acute Pericarditis
- Rare. Give ASA. No NSAIDs or steroids b/c they interfere with scar formation.

6) Dressler Syndrome
- See other cue card
- Immune-based syndrome occurring weeks to months after MI
- Tx is ASA

13

Dressler Syndrome

1) What is it?
2) Presenting symptoms?
3) When does it happen?
4) Tx?

1) Immunologically-based syndrome occurring post-MI. AKA "post-MI syndrome".

2) Pw
- Fever
- Malaise
- Pericarditis
- Leukocytosis
- Pleuritis

3) Weeks to months after MI

4) ASA

14

Cardiogenic and Vascular causes of CP

1) Stable or Variant Angina

2) Unstable Angina/NSTEMI

3) STEMI

4) Pericarditis

5) Aortic Dissection

15

Pulmonary causes of CP

1) PE

2) Pneumothorax

3) Pleuritis

4) Pneumonia

5) Status Asthmaticus

16

GI causes of CP

1) GERD

2) Diffuse Esophageal Spasm

3) PUD

4) Esophageal Rupture

17

Chest Wall causes of CP

1) Costochondritis (acute inflammation of costal cartilage)

2) Muscle Strain

3) Rib #

4) HZV

5) Thoracic Outlet Syndrome

18

Psychiatric causes of CP

1) Panic attack

2) Anxiety

3) Somatization

19

Classic drug that causes CP

1) Cocaine

20

What is unstable angina?

Decrease in blood supply to heart (contrast to stable angina which is an increased myocardial O2 demand).

1) Angina that is increasing in frequency, duration, or intensity of CP.

2) New onset angina that's severe and getting worse.

3) Angina AT REST.

21

Frank-Starling Principle

Increased preload to heart will result in increased contractility

22

CHF

1) Basic idea
2) Causes of systolic dysfunction
3) Causes of diastolic dysfunction
4) What's "High Output Heart Failure?"

1) Heart can't meet demands of body.

2) Impaired contractility (systolic dysfunction)
- Ischemic heart disease
- HTN leading to cardiomyopathy
- Valvular heart disease
- Myocarditis (post-viral)
- Less common: EtOH, RADs, Hemochromatosis, Thyroid disease

3) Impaired relaxation (diastolic dysfunction)
- HTN leading to myocardial hypertrophy
- AS
- MS
- AR
- Restrictive cardiomyopathy (amyloidosis, sarcoidosis, hemochromatosis)

4) Something in periphery is causing the body to need more O2. If they're present and the heart has underlying disease, it could precipitate CHF.
- Chronic anemia
- Pregnancy
- Hyperthyroidism
- AV fistula
- Paget's
- MR
- AI
- Wet beriberi

23

Symptoms of Left-Sided CHF

1) Dyspnea

2) Orthopnea (SOB while recumbent)

3) PND

4) Nocturnal cough

5) CONFUSION + MEMORY IMPAIRMENT: Late CHF. Due to inadequate brain perfusion.

6) Diaphoresis and cool extremities at rest

24

Signs of Left-Sided CHF

1) Point of maximal impulse displaced left

2) S3: Due to rapid filling into non-compliant LV.

3) S4 Gallop: Sound of atrial systole into non-compliant LV.

4) Crackles due to pulmonary edema

5) Dullness to percussion

6) DECREASED tactile fremitus (due to decreased transmission of sound)

7) Strong S2 (indicates pulmonary HTN)

25

Signs of Right-Sided CHF

1) Peripheral edema

2) Nocturne

3) Jugular venous distention

4) Hepatomegaly/Hepatojugular reflux

5) Ascites

6) RV heave

26

Signs of CHF on CXR

1) Congestion

2) Kerley B lines

3) Shadow of Azygous visible in RUL on frontal view

4) Shadow of Bronchus Intermedium visible in LUL on frontal view

27

What is BNP?

1) When is it released?
2) What does a high level tell you?

B-Type Natriuretic Hormone

1) Released in response to ventricular volume expansion.

2) Levels over 150 pg/mL correlate strongly with presence of decompensated CHF. Useful if trying to differentiate between COPD and CHF.

28

Tests to do to investigate CHF

1) CXR

2) Echo: Identifies cause, chamber dilation, and EF ( 40%).

3) ECG can show previous MI.

4) Multicoated Acquisition Test (MUGA) to look for ischemia. Uses Tec-99.

5) Cardiac Cath: Can tell you about systolic vs. diastolic dysfunction.

6) Stress test: Identifies ischemia and/or infarction. Quantifies conditioning. Differentiates between pulmonary vs. cardiac dyspnea.

29

Tx of CHF

1) Lifestyle
- Na restrict (

30

Signs of Digitalis Toxicity

1) CNS
- Confusion
- Visual disturbances

2) GI
- N + V
- Anorexia

3) Cardiac
- Ectopic beats
- AV BLOCK
- ATRIAL FIBRILLATION
- PAROXYSMAL ATRIAL TACHYCARDIA WITH 2:1 BLOCK

31

NYHA Classification for CHF

1) Class I?
2) Class II?
3) Class III?
4) Class IV?

1) Disease but no symptoms and no limitations.

2) Mild symptoms. Slight limitation to normal activity.

3) Marked limitation, and only able to do a small amount of activity. Comfortable only at rest.

4) Severe symptoms, that are present at rest.

32

Acute Decompensated HF

1) What is it?
2) How do you treat it?

1) Acute dyspnea and elevated LV filling pressures, +/- pulmonary edema.

2)
- O2
- Diuretics: MOST IMPORTANT TX!
- Na restrict
- Nitrates: ONLY IF NO HYPOTENSION.
- If have pulmonary edema despite the above, add an INOTROPE (ex = Dobutamine).

- No role for Digoxin as it takes weeks to kick in.

33

Premature Atrial Beats

1) Signs on ECG?
2) Significance?
3) Tx?

1) Early P waves that look different than normal P waves.

2) Not significant in normal heart. May be precursor to ischemia in diseased heart.

3) Beta blocker if symptomatic.

34

Premature Ventricular Beats

1) Signs on ECG?
2) Significance?
3) Tx?

1) Wide QRS without P waves (they're buried within the QRS).

2)
- Associated with increased mortality even in normal hearts.
- If frequently occurring, require w/u for structural disease.
- If frequent PVCs AND underlying heart disease, at risk for sudden death due to arrhythmia. May benefit from ICD.

35

Atrial Fibrillation

1) Causes
2) Signs + Symptoms
3) Tx principles (see other flashcard)

1)
- Heart disease
- Pericarditis or pericardial trauma
- Pulmonary disease
- Thyroid conditions
- Systemic illness
- Stress to body
- EtOH
- Sick Sinus Syndrome: A group of conditions where the SA node is not functioning properly. Example = Tachy-Brady syndrome (alternating tachycardia and bradycardia)
- Pheochromocytoma

2)
- Fatigue
- Exertional dyspnea
- Palpitations
- Dizziness
- Syncope
- Irregularly irregular pulse

36

Tx of A FIB.

1) Hemodynamically unstable
2) Hemodynamically stable
3) Chronic
4) Different choices for cardioversion

1) Immediate electrical cardioversion

2)
- Is rate over 100? If so, need to control with Beta blocker.
- Once rate is controlled, must find out how long patient has been in A FIB for:
a) If > 48 hours, significant risk that clot has formed in atrium, which can dislodge and cause stroke. Can do an echo to see, or you can anticoagulate for 3 weeks and then cardiovert. Need 4 weeks of anticoagulation afterwards. Goal is INR of 2-3.

b) If

37

Atrial Flutter

1) Causes
2) ECG
3) Tx

1)
- Heart disease
- COPD
- ASD

2)
- Saw tooth baseline
- 2-3 P waves per QRS

3)
- See A FIB

38

Multifocal Atrial Tachycardia

1) What is it?
2) Normally associated with?
3) ECG changes?
4) Tx?
5) Distinction from "Wandering Atrial Pacemaker?"

1) Multiple parts of heart controlling pace.

2) COPD or other severe resp conditions.

3) At least 3 different P wave morphologies + Tachycardia.

4) Tx underlying disease. Improve O2.
- If LV function preserved, use Beta Blocker.
- If LV function not preserved, use Amiodarone or Digoxin.
- NO ROLE FOR ELECTRICAL CARDIOVERSION.

39

PSVT

1) Types
2) Causes
3) Tx

1)
a) AV Node Reentrant
- Reentrant circuit is in AV node
- Most common out of the SVTs
- Narrow QRS with buried P waves: Occur b/c impulses exit and activate atria and ventricles simultaneously.

b) Orthodromic AV Reentrant
- Accessory pathway in between atria and ventricles
- Narrow QRS +/- buried P

2)
- Ischemic heart disease
- Digoxin toxicity
- AV reentry
- Atrial flutter
- Accessory pathway
- Excessive caffeine or EtOH

3)
- Maneuvers to stimulate the vagus, which will delay AV conduction and therefore block reentrant circuit: Valsalva, carotid massage... etc.
- Acute Tx: Adenosine, which terminates the SVT.
- Preventive: Beta blocker
- If recurrent, use catheter ablation to destroy reentrant circuit.

40

Wolff-Parkinson White

1) What is it?
2) ECG changes?
3) Tx?

1) Accessory pathway through Bundle of Kent allows premature ventricular excitation. Can cause paroxysmal tachycardia in two different ways:

a) Orthodromic reciprocating tachycardia: No delta waves.
b) Supraventricular tachycardia (A FIB or A Flutter).

I don't think the above is important. Look for tachycardia + delta waves.

2) Narrow complex tachycardia + Delta waves

3)
- DO NOT GIVE BETA BLOCKERS OR CCBs OR ANYTHING THAT ACTS ON THE AV NODE. Will accelerate conduction through accessory pathway.
- Catheter ablation of accessory pathway

41

V Tach

1) What is it?
2) Causes
3) What is "sustained VT?" Tx?
4) What is "unsustained VT?" Tx?
5) Clinical Features?
6) ECG features?
7) Important to distinguish from? How do you do this?

1) 3 or more PVCs in a row with a rate > 100.

2)
- CAD with prior MI (most common cause)
- Active ischemia
- Active Hypotension
- Cardiomyopathy
- Congenital defects
- Prolonged QT Syndrome
- Drug toxicity

3) Lasts for > 30 seconds and doesn't stop.
- Symptomatic (IE hemodynamic compromise and/or ischemia)
- Life-threatening
- Can progress to V FIB if untreated
- Tx
a) Hemodynamically stable with mild symptoms: IV Amiodarone
b) Hemodynamically unstable or severe symptoms: Immediate synchronous electrical cardioversion + IV Amiodarone (to maintain sinus). ICD implantation later.

4) Brief and self-limited.
- Asymptomatic
- If CAD or LV dysfunction are present, this is a significant risk factor for sudden death. W/U patient for these conditions.
- Tx
a) If asymptomatic and no underlying disease: No Tx
b) If underlying disease, or symptomatic: ICD implantation

5)
- Palpitations
- Syncope
- Dyspnea
- Cardiogenic shock
- Canon A waves in neck (from atria contracting against a contracting ventricle).

6) Wide and bizarre QRS complexes at rapid rate.

7) SVT with Aberration. The only real difference is that VT occurs in those with Hx of structural heart disease while SVT with Aberration does not.

42

Causes of Prolonged QT

1) Long QT Syndrome

2) TCAs

3) Anticholinergics

4) Electrolyte abnormalities

5) Ischemia

43

V FIB

1) What is it?
2) Recurrence risk?
3) Causes?
4) PW
5) Dx?
6) Tx?

1) Multiple foci in ventricles fire rapidly leading to zero CO.

2)
- If associated with MI, risk is low
- If not associated with MI, risk is high (30%). Require prophylactic amiodarone or implantable defibrillator.

3)
- Ischemic heart disease
- Anti-arrhytmics that prolong QT
- A FIB with rapid ventricular rate as in WPW

4)
- Absent heart sounds and pulse
- Unconscious
- Leads to SCD (death within 1 hour of symptom onset secondary to cardiac cause) if untreated

5) No waves on ECG. Just looks like erratic mountains.

6)
- Immediate UNSYNCHRONIZED defib + CPR.
- Give IV epi.
- Give IV Amiodarone if this doesn't work.
- If pt returns to normal after caridioversion, continuous IV amiodarone. Implantable defibrillator when able, otherwise long-term amiodarone.

44

Does defib work for asystole?

No. Give epi and CPR.

45

Sinus bradycardia

1) Definition
2) Causes
3) PW
4) Tx

1) Rate persistently under 45.

2)
- Ischemia
- Increased vagal tone
- Anti-arrhythmic drugs

3)
- Fatigue
- Exercise intolerance
- Angina
- Syncope

4)
- Pacemaker
- Atropine to block vagal stimulation

46

Sick sinus syndrome

1) Definition
2) PW
3) Tx

1) Persistent spontaneous sinus brady.

2)
- Dizziness
- Confusion
- Syncope
- Fatigue
- CHF

3) Pacemaker

47

AV Block

1) 1st degree?

2) 2nd degree (Mobitz I)

3) 2nd degree (Mobitz II)

4) 3rd degree

1) PR > 0.20. No Tx.

2) Wenckebach. PR large, increases in length, then dropped beat. No Tx.

3) NORMAL PR INTERVAL but dropped beats. Pacemaker.

4) AV dissociation. Pacemaker.

48

Dilated Cardiomyopathy

1) Definition
2) Causes
3) PW
4) Dx
5) Tx

1) Insult causes dysfunction of LV contractility

2)
- 50% = Idiopathic
- CAD + Previous MI
- Alcohol
- Thiamine deficiency
- Viral
- Thyroid disease
- SLE, scleroderma
- Pheo
- Familial/genetic

3)
- Signs of L and R CHF
- S3 and S4
- Murmurs (MS or TR)
- Cardiomegaly
- Coexisting arrhythmia
- Sudden death

4)
- Treat like CHF (diuretics, vasodilators... etc.)
- Anti-coagulate

49

HOCM

1) Inheritance
2) Pathophys
3) PW
4) Signs
5) Murmur characteristics
6) Dx
7) Tx

1) AD

2) Diastolic dysfunction due to stiff heart. Can't refill due to high diastolic filling pressures. May involve dynamic outflow obstruction due to asymmetric hypertrophy of septum.

3)
- Dyspnea
- CP
- Syncope
- Palpitations
- Arrhythmia
- Cardiac failure
- Sudden death

4)
- Loud S4
- Systolic ejection murmur.

5)
- Decreased with squatting (which decreases outflow obstruction). UNIQUE TO HOCM AND MVP. THIS WILL INCREASE THE INTENSITY OF ALL OTHER MURMURS.
- Decreased with sustained hand grip (which raises SVR, and therefore lowers the pressure difference across the aorta).
- Increased by valsalva and standing (decrease LV size and thus increases outflow obstruction). THIS IS UNIQUE, AS ALL OTHER MURMURS EXCEPT MVP ARE DECREASED BY THIS.

6) Echo

7)
- None if asymptomatic
- Avoid strenuous exercise
- Beta blockers (slow HR and therefore increase diastolic filling time)(reduce heart contractility and therefore O2 consumption).
- Verapamil if BB doesn't work.
- Myomectomy to remove part of septum (if severe disease)

50

Restrictive Cardiomyopathy

1) Pathophysiology
2) Causes
3) PW
4) Dx
5) Tx

1) Infiltration of myocardium leads to decreased ventricular compliance which leads to reduced diastolic filling. Systolic function occurs in severe disease.

2)
- Amyloidosis
- Sarcoidosis
- Hemochromatosis
- Scleroderma
- Carcinoid syndrome
- Chemo or RADs
- Idiopathic

3) Elevated filling pressures cause...
- Dyspnea
- R sided signs

4)
- Echo: Thick myocardium.
- ECG: Low voltages.
- Bx diagnostic

5)
- Tx underlying disorder
- Beware of diuretics and vasodilators: Reduce preload, which might drop CO.

51

Myocarditis

1) Pathophysiology
2) Causes
3) PW
4) Dx
5) Tx

1) Inflammation of myocardium

2)
- Viral
- Bacterial
- SLE
- Meds
- Idiopathic

3)
- Can be asymptomatic
- Fatigue
- Fever
- CP
- Pericarditis
- CHF
- Arrhythmia
- Death

4) Elevations in cardiac enzymes and ESR

5) Supportive

52

Acute Pericarditis

1) Pathophysiology
2) Causes
3) Clinical features
4) CP in detail
5) Dx
6) Tx

1) Inflammation of pericardial sac

2)
- Post-viral
- Viral (Coxsackie, EBV, Hep A and b)
- Bacterial (TB)
- Fungal
- Acute MI
- Uremia
- Collagen vascular disease
- Neoplasm (esp. Hodgkin's Lymphoma)
- Post-MI (Dressler's)
- Post cardiac Sx
- Amyloidosis
- RADs
- Trauma

3)
- CP
- Fever + Leukocytosis
- Pericardial friction rub (high pitched)

4)
- PLEURITIC
- RELIEVED BY SITTING UP AND LEANING FORWARD
- MADE WORSE BY LAYING FLAT, COUGHING, SWALLOWING
- Radiates to neck and traps

5) Diffuse ST elevation and PR depression

6) Most = Self-limiting. Give NSAIDs. If minor, can Tx as outpatient. If severe, Tx as inpatient.

53

Constrictive pericarditis

1) Pathophys
2) Cause
3) PW
4) Signs
5) Dx
6) Tx

1) Fibrous scarring interferes with diastolic filling. Ventricles can fill a bit, but are abruptly stopped.

2)
- Idiopathic (likely post-viral)
- Several other causes listed.

3)
- VERY ILL LOOKING
- Fluid overload (edema, ascites, pleural effusions... etc.)
- Diminished CO (dyspnea on exertion, fatigue... etc.)

4)
- JVP distention
- KUSSMAUL SIGN (JVP doesn't go up during inspiration)

5)
- ECG: Low QRS voltages
- Echo: Increased pericardial thickness. SHARP HALT IN VENTRICULAR DIASTOLIC FILLING.
- Cardiac Cath: ELEVATED AND EQUAL DIASTOLIC PRESSURES IN ALL CHAMBERS.

6) Tx underlying condition. May need Sx (pericardiectomy)

Aside: Hard to differentiate between this and Restrictive pericarditis (infiltrate that prevents diastolic filling). Can be done with echo or cardiac cath.

54

Pericardial Effusion

1) Pathophys
2) PW
3) Dx
4) Tx

1) Acute or chronic exudation of fluid into pericardial space.

2) Non-specific, but...
- Muffled heart sounds
- Friction rub
- Dullness at left lung base

3)
- Echo: Test of choice (sens + spec)
- CXR: Enlarged heart if effusion is large
- ECG: Low voltages. Electrical alternans if severe.
- Pericardial fluid analysis: Can ID cause.

4)
- Pericardiocentesis only if evidence of tamponade.
- If small and clinically insignificant, re-order echo in 1 week.

55

Cardiac Tamponade

1) Pathophysiology
2) Causes
3) PW + Signs
4) Dx
5) Tx

1)
- Accumulation of fluid in pericardial sac.
- RATE is important, NOT AMOUNT.
- 200 mL rapidly = Tamponade
- 2 L that develops slowly = Tamponade
- Fluid mechanically impairs diastolic filling of ventricles

2)
- Penetrating trauma
- Iatrogenic
- Pericarditis
- Post-MI with free-wall rupture

3)
- BECK'S TRIAD: HYPOTENSION, MUFFLED HEART SOUNDS, JVP DISTENTION.
- Narrowed pulse pressure (systolic-diastolic)
- PULSUS PARADOXUS (10 mm Hg drop in BP on inspiration)(Clinically, pulse is strong on expiration and weak on inspiration).
- Tachypnea
- Tachycardia
- Cardiogenic shock

4)
- Echo: Best test
- CXR: Enlargement
- ECG: Electrical Alternans (different QRS wave heights)
- Cardiac Cath: EQUALIZATION OF PRESSURES IN ALL CHAMBERS.

Aside: Chamber pressure equalization also happens in constrictive pericarditis.

5)
- Non-hemorrhagic, Hemodynamically stable: Monitor
- Non-hemorrhagic, Hemodynamically unstable: Pericardiocentesis
- Hemorrhagic secondary to trauma: EMERGENT SX. Pericardiocentesis is ONLY A TEMPORIZING MEASURE IN THIS SCENARIO.