Pericardial Disease Flashcards by Kyra Porter

jugular venous pulsation

*patient lying down in bed around a 45 degree angle, head facing left, looking at the right side of the neck, particularly at the IJ
*recall: there is no valve between the right atrium and the SVC

*estimated right atrial pressure (RAP, in cm of water) = (JVP height) + 5 cm
*normal: 6-8 cm H2O

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jugular venous pulsation (JVP) - measurements

*A wave = atrial contraction
*C = tricuspid valve closure/systole
*X descent = atrial relaxation
*V wave = venous return
*Y descent = opening of tricuspid valve

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jugular venous waveform

*A wave = atrial contraction
*C = tricuspid valve closure/systole
*X descent = atrial relaxation
*V wave = venous return
*Y descent = opening of tricuspid valve

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differentiating JVP from carotid pulse

*for each heartbeat, there are 2 pulsations in the JVP but only 1 in the carotid
*note - if we have atrial fibrillation, there will be no significant “a” wave in the JVP (b/c no p-wave in atrial fibrillation)

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pericardium - review

*visceral and parietal layers are chief components and separated by the fluid layer
*fibrous/parietal layer innervated by phrenic nerve (visceral layer has no significant innervations)

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pericardial agenesis

*an extremely rare condition in which the pericardium does not form
*the heart tends to be more translocated into the left side of the chest
*note that people without a pericardium may not have any significant impacts

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possible reasons for the pericardium

*maintain proper anatomic orientation
*prevent acute dilation of the left ventricle when sudden increase in cardiac volume
*prevent spread of infection from adjacent structures

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acute pericarditis - overview

*inflammation of the pericardial layers (visceral & parietal)
*most common pericardial ailment

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acute pericarditis - symptoms

*SHARP STABBING CHEST PAIN, usually located in the precordium, that WORSENS WITH INSPIRATION or lying down (supine)
*fever
*pay particular attention to recent history

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acute pericarditis - pathophysiology of symptoms

*chest pain worsening with INSPIRATION: expanding lungs rub against an inflamed pericardium
*chest pain worsening when SUPINE: more blood returns to the heart (i.e. heart size increases), and the heart rubs up against an inflamed pericardium

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acute pericarditis - physical exam findings

*may have a pericardial friction rub caused by the different layers of the inflamed pericardium rubbing against each other
*of note, some rubs have different components: ventricular contraction, ventricular relaxation, atrial contraction

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acute pericarditis - diagnostic studies

1) 12-lead EKG:
-diffuse ST segment elevation
-PR segment depression (recall line b/w T and P is our baseline)

2) C-Reactive Protein

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acute pericarditis - causes

*infectious: viral (HIV, COXSACKIE), TB, bacterial
*non-infectious: POST-MI, post-cardiotomy (POST-CABG), uremic (renal failure related), neoplastic
*radiation induced
*connective tissue disease (LUPUS, rheumatoid arthritis, systemic sclerosis)
*drug-related (procainamide, hydralazine, anthracycline chemotherapy, minoxidil)

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top causes of acute pericarditis

*coxsackie virus
*post-myocardial infarction
*post-CABG
*lupus

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acute pericarditis - treatment options

*aspirin
*NSAIDs (ibuprofen)
*colchicine
*check an echo to see whether pericarditis may be complicated by a pericardial effusion

note - avoid steroids, as they increase the likelihood that the pericarditis will return

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pericardial effusion - overview

*abnormal accumulation of fluid in the pericardial cavity, between the visceral and parietal pericardium

note - normally there is 15-50 mL of serous fluid in the pericardial space

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3 factors which determine clinical symptoms of pericardial effusion

pericardial volume
rate of fluid accumulation (acute vs. chronic)
stiffness of the pericardium

pericardial pressure & the RIGHT heart in pericardial effusion

*when pressure in pericardium > right atrial pressure, you start to have RIGHT ATRIAL INVERSION (pericardial effusion pushes against and collapses part of the RA)

*when the pressure in pericardium > right ventricular pressure, you start to have DELAYED RIGHT VENTRICULAR FILLING (filling predominantly occurs in late diastole - think P wave)

pericardial pressure & the LEFT heart in pericardial effusion

*as flow decreases through the right chambers, the left-sided filling starts to exhibit more respiratory variation; right-sided diastolic pressures exceed left-sided → septum deviates toward LV → DECREASED STROKE VOLUME

*as flow decreases through the right chambers, the cardiac output on the left side starts to go down; pt becomes hypotensive, and the body responds by increasing heart rate (becoming tachycardic); this is cardiac tamponade (large effusion compromising CO in a significant way)

cardiac tamponade - overview

*compression of the heart by fluid (e.g. blood, pleural effusions) → DECREASED CARDIAC OUTPUT
*equilibration of diastolic pressures in all 4 chambers
*should be suspected in any patient with pericarditis, known effusion, or chest trauma who develops volume overload and has signs of decreased cardiac output

cardiac tamponade - physical exam findings

jugular venous distension
hypotension with pulsus paradoxus
decreased/muffled heart sounds
sinus tachycardia

note: findings 1-3 are known as BECK’S TRIAD

cardiac tamponade: JVD

*with cardiac tamponade, the X descent (atrial relaxation) is unaffected
*the Y descent is ABSENT (decreased atrial pressure with opening of the tricuspid valve) because:
-the large pericardial effusion is pushing against the right ventricle and making it very difficult to fill

cardiac tamponade: PULSUS PARADOXUS

*normally, there is a < 10 mmHg drop in systolic BP during inspiration
*in TAMPONADE: there is a drop > 10 mmHg in systolic BP DURING INSPIRATION because of the profound effect of the effusion limiting the size of both the right & left ventricles

pulsus paradoxus vs. pulsus alternans

*recall: pulsus alternans is when the pulse is stronger every other beat (seen in patients in heart failure with reduced ejection fraction)

*pulsus paradoxus is when you take in a breathe, it shifts the septum toward the left and the pressure goes down, whereas when you breathe out, the pressure goes up

cardiac tamponade: pulsus paradoxus - physiology

*when one breathes in, there is increased venous return, which means there is increased pressure on the right side to overcome the tamponade squeeze *because the RV diastolic pressure > LV diastolic pressure, both ventricular and atrial septa bow toward the left

cardiac tamponade: electrical alternans

*varying heights of the QRS (look at lead II rhythm strip) *results from the heart "swinging" as a result of the surrounding fluid

cardiac tamponade & obstructive shock - pathophysiology

cardiac tamponade → reduced filling → low cardiac output → decreased arterial pressure → shock → multiple organ system failure

cardiac tamponade - causes

*vast majority caused by any kind of acute pericarditis *additionally, acute hemorrhage into the pericardium, which can be caused by: -blunt force trauma -LV free wall rupture secondary to STEMI -acute aortic dissection

cardiac tamponade - treatment

*pericardiocentesis (echo-guided) to remove fluid *often leave in a drain to prevent re-accumulation note - do NOT drain fluid if the tamponade is due to acute aortic dissection

pericardial constriction - overview

*scarring and fibrosis of the pericardium with possible calcification → pericardium is extremely stiff

pericardial constriction - causes

*tuberculosis was the #1 cause in the early 20th century *now, it is idiopathic; recurrent bouts of pericarditis & left-sided chest radiation are common culprits

pericardial constriction - pathophysiology

*during filling in the normal heart/pericardium, both can expand *in pericardial constriction, the stiffness of the pericardium may actually limit the filling of the heart because the pericardium does not expand with the heart *as blood passes from the right atrium into right ventricle, the RV expands until it reaches the limit imposed by the stiff pericardium; as a result, venous return stops, and venous pressure increases *if left ventricular expansion is limited, it may limit stroke volume & cardiac output→ low blood pressure

pericardial constriction - signs/symptoms

*JVD, hepatomegaly, ascites, peripheral edema *pulmonary rales *dyspnea *hypotension & reflexive tachycardia *KUSSMAUL'S SIGN

pericardial constriction - Kussmaul's Sign

*normally when you inhale, more blood should get into the thoracic cavity *in CONSTRICTION, when the pt inhales, the jugular veins distend b/c the stiff pericardium will not allow more blood to enter the right side of the heart *SIMPLE: increase in jugular veinous pressure (distention of jugular veins) during inhalation note - Kussmaul's sign is NOT part of cardiac tamponade

pericardial constriction: pericardial knock

*in constriction, a pericardial knock occurs when the ventricles hit the stiff, calcified pericardium and can no longer expand *"knock" is heard after the S2 heart sound

what is Kussmaul's sign associated with?

PERICARDIAL CONSTRICTION note: Kussmaul's sign is distention of the jugular veins/increased JVP during INHALATION

pericardial constriction: jugular venous pulsation

*in constriction, there is a VERY STEEP Y-DESCENT, which indicates pressure really drops when blood moves forward through an open tricuspid valve

contrast pericardial constriction vs. cardiac tamponade

*jugular venous pulsation: -STEEP Y-descent = constriction -absent/decreased Y-descent = tamponade *Kussmaul's sign = constriction *pericardial knock = constriction *pulsus paradoxus can occur in both, but is more likely in tamponade

ventricular interdependence in pericardial constriction

*during inspiration, the septum shifts to the left to allow more blood on the right side of the heart (LV becomes smaller, RV becomes larger) *during expiration, the septum shifts to the right to allow more blood on the left side of the heart

pulsus paradoxus in pericardial constriction

*NORMAL: when you inspire, blood stays in lungs; normally, LA expands → lowers LA pressure → maintains forward flow to LA *in CONSTRICTION: LA can't expand during inspiration → pressure stays elevated → pressure in pulmonary veins drops → lower pressure gradient from lungs to LA → lower left sided stroke volume

treatment of significant pericardial constriction

*pericardial stripping (pericardial window)