Pericardial Disease Flashcards
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
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
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
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)
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)
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
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
acute pericarditis - overview
*inflammation of the pericardial layers (visceral & parietal)
*most common pericardial ailment
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
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
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
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
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)
top causes of acute pericarditis
*coxsackie virus
*post-myocardial infarction
*post-CABG
*lupus
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
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
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)
