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112 Cards in this Set
- Front
- Back
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Two Types of Hypertension |
1. Primary: Most common (90%), unknown idiology (mostly linked to lifestyle) 2. Secondary: Caused by underlying disease (kidney, glandular, arterial, sleep apnea |
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Systemic Hypertension Normal/Abnormal Value Ranges |
Normal: <120 / <80 Prehypertension: 120-139 / 80-89 Mild HTN: 140-159 / 90-99 Moderate HTN: >160 / >100 Severe HTN (hypertensive crisis): >180 / >110 |
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How does systemic HTN eventually lead to hypertensive heart disease? |
SystemicHTN causes: - Anincreasein vascular resistanceand LVafter load - Whichleads to LVH - Whichthen leads to Diastolic Dysfunction - Whichthen leads to Systolic Dysfunction |
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2D Echo Findings of Hypertensive Heart Disease |
- LV pressure overload with normalLV size and normal LVF - Concentric LVH - Aorta enlargement /calcification / dissection - LAE due to elevatedLVEDP and MR - Sclerotic AV - Mitral annular calcification(MAC) |
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M-Mode Findings of Hypertensive Heart Disease |
- Concentric LVH with normal LV size and LVF MildLVH (wall thickness 1.2-1.4 cm) Moderate LVH (wall thickness 1.4-1.9cm) Severe LVH (wall thickness >2.0 cm) - Increasein LV Mass - LAenlargement due to elevated LVEDP and MR - Aorta enlargement /calcification / dissection |
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Doppler Findings of Hypertensive Heart Disease |
Diastolic Function: - Impaired Early Relaxation Pattern (SmallE / Big A/ Long DT) Systolic Function : - Mid-cavitary high velocity jet - Without SAM (can also get SAM due to super thick walls) - Velocity will be increased with hypovolemia or increased contractility Valvular Doppler Findings - MR,AR |
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End Stage Hypertensive Heart Disease |
- LV enlargement with decreased LV hypertrophy - Looks similar to Dilated CMO (enlarged LV, decreased systolic function) |
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Chronic HTN |
Patient may present with symptoms of heart failure due to: - Diastolic or systolic dysfunction - CAD - Valve disease |
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Limitations and Pitfalls in Assessing Hypertensive Heart Disease: |
- LV mass calculation 2D vs. M-mode (need wall definition) - May be confused with HCM or RCM |
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Treatment of Hypertensive Heart Disease |
- Modify lifestyle - Medical therapy (beta blockers, calcium channel blockers, diuretics) * Serial BP readings to assess medical therapy |
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Hypertensive Hypertrophic Cardiomyopathy |
- NOT a true CMO - Severe organ damage due to HTN - Patients present with heart failure - Normal to hyperdynamic LVF - Concentric LVH - Diastolic dysfunction - Cavity obliteration with mid-cavitary high velocity jet |
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Pulmonary Heart Disease |
- Cor Pulmonale (right heart failure) - Shortness of breath - Wheezing - Edema - Ascites - Disease of the heart characterized by RVH and RVE and secondary to disease of the lungs or their blood vessels - Pulmonary heart disease's main component is pulmonary HTN |
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Pulmonary Hypertension |
- PHTN caused by increased pressure in the pulmonary arteries/lungs - Increase in pulmonary artery pressure (>30 mmHg) due to: reduced size of pulm. vasculature and/or increase in pulmonary blood flow |
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Types of PHTN |
Primary: - Idiopathic Secondary: - Aquired heart disease (CAD, LV failure, AV/MV disease, CMO) - Pulmonary disease (emphysema, COPD, bronchitis) - Congenital heart disease (anomalies with extra blood flow to the lungs |
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Underlying Pathophysiology of PHTN |
- RV ejecting into a highresistance pulmonary bed ---> chronic RV pressure overload - Initially results in RVH withnormal RV function - Progresses to: DecreasedRV function, RVenlargement (occurs early on), Moderateto severe TR, RAenlargement |
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2D Echo Findings of PHTN |
- RVH,RV enlargement, decrease RV function - FlattenedIVS or “D” shaped LV - RAenlargement ìMPAdilatation - Dilatationof the IVC / hepatic veins - Decreasecollapse of IVC with inspiration - IASbowed toward the LA – high RA pressure - PFO– bubble study to assess for shunt |
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M-Mode Findings of PHTN |
- Reducedor absent “a” wave – PV M-Mode dueto increased PA end diastolic pressure - “FlyingW” – PV M-Mode (mid-systolicclosure of the PV due to high pressure in the PAs/lungs) - RVH/ RVE - Paradoxicalseptal motion (IVSmoves opposite from normal) |
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TV Annulus M-Mode (TAPSE) |
TAPSE: Tricuspid Annular Plane Systolic Excursion - M-Modethrough RV free wall of TV annulus – Apical 4 chamber - Measuredisplacement of TV annulus from end-diastole to end-systole - Reflectslongitudinal RV movement – indicator ofRV systolic function - NormalTAPSE – > 1.6 cm - TAPSE< 1.6 cm – indicates poor PHTN prognosis or RV systolicdysfunction |
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Doppler Findings of PHTN |
~Mid-systolic notching of RVOT /PA signal (seen in severe PHTN) - Correlateswith “flying W” on PV M-Mode ~Assess TR velocity for RVSP - RVSP(PAP) = 4 (TR vel)2 + RAP - TR velocity relates to pressure differenceof RV / RA - Volume/severity of TR representedby intensity of TR signal ~Assess PR for PAEDP (Normal = 4 –12 mmHg) ~Assess acceleration time of RVOT |
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RVOT Acceleration Time |
Measure time from beginning of signal to peak of signal - Normal: > 120 msec - PHTN: <90 msec |
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RVSP Grading of PHTN |
(RVSP/PAP) NormalPAP: 15 – 30 mmHg MildPHTN: 30 – 40 mmHg ModeratePHTN: 40 – 70 mmHg SeverePHTN: > 70 mmHg Eisenmenger’s: > 120 mmHg |
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IVC -- Estimated RA Pressure |
< 2.0 cm andcollapses > 50% with inspiration - EstimatedRAP = 5 mmHg or 3 mmHg (newASE guideline) < 2.0 cm andcollapses < 50% with inspiration - EstimatedRAP = 10 mmHg or 8 mmHg (newASE guideline) > 2.0 cm and collapses < 50% withinspiration - EstimatedRAP = 15 mmHg or 8 mmHg (newASE guideline) > 2.0 cm with noinspiratory collapse - EstimatedRAP = 20 mmHg or 15 mmHg(newASE guideline) |
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Pitfalls/Limitations: PHTN |
- Difficultto image due to lung disease - Notbeing parallel to TR jet - Notobtaining good TR envelope or PR - Needto try additional ways to bring out TR to estimate PA pressure (legraises, inspiration, contrastecho, agitatedsaline) |
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Treatment for PHTN |
- Treat underlying etiology if secondary PHTN - Primary PHTN: pulmonary vasodilators (flolan, bosentan) - IVC filter if PHTN due to pulmonary emboli - Lung and/or heart-lung transplant |
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Eisenmenger's Syndrome |
- Reversalof any congenital shunt from left-to-right to right-to-left (ASD,VSD, PDA) - Occursdue to irreversible elevation of pulmonary vascular resistance and severe PHTN - Classifiedas a cyanotic heart defect– oxygen level in blood is lower than normal due to mixingof oxygenated and deoxygenated blood - Clinicalfindings: DOE,cyanosis, clubbing of fingers |
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M-Mode and 2D Findings of Eisenmenger's |
M-Mode findings same as PHTN 2D findings same as PHTN inaddition to: - Determineetiology of Eisenmenger’s - Typeof shunt – ASD, VSD, PDA - Assessventricular dimensions and systolic function |
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Eisenmenger's Doppler Findings |
- Assess TR and PR velocities for RVSP and PAEDP - Assess the shunt: ASDshunt from RA to LA VSDshunt from RV to LV PDAshunt from PA to Aorta Whatis the velocity and the volume of the flow? |
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Eisenmenger's Treatment |
- Heart-Lung Transplant |
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Pulmonary Emboli |
- Blood clot to lungs, commonly from legs (DVT) - Sudden dyspnea - Angina - Cough - RV enlargement - Decreased RV function - TR - Assess for thrombus in RA, RV, MPA |
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McConnell's Sign |
- Distinct echo finding suggestive of a patient having an acute pulmonary embolism - Akinesis of mid-ventricular RV free wall - Normal, preserved motion of RV apex |
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Reasons for Transplant |
¤ IschemicHeart Disease¤ ¤ Cardiomyopathy (DCM #1 reason) ¤ Valvular Heart Disease¤ ¤ CongenitalHeart Disease |
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Contraindications for Transplant |
¤ Renalor hepatic disease ¤ SignificantPHTN ¤ Diseasesthat will reduce life expectancy ¤ ActiveInfection ¤ Unresolveddrug and/or alcohol abuse ¤ Extremeobesity ¤ Overage 65 |
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Pre-Transplant Evaluation |
¤ Heartcatheterization (receiver and donor) ¤ Treadmillexercise testing ¤ Pulmonaryfunction tests ¤ Renalfunction tests ¤ Bloodand tissue typing ¤ Echocardiogram |
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Selection Criteria for Transplant |
¤ End stage heart disease(prognosis of less than 6-12 months) ¤ NYHA class III or IV ¤ Ineffective conventional medicalor surgical therapy ¤ Age criteria is flexible: based on “physiologic age” rather thanabsolute chronologic age ¤ Psychosocial stability |
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Who performed the first adult human heart transplant in the US? |
- 1968– Norman Shumway, Stanford Medical Center - Performedfirst adult human heart transplant in the United States |
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What drug is used for anti-rejection? |
Cyclosporine: immunosuppressive drug, isolated from a soilfungus |
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Orthotopic Heart Transplant |
- Removalof diseased heart and replacing with new, donor heart - Sutured into place to the pulmonary trunk |
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Orthotopic Heart Transplant: Donor |
- Procedurefor donor - Heartis rapidly cooled and arrested with cardioplegia solution - Acquiredonor heart be severing SVC, IVC, pulmonary veins, aorta, and pulmonary trunk - Heartplaced in preservative and placed on ice - Immediatetransportation (not to exceed 5 hours) |
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Orthotopic Heart Transplant: Recipient |
- Sternotomy performed and cardiopulmonarybypass started - Suitabilityof donor organ confirmed before surgery continues - Pulmonarytrunk and aorta are resected above their semilunar valves - Posteriorportions of atrial walls and interatrial septum are left intact inpreparation to connect donor heart - Recipientheart is excised - Donorheart is placed in pericardial cavity and aligned with interatrial septum, and RA and LA wallremnants of recipient’s heart |
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Heterotopic Heart Transplant |
- Donorheart is placed in the right chest alongside recipient heart (piggy-back) NO LONGER PERFORMED - Limited role because therecipient’s native heart function continues to deteriorate, producingsymptomatic deterioration of patient - Givespatient’s original heart a chance to recover - Ifdonor heart fails/is rejected, can be removed - Ifthe recipient’s body significantly larger than donor’s, donor heart not strongenough to function by itself |
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Xenotransplantation |
- Replacinga human heart with the heart of another species - Usuallythe heart of a chimpanzee or baboon - Beinginvestigated as a potential supply of donor organs |
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Main Complications of Cardiac Transplant |
- Rejection - Coronaryartery disease - Infection |
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Rejection |
- Major threat to long-term survival - Responseof the recipient’s immune system to foreign antigens - Attack myocardial cells - Confirmedby RV biopsy |
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Right Ventricular Biopsy |
- Performedin cath lab – catheter into femoralvein, IVC, RA, across TV to RV, biopsy taken from IVS (used to confirm rejection) - Invasive,expensive - Samplingerror - Tricuspidvalve damage - Scartissue secondary to multiple biopsies - Uncomfortablefor patient |
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Other Complications of Transplants |
- Post-transplantmalignancies - Alteredconduction pathways - Mayresult in pacemaker - Denervationof the heart - Interruptionof nerve impulse route due to excision of the heart - Delayedresponse to exercise - Chestpain receptors are cut, resulting in inability to feel angina |
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Echo Findings in Cardiac Transplant |
- Biatrial enlargement - Pericardialeffusion - Paradoxicalseptal motion - IVSmoving toward RV in systole - IncreasedLV wall thickness - IncreasedRV dimension - Tricuspidregurgitation |
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Echo Findings in Cardiac Transplant Rejection |
- Increased LV wall thickness (progressivelyincreasing) - Increasein LV mass - Decrease in LV systolic function - Pericardialeffusion - Restrictivefilling: BigE / Small A / Short DT |
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LVAD |
- Left Ventricular Assist Device - Implantablemechanical pump that helps pump blood from the left ventricle to the aorta - Usedfor: bridgeto heart transplant, toolto use so heart can become strong enough to pump on its own - Long-termtreatment |
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LVAD Risks |
- Bloodclots – may form as blood moves through VAD - Bleeding– requires open heart surgery and this increases risk of bleeding afteroperation - Infection– VAD connected through port - Devicemalfunction – power failure - Rightheart failure – with LVAD, left heart may pump more than what right heart wasused to |
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Pericardium |
- Pericardium is a loose, double wall sac of elastic connective tissue - Fibrous pericardium is the OuterLayer - Serous pericardium is the InnerLayer * Twolayers: Parietal & Visceral(epicardium) * Pericardialfluid located between inner layers (10-50 ml is normal) - PericardialReflection occurs where the parietal andvisceral pericardium meet |
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What does the pericardium do? |
- It Restricts theanatomical position of the heart *Restrainingeffect on cardiac filling - It Minimizes thefriction between the heart and adjacent structures *Lubricatingfunction to allow normal rotation, translation - It Preventsdisplacement of the heart and kinking of the great vessels *Separatesheart from mediastinum, lungs, and pleural space |
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Theproximal ascending aorta is: |
INTRApericardial |
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Thepulmonary veins are: |
EXTRApericardial |
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Pericarditis |
- Inflammationof the pericardium - ClinicalDiagnosis: pericarditisis not thesame as pericardial effusion - Causes: Idiopathic, bacterialor viral infection, trauma, transmural MI, uremia(kidney failure) |
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Symptoms/Presentation of Pericarditis |
- Positionalchest pain (CPworse lying down or with inspiration/CPrelieved by sitting up & bending forward) - Dyspnea - EKGchanges (ST elevation) - Newor increasing pericardial effusion - Pericardialrub/friction rub (Pericardialsurfaces rubbing together--hurtswhen you take a deep breath in) |
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Echo Assessment in Pericarditis |
Needto Assess Pericardium for: Thickening - Brightappearance - Multipleechoes - ConsiderPericardial Constriction Effusion - ConsiderCardiac Tamponade |
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Pericardial Effusion |
- Fluidaccumulation between visceraland parietal layers of the pericardium - Canbe blood or clear fluid - Physiologic effect depends on amountof fluid and rateof accumulation - Otherdisease states can cause pericardial effusion |
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Differential Diseases with Echo Findings of Pericardial Effusion |
- MalignantDiseases (lungcancer, breast cancer, lymphoma, melanoma) - InflammatoryDiseases (Lupus,scleroderma, uremia) - Intracardiac-Pericardial communications (Bluntchest trauma, post-cath, MILV rupture, aortic dissection) - InfectiousDiseases (viral,bacterial, ex: tuberculosis) |
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Echo Findings of Pericardial Effusion |
- Diffuse Effusion (echofree space symmetrically surrounding the heart) - FatPad – can be confused with an effusion (isolated anterior echo free space) - Posterior Systolic Separation (normalfinding, need~ 25cc of fluid for systolic and diastolic free space) - Fibrinous Stranding (echo dense structures within the pericardial fluid) - Loculated Effusion (localized,caused by adhesions, postcardiac surgery, recurrent effusions, rare– mets to pericardium)
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Pericardial Effusion Severity Scale |
- Physiologic: clearspace posteriorly in systole only (NORMAL) - Smalleffusion: <100cc, clearspace in systole and diastole posteriorly only and < 1 cm - Moderateeffusion: 100-500cc, posteriorclear space maintained in systole and diastole and is 1 to 2 cm in width - Largeeffusion: >500cc, clearspace seen in systole and diastole, surrounds the whole heart and is > 2 cmin width |
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Pitfalls in Assessing Pericardial Effusion |
- Mistaking dilated Coronary Sinus or Desc Aorta for a located effusion - Mistaking a Pleural Effusion for Pericardial Effusion - Pleural Effusion (it is posterior to the descending aorta in PLAX, and superior to RA from A4C) - Pericardial Effusion (it is anterior to descending aorta from PLAX , and pericardia leffusion is rarely located anteriorly alone due to gravity) - Needto assess in many and all views!! |
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Treatment for Pericardial Effusion and Pericarditis |
- Anti-inflammatoryAgents: Aspirin - Analgesics: Painkillers - Steroids: Prednisone |
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Pericardial Cyst |
- Rare,benign abnormality of the pericardium - Cystappears (typically) adjacent to RA in right costophrenicangle; echo-free appearance - Usuallyfound incidentally on CXR with no symptoms, but cysts have been found to causechest discomfort or rhythm disturbances - Diagnosisbest confirmed by MRI or CT |
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Cardiac Tamponade |
- Existswhen sufficient pericardial fluid has accumulated to impair ventricular fillingand decrease cardiac output - Pressurein the pericardium EXCEEDS the pressure in the cardiac chambers resulting inimpaired cardiac filling |
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Tamponade Physiology |
- Increasein pericardial pressure--Impairedfilling of cardiac chambers - Compressionof free walls--Whenpericardial pressure exceeds chamber pressure when it’s at its lowest (diastolefor ventricles, systole for atria) - Eventually,diastolic pressures in all chambers are equal and elevated - Intrapericardialpressure influenced by boththe volume of fluid and the rate at which it accumulates - A lotof fluid can accumulate slowly with no compromise or a small amount of fluidcan accumulate rapidly with compromise |
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Is cardiac tamponade a clinical or an echo diagnosis? |
Clinical |
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What are the steps on the path to tamponade? |
- Extra pericardial space is filled - Pericardialspace continues to fill with fluid at a faster rate than the pericardium canstretch - Whenthe rate is exceeded, the pressure increases in the pericardial space (resultsin pericardial space pressure higher than the intracardiacpressures) |
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Compensatory Mechanisms on Tamponade |
3Principal Features:
- Elevated intrapericardial pressures - Limitation of ventricular filling throughout diastole - Reduction of Cardiac Output |
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Clinical Features of Tamponade |
- Dyspnea - Orthopnea - Tachypnea - Tachycardia - Normalt o decreased blood pressure with narrow pulse pressure - Kussmaul’s sign - Beck’s triad - Chestdiscomfort - Shock - Diminished heart sounds - Pericardial friction rub - Localized effusion - Pulsus paradoxus - Electricalalternans - ElevatedJVP |
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Kussmaul's Sign |
- Rarein Tamponade - Usuallyseen in Constriction - The paradoxic riseor absence of inspiratory fall in the level of JVP during inspiration - Dueto the insulating effects of the fluid - Normal– usually see a decrease in JVP with inspiration - In tamponade/constrictionthere is an increasein the level of the JVP during inspiration |
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Beck's Triad |
- Hypotension - IncreasedJVP (withinspiration) - Small,quiet heart (decrease heart sounds) - Featuresare typically seen with rapid accumulation of fluid/blood |
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Pulsus Paradoxus |
- Exaggerationof the normal small decline in systolic blood pressure that occurs duringinspiration (Dropin systolic BP > 10 mm Hg with inspiration) - Definedas: the difference in systolic cuffpressure from the point at which sounds are heard intermittently duringrespiration and the point at which sounds are heard throughout the respiratorycycle |
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Electrical Alternans |
- Alternatingamplitude of QRS complex due to “swinging” heart within the pericardial fluid - Increased QRS voltage alternating with decreased QRS voltage |
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Tamponade Effects of LV |
- Impaired LV filling - Increase in LV diastolic pressure - Decrease in SV - Increase in HR in an attempt to maintain CO |
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Tamponade Effects of RV |
- Impaired RV filling - Increase in RV pressures - Increase in IVC & hepatic vein diameter |
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Symptoms/Presentation of Tamponade |
- Beck’s Triad - Symptoms of low CO - Tachycardia - Pulsus Paradoxus - Friction Rub - Hepatomegaly and spleen enlargement |
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Tamponade Findings on EKG and X-ray |
EKG: - Electrical Alternans - ST and T wave elevation in all leads, except AVR and V1 - Sinus Brady-->Cardiac Arrest (from exhaustion)
ChestX-ray: - Cardiomegaly |
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Echo Findings of Cardiac Tamponade in RA |
- RA collapses in late diastole/early systole - Very reliable predictor of tamponade - Intrapericardial pressures > RA pressure - Brief collapse may be normal - Inversion> 33% of R-R interval (Sensitivity94%, Specificity100%) |
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Echo Findings of Cardiac Tamponade in RV |
RV diastolic Collapse - Very reliable predictor of tamponade - Intrapericardial pressure > RV diastolic pressure - Absentin RVH or infiltrative disease - Bestseen in PLAX and/or SC with M-mode (Sensitivity60-90%, Specificity85-100%) |
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Echo Findings of Cardiac Tamponade with Inspiration/Expiration |
- Use respirometerduring echo – demo insp. + exp. - Ifemergent echo & suspect tamponade contact doctor - Changesin Ventricular Volume & Size - Inspiration (increasein RVID diastole, decreasein LVIDd, septumtoward LV in diastole & RV in systole, big non collapsing IVC) - Expiration (decreasein RVIDd, increasein LVID diastole, normalizationof septal motion) - Correlateswith Pulsus Paradoxus |
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RVIF TV E Velocity |
- Increase with inspiration
- Decrease with expiration - > or = to a 40% change needed between inspiration and expiration for a positive result |
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Hepatic Vein Flow |
- Increase diastolic reversal with Expiration - Decrease diastolic flow with Expiration |
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LVIF– MV E velocity |
- Decrease with Inspiration - Increase with Expiration - >or = to a 25% change needed between inspiration and expiration for positiveresult (MV) |
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Pulmonary Vein Flow |
- Increasein diastolic flow with expiration |
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Echo in the Diagnosis ofPericardial Effusion / Tamponade |
Pro: highsensitivity, procedureof choice for effusion, usesmultiple windows/views Con: cannotdetermine etiology, missinga locatedeffusion, noEcho finding has 100% predictive value |
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Treatment of Pericardial Tamponade |
- OftenEmergent - Hypotensioncan lead to shock and death - Pericardiocentesis –most effective treatment - Aka –Pericardial Tap or Tap - PericardialWindow - Pericardiectomy |
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Pericardial Constriction |
Conditionwhen the visceral and parietal layers of the pericardium are adherent,thickened, and fibrotic resulting in impaired diastolic filling. (also known as constriction, constrictive pericarditis, restrictive pericarditis) |
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Etiology of Pericardial Constriction |
CommonCauses: Idiopathic(unknown), repeated episodes of pericarditis, post cardiac surgery (Iatrogenic), post radiation therapy (Iatrogenic), infectious– bacterial (TB) or viral Less Common Causes: infectious– fungal, postMI, trauma, neoplasms, connectivetissue disease, lupus, scleroderma, rheumatoid Arthritis |
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Irradiation |
- Radiationto the chest - Affectscan be 1-30 years later - Usually15-16 years post radiation therapy |
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Post Myocardial Infarction |
Dressler’sSyndrome: - Delayedform of pericarditis - Immunesystem’s response following heart damage - Usuallyoccurs 1 to 12 weeks afteran MI - Commonto reoccur - Evaluatefor RWMA, Constrictive Pericarditis, and Pericardial Effusion - Rarefor Cardiac Tamponade tooccur |
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Symptoms and Clinical Findings ofPericardial Constriction |
- OftenNon-Specific and Subtle - Fatigue,weakness--dueto low CO - Generalmalaise - Jugularvenous distension - Distantheart sounds - Hepatomegaly,Ascites (late in disease state) - Peripheraledema (late in disease state) |
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ClinicalSigns and Symptoms |
Kussmaul’sSign: Paradoxic riseor absence of inspiratory fall in the level of the jugular venous pressureduring inspiration DiastolicPericardial Knock: FollowsS2 (closure of AV +PV) – mid to late diastole, dueto loss of pericardial elasticity Hepatosplenomegaly –liver & spleen enl.¤Dueto venous congestion |
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EKG findings with Pericardial Constriction |
- Flator inverted T waves - Lowvoltage QRS in all leads - Atrialfibrillation/flutter - NonspecificS-T/T wave changes - SinusTachycardia |
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Chest X-ray findings with Pericardial Constriction |
- Normalto slightly increased cardiac silhouette - Calcifiedpericardium |
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Physiology of Pericardial Constriction |
- ImpairedDiastolic Filling- dueto constrictive nature of pericardium - Pericardiumacts like a rigid container that the heart is placed in - Systolic function fairlynormal - Diastolic function impaireddue to rigid pericardium - Abruptcessation of diastolic filling |
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Right Heart and Left Heart Physiology of Pericardial Constriction |
RightHeart: Venousreturn to right heart decreases, systemicvenous pressures rises, rightsided failure ensues LeftHeart: Reductionin stroke volume, cardiac output, and blood pressure |
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2D and M-Mode Findings of Pericardial Constriction |
- AbnormalLVPW on M-Mode - LVPWflat in diastole – due to impairment of diastolicfilling; results in a flat pattern of posterior wall motion - DilatedIVC and Hepatic Veins--Reflectingelevated RA pressure, increasein hep veinflow with inspiration - Pericardialthickening -- Increasedor prominent - Abnormalseptal motion: Respiratoryvariations in RV and LV sizes with septal shift (Paradoxicalon M-mode, “Septalbounce” on 2D) |
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Hemodynamics with Pericardial Constriction |
- Disassociationbetween intrathoracicand intracardiacpressures - ExaggeratedVentricular Interdependence - Inspiration: Rightheart fills more, Leftheart fills less - Expiration: Rightheart fills less, Leftheart fills more |
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Echo Findings of Pericardial Constriction |
- AssessAtrial Filling Patterns - Rightupper pulmonary vein & hepatic vein - VentricularInflow Patterns - Increasein E point – rapid, early diastolic filling due to initial highatrial-to-ventricular pressure difference - ShortDecel Time – filling abruptly ceases due to high LV pressure - DecreasedA point – due to elevated LV diastolic pressure |
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Respiratory Changes with Pericardial Constriction |
Expiration: Decreaseof RVIF velocity, Increaseof LVIF velocity Inspiration : Intrapleural pressure becomes more negative causing: * Increase of RVIF velocity * Decrease of LVIF velocity >or = to a 25% change needed for positiveresult (MV) >or = to a 40% change needed for positiveresult (TV) %change between inspiration (E wave) and expiration (E wave) |
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Doppler Findings of Pericardial Constriction |
- Inspiration: * MitralE velocity: Decreaseof greater than or equal to 25% * TricuspidE velocity: Increaseof greater than or equal to 40% * Decelerationtimes shortenedto less than or equal to 160 sec * IVRTis prolonged - SVCflow does not change significantly respiration - Highpreload can mask respiratory changes |
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Hepatic Doppler Findings of Pericardial Constriction |
Inspiration: Slightincrease in diastolic forward flow Expiration: Decrease,disappearance or reversal of diastolicforward flownIncreasein diastolic flow reversals |
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Pulmonary Doppler Findings of Pericardial Constriction |
Inspiration: Slightdecrease or reversal in diastolic forward flow Expiration: Increasein diastolic forward flow |
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Complications of Pericardial Constriction |
- DecreasedCO and SV - CHF: dueto diastolic dysfunction - Canbe fatal ifnot diagnosed early |
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Management and Treatment of Pericardial Constriction |
Causeshould try to be identified and treated: - Diuretics,antibiotics Pericardiectomy: - typicallya surgical removal of parietal pericardium - Maysee “swinging heart” on echo - Signsand symptoms may not resolve immediately - Potentiallycurable – complete removal - 90%of patients see eventual symptomatic improvement - 5-15%mortality rate |
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Right and Left Heart Cath for Diagnosing Pericardial Constriction |
Rightand Left Heart Cath– Method of Choice - Ableto assess left and right sided pressures simultaneously - Allpressures will be elevated and equal “Squareroot” sign: - Typicalfinding on LV/LA pressure tracings - Brief,rapid fall of ventricular pressure in early diastole followed by a highend-diastolic pressure plateau (equalization of all chamber pressures) |
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"Square Root" Sign for Diagnosing Pericardial Constriction |
“Square root” sign: - Typical finding on LV/LA pressure tracings - Brief, rapid fall of ventricular pressure in early diastole followed by a high end-diastolic pressure plateau (equalization of all chamber pressures) |
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Chest X-Ray/CT/CMR for Diagnosing Pericardial Constriction |
ChestX-Ray, CT, or CMR - Calcificationof the pericardium - Slightlyincreased or normal cardiac silhouette - CMR/CT– accurate measurement of pericardial thickness |
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Constriction vs. COPD SVC Flow Velocity |
Constriction - SVCflow does not change significantly with respiration COPD - SVCflow is markedly increased with inspiration dueto intrapleuralpressure becoming more negative with inspiration-->RApressure decreases --> augmentation of SVC flow |
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Constriction vs. COPD Mitral E Velocity |
Constriction: Increasein LVIF velocity occurs immediately after the onset of expiration COPD: Increasein LVIF velocity occurs toward the end of expiration (velocities graduallyincrease and decrease; first beat may not have maximal change) - MVinflow not typically restrictive_____________ Obesity: May also mimic constriction - Workharder to breathe - Increase in intrathoraicpressure - Respiratory variation |
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Constriction vs. Restriction |
Constriction: - Thickenedand noncompliant pericardium - Respiratoryvariation of ventricular filling and interdependence - Septal bounce present Restriction: - Stiffand noncompliant ventricular myocardium - Mitralinflow rarely shows respiratory variation - Rapidearly filling and restrictive Doppler filling pattern |
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Constriction vs. Restriction Tissue Doppler E |
Restriction - e’markedly decreased (< .8 m/s) Constriction - e’relatively well preserved (> .8m/s) |
