UWorld 3 Flashcards
Acute pain, parasthesia, pallor and pulselessness of lower legs in patient with AFib
Acute arterial occlusion of lower extremity likely due to thromboembolism in setting of AFib.
If patient’s CHA2DS2VASC score is at least 2, he should be anticoagulated to reduce long term risk of systemic embolization
As far as choice of anticoagulation, ASA or ASA plus clopidogrel is significantly less effective than warfarin or target-specific oral anticoagulants like apixaban, dabigatran, rivaroxaban
Reflex syncope
AKA situational syncope. Neurally mediated syncope associated with specific triggers like micturition, defecation, cough. The triggers cause an alteration in the autonomic response and can precipitate a predominant cardioinhibitory, vasodepressor or mixed response.
Increased parasympathetic stimulation (cardioinhibitory) can manifest as profound bradycardia, varying degrees of AV block or asystole
Decreased sympathetic output can lead to vasodilation, hypotension or syncope.
What kinds of murmurs should worry us?
Diastolic and continuous murmurs are usually due to underlying pathology. Their presence should prompt further evaluation with a transthoracic echo which can find valvular regurgitation and evaluate for any associated structural abnormalities or hemodynamic consequences.
Midsystolic murmurs in otherwise young, ASx adults are usually benign and do not require further evaluation
High pitched blowing murmur. Gradually decreasing diastolic murmur. (decrescendo). Best heard along LSB at 3rd and 4th IC spaces with patient sitting up and leaning forward while holding breath in full expiration.
Aortic Regurgitation
Paroxysmal SVT
The most common paroxysmal tachycardia in people without structural heart disease.
Attacks begin abruptly and are characterized by HRs between 160-220 bpm. Most common mechanism underlying PSVT is re-entry into the AV node.
Mechanical and medical therapies for PSVT decrease AV node conduction.
Vagal maneuvers like valsalva, carotid sinus massage and immersion in cold water increase vagal tone and decrease conduction through AV node. This slows HR and can often break the rhythm.
Adenosine is a very short acting AV nodal blocker that is often used as well.
Atrial premature beats
AKA premature atrial complexes. Occur when there is premature activation of the atria originating from a site other than the SA node.
ECG will show early P wave. PACs by themselves represent a benign arrhythmia that can occur in healthy individuals and in patients with a variety of cardiovascular and systemic diseases.
They may occur singly or in a pattern of bigeminy. PACs are usually ASx. Sometimes, they can cause symptoms of “skipped” beats or palpitations. Sometimes they can precede AFib.
Tx is required only when symptoms cause distress or when there is SVT. B blockers are often helpful. Even in ASx patients, precipitating factors like tobacco, alcohol, caffeine and stress should be avoided.
Amiodarone side effects (10)
It is a class 3 antiarrhythmic drug. Often used for management of ventricular arrhythmias in patients with CAD and ischemic cardiomyopathy. Long term monitoring of PFTs and TFTs is recommended for early detection and recognition of potential side effects.
Cardiac
1) Sinus brady, heart block
2) Risk of proarrhythmias - QT prolongation and torsades
Pulm
1) Chronic interstitial pneumonitis (cough, fever, dyspnea, pulmonary infiltrates) most common
Endo
1) Hypothyroid
2) Hyperthyroid
GI/Hep
1) Elevated transaminases, hepatitis
Ocular
1) Corneal microdeposits
2) Optic neuropathy
Derm
1) Blue-grey skin discoloration
Neuro
1) Peripheral neuropathy
Pulm toxicity of amiodarone
A serious adverse effect of long term use that usually presents with chronic insterstitial pneumonitis (most common) but can cause ARDS.
Pulm toxicity correlates with total cumulative dose and usually occurs months to several years after initiation of drug.
Baseline CXR and PFTs are usually obtained prior to starting therapy and long-term surveillance is guided by development of signs of symptoms (cough, fever, dyspnea) suggestive of pulmonary toxicity
Apixiban mechanism
Oral factor 10a inhibitor (Stuart-Prower Factor)
How does CHF lead to hyponatremia?
Low CO along with decreased perfusion pressure at the baroreceptors and renal afferent arterioles leads to neurohormonal activation with the release of renin, NE and secretion of ADH.
ADH binds to V2 receptors in renal collecting ducts and promotes water reabsorption, while renin (via ATII) and NE increase proximal Na and water reabsorption and limit water delivery to the distal tubules.
These actions promote free water retention and lead to dilutional hyponatremia. This also contributes to hyperK.
Tx involves fluid restriction, ACEIs and loop diuretics.
Avoid salt tabs in edematous patients due to volume overload. Salt tabs are only used for hypoNa due to SIADH.
Mechanism for nitrates relieving pain in angina
Nitrates exert their effect by direct vascular smooth muscle relaxation causing systemic venodilation and an increase in peripheral venous capacitance.
Their primary anti-ischemic effect is mediated by systemic vasodilation (!!!) and decrease in cardiac preload (!!!) resulting in decreased LV EDV and LV ESV.
This leads to reduction in LV wall stress (!!!) which reflects afterload and is proportional to (pressure x radius all divided by thickness). Also, this decreases myocardial O2 demand (!!!) resulting in relief of anginal symptoms.
Monomorphic VTach
QRS complexes are wide and all match each other
Fusion beats
Capture of electrical signal though both the atrium and ventricle briefly leading to a hybrid of a normal and wide QRS complex (P waves precede fusion complex)
These are basically diagnostic for sustained monomorphic VTach (SMVT)
Management of patients with SMVT
Depends on symptoms and hemodynamic stability.
Patients with SMVT who are clinically and hemo stable can be initially managed with antiarrhythmic drugs. IV amiodarone is usually preferred, and other agents (procainamide, sotalol. lidocaine) are reserved for patients who do not respond to amiodarone.
Antiarrhythmics can convert SMVT to sinus rhythm and avoid need for urgent electrical cardioversion.
Synchronized electrical cardioversion is indicated for patients with persistent tachyarrhythmia who are severely symptomatic (AMS, acute HF or pulm edema, ischemic chest pain) or hemodynamically unstable (hypotension, signs of shock)
Meds to withhold prior to cardiac stress testing
1) Hold for 48h - B blockers, CCBs, nitrates. Should be continued though in patients with known CAD undergoing stress test to assess efficacy of antiangianal therapy.
2) Hold for 48h prior to vasodilator stress test - Dipyridamole
3) Hold for 12h prior to vasodilator stress test - Caffeine containing foods or drinks
4) Continue - ACEIs, ARBs, Digoxin, Statins, Diuretics
Gold standard for diagnosis of CAD
Coronary angiography - BUT it is expensive and invasive so first line in someone with low to intermediate probability pretest of CAD is stress testing.
DDx and features of various types of chest pain
CAD
1) Substernal
2) Radiation to arm, shoulder or jaw
3) Precipitated by exertion*
4) Relieved by rest* or nitro*
Pulm/pleuritic (pleurisy, pneumonia, pericarditis, PE)
1) Sharp/stabbing pain
2) Worse with inspiration
3) Pericarditis - worse when lying flat
4) PE, pneumothorax - respiratory distress, hypoxia
Aortic (dissection, intramural hematoma)
1) Sudden, severe tearing pain
2) Radiates to back*
3) Elderly men
4) HTN and risk factors for atherosclerosis
GI/esophageal
1) Nonexertional, relieved by antacids
2) Upper abdominal and substernal
3) Associated with regurgitation, nausea, dysphagia
4) Nocturnal pain*
5) Prolonged CP lasting more than an hour***, postprandial symptoms, associated heartburn or dysphagia (all point to esophageal etiology)
Chest wall/MSK
1) Persistent and or prolonged pain
2) Worse with movement or change in position
3) Often follows repetitive activity
AAA
Usually ASx and discovered incidentally. Found as a pulsatile abdominal mass.
AAA rupture is life threatening. All incidentally discovered aneurysms require close f/u.
Imaging modality of choice is abdominal US. It is nearly 100% sensitive and specific, allows size measurement, and can show presence of any associated thrombus.
AAA rupture
Patient with pulsatile abdominal mass, hypotension and abdominal pain. Forego imaging and get to OR right away.
CYP450 inhibitors (8)
Increase Warfarin effect (increased bleeding risk)
1) Acetaminophen, NSAIDs
2) ABx/Antifungals (metronidazole)
3) Amiodarone
4) Cimetidine
5) Cranberry juice, Ginkgo biloba, Vitamin E
6) Omeprazole
7) Thyroid hormone
8) SSRIs (fluoxetine)
CYP450 Inducers (5)
Decrease warfarin effect (lower efficacy)
1) Carbamazepine, phenytoin
2) Ginseng, St Johns Wort
3) OCPs
4) Phenobarbital
5) Rifampin
Ventricular aneurysm
Post MI complication (5d to 3mo) consisting of thin and scarred or fibrotic myocardium in remodeled areas affected by an ST segment elevation or a transmural MI. Patient presents with progressive decompensated CHF.
Usually, ST segment elevations go away within a few weeks of an MI. VAs present with ECG findings of persistent ST elevation after recent MI and deep Q waves in the same leads.
Large VAs can lead to progressive LV enlargement, causing heart failure, refractory angina, ventricular arrhythmias, mural thrombus with systemic arterial embolization, or mitral annular dilation with MR.
Dx confirmed by echo (thinned, dyskinetic LV portion in the area of prior MI)
Dressler
Acute pericarditis can present in first several days after MI and can cause diffuse ST segment elevation.
Post-cardiac injury syndrome (Dressler) is an immune-mediated pericarditis that can occur weeks to months post MI.
What might raise suspicion for free wall rupture after MI?
Large pericardial effusion. Usually causes cardiac tamponade (dyspnea, hypotension, pulsus paradoxus, high jugular pressure) and can progress rapidly to pulseless electrical activity.
Papillary muscle rupture following MI
Mechanical complication typically occurring 2-7d post MI. Presents dramatically with acute severe MR (hypotension, pulm edema, cardiogenic shock) and does not cause persistent ST segment elevations
Lung fields in setting of RV infarct
Clear. They usually have elevated JVPs and hypotension.
Hypertensive complications (urgency vs emergency)
Urgency
1) Severe HTN (usually at least 180/120) with no symptoms or acute end organ damage
Emergency - Severe HTN with acute, life threatening end organ complications
1) Malignant - Severe HTN with retinal hemorrhage, exudates or papilledema
2) Hypertensive encephalopathy - severe HTN with cerebral edema and non-localizing neuro symptoms and signs
Development of AV block in patient with infective endocarditis should raise suspicion for what?
Perivalvular abscess extending into adjacent cardiac conduction tissues. Aortic valve endocarditis and IV drug abuse are associated with an increased risk of periannular extension of endocarditis.
Perivalvular abscess is seen in about 30-40% of patients with IE at time of surgery or autopsy.
Location of AR murmur
When it is due to valve disease the early diastolic murmur is best heard along LSB (3rd and 4th IC space)
When it is due to aortic root disease, it is best heard along RSB
When should renovascular HTN (Renal artery stenosis) be suspected?
Suspect and evaluate if:
1) Elevation in serum Cr more than 30% from baseline after starting ACEI or ARB
2) Severe HTN in patients with recurrent flash pulm edema
3) Severe HTN in patients with diffuse atherosclerosis
4) Onset of severe HTN after age 55
5) HTN in a patient with asymmetric kidney size or a small atrophic unilateral kidney
6) Presence of abdominal bruit (high specificity)
Summary: Suspect in all patients with resistant HTN and diffuse atherosclerosis, asymmetric kidney size, recurrent flash pulm edema or elevation of serum cr by more than 30%
What other conditions is variant angina often associated with?
Other vasospastic disorders like Raynaud’s and migraine HAs.
Most common cause of MR in developed countries
MVP - mild MR with mid systolic click and mid to late systolic murmur.
Adverse effects of phosphodiesterase 5 inhibitors
CV
1) Hypotension (esp with nitrates, alpha blockers like doxazosin)
Ocular
1) Blue discoloration of vision
2) Nonarteritic anterior ischemic optic neuropathy
GU
1) Priapism
Other
1) Flushing
2) HA
3) Hearing loss
Ventricular remodeling after MI
Following a MI, ventricular remodeling occurs and gradually causes dilatation of the LV with thinning of the ventricular walls. This can result in CHF.
Ventricular remodeling occurs in the weeks to months following a MI; therefore it is often missed on the discharge echo.
ACE Inhibitors have been shown to limit ventricular remodeling. An ACEI should be started within 24h of MI in all patients without a contraindication.
AFib with RVR tx
Rate control should be tried first with beta blockers or CCBs. Immediate synchronized electrical cardioversion is indicated is indicated in hemodynamically unstable patients with rapid AF
Features of constrictive pericarditis
Etiology
1) Idiopathic or viral pericarditis
2) Cardiac surgery or radiation therapy*
3) TB pericarditis (in endemic areas)
Clinical presentation
1) Fatigue and dyspnea on exertion
2) Peripheral edema and ascites
3) Increased jugular venous pressure
4) Pericardial knock may be heard
5) Pulsus paradoxus
6) Kussmaul’s sign
Diagnostic findings
1) ECG may be nonspecific or show atrial fib or low-voltage QRS complex
2) Imaging shows pericardial thickening and calcification
3) Jugular venous pulse tracing shows prominent x and y descents
Hodgkin lymphoma cardiac complications
Acute or delayed pericardial disease, myocardial ischemia/infarction, restrictive cardiomyopathy, CHF, valvular abnormalities, and conduction defects
Survivors are at increased risk for cardiac disease that can present as much as 10-20 years or more after mediastinal irradiation and/or anthracycline therapy
What causes constrictive pericarditis
It’s the result of scarring and subsequent loss of normal elasticity of the pericardial sac. The inelastic pericardium prevents venous return to the right heart during inspiration and leads to R HF.
Patients typically present with peripheral edema, ascites, and hepatic congestion with hepatomegaly, which can progress to cirrhosis (cardiac cirrhosis).
Patients may have pericardial calcifications on CXR. Echo confirms dx and typically shows increased pericardial thickness, abnormal septal motion, and biatrial enlargement.
Diuretics provide temporary relief, and pericardiectomy is definitive treatment for patients with refractory symptoms.
Dipyridamole
Can be used in myocardial perfusion scanning when exercise testing is not possible (amputee for example). It is a coronary vasodilator (like adenosine).
Infusion of these substances in patients without CAD increases coronary blood flow 3-5 times above baseline levels. However, in patients with CAD, the diseased vessels distal to the obstruction are already maximally dilated and their ability to increase myocardial perfusion is limited.
Therefore, redistribution of coronary blood flow to non-diseased areas occurs, and the perfusion of “diseased” segments diminishes. This phenomenon demonstrated by dipyridamole is called coronary steal and is used to diagnose ischemic heart disease.
3 most common causes of aortic stenosis in general population
Senile calcific aortic stenosis, bicuspid aortic valve, and RHD.
A bicuspid aortic valve is the cause of AS in majority of patients under 70 years old.
Chronic venous insufficiency
A common cause of peripheral edema. Suspect in patients with isolated lower extremity edema and/or dilated veins with otherwise normal physical exam. Presentation may look like this: bilateral lower extremity pitting edema, varicose veins and venous ulcer.
May have normal JVP (less than 3cm above sternal angle) indicating that HF is not likely.
Patients may present with leg discomfort, pain, or swelling that typically worsens with prolonged standing and improves after walking or limb elevation.
Depending on severity, leg exam may show abnormal venous dilation (telangiectasia, varicose veins), pitting edema, skin discoloration, dermatitis/eczema, lipodermatosclerosis, or skin ulcerations such as a medial ankle ulcer.
Initial treatment of chronic venous disease includes leg elevation, exercise and compression stockings.
Patients not responding require venous duplex US to identify venous reflux or insufficiency. Patients with persistent symptoms and documented reflux should be referred for endovenous ablation
Stress-induced (Takotsubo) cardiomyopathy
AKA apical ballooning syndrome AKA Broken Heart Syndrome
Refers to transient systolic dysfunction of apical and/or mid segments of the LV with hyperkinesis of the basal segments causing a balloon like appearance of LV in systole. Seen usually in older adults in response to intense physical or emotional stress or acute medical illness (unexpected death of relative, grave medical diagnosis, arguments, significant loss)
Statin mechanism
Inhibit an intracellular synthesis pathway
They inhibit HMG-CoA reductase enzyme, prevent conversion of HMG CoA to mevalonic acid and increase the number of cell membrane LDL receptors.
Statins also decrease Coenzyme Q10 synthesis, which is involved in muscle cell energy production and possibly contributes to statin-induced myopathy
Supravalvular AS
Second most common type of AS. Usually refers to congenital LV outflow tract obstruction due to discrete or diffuse narrowing of the ascending aorta.
This causes a systolic murmur similar to that seen with valvular AS; however the murmur is usually best heard at the first right IC space, higher than where the valvular As murmur is best heard.
Patients may also have unequal carotid pulses, differential BP in upper extremities (high pressure jet in ascending aorta) and a palpable thrill in suprasternal notch.
Patients with significant supravalvular AS develop LVH over time and can also have coronary artery stenosis as an associated anomaly. These changes, along with the increase in myocardial oxygen demand during exercise can lead to subendocardial or myocardial ischemia, which can cause anginal symptoms during exercise
AAA screening
USPSTF recommends screening male active or former smokers aged 65-75 years with a one-time abdominal US to evaluate for an AAA. No recs for people who have never smoked.
Screening and surgical repair of large AAAs (5.5cm or greater) have been found to decrease AAA-specific mortality in this population.
Uremic pericarditis
Sharp and pleuritic CP, pericardial friction rub, uremia.
UP occurs in 6-10% of renal failure patients, typically in those with BUN above 60. However, the degree of pericarditis does not always correlate with degree of serum BUN or Cr elevation.
UP does not usually present with the classic ECG findings of pericarditis (like diffuse ST segment elevations) as the inflammatory cells do not penetrate the myocardium
Dialysis is the most effective treatment for UP and can resolve symptoms and decrease the size of any pericardial effusion.
Systemic anticoagulation (heparin) can cause hemorrhage into pericardial space and should be avoided during hemodialysis.
Etiologies of pericarditis (6 big groups)
1) Infection - viral (most common), bacterial
2) Iatrogenic - Surgery, trauma, radiation and drug-related
3) Connective tissue disease - RA, SLE
4) Cardiac - Dressler syndrome (post MI pericarditis), usually 1-6w after MI
5) Uremic - Serum BUN usually above 60, but degree of pericarditis does not always correlate with degree of elevation
6) Malignancy - Can be due to cancer (lung and breast, Hodgkin) or treatment (radiation, chemo)
Pathognomonic ECG finding for pericardial effusion
Electrical alternans (Varying amplitude of QRS complexes). It is due to swinging motion of heart in the pericardial cavity that causes a beat-to-beat variation in QRS axis and amplitude.
Electrical alternans with sinus tachy is highly specific for pericardial effusion, but not sensitive
Patients with cardiac tamponade and hemodynamic compromise should have emergency pericardiocentesis
Risk factors for developing AAA
1) Older age (over 60)
2) Smoking
3) FHx
4) White
5) Atherosclerosis
Strongest predictors of AAA expansion and rupture
1) Large diameter
2) Rapid rate of expansion
3) Current smoking
Current indications for operative or endovascular AAA repair
1) Aneurysm size above 5.5cm
2) Rapid rate of expansion (more than 0.5cm in 6 months or more than 1cm in 1 year)
3) Presence of symptoms (abdominal, back, flank pain; limb ischemia) regardless of size
Second degree AV block. Mobitz 1 vs 2
Level of block
1) Usually AV node
2) Below the level of AV node like in Bundle of His
ECG
1) Progressive prolonged PR interval leads to a nonconducted P wave (group beating)
2) PR interval remains constant with intermittent nonconducted P waves
QRS
1) Narrow
2) Narrow or wide
Exercise or atropine
1) Improves it
2) Worsens it
Vagal maneuvers (carotid sinus massage)
1) Worsens it
2) Paradoxically improves it
Risk of complete Heart block
1) Low (it’s a benign rhythm)
2) Higher risk, indication for pacemaker
First degree AV block
Due to delayed impulse transmission from atria to the ventricles leading to a prolonged PR interval greater than 0.2s.
The PR interval remains constant and there is a QRS complex present for every P wave
If patient has normal QRS duration there is no further evaluation needed. If patient has prolonged QRS then they likely have a conduction delay below AV node and should have electrophysiology testing to determine its nature.
Third degree AV block (complete block)
Refers to complete failure of impulse conduction from atria to the ventricles. On ECG rhythm strip, P waves are entirely unrelated to QRS complexes and can be found before, after, or even buried in QRS complexes.
Reversible causes of pulseless electrical activity
5 Hs and Ts
1) Hypovolemia
2) Hypoxia
3) Hydrogen ions (acidosis)
4) Hypo or hyperK
5) Hypothermia
6) Tension pneumo
7) Tamponade, cardiac
8) Toxins (narcotics, benzos)
9) Thrombosis (pulm or coronary)
10) Trauma
Isolated systolic HTN
SBP above 140 with diastolic BP below 90. It is associated with severalfold increase in risk for CV mortality and morbidity. Similar to way that primary HTN is managed, treatment should include lifestyle mods and pharm.
It is an important cause of HTN in elderly patients and is caused by increased stiffness or decreased elasticity of the arterial wall. This change reduces ability of arteries to dampen the systolic pressure and leads to an increased pulse wave velocity and pulse wave reflection in systole.
What percentage of patients with Mitral Stenosis develop AFib?
70%. This is due to LA dilatation.
Indications for urgent dialysis
AEIOU
1) Acidosis - metabolic acidosis - pH less than 7.1 refractory to medical therapy
2) Electrolyte issues - Symptomatic hyperK (ECG changes or ventricular arrhythmias), Severe hyperK (K above 6.5 refractory to medical therapy)
3) Ingestion - Toxic alcohols (methanol, ethylene glycol), Salicylate, Lithium, Sodium vaproate, carbamazepine
4) Overload - volume overload refractory to diuretics
5) Uremia - Symptomatic (Encephalopathy, Pericarditis, Bleeding)
Risk factors and clinical features of atheroembolism (cholesterol crystal embolism)
Risks
1) Comorbid conditions (hypercholesterolemia, HTN, T2DM)
2) Cardiac cath or vascular procedure
Clinical
1) Derm (livedo reticularis), ulcers, gangrene, blue toe syndrome
2) Renal (acute or subacute kidney injury)
3) Central nervous system (stroke, amaurosis fugax)
4) Ocular involvement (Hollenhorst plaques)
5) GI (intestinal ischemia, pancreatitis)
Dx of atheroembolism
Labs
1) High serum Cr, eosinophils, hypocomplementemia
2) UA - typically benign with few cells or casts, may have eosinophiluria
Skin or renal biopsy
1) Biconvex, needle shaped clefts within occluded vessels
2) Perivascular inflammation with eosinophils
Treatment for stable chronic angina
Antianginal
1) Beta blocker
a) 1st line for anginal symptoms, improves exercise tolerance
b) relieves angina by decreasing myocardial contractility and HR
c) improves survival in those with MI
2) CCB
a) Can combine with BB if angina persists or as alternate therapy
b) Improves angina by causing peripheral and coronary vasodilation
3) Nitrates
a) Short acting form is used in the acute setting
b) Long acting is an add-on therapy for persistent therapy
Preventive
1) ASA
2) Statin
3) Smoking cessation
4) Regular exercise and weight loss
5) Control of BP and diabetes
Cor Pulmonale
CP refers to impaired function of the RV caused by pHTN that occurs due to underlying diseases of the lungs (COPD, ILD), pulmonary vasculature (Idiopathic PAH) or OSA. By convention, RV dysfunction due to L heart disease or congenital heart disease is NOT considered Cor Pulmonale.
Patients with Cor Pulmonale typically present with exertional symptoms (dyspnea, angina, syncope), anorexia or abdominal pain (due to hepatic congestion), and peripheral edema.
Exam may show loud P2 (pulmonic component of S2) and a RV 3rd heart sound, tricuspid regurg murmur (holosystolic at LSB, augments with inspiration), elevated JVP with hepatojugular reflux, hepatomegaly with pulsatile liver, and occasionally ascites or pleural effusion.
Dx of CP is based mainly on clinical features and echo findings (RVH, tri regurg with RA enlargement). If needed, definitive dx can be made using R heart cath showing pulm artery systolic pressure above 25.
Acute limb ischemia after MI
Suggests possible embolus from LV thrombus. Management includes immediate anticoagulation, vascular surgery consult, and TTE to screen for LV thrombus and evaluate LV function
Hepatojugular reflux
Useful clinical tool that can differentiate between cardiac and liver disease related causes of lower extremity edema.
Patients with peripheral edema due to heart failure have elevated JVP and positive HJR.
Those with peripheral edema due to primary hepatic disease and cirrhosis have reduced or normal JVP and negative HJR.
HJR is elicited by applying firm and sustained pressure for 10-15s over upper abdomen. Positive response is sustained elevation of JVP greater than 3cm during continued abdominal compression. It is reflection of failing RV that cannot accommodate an increase in venous return with abdominal compression
Most common causes of a positive HJR
Constrictive pericarditis, RV infarct, and restrictive cardiomyopathy
Look out for history of TB (constrictive pericarditis)
What should be done in all patients who undergo central venous cath?
CXR to confirm correct placement before giving any drugs or agents through the catheter.
Pericardial effusion on CXR
Appears as enlarged, water bottle shaped cardiac silhouette on CXR. Exam findings of effusion without tamponade include diminished heart sounds on auscultation and a maximal apical impulse that is hard to palpate
