Cardiac Tumours

Epidemiology

• Primary cardiac tumours are extremely rare
  • Metastatic tumours are 30-40 times more prevalent
  • Of all the primary tumours, myxoma is the most common, accounting for up to half of all primary benign tumours in adults
    • In children, rhabdomyomas are more common

Types

• Benign Primary tumours
  • Myxoma
    • The majority seem to be located in the left atrium and are pedunculated.  They may prolapse through the mitral valve during diastole and prevent ventricular filling.
    • They can be smooth/firm or friable/irregular.  The latter can often present with systemic embolism.
  • Papillary fibroelastomas
    • Avascular papillomas usually occurring on the mitral or aortic valves.  They don’t often cause any valvular disruption but present instead with embolic disease.  Usually found in older people.
  • Rhabdomyomas
    • Most common heart tumour in children, and commonly associated with Tuberous Sclerosis.  Most are located intramurally or free wall of the left ventricle, and can affect the conduction system.  They can regress with age but a minority can develop tachyarrhythmias/heart failure due to outflow obstruction.
  • Other types of benign tumours include fibromas (often found in childhood and associated with renal tumours or basal cell naevus syndrome); Haemangiomas; Teratomas; Lipomas; Paragangliomas (including phaeochromocytomas) and Pericardial cysts)
• Malignant tumours
  • Sarcoma
    • 2nd most common primary tumour and most common malignant primary- it affects mainly middle-aged adults and originate in the right atrium, involving the pericardium and can cause right ventricular inflow obstruction and pericardial tamponade.  It frequently metastasises to the lung.
  • Other types include lymphoma and pericardial mesothelioma.
• Metastases
  • Most common although rare in general- usually from the lung, breast or kidney cancers.

Symptoms/Signs

• Many patients can be asymptomatic (found incidentally on imaging)
• Symptoms largely depend on the size, location and character of the tumour, but there may be a triad of features
  • Valvular obstruction
    • I.e. left or right sided heart failure
      • Left sided: shortness of breath; orthopnoea; pulmonary oedema
      • Right sided: peripheral oedema; ascites; raised JVP
  • Embolic events
    • Most tend to be left sided and therefore systemic embolic events
      • Stroke or tissue/organ ischaemia
  • Constitutional symptoms
    • Weight loss, fatigue, weakness, fever, arthralgia
    • May resemble infective endocarditis
• A diastolic murmur may be audible with myxomas, and an audible ‘tumour plop’ may be heard too as the tumour passes through the mitral valve.

Investigation

• Due to the rarity of these tumours- often symptoms are investigated for other causes and diagnosis may be delayed
• Echocardiogram may detect tumours
• Cardiac MRI is used to stage tumours

Management

• Depends on the tumour type, individual patient and predicted outcome
• In general
  • Benign primary tumours should be offered excision (note that this is entirely dependent on individual and their functional status
  • Malignant primary tumours are general palliative
  • Metastatic disease should be treated depending on the primary

Brugada Syndrome

An ECG abnormality with a high incidence of sudden death in patients with structurally normal hearts.

Aetiology

• Most cases due to a mutation in a cardiac sodium channel gene (sodium channelopathy)
  • Most are spontaneous but occasionally there are hereditary cases

Features/Diagnostic criteria

• NB Can be transient and/or can be unmasked/augmented by a number of factors e.g. fever, ischaemia, drugs (notably sodium channel blockers e.g. flecainide; calcium channel blockers; alpha receptor agonists; beta blockers; nitrates; cocaine; alcohol), hypokalaemia, hypothermia, cardioversion
• ECG findings
  • Type 1
    • Coved ST segment elevation >2mm in >1 of V1-V3, followed by a negative T wave (Brugada sign)
  • Note that this is the only sign that is potentially diagnostic.  It must be associated with one of the following to make the diagnosis:
    • Episode of VF or polymorphic VT
    • Family history of sudden cardiac death <45 years old
    • Coved type ECGs in family members
    • Inducibility of VT with programmed electrical stimulation
    • Syncope
    • Nocturnal agonal respiration
  • Type 2 sign has >2mm of saddleback shaped ST elevation and type 3 can be either morphology but with <2mm elevation

Other investigations

• Where the patient is asymptomatic, it may be appropriate to carry out electrophysiological testing to try and induce VT in patients with ECG changes.  However, this is often not conclusive and does carry significant risk.
  • Alternatively, attempting to induce VT with a dose of flecainide may also help with diagnosis, but has similarly poor diagnostic capability and can be dangerous.

Management

• The only proven management for Brugada syndrome is an ICD device.

Arrhythmogenic right ventricular cardiomyopathy

Background

• Autosomal dominant condition characterised by abnormal cardiac proteins (potentially desmosomal proteins) which causes breakdown of the hear muscle and replacement with fibrous/fatty tissue
  • Usually affects the right side but can affect both
  • Uncommon 1:2000
• These patients are at increased risk of ventricular arrhythmias, sudden death (serious cause of sudden death in <35 year group- and accounting for around 20% of sudden cardiac deaths) and right heart failure

Pathogenesis

• Four phases
  • Concealed phase
    • Small changes to the right side of the heart.  Patients are asymptomatic
  • Overt phase
    • Symptomatic right ventricular arrhytmias associated with functional and structural changes
  • Right heart strain/failure
    • Disease affecting the entire right ventricle
  • Left ventricular impairment

Presentation

• Usually presents in young adult males
• Occasionally, patients may present with symptoms such as
  • Arrhythmias e.g. syncope, palpitations, light-headedness/dizziness
  • Shortness of breath
  • Leg swelling/abdominal distention/ascites (Right heart strain)
• Unfortunately, many patients are asymptomatic until sudden cardiac death (diagnosis made at autopsy)

Investigations

• ECG may show a slightly broad QRS complex and inverted T waves in the right precordial leads (II < III; V1 > V2)
  • Left bundle branch block is common
• ECHO and MRI scans can confirm the diagnosis (fatty deposits seen on MRI)

Management

• Implantable defibrillator is an option for patients at risk of sudden death (drug treatments such as sotalol or amiodarone + beta blocker may help)

Evaluating Cardiac Murmurs

Once you have identified which murmur…

• A murmur is (technically) NOT a diagnosis but a sign.  Therefore you should ask WHY is there a murmur.  This may involve further investigation e.g.
  • Echocardiogram – will often further evaluate the severity and impact of a murmur but may not provide a cause.
  • Imaging- e.g. CTPA (particularly if SOB and pulmonary regurgitation- to rule out PE as cause)
  • ECG- may show signs of past infarction which may explain a murmur
• Management of murmurs really depends on the underlying cause and whether it is reversible.  It also depends on the impact of the murmur on cardiac function.  A large number are managed conservatively (particularly idiopathic aortic stenosis), although it is a good idea to manage any underlying risk factors for cardiac disease e.g. cholesterol, blood pressure, weight, etc.

Varicose Veins

Background

• Valve insufficiency in the veins (usually in the leg) cause a back up of pressure in the venous system.  Thin walled superficial veins are unable to cope with higher pressures and so dilate and become tortuous.
  • The most common valves involved are located at the sapheno-femoral junction
• Varicose veins are extremely common, with an incidence of around 2.5% of women and 2% of men.
  • Age, pregnancy, liver disease, previous DVT and family history all seem to increase the risk of varicose veins

History

• Quite often patients present without any symptoms – veins are bothering them because of aesthetic reasons
  • Important to ask about symptoms e.g. itching, discomfort, heaviness of the legs, night cramps, oedema, burning, paraesthesia, excercise intolerance, weakness, restless legs etc.
    • Classic picture is of dull ache which is worse with prolonged standing
  • Check SOCRATES i.e. onset, duration, timing/change, exacerbating/alleviating factors etc
• Make sure also to ask about
  • PMHx- Varicose veins (and any previous assessments/management), DVT, trauma, oedema, liver problems, cardiovascular disease; and Drug history
  • Social history- in particular, occupation that may involve prolong standing

Examination

• Inspection
  • Inspect both legs fully exposed with the patient standing first
    • Usually inspect from the anteromedial aspect of the thigh to the lateral aspect of the leg (long saphenous vein route); and then the back of the calf (short saphenous)
    • Look also for skin changes e.g. haemosiderin deposition, eczema, ulcers, thinned skin etc
• Palpation
  • Palpate the varicosities for tenderness (thrombophlebitis- normally should be painless); if they are hard this may suggest thrombosis
    • See if the veins will empty and refill with palpation
  • Palpate the skin if there any changes
  • Cough impulse test (whilst standing- tests for saphenofemoral insufficiency)
    • Locate the saphenofemoral junction by locating the femoral pulse then moving medially (vein) then two fingerbreadths inferiorly
    • Compress the area and ask the patient to cough
      • If a ‘thrill’ is felt, suggests that the valve here is incompetent
  • Elevate the leg to around 15 degrees and check the rate of vein emptying
• NB Other special tests e.g.
  • Trendelenberg test (tests for the location of the incompetent valve using a tourniquet at the level of the saphenofemoral junction to prevent refilling on standing- shows incompetence at the level of the SFJ; Note the tourniquet can be applied lower down the leg to check at which level the incompetence arises)
  • Perthes’ manoeuvre (using a tourniquet to prevent superficial filling and asking the patient to activate calf muscles by standing on tip toes repeatedly- normally emptying the varicosities by paradoxically filling in deep vein obstruction) have been used in the past but have now become surplus due to evaluation by Doppler USS.
• You should also auscultate varicosities and check for pitting oedema and peripheral pulses (a JVP assessment may also be appropriate where oedema is present).

Management

• Lifestyle – although unlikely to reverse the process, losing weight and exercise will prevent deterioration and further varicosities
  • NB Compression stocking may also prevent further varicosities but are not recommended for management unless further management (intervention) is not possible)
• Interventional management
  • Endothermal ablation
  • USS guided foam sclerotherapy
  • Avulsion
  • Ambulatory phlebectomy
  • Injection sclerotherapy

ECG Interpretation

Below is a systematic approach to the interpretation of the ECG.

1. Check Patient Details
   1. Name, DOB (and age), patient number
2. Rate
   1. Calculate either by
      1. 300 divided by the number of large squares between each QRS complex (if the rhythm is regular)
      2. or by multiplying the total number of QRS complexes in a rhythm strip (usually 10 seconds) by 6
3. Rhythm
   1. Is the rhythm regular or irregular?
      1. Regularly irregular (heart block)
      2. Irregularly irregular (Atrial fibrillation)
4. Axis
   1. The most accurate way of determining the axis is by REMEMBERING THIS DIAGRAM
      1. I.e. lead I (0°); lead II (60°); lead III (120°); aVF (90°); aVR (-150°) and aVL (-30°).  Also -30-90° is normal; >90° is RAD; <-30° is LAD
      2. You then can calculate the axis by finding the iso-electric lead and +/- 90°.  Depending on the positive leads, you can determine the axis.
         1. e.g. if the isoelectric lead (biphasic lead with similarly sized positive and negative deflections) is lead aVL (-30°), the axis will either be 60° or -120°.  If leads I (0°), II (60°) and aVF (90°) are all positive, we know it must lie within this range, so it has to be 60° (normal axis).
      3. In short the axis is always in the direction of positive leads, away from negative leads and 90° to isoelectric leads.
   2. Alternatively, 
   3. RAD suggests right ventricular hypertrophy e.g. Pulmonary hypertension; mitral stenosis; PE (note there can also be the classic prominent S wave in lead I and prominent Q wave in lead III and inverted T wave in lead III (S1Q3T3)); cor pulmonale; right ventricular cardiomyopathy.
   4. LAD can be due to left ventricular hypertrophy but is more commonly seen in LBBB, inferior MIs and other conduction defects e.g. WPWS
5. Go through the waveform systematically
   1. P-waves: Present/Absent (Atrial fibrillation/flutter)
   2. PR interval (0.12-0.2 secs/3-5 small boxes): Normal/prolonged (see heart block)
   3. QRS complex (<0.12 secs): Narrow (normal) or broad (Ventricular arrhythmias; bundle branch block)
   4. ST-segment: elevated/normal/depressed (ischaemic changes (see ACS))
   5. T waves: normal/inverted/tall (old ischaemic changes or acute MI/hyperkalaemia)

Warfarin Prescribing and Counselling

NB- Make sure to follow local guidance on warfarin prescribing (there are often slight differences- not all guidance is the same)

Indications

• Venous thromboembolism (DVT/PE)
• Atrial Fibrillation (and pre/post-cardioversion)
• Valvular heart disease and valve replacements
• Mitral stenosis/regurgitation (with AF or history of systemic embolism/left atrial thrombus/enlarged left atrium)
• Dilated cardiomyopathy

Contraindications

• Haemorrhagic stroke
• Bleeding disorders (including liver failure/renal failure)
• Potential bleeding lesions e.g. peptic ulcer, varices, aneurysm, proliferative retinopathy, recent trauma
• Uncontrolled severe hypertension (SBP>200mmHg; DBP>120mmHg)
• Pregnancy

Counselling patients about warfarin

• WIPE (Wash hands, Introduce self, Check Patient details, Explain why you are there)
  • It is good to check understanding of warfarin, patient’s condition, risks and benefits, any contraindications (double check consent)
  • Explain
    • Side effects e.g. Bleeding/bruising, rash, alopecia, nausea/diarrhoea
      • Explain when to contact doctor/medical attention e.g. blood in urine, in vomit, in sputum/cough, excessive nose bleeds, excessive PV bleeding, prolonged wound bleeding (generally >5 mins for small cuts)
    • Drug interactions
    • Monitoring
• Explain how to take/compliance
  • Try to take at same time every day (e.g. 6pm in the evening)
    • Take missed dose ASAP (within 6 hours of missed dose)- do not double up doses
  • Explain the different warfarin doses/tablets (colours) and how to make up the dose
  • Explain the yellow book (or equivalent) and alert card
  • Explain the importance of not running out of tablets.
  • Explain duration of therapy
    • For single VTE (with explanation)- 3 months; (without explanation)- 6 months
    • For recurrent VTE – usually long term
    • For AF – as long as the condition persists
    • Valve replacements- lifelong
    • Cardioversion – 4 weeks before and after
  • Explain monitoring- measure INR initially every few days/every week; if the INR is stable on a good maintenance dose, the frequency can be reduced
• Explain lifestyle changes
  • Advise against contact sports
  • Advise re certain foods e.g. broccoli, sprouts, cabbage, liver, pork, cranberry juice, grapefruit juice- try to limit/avoid
  • If a heavy drinker, recommend cutting down (make sure to check LFTs/clotting prior to initiation).  Ideally, minimal alcohol intake.
  • Discuss appropriate contraception- in general try to avoid oestrogen containing preparations.  Reinforce importance of contraception and warfarin in pregnancy.
  • Advise about falling ill/going to hospital- letting staff know about the prescription.  Also re: drug interactions (don’t take aspirin, seek advice before starting herbal/alternative preparations, inform doctor before starting any new drugs/change of dose- may require more frequent INR monitoring)
    • Also important to inform your dentist
• Explain initiation
  • 2 kinds- fast/rapid (for acute VTE/valve replacement) and slow (for AF/valve disease)
  • Fast initiation
    • Usually used in combination with LMWH (for 4 days minimum and until INR>2)
    • ‘Loading dose’ of warfarin is usually 5mg (can be 10mg if there are no risk factors: age>60; body weight <50kg; liver disease; cardiac failure; low albumin; known bleeding risk; taking drugs that affect warfarin; previously anticoagulated at maintenance dose <2mg)
    • Subsequent doses are as follows (refer to local guidelines)
    • 
  • Slow Initiation
    • Once initial checks (e.g. contraindications/bloodwork) has been carried out, start on a low dose of warfarin (e.g. 2mg/day; 1mg if patient is unwell/potential for drug interactions) for a week.
    • Check INR after this and adjust dose as required:
    • 
    • In general, if the patient is taking an antiplatelet, this can be continued until the INR is in therapeutic range and then stop.  NB patients who have had an ACS in the past 12 months or have got a stent may require dual anticoagulant/antiplatelet therapy
•  Explain monitoring/dose adjustments (once INR therapeutic and maintenance dose reached)
  • If INR is abnormally high or low (i.e. sub- or supra-therapeutic)- consider a change in dose (see below) and recall in 7-14 days
  • In general, if the INR is within therapeutic range, the patient can be monitored by increasing weekly intervals (i.e. 1 normal measurement- 1 week; 2 normal measurements- 2 weeks etc).
    • More than 5 therapeutic INRs suggest stable therapy and patients can be seen every 8-12 weeks following this
  • If the patient becomes unwell or there is any other reason to increase the frequency of monitoring- ensure the patient understands the importance of notifying the doctor/clinic.
  • Dose adjustments
    • For target INR 2-3 (2.5)
      • If low-
        • increase dose by 10% of total weekly dose (e.g. if the patient takes 21mg/week- increase the dose by 2mg/week) if the INR is consistently slightly low (1.8-1.9) or if the INR is low (1.6-1.8) at any time
          • This may mean alternating daily doses.
          • Also review INR in ~2 weeks
        • consider a loading dose (150% of maintenance dose) and increasing dose if the INR is lower than 1.6 (e.g. if the patient normally takes 6mg/day- consider a one-off dose of 9mg and increasing the dose by 4-5mg/week)
          • review INR in several days/one week
      • If high
        • decrease dose if the INR is consistently slightly high (3-3.2) or if the INR is ever high (3.4-3.9)
          • Review INR in ~2 weeks depending on severity
        • if the INR is significantly high (4-5), consider omitting one dose and reducing overall dose.  If >5, it may be appropriate to omit >1 dose.
          • Review INR in a few days
        • If the INR >6, stop warfarin until INR <5 and consider vitamin K reversal
          • Review INR next day if the patient is stable and not bleeding (oral vit K (1mg) is suitable)
          • If the patient is bleeding, admit for IV vitamin K (usually 1mg if not compromised; 5mg if in haemodynamic compromise +/- clotting factors/prothrombin (or FFP if not available))

Anti-arrhythmic Drugs

Classification

• Antiarrhythmic drugs can be classified either by their mechanism of action or by what they are commonly used to treat.

Mechanism of Action

1. Membrane stabilising agents- Sodium channel blockers
   1. Those that act to prolong the action potential (can be used in atrial fibrillation, flutter; supraventricular and ventricular tachyarrhythmias)
      1. examples include procainamide, dispyramide and quinidine
         1. The only which is used in Tayside is disopyramide (rarely used- only with specialist guidance)
   2. Those that act to shorten the action potential (ventricular tachyarrhythmias)
      1. Examples include lidocaine and mexiletine (latter not used in Tayside routinely)
   3. Those that have no effect on action potential but have the greatest reduction in the phase 0 slope (SVT and VT)
      1. Examples include flecainide; propafenone
   4. 
2. Beta-blockers (mainly used in AF/Flutter and to prevent SVT/VT)
   1. Non-selective (β1 and β2 antagonists)
      1. Propanolol is the most commonly used one
   2. Selective (myocardial β1 antagonist)
      1. bisoprolol
   3. Sotalol
      1. Mixture of non-selective beta-blocker and a class III antiarrhythmic (d-sotalol).
3. Potassium channel blockers
   1. Act to increase the QT interval- particularly useful in tachycardias involving re-entry phenomenon
   2. Most widely used drugs are amiodarone and sotalol (see above)
      1. NB Amiodarone also has class I, II and IV activity (complex mechanism of action)
   3. 

   4. Side effects of amiodarone include hypothyroidism (resembles thyroxine); corneal micro-deposits; optic neuropathy; deranged LFTs (rarely hepatic impairment e.g. jaundice, hepatomegaly); long-term use can cause blue-grey discolouration of the skin and photosensitivity; peripheral neuropathy; gynaecomastia and interstitial pulmonary fibrosis.

4. Calcium channel blockers
   1. Dihydropyridines (smooth muscle selective- not used as anti-arrhythmic drugs but used in high blood pressure to increase vasodilation.  Examples include amlodipine; nifedipine)
   2. Non-dihydropyridines
      1. Examples include verapamil (fairly cardioselective- most commonly used for arrhythmias/angina)
      2. Diltiazem is an intermediate and is both rate-limiting and has vascular effects (better for blood pressure)

Other antiarrhythmic drugs

• Atropine sulphate- increases sinus rate and SA/AV conduction
  • Treatment mainly for bradycardias due to vagal overactivity
  • Also used in the acute setting as part of resuscitation measures
• Adenosine (IV)- main action is to slow atrioventricular conduction (also decreases rate)
  • Can be used in attempting to halt SVT (particularly where the AV node is involved in re-entry e.g. WPWS)
  • It can also be used to help differentiate AF/flutter from VT
    • AF/flutter will produce a transient AV block
    • In VT, no change will occur
  • Avoid in asthmatics if possible (bronchospasm)
• Digoxin

See also arrhythmias and their managment

Calcium Channel Blockers

Mechanism of Action

• Promote vasodilator activity (reducing blood pressure) by reducing calcium influx into vascular smooth muscle cells by interfering with voltage operated calcium channels (and to a lesser extent receptor-operated channels) in the cell membrane.
• This also has an extra effect on cardiac myocytes- causing negative inotropy (decreased cardiac output) and, to a certain extent, negative chronotropy and dromotropy (slowing of cardiac conduction), depending on the CCB.

Classes of CCBs

• Dihydropyridine derivatives (namely amlodipine)
  • Pronounced vasodilator properties; intense reflex cardiac stimulation usually overcomes any direct cardiac effects
• Rate-limiting CCBs (usually verapamil or diltiazem)
  • More noticeable cardiac effects

Indications

• Stable angina where beta-blockers are contraindicated (rate limiting CCB- diltiazem)
• Hypertension in older people (dihydropyridine class- amlodipine)
  • NB Dihydropyridines can also be used in angina
• May also be used in the symptomatic treatment of Reynaud’s
• Occasionally used for management of AF (again, where beta-blocker is contraindicated; verapamil is commonly used)
  • NB the BNF says that verapamil is contraindicated where an accessory pathway is involved (risk of acceleration).  However, they remain in use as antiarrhythmic drugs for SVTs (often second or third line)
• Special CCBs can be used under certain circumstances e.g. nimodipine for prevention/treatment of vascular spasm after subarachnoid haemorrhage

Contraindications

• Rate-limiting CCBs should be avoided in heart failure (may worsen symptoms/ cause deterioration)
• Rate-limiting CCB should be avoided with concomitant beta blocker use or in severe bradycardia; 2nd/3rd degree heart block; sick sinus syndrome;
  • Also avoid in the acute phase of an MI (bradycardia; hypotension; LVF)
• Cardiogenic shock, unstable angina and significant aortic stenosis
  • Hypotension is a relative contraindication

Cautions

• Hepatic impairment- may need to reduce dose; renal impairment- consider starting at a lower dose
• It is not recommended to stop CCBs suddenly (risk of rebound tachycardia)

Side effects

• Common
  • Abdominal pain; nausea; constipation (particularly verapamil)
  • Palpitations (reflex response for dihyrdopyridines); flushing; oedema (NB diuretics are often not helpful, but ACEIs/ARBs may be helpful)
    • RLCCBs also can cause bradycardia; SA block/AV block;
  • Headache; dizziness; sleep disturbance; fatigue/malaise; hypotension
• Less commonly
  • GI disturbance (usually constipation due to effect on GI CC receptors); weight change
  • Dry mouth; taste disturbance
  • Hypotension; syncope; chest pain; dyspnoea;
  • Rhinitis
  • Mood changes
  • Muscle weakness; tremor; paraesthesia; myalgia; muscle cramps; back pain; arthralgia
  • Urinary disturbance; impotence; gynaecomastia
  • Visual disturbance; tinnitus
  • Rash (including erythema multiforme); pruritus; sweating; alopecia; purpura; skin discolouration
• Very rarely
  • Gastritis; pancreatitis; hepatitis; jaundica; cholestasis; gingival hyperplasia (particularly for rapid onset/short acting)
  • Myocardial infarction; arrhythmias; tachycardia; vasculitis;
  • Coughing
  • Peripheral neuropathy; hyperglycaemia
  • Thrombocytopenia;

Jugular Venous Pressure

Examination Technique

• Get the patient to relax.  Make sure not to use too many pillows (best seen with the head lying directly against the bed)
  • With the patient lying at around 45°, ask the patient to gently turn their head to the left.  The JVP may be seen rising from the clavicle, between the heads of the sternocleidomastoid muscle.

• To differentiate between pulsations from the carotid pulse-
  • JVP will sink into the clavicle as you raise the bed, or with patient inspiration
  • JVP is not palpable
  • JVP usually has a bifid waveform (see below)
  • JVP will usually rise in response to ‘hepatojugular reflex’
  • deep pressure is applied to the RUQ (better during expiration)
• Measure the JVP as the vertical height from the sternal angle to the top of the JVP
  • Usually < 3cm

NB ‘c wave’ is almost never visible

• In AF there is no effective atrial contraction and so no ‘a wave’.
• In Tricuspid regurgitation, there are ‘systolic cv waves’ (prominent v waves) due to the right ventricular impulse being transmitted through the incompetent tricuspid valve during systole.
• In pulmonary hypertension (e.g. in pulmonary embolic disease); the JVP will be elevated with large ‘a waves’ as the right atrium tries to overcome the high pressures
• In complete heart block, the atria and ventricles contract out of synchrony.  Occasionally, atrial systole will occur just before ventricular systole and cause an extra large ‘cannon a wave’ as the right atrium contracts against a closed tricuspid valve. (Can also occur in tricuspid stenosis)
• Things that don’t effect JVP:
  • Mitral regurgitation; small VSDs
• Kussmaul’s sign is a JVP that rises (paradoxically- usually shortens) with inspiration.  May be caused by conditions which restrict the heart e.g. pericardial effusion/tamponade; contrictive pericarditis ; restrictive cardiomyopathy; as well as right heart failure