Heart Lectures Flashcards
BP = ?
BP = CO x SVR
What determines 85% of systemic vascular resistance?
Pressure in the pre-capillary arterioles
Describe the RAAS system
What controls BP?
Hormonal influences (RAAS and SS)
Neurological control
What does SS activation of the following receptors do?
- α 1 receptors in systemic arterioles
- β 1 receptors
- β 2 receptors in musculature arterioles
α 1 = vasoconstriction of systemic arterioles
β 1 = inc force and rate of heart contraction
β 2 = vasodilation of arterioles in muscles
What is NOR an agonist of?
Mostly α receptors
What is ADR an agonist of?
α and β receptors
Where are baroreceptors for neurological control of BP found?
Carotid sinus
Aortic arch
What can cause secondary HT?
What causes primary HT?
Which drugs can cause HT?
Oral contraceptives
NSAIDs
Corticosteriods
OTC decongestants
Stimulant recreational drugs
Hermal remedies
Some SSRIs - Venlafaxine
How can you tell if a P has renal artery stenosis clinically?
Bruit of the renal artery?
Sudden deterioration of renal function after starting ACEIs
Flash pulmonary oedema
How is renal artery stenosis treated?
Standard medical treatment is first line
If it doesn’t respond - can consider renal artery stenting
How do you treat HT with CKD?
Aggressive standard medical Rx - aim to get BP <130/80
Which drugs can reduce CKD progression?
What do you need to beware of when using these drugs?
ACEIs
Need to beware of using with drugs that exacerbate hyperkalaemia as ACEIs block aldosterone (aldosterone inc Na reabsorption and expense of K+ which is excreted in the urine - this is prevented with ACEIs = hyperkalaemia)
Which diuretic can cause hyperkalaemia?
Spironolactone
Which diseases are phaechromocytoma associated with?
Neurofibromatosis
Multiple Endothelial Neoplasia Type 2
What are the symptoms of a pheochromocytoma?
Anxiety, palpitations, tremor, sweating, headache, diarrhoea, Raynaud’s, chest pain
Catecholamines are secreted in bursts - therefore symptoms occur in “attacks”
What are the signs of a pheochromocytoma?
HT - ?postural hypotension
Tachycardia, fever, glycosuria, pallor, flushing
What are the tests for phaechromocytoma?
24hr urinary catecholamines
CT / MRI
PET scan
What is the Rx for a phaemochromocytoma?
α and β blockade
Can do surgical excision
What causes Cushing’s disease?
Pituitary adenoma secreting ACTH
When should you suspect Cushing’s
Obese with thin skin & easy bruising
Proximal myopathy
Low K+ and high Na+
What are the tests for Cushing’s?
24hr urinary cortisol
Low dose dexamethasone suppression test
Dexamethasone is a man-made version of cortisol. After you take a dose of it, your body should make less cortisol. That’s the idea behind the test – take some dexamethasone and see whether your cortisol level drops.
In the adrenal gland, where do the following come from?
- Catecholamines
- Cortisol
Catecholamines = medulla
Cortisol = adrenal cortex
What causes Conn’s syndrome?
Adenoma or hyperplasia of the adrenal cortex
When should you suspect Conn’s syndrome as a cause of HT?
If the P has HT and low K+ (beware if on drugs which lower K+; also beware if on drugs that raise K+ back to normal ranges)
Also if there is a high aldosterone:renin ratio
How is Conn’s diagnosed and treated?
Diagnosed = CT or MRI, or venous sampling from the adrenal veins
Tx = spironolactone, adrenalectomy if unilateral
Where is aortic coarctation usually found?
Distal to left subclavian artery
How is aortic coarctation recognised clinically?
Weak femoral pulses
Radio femoral delay
Palpable collaterals over posterior ribs (can appear as notching on ribs on XRAY)
Murmur of AR
How is aortic coarctation diagnosed?
CT or MR aortography
What is the protocol for treating HT in the following Ps:-
- Clinic BP under 140/90
- Clinic BP between 140/90
- Clinic BP over 180/120
> 140/90 = offer ABPM or HBPM
If >80 and >150/90 - lifestyle advice and poss drug Rx
If 80-40 = lifestyle advice and drug Rx
> 180/120 = assess for target organ damage. If none - repeat within 7 days, give ABPM or HBPM.
If retinal haemorrhage, papilloedema, life-threatening Sx or suspected pheochromocytoma - needs same day specialist review!
What is the second commonest cause of HF?
HT
What are the possible effects of chronic HT?
Heart muscle damage
Large vessel damage (AA, CVD, CAD, PVD)
Micorvascular damage (CKD, brain dysfunction, exacerbation of diabetes effects)
What are the acute effects of severe HT?
What lifestyle advice for HT should you give in relation to:
- Alcohol
- Salt
- Exercise
- Smoking
- Caffeine
What lifestyle advice for HT should you give in relation to:
- Weight
- Diet
What physical things should you examine in a P with HT?
How is hypertensive retinopathy graded?
What blood tests can indicate a high alcohol excess?
High MCV
High GGT
What is the second commonest cause of renal dysfunction?
HT
What blood tests should you do in HT?
How do
- Conn’s syndrome
- Cushing’s syndrome
- Acromegaly
appear on blood tests?
Conn’s = can cause low K+ and high aldosterone : renin ratio
Cushing’s = can cause high Na+ and low K+, can also cause high glucose
Acromegaly = can cause high glucose levels
What abnormalities can HT cause on an ECG?
Can cause LV hypertrophy
- get tall QRS complexes.
Can also cause lateral T wave inversion = strain pattern
May also cause LBBB
Which criteria is used to identify LV hypertrophy on ECG?
What do you need to remember about this criteria?
Sokalov-Lyon criteria
= Tallest R wave in V5 or 6 + S wave in V1 is greater than 35mm
Is not v sensitive - may be caused by young, thin Ps
Conversely - older and fatter Ps may not show these signs on ECG even though they have LVH.
What does this ECG show?
LV hypertrophy with strain - shows tall QRS complexes with lateral T wave inversion.
Name
- 3 ACEIs
- 2 ARBs
- 1 α blocker
- 3 β blockers
- 3 calcium channel blockers
- 1 direct acting vasodilator
- 2 nitrates
- 2 loop diuretics
- 1 thiazide like diuretic
- 1 thiazide diuretic
- 1 aldosterone antagonist
What is Step 1 of the hypertensive medication ladder?
If T2DM or <55 and not A/AC descent = ACEi or ARB
If >55 & no T2DM or A/AC descent = give CCB
What is Step 2 of the hypertensive medication ladder?
Add on an ACEi/ARB or CCB depending on what was used for Step 1
What is Step 3 of the hypertensive medication ladder?
ACEi or ARB + CCB + Thiazide-like diuretic
What is Step 4 of the HT medication ladder?
Confirm is elevated with A or HBPM
Get expert advice
- Can add spironolactone if K+ is <4.5 or an α or β blocker if blood K+ is >4.5
When is HT diagnosed as chronic or gestational in pregnancy?
Chronic HT if it occurs before 20w
Gestation if it occurs after 20w
When do you treat HT in pregnancy?
If >140/90
What drugs should you avoid to treat HT in pregnancy and why?
Need to avoid
- ACEIs
- ARBs
- Diuretics
They reduce placental blood flow
Which drugs are safe to treat HT in pregnancy?
Labetalol (α and β blocker)
Nifedipine (Ca channel blocker)
Methyldopa (acts on BP control centre in the medulla)
When is rapid HT control required?
If there is
- accelerated HT (headaches, visual disturbances)
- hypertensive encephalopathy
- acute HF (pul oedema)
- aortic dissection
- pre-eclampsia / eclampsia
What Rx is given for hypertensive emergencies?
IV Labetalol, Nitrate (GTN, isosorbide dinitrate) and sodium nitroprusside
Also - BP monitoring - dont want to reduce too fast - want to reduce over a period of time - immediate reduction
What did the seven countries study show regarding hyperlipidaemia?
That there was an exponential association between cholesterol levels in the blood and cardiovascular mortality
Rise from 4mmol to 8mmol linked to a 5fold inc in CHD mortality
What are the two pathways to make cholesterol in the body?
Exogenous = broken down from food taken in
Endogenous = made from HMG-CoA in the liver
Which enzyme is involved in making cholesterol in the liver?
HMG-CoA Reductase
How do statins work?
Inhibit HMG-CoA Reductase - thus reducing cholesterol by the liver.
Lowers LDL, total cholesterol and 3Gs, increases HDL
Which Rx is first line for Ps with elevated cholesterol?
What is good about this Rx?
Atorvastatin
Simvastatin
They have been proven to reduce all cause mortality in CVD.
Why do statins reduce all cause mortality?
As well as reducing cholesterol levels, they lower inflammatory cytokine levels in atherosclerotic plaques.
This prevents progression of atherosclerosis and stabilises the plaques that are already there.
What are statins used for in secondary prevention?
What dosage is used?
Used in Ps who have had a CVD to prevent recurrence = secondary prevention.
High dose starting therapy = Atorvastatin 80mg OD
What is the ideal lipid profile?
- Cholesterol
- LDL
- 3Gs
- HDL
- Total:HDL Ratio
Cholesterol <5
LDL <3
3Gs = 0.5-2
HDL = >1.5
Total: HDL ratio = <3.5
What can cause secondary dyslipidemia?
DM
Hypothyroidism
CKD
Chronic liver disease
Obesity
Smoking
Alcohol XS (inc 3Gs)
Medications (thiazide diuretics)
How does lifestyle advice differ from hyperlipidemia to HT?
Hyperlipidemia - advice omits any guidance about caffeine
When are statins recommended for primary prevention?
What Rx are Ps started on?
If the 10 year risk of CVD is >10% based on Q-risk
Start on Atorvastatin 20mg OD for 3months - aim for non-HDL reduction of >40%
If statins do not reduce cholesterol levels sufficiently, what other Rx can be considered?
Ezetimbe (inhibits absorption of cholesterol by small intestine)
Evolocumab (PCSK9 inhibitor - reduces cholesterol)
Bezafibrate (for high 3Gs - activates lipoprotein lipase)
On a parasternal long axis view of an echocardiogram - which chamber is
(a) most anterior
(b) most posterior?
Most anterior = right ventricle
Most posterior = left atrium
What views can be seen during an echocardiogram?
Parasternal long axis
3 x Parasternal short axis - aortic valve, mitral valve and heart muscle levels
Apical 4-chamber view
Apical 3-chamber view
How can you identify the aortic valve in cross section on an echo?
Looks like the Mercedes Benz sign
Which leaflet of the mitral valve is bigger - anterior or posterior?
Anterior leaflet has bigger area (approx twice as big)
Which chamber of the heart is often lacerated in stabbings?
Right ventricle
What causes aortic stenosis?
Calcium deposits on aortic valve leaflets
How is the doppler principle used in echo?
Can be used to calculate pressure differences between chambers, valve gradients, pulmonary artery pressures, right atrium pressure and to quantify intra-cardiac shunts
Apart from echo - what is another way to estimate right atrial pressure?
By the jugular venous pressure
What is echo used as the first line imaging modality for?
Pretty much all cardiac Ps - inc HF, cardiomyopathy, valve disease, pericardial effusion and congenital heart disease
What is the first line investigation for endocarditis?
Trans-oesophageal echocardiography
What are the pros and cons of cardiac MRI compared to echocardiogram?
What isotope can be used for enhancement on echocardiogram?
Gadolinium
When is cardiac MRI the investigation of choice?
When you need to characterise the myocardium -
- Cardiomyopathies (DCM, HCM, ARVC)
- Myocarditis v. MI
- Amyloid heart disease
- Cardiac sarcoid
- Haemochromatosis
What do we look for on a cardiac stress test ECG? Which protocol is used for these?
Bruce protocol
Exercise ECG is still used but is not recommended by nice, and is becoming less utilised. When is it still utilised in the UK?
How does myocardial perfusion scanning work?
How does stress echocardiography work?
When is functional imaging used?
Investigating recurrent angina cause in Ps with known CAD
For objective evidence of ischaemia
What investigation is first line for suspected angina?
CT Coronary Angiography
What are the pros and cons of CT Coronary Angiography?
When is ambulatory ECG monitoring used?
When you are concerned the P may have an arrhythmia
- Sx of palpitations, dizzy spells, syncope, episodic chest pain, SOB
What does cardiac catheterisation provide us with?
What is cardiac catheterisation used for?
First line for unstable patients and stable angina as a prelude to PCI procedures
For measuring pressures in suspected pulmonary HT
For shunt calculations
Difficult haemodynamic diagnoses
Assessment of valve regurgitation
If the SAN fails - what happens?
The atrial muscle can generate a heartbeat of 60 bpm (autotonicity)
If that fails - the AVN can generate a heartbeat of 40bpm
If that fails the ventricular myocardium can generate a heartbeat of 30 bpm
What is seen on this ECG?
The broad extra beats on II are ectopic beats - because they look different from the normal complexes - is likely they are coming from the ventricular myocardium = ventricular ectopic beats
When are ectopic beats not benign?
When they have a very high frequency
If you get R on T ventricular ectopics - can induce VF
How are ectopic beats managed?
Exclude underlying heart disease
Ensure they are low frequency
Lifestyle changes
Drug Rx = try to avoid but if necessary - propanol PRN and bisoprolol regularly
What are the principles of arrhythmia management?
Document with ECG
Exclude / identify underlying pathology
Assess risk
Lifestyle, Rx
Can use ablation or device therapy
What is the re-entry mechanism of arrhythmias?
For sustained tachycardias - the re-entry mechanism can be the cause.
For re-entry to occur there have to be 2 simultaneous pathways - either anatomically separated - e.g. from scar from MI, or functionally - e.g. within part of the cardiac conduction tissue. One of the pathways must be faster = slow and fast pathways
Slow pathway can continue round and round in diagram 2 - setting up a short circuit - can make the heart beat very quickly - even in excess of 200bpm - will continue until something blocks it - e.g. another ectopic beat. One place this happens is AVN - 2 pathways are not anatomically separated. Called functional micro reentry.
In contrast to entry around a scar = anatomical macro reentry.
What is seen in this ECG?
Rapid narrow complex tachycardia - approx. 160-170bmp = form of supra ventricular tachycardia
Is some ST segment depression = rate related ischaemia - heart going fast - generating some subendocardial ischaemia.
What are the 3 main causes of SVT?
AVNRT - AV node reentry tachycardia = short circuit reentry occurring in the AV node. Because the atria and ventricles are activated at exactly the same time, the P wave is buried in the QRS.
AT - Paroxysmal Atrial Tachycardia - focus of arrythmia is in the atrium themselves - sometimes are reentry arrythmia, sometimes due to increased autotonicity. Atria are activated before the ventricles - there are P waves - PR interval is short because the focus of the arrythmia is closer to the AV node than the SAN. There is a P wave before the QRS
AVRT - Atrio-ventricular reentry tachycardia - P wave comes after the QRS -occurs through accessory pathway between atrium and ventricles - macro reentry - P wave is sometimes buried in the T-wave after the QRS.
Which condition is an example of functional macro re-entry SVT?
WPW - P has a second connection between the atrium and the ventricles. Normally the AVN is the only connector. In WPW - signal can go down the normal pathway, back up the ventricles, through the accessory pathway in the atria and then down the normal pathway again = more beats.
Macro re-entry - can conduct very quickly.
What does this ECG show?
See short PR interval - less than 3 little squares and there is slurring of the upslope on an R wave or slurring of the downslope of the S wave. Slurred upstreak on R wave = delta wave + broad QRS complexes = WPW
Is also sometimes a cause of dominant R waves in lead I.
How is SVT managed?
Exclude underlying heart disease
Lifestyle factors
Acute Rx (if sustained arrhythmia) = vagotonia manoeuvres, AV node blocker (adenosine or verapamil), DC cardioversion
How is SVT prevented?
If atrial cause of tachycardia = Bisoprolol (stabilises the atria)
If there is an AVN reentry cause - AV node blocker such as Bisoprolol or Verapamil
WPW = use Flecainide (is an accessory pathway blocker)
What has a 90% cure rate for most forms of SVT?
Electrophysiological study and Ablation
What normally causes sinus tachycardia?
Usually reactive to something (fever, pain, emotional stress/anxiety, dehydration, stimulants, low BP)
Also - thyroxtoxicosis, severe anaemia, PE
Rare cause - intrinsic sinus node dysfunction
What does this ECG show?
Sinus tachycardia
Narrow complexes, tachycardia (130bpm), but complexes look normal - normal P wave and QRS
What is the commonest serious arrhythmia?
AF
What is the pathophysiological cause of AF?
Multiple macro re-entry circuits in the atria
What does this ECG show?
Rapid, irregular - because the atria are not beating in a coordinated way
No P waves
How does AF present?
AF can be classified by the 3Ps. What are these and how can you tell the difference between them?
Paroxysmal - comes and goes spontaneously
Persistent - there all the time unless treated
Permanent - nothing gets rid of it
What risk can be caused by AF?
What can be used to calculate the risk?
Risk of thrombosis
- often from LA appendage
- is cause of approx 10% of acute strokes
CHA2D2SVASc score (for F - need a score of more than 2 - dont get anticoagulated just for being female)
What investigations should we do for AF?
Hx
Bloods - inc thyroid, MCV, GGT
CXR - underlying disease?
Echocardiogram - valve disease, cardiomyopathy, CHF
Screen for IHD
How do we manage paroxysmal AF?
Maintain sinus rhythm
Treat underlying cause, address lifestyle issues
Can use amiodarone (best) or flecainide or bisoprolol (less effective but less toxic)
Can consider ablation of drugs dont work (law of 1/3rds - 1/3 cured, 1/3 better, 1/3 no better and need repeat)
Irrespective of ablation - continue anticoagulants if indicated as high risk of recurrence
How can we manage persistent AF?
Cardioversion + atrial stabilising agent
What do we do for permanent AF when cardioversion fails?
Control ventricular rate with AVN blocking drugs
- HR < 110
- control symptoms
Dont give more than 2 AV blockers at a time
Bisoprolol + Amiodorone or Digoxin
What is seen on this ECG?
Atrial flutter = zig zag sawtooth baseline
What is AF with 4:1 conduction?
Short circuit is occurring 4x per heart beat - only 1 in 4 signals are conducted down = 75 bpm - appear to have normal pulse
Can also have 2:1 conduction = 150 bpm and 1:1 conduction = 300 bpm
What is seen on this ECG?
Ventricular tachcardia (sustained, monomorphic - sustained because it goes on for the whole length of the ECG, monomorphic because the complexes look like each other)
What types of ventricular tachycardia are there?
Monomorphic
Polymorphic (Torsade de Pointes)
What is seen on this ECG?
Ventricular fibrillation - chaotic, no discernible complexes
Ventricular tachycardia is serious and potentially fatal. Is often poorly tolerated, esp if the P has HF.
How is this condition managed?
Need to restore sinus rhythm ASAP.
Amiodarone or emergency DC cardioversion (Can also do cardiac pacing - pace faster than the VT to break the short-circuit and then dial it back).
Keep K+ >4.5, replace Mg
Diagnose and treat underlying disease
Ventricular stabilising drugs - β blockers amiodarone, IV lignocaine
What is the risk of prolonged QT intervals?
Carry a risk of polymorphic ventricular tachycardia, syncope and death.
What can cause acquired QT Prolongation?
Hypokalaemia
Hypomagnesaemia
Anti-arrhythmics - amiodarone, flecainide
ABx - clarithromycin, erythromycin
Antifungals -fluconazole
Antimalarials - chloroquine
Antidepressants - Citalopram
Antipsychotics - clozapine, risperidone
On some ECGs for bradycardia there are some heartbeats without P waves - why is this?
Because the sinus node is failing to fire and therefore the beat is coming from the AVN.
What is seen on this ECG?
How can you identify LBBB on an ECG?
You get an “M” in V6 and a “W” in V1.
WilliaM
If QRS mostly goes down in V1 and it is broad = LBBB
Can also get lateral ST depression and T wave inversion
What is seen on this ECG?
LBBB
What causes LBBB?
Can indicate cardiac pathology - IHD, HT heart disease, cardiomyopathy
How does RBBB appear in ECG?
Upward deflection in V1 and downward deflection in V6
Wide complexes >3 squares
Deep slurred S wave in lateral leads
What is seen on this ECG?
RBBB
What can cause RBBB?
Right heart strain = chronic lung disease, pul HT, PE, congenital heart disease
Also IHD
What is seen on this ECG?
First degree heart block - gap between P and QRS is longer than 200ms (1 large square)
What does this ECG show?
Increasing gaps of PR interval due to progressive fatigue of the AVN.
1st degree = no dropped complexes
2nd degree = get some dropped complexes
What does this ECG show?
PR interval stays the same - broad complexes. Get intermittent dropped beats.
What does this ECG show?
A lot more P waves than QRS complexes - is no fixed relationship between them - AVN is not getting through
How do patients with bradycardia present?
The more severe the heart block, the more likely they are to have symptoms
How is bradycardia treated?
If low grade / asymptomatic = reassurance
Acute - atropine, isoprenaline infusion, temporary pacing
Long-term = permanent pacing
What is seen on this ECG?
How are pacemakers named?
What two things are needed for endocarditis to occur?
Bacteraemia
Endovascular abnormality
Which valves are most commonly affected in endocarditis?
Usually is left sided heart valves - pressure on LHS tends to be higher - but in IV drug uses - the bacteria from the syringe hit the tricuspid valve first - therefore right sided valves more commonly affected
Why are valves susceptible to endocarditis?
Because they are avascular structures = limited efficacy of immune system
At what size to vegetations have a significant risk of embolisation?
High risk if >10mm
Which the most common organism for infective endocarditis?
Viridans streptococci (commensals of the mouth)
Which is the most destructive organism for infective endocarditis?
Staph aureus
If there has been rapid destruction of the valve - think S aureus.
Which organism is most likely to cause endocarditis in a patient who has bowel malignancy?
Strep bovis
Which is the most common cause of endocarditis in IV drug users?
Staph aureus
What percentage of Ps will not grow an organism on blood cultures?
5-10%
What are the clinical features of endocarditis?
Vast majority will have fever, murmur and haematuria. If none of these is unlikely to be endocarditis.
When do you get Ps with clubbing and splenomegaly in endocarditis?
Rarely - when they have chronic untreated endocarditis but Ps in the UK tend to be treated quickly
Why do the vast majority of patients get haematuria with endocartiditis?
This is due to micro emboli that enter the renal circulation
What investigations can you do for suspected infective endocarditis?
Bloods (FBC, U&E, CRP, LFTs)
Urinalysis
Blood cultures - 3 sets, 3 sites, 3 occasions
ECG (?PR prolongation)
CXR
TTE
TOE
PET
What criteria are used to determine whether a P has infective endocarditis?
Duke criteria
What are the DUKE criteria?
BE TIMER
B - Blood culture positive x 2, 12 hrs apart
E - Echocardiographic évidence
T - Temp >38
I - Immunological phenomena (Osler’s nodes, Roth spots)
M - Microbiological evidence (+ve blood culture not meeting major criteria)
E - Embolic phenomenon (arterial emboli, septic emboli, conjunctival haemorrhage & painless skin lesions)
R - RF = Congenital, IVDU
Definitive diagnosis = 2 major OR 1 major + 3 minor OR 5 minor
Possible = 1 major + 1 minor OR 3 minor
When should you consider surgical intervention for infective endocarditis?
- Rx fails
- Staph aureus or fungal cause
- Prosthetic valve
- Large vegetation (>1cm = risk of embolisation)
- Aortic root abscess - very difficult to eradicate with Abx alone
How complications can arise from infective endocarditis?
HF
Multi organ failure (Sepsis)
Embolism = stroke / acute limb ischaemia / discitis Can cause acute back pain - esp S aureus - can embolise to the discs in the spine - very serious - spinal infection can progress to spinal abscess.
Sometime underlying endocarditis diagnosis is missed - rather seen as discitis.)
Aortic root abscess - can involve AV node - HB = PR prolongation
When do we use Abx prophylactically for endocarditis?
Little evidence of benefit
Used if very high risk of dying if they get endocarditis
= Dental procedure + prosthetic valve / previous Hx / complex cogenital heart disease
When can you get “Marantic” endocarditis?
Disseminated end stage cancers (esp mucous secreting adenocarcinomas)
What is pulmonary HT defined as?
Mean pul a. pressure >20mmHg
What makes pul pressures high?
Inc pul vascular resistance
PA pressure = CO x PVR
What is the most common cause of pulmonary hypertension?
Left heart disease (70%)
Most common LHD = HFpEF (abnormality of the left heart)
1 = primary condition of the lung vasculature - can occur from AI (SLE) or as a reaction to appetite suppression drugs
3 = Cor pulmonale
What are the symptoms and signs of pulmonary hypertension?
Why do you get a parasternal heave in pulmonary hypertension?
The pulmonary pressure goes back within the system and makes pressure in the right ventricle very high
Why can you get a murmur in pulmonary hypertension?
Can get valve regurgitation on the right side = systolic murmur (tricuspid regurg) or diastolic murmur (pulmonary regurg) - sounds similar to aortic regurg murmur
What ECG changes are see in pulmonary hypertension?
P pulmonale (tall P waves)
Right axis deviation
RV Hypertrophy - dominant R wave in V1, T wave inversion in anterior leads
What investigations can be done for pulmonary arterial HT?
What can you see on CXR in pul a. HT?
Prominent pulmonary arteries
In this CXR - pulmonary artery is bigger than the aorta - normally the other way around.
Why do we do a CTPA in possible pul a. HT cases?
Ensure they dont have chronic thromboembolic pulmonary HT
What is the treatment for pul. a. HT?
Supportive therapy (diuretics)
?Pulmonary vasodilator therapy
Pulmonary vasodilators - Ca channel blockers etc
What is chronic thromboembolic PHT
How can you possibly differentiate between chronic thromboembolic PHT and PHT?
Resting hypoxia - may be present in PS with chronic thromboembolic and not PHT
Clinically - Ps who have pul a. HT normally have resting normal O2 sats, whereas Ps with resting chronic thromboembolic PHT may have a resting hypoxia.
How is chronic thromboembolic PHT treated?
Anticoagulant - Apixaban
Supportive measures (diuretics, LTOT)
In general, pulmonary arterial vasodilators do not work for chronic TE PHT - problem is not the pulmonary microvasculature, problem is big lumps of clot.
Can consider surgery to remove clot (pulmonary endartectomy) but carries high surgical risk
Why does left heart dysfunction cause Pul HT?
Elevated pressures in the circulation are transmitted backwards - any form of LH dysfunction will eventually cause elevated pressure in the LA.
HF, left valve disease (aortic, mitral) - have common mechanism to elevate LA pressure - transmitted back through the pulmonary system. Eventually causes remodelling of the pulmonary veins - become like systemic arteries = elevation of pressures in the right side of the heart = right heart strain.
What problems in the left ventricle can cause Pul HT?
Left ventricular dysfunction = HFrEF and HFpEF
Valve disease - mitral more common - esp mitral stenosis
ASD, VSD and Patent ductus arteriosus
What is Eisenmenger Syndrome?
PHT due to an intra-cardiac shunt
Right sided pressures rise, get bigger than left-sided pressures
Causes deoxygenated blood to enter the systemic circulation
Signs = clubbing, central cyanosis, elevated JVP, parasternal heave, loud S2
What is right sided heart failure due to chronic lung disease called?
Cor pulmonale
(Caused by OSA, COPD, pulmonary fibrosis)
What are signs and symptoms of cor pulmonale?
Elevated JVP
RV+
Loud P2
Tricuspid regurg murmur
Hepatomegaly
