Cardiovascular Flashcards
What are the symptoms of an aortic dissection?
- Chest pain- sudden, tearing, severe, anterior or interscapular
- Dizziness
- SOB
- Sweating
- Neuro deficit
What are the signs of an aortic dissection?
Unequal radial pulses
Tachycardia
Hypo/hypertension
Difference in BP between arms >15mmHg
Aortic regurgitation
Pleural effusion
Neurological deficit if carotid artery dissection
What urgent investigation would you do for a suspected aortic dissection?
Urgent CT aorta
What might a CXR show in aortic dissection?
Widened mediastinum >8cm (rare)
Irregular aortic knuckle
Small left pleural effusion
What is the acute treatment of aortic dissection?
Senior help
If HYPOtensive - oxygen, 2x large bore cannulae, Xmatch, IV opioids
If HYPERtensive - keep systolic BP <100mmHg
BOTH - Surgery (Type A, involving ascending aorta) or conservative management (Type B, involving descending aorta only)
What are the risk factors for an aortic dissection?
Smoking, obesity, diabetes, HTN, high cholesterol, family hx, previous IHD
What is the definition of an aneurysm?
A permanent and irreversible dilatation of a blood vessel by at least 50% of the normal diameter
What are the 2 types of aortic aneurysm and which is most common?
Abdominal and thoracic
Abdominal most common
What is the normal diameter of the abdominal aorta and what diameter would be classed as a AAA?
Normal= 2cm
AAA= 3cm +
Where do most AAA’s arise from?
Below the level of the renal arteries
What are the symptoms/signs of an unruptured AAA?
- Most are asymptomatic
- Back/loin/groin pain
- Pulsatile swelling on examination
- Distal embolisation- gives features of limb ischaemia but with easily palpable pulses
- Uterohydronephrosis
- Severe recent onset lumbar pain may indicate impending rupture!
What is the monitoring requirement for AAAs? At what diameter would surgery be recommended?
3-4.4cm annual US
- 5-5.4cm 3 monthly US
- 5cm or bigger consider surgery
What are the surgical options for AAA repair?
Open surgery
Endovascular repair: stent-graft introduced through femoral arteries
What is the NHS screening for AAA and when/to whom is it offered?
One US offered to men aged 65- if negative, rules out AAA for life
What are the symptoms of pericarditis?
Pleuritic chest pain, worse on lying flat/deep inspiration, better when sat forwards Fever
Recent viral illness
What signs may be found in pericarditis
None, or pericardial rub
What would a saddle shaped ST segment on ECG suggest?
Pericarditis
What investigations would you do for suspected pericarditis and what would they show?
Bedside- temp
Bloods- Raised WCC and CRP, troponin
ECHO- bright pericardium +/- pericardial effusion
What is the management of acute pericarditis?
Reassurance
Paracemtaol/NSAIDs
If continues >14d, use colchicine/steroids
What is constrictive pericarditis?
Chronic inflammation of the pericardium resulting in a thickened, scarred pericardium which impairs heart function
What are the signs/symptoms of constrictive pericarditis?
Similar to R heart failure- SOB, peripheral oedema, raised JVP with Kussmaul’s sign
Pulsatile hepatomegaly (70%)
Pericardial knock
What investigation would distinguish constrictive pericarditis from restrictive cardiomyopathy?
ECHO
What is the management of constrictive pericarditis?
Treat cause
Anti-inflammatories
Pericardiectomy
What are the causes of cardiac tamponade?
Pericarditis, aortic dissection, haemodialysis, warfarin, trans-septal puncture during cardiac catheterisation, post cardiac biopsy
What are the signs of cardiac tamponade?
Tachycardia
Hypotension
Pulsus paradoxus
Raised JVP
Kussmaul’s sign
Muffed S1/2
What investigations would you do for cardiac tamponade? What would they show?
CXR: large globular heart
ECG: low voltage QRS +/- electrical alternates
ECHO is DIAGNOSTIC: echo-free zone around heart +/- diastolic collapse of right atrium and ventricle
What is the management of cardiac tamponade?
Urgent drainage of pericardial effusion
What is cardiac tamponade? What is its pathogenesis?
Accumulation of pericardial fluid, resulting in increased intrapericardial pressure causing poor ventricular filling and reduced cardiac output
What are the clinical features of pericardial effusion?
SOB
Raised JVP (with prominent x descent)
Bronchial breathing at left base
Signs of cardiac tamponade
What is the management of pericardial effusion?
Treat cause
Pericardiocentesis (diagnostic/therapeutic)
What would CXR, ECG and ECHO show in pericardial effusion?
CXR: enlarged globular heart
ECG: low voltage QRS and electrical alternans
ECHO: echo-free zone around heart
What is the target BP for those without diabetes age >80 and <80?
<80 = <140/90
>80 = <150/90
What rise in creatinine/decrease in eGFR is acceptable when on an ACEi?
eGFR decrease up to 25%
or
Creatinine rise up to 30%
What 4 things could cause hypertension with low potassium?
Conn’s
Cushing’s
Renal artery stenosis
Liddle’s
What is the first line treatment for HTN in a diabetic?
ACEi
What is the treatment for resistant hypertension if further diuretics are not tolerated, contraindicated or ineffective?
Consider alpha blocker or beta blocker
What should an adult <80yrs with stage 1 HTN, no end organ damage and a QRisk >10% but <20% be treated with?
Lifestyle advice PLUS a statin
Antihypertensive drug treatment should be offered to those <80yrs with stage 1 HTN if they have 1 or more of???
Target organ damage
Established CV disease
Renal disease
Diabetes
10yr CV risk >20%
If HTN is uncontrolled on ACEi, Ca channel blocker and thiazide diuretic what is the next step?
If K+ <4.5 = spiro
If K+ >4.5 = increase dose of thiazide
What are the sx/signs of idiopathic intracranial HTN?
Headache
Blurred vision
Papilloedema
Enlarged blind spot
+/- 6th nerve palsy
What are the risk factors for idiopathic intracranial HTN?
Obesity
Female
Pregnant
Drugs: COCP, steroid, vit A, lithium, tetracycline
What is the management of idiopathic intracranial HTN?
Weight loss
Diuretics e.g. acetazolamide
Topiramate
Repeated LPs
Surgery
What is aleading cause of sudden cardiac death in young athletes?
Hypertrophic obstructive cardiomyopathy
What would an ECHO show in hypertrophic obstrcutive cardiomyopathy?
Mitral regurg
Systolic anterior motion of anterior mitral valve
Asymmetric septal hypertrophy
What is the inheritance of HOCM?
Autosomal dominant
What are the causes of dilated cardiomyopathy?
Alcohol
Coxsackie B virus
Doxorubicin
Wet beriberi
What are the causes of restrictive cardiomyopathy?
Amyloidosis
Post-radiotherapy
Loeffler’s endocarditis
What is the name for stress-induced cardiomyopathy?
Takotsubo
What is the management of Takosubto cardiomyopathy?
Supportive
What do new widening QRS complexes and an RSR pattern in v1 suggest?
RBBB
What would widened QRS complexes and a notched morphology of the QRS complexes in the lateral leads suggest?
LBBB
What are the risk factors for mitral regurg?
Female
Low BMI
Prior MI/mitral stenosis/valv prolapse
Collagen disorders e.g. Marfans, Ehlers-Danlos
What wpuld a pan-systolic blowing murmur heard best at the apex, radiating to the axilla suggest?
Mitral regurgitation
Secondary causes of HTN
- Renal disease
- Primary hyperaldosteronism
- Phaeochromocytoma
- Cushing’s
- Acromegaly
- Hyper/hypothyroidism
- Alcohol
- Connective tissue disorders
- OSA
- Coarctation of aorta
- Renal artery stenosis
Annual review for HTN
- Check blood pressure
- Check renal function by measuring creatinine, electrolytes and EGFR
- Dip urine to check for proteinuria
- Q risk
What is accelerated hypertension?
Blood pressure >180/110 mmHg with signs of papilloedema and/or retinal haemorrhage
Complications of hypertension
- Heart Failure
- Coronary artery disease
- Stroke
- Chronic kidney disease
- Peripheral arterial disease
- Vascular dementia
Symptoms of postural hypotension
Dizziness
Lightheaded
Blurred vision
Weakness
Fatigue
Nausea
Palpitations
Headache
Less common; syncope, dyspnoea, chest pain, neck/shoulder pain
Positive tilt table test
Systolic BP falls below 20mmHg and diastolic BP below 10mmHg of baseline
What is the tilt table test for orthostatic hypotension
Tilt testing to an angle between 60 and 80° for three minutes
First line drug for orthostatic hypotension
Fludrocortisone
Symptoms of hypotensive shock
- Feeling cold, unwell, anxious, faint, short of breath
- Fainting
- Patient may look pale and sweaty
- Tachypnoea
- Tachycardia
- Fall in blood pressure
- Late features include confusion, coma
Causes of hypovolaemic shock
- Loss of blood
- Trauma
- Burns
- Severe loss of water and salt from heat, poor intake, diarrhoea and vomiting, inappropriate diuresis
Investigations for hypovolaemic shock
Bedside – monitor urine output with catheter, may need CVP monitoring
Bloods – Hb, U&Es, LFTs, group and save, crossmatch, coagulation screen, blood gas
Imaging- ultrasound vena cava to distinguish hypovolaemic vs cardiogenic shock
Stages of loss of blood volume
Class 1: 10-15% blood loss; physiological compensation
Class 2: 15-30% blood loss; postural hypotension, generalised vasoconstriction, reduction in UO to 20 to 30ml/hour
Class 3: 30-40% blood loss; hypotension, tachycardia, tachypnoea, UO under 20ml/hour, patient confused
Class 4: 40% blood loss; marked hypotension, tachycardia and tachypnoea, no UO, patient comatose
Management of hypovolaemic shock
Oxygen
Venous access
Crystalloid e.g. Hartmann’s, normal saline (or blood if haemorrhage)
IV analgesia if pain
Surgery if bleeding
Complications of hypovolaemic shock
AKI
Gut ischaemia
Hypoxia
Metabolic acidosis
Cardiac arrhythmias/arrest
Haemoconcentration- smudging and venous sinus thrombosis
Virchow’s triad of risk factors for thrombophlebitis
Damage to vessel wall (due to infection, inflammation or trauma)
Stasis of blood flow
Hypercoagulability of blood
Risk factors for thrombophlebitis
- Obesity
- Thrombophilia
- Smoking
- Oral contraceptives
- Pregnancy
- IVDU
- IV infusion
Signs of thrombophlebitis
Painful, hard lump, often with surrounding erythema
Management of superficial phlebitis
Topical anti-inflammatory
Resolves spontaneously in 10-14 days
Mitral stenosis murmur
Mid diastolic murmur heard best with patient leaning to left side
Causes of mitral stenosis
Rheumatic fever
Degenerative calcification
Congenital
SLE
RA
Carcinoid
Infective endocarditis
Amyloid deposition
Signs associated with mitral stenosis
Malar flush
Raised JVP
Laterally displaced apex beat
RV heave
Loud SI with opening snap in early diastole
A mid-late diastolic murmur, heard best with patient in left lateral position, with the bell of the stethoscope
AF
Signs of RV failure including hepatomegaly, ascites and peripheral oedema
What does this ECG show?

LBBB
ECG features in RBBB
QRS duration >120ms
An “M-shaped” QRS complex in V1 (rSR pattern)
Wide, slurred S wave in lateral leads (aVL, V5-6)

ECG features in LBBB
QRS duration >120ms
Broad R wave in I, aVL and V6
Lack of septal Q waves in I and V6
Causes of RBBB
Normal variant- more common with increasing age
RVH
Cor pulmonale
PE
MI
Atrial septal defect
Cardiomyopathy
Myocarditis
Causes of LBBB
Acute anterior MI
Coronary artery disease
LVH
Heart failure
Idiopathic
Hyperkalaemia
Digoxin toxicity
ECG findings in atrial flutter
- ‘sawtooth’ appearance
- as the underlying atrial rate is often around 300/min the ventricular or heart rate is dependent on the degree of AV block. For example if there is 2:1 block the ventricular rate will be 150/min
- flutter waves may be visible following carotid sinus massage or adenosine
Clinical features of complete heart block
- syncope
- heart failure
- regular bradycardia (30-50 bpm)
- wide pulse pressure
- JVP: cannon waves in neck
- variable intensity of S1
Describe atrial flutter and its pathophysiology
Due to re-entry circuit in the atrium
Atria contract at 300-400bpm
Refractory period of AV node means not every P is conducted
The result is that there are several P waves and then a QRS which is conducted regularly e.g. 3 P waves then a QRS complex is 3:1
Describe the ECG features of atrial fibrillation and its pathophysiology
Supraventricular tachycardia
Indiscernable P waves
Irregularly irregular pulse
Narrow irregular QRS complex
Due to uncoordinated atrial activation resulting in an irregular ventricular response
Management of atrial fibrillation
1st line treatment is rate-control with beta blocker or rate-limiting calcium channel blocker
Assess stroke risk with CHA2DS2VASc score
If 2 or more (F) or 1 ore more (M) need anticoagulation
Assess risk of major bleed using HAS-BLED tool
Anticoagulants: apixaban, dabigatran, rivaroxaban, Vit K antagonist (e.g. warfarin)
Risks associated with AF and atrial flutter
Ineffective contraction of atria results in stasis of blood and promotes clot formation, increasing the risk of stroke and other thromboembolic complications
Acute and long term management of atrial flutter
Acute:
Rate control with beta blocker or Ca channel blocker
DC cardioversion for immediate restoration of sinus rhythm- if patient is hypotensive, or 1:1 AV conduction
Elective restoration of sinus rhythm: antiarrythmic drug, DC cardioversion or rapoid atrial pacing
Long term:
Anticoagulation to prevent clots
Catheter ablation usually curative
Pathophysiology of ectopic beats (ventricular ectopics/premature beats)
- Ectopic firing of a focus within the ventricles bypasses the His-Purkinje system and depolarises the ventricles directly.
- This disrupts the normal sequence of cardiac activation, leading to asynchronous activation of the two ventricles.
- The consequent interventricular conduction delay produces QRS complexes with prolonged duration and abnormal morphology.
ECG features of premature ventricular ectopics
- Broad QRS complex (≥ 120 ms) with abnormal morphology.
- Premature — i.e. occurs earlier than would be expected for the next sinus impulse.
- Discordant ST segment and T wave changes.
- Usually followed by a full compensatory pause.
- Retrograde capture of the atria may or may not occur.
What is cardiogenic shock?
Occurs when there is failure of the pump action of the heart, resulting in a decrease in cardiac output causing reduced end-organ perfusion. This leads to acute hypoperfusion and hypoxia of the tissues and organs, despite the presence of an adequate intravascular volume.
Defined as:
- Sustained hypotension (systolic blood pressure (BP) <90 mm Hg for more than 30 minutes)
- Tissue hypoperfusion (cold peripheries, or oliguria <30 ml/hour, or both)
(Despite adequate LV filling pressure)
Most common cause of cardiogenic shock
MI
Symptoms of varicose veins
aching legs
discomfort or itching over the veins
swollen feet and ankles
Management of varicose veins
Weight loss, light activity
Most common cause of infective endocarditis
Staph aureus
Valves most commonly affected by infective endocarditis
Mitral
Aortic
Mitral + aortic
Tricuspid
Pulmonary (rare)
Signs and symptoms of infective endocarditis
Signs:
- Heart murmur (may be new)
- Splinter haemorrhages
- Osler’s nodes (small tender red-purple nodules on terminal phalanges)
- Janeway’s lesions (irregular painless erythematous macules on thenar and hypothenar eminence)
- Roth’s spots (retinal haemorrhages with pale centres)
- Cerebrovascular accident
- Arthritis
- Splenomegaly (long standing disease)
- Meningism
Symptoms:
- Infection e.g. fatigue, fever, flu-like symptoms, pain, anorexia, weight loss
- May present as an acute rapidly progressive infection
Risk factors for infective endocarditis
Valvular heart disease
Valve replacement
Structural congenital heart disease
Previous infective endocarditis
Hypertrophic cardiomyopathy
Drug abuse
Invasive vascular procedures
Investigations for endocarditis
Bloods- CRP, FBC
Blood cultures
CXR
ECG
ECHO (TTE is initial investigation of choice)
Diagnostic criteria for infective endocarditis
2 major or 1 major + 3 minor or 5 minor criteria
Major criteria:
- Positive blood cultures
- Evidence of endocardial involvement (e.g. positive ECHO)
Minor criteria:
- Predisposition: predisposing heart condition or intravenous drug use.
- Fever: temperature >38°C.
- Vascular phenomena: major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial haemorrhage, conjunctival haemorrhages and Janeway’s lesions.
- Immunological phenomena: glomerulonephritis, Osler’s nodes, Roth’s spots and rheumatoid factor.
- Microbiological phenomena: positive blood culture but does not meet a major criterion as noted above or serological evidence of active infection with organism consistent with IE.
- PCR: broad-range PCR of 16S (polymerase chain reaction using broad-range primers targeting the bacterial DNA that codes for the 16S ribosomal subunit).
- Echocardiographic findings consistent with IE but do not meet a major criterion as noted above.
Management of infective endocarditis
Empirical antibiotics whilst awaiting cultures:
native valve, indolent presentation- amoxicillin
native valve and sepsis- vancomycin AND gentamicin
prosthetic valve- vancomycin + gentamicin + rifampicin
Staphylococcal endocarditis- flucloxacillin IV 4 weeks
Streptococcal- benzylpenicillin or ceftriaxone
Surgery if heart failure or inadequate response to antibiotic treatment
Management of MI (long-term)
Lifestyle advice:
- Stop smoking
- Cardioprotective diet (salt <6g/d, minimise refined sugars, wholegrain, 4-5 30g portions nuts/seeds per week, fish 2x per week, 5 a day, olive oil, reduce fat and sat fat)
- Regular exercise- ideally 150mins per week of moderate intensity aerobic activity and muscle strength on 2 or more days per week
- Weight loss if overweight
- <14 units alcohol per week
- Cardiac rehabilitation programme
- Annual influenza vaccine
Medication:
- ACEi
- Dual antiplatelet therapy (aspirin + clopidogrel or ticagrelor)
- Beta-blocker
- Statin
Source: https://cks.nice.org.uk/mi-secondary-prevention#!scenario
Management of acute myocardial infarction
Morphine 10mg IV (+metoclopramide IV)
Oxygen (to keep O2 sats >94%)
Nitrates
- sublingual GTN (2 sprays) if not hypertensive, then prn
- IV GTN/IV isosorbide dinitrate
Aspirin 300mg loading then 75mg OD lifelong
Clopidogrel 300mg loading then 75mg for 12 months OD/Ticagrelor/Prasugrel*
+ LMWH or fondaparinux
+ beta blockers (if no contra-indications)
+ statin
If STEMI- refer for PCI or thrombolysis (if PCI not possible within 90mins, give thrombolysis plus LMWH/fondaparinux)
Investigations for ACS
- 12 lead ECG (then continuous cardiac monitoring)
- Bloods: usual bloods (FBC, U&Es, LFTs, CRP, glucose) plus cardiac enzymes (STAT and again at 10-12 hours post- pain onset), magnesium, phosphate, lipid profile
- Chest X-ray (LVF signs?)
Symptoms suggestive of ACS
Pain in chest (or arms/back/jaw) lasting >15mins
Associated with nausea & vomiting, sweating, or breathlessness
Associated with haemodynamic instability
Pain is new-onset, or an abrupt deterioration of stable angina
ECG features indicative of ischaemia/previous MI
Pathological Q waves
LBBB
ST-segment and T-wave abnormalities
*a normal ECG does not confirm or exclude a diagnosis of ACS*
When is serum troponin normally detectable after a myocardial infarction?
Within 3-6 hours
What is the definition of angina?
Chest pain (or constricting discomfort) caused by an insufficienct blood supply to the heart muscle
The 3 types of angina and their definitions
Stable- occurs with exertion or stress, relieved within minutes of rest or with GTN spray.
Unstable- new onset angina, or abrupt deterioration in stable angina, often occuring at rest. Requires immediate admission.
Prinzmetal’s variant (aka coronary artery vasospasm)- rare angina due to narrowing/occlusion of proximal coronary arteries due to spasm. Occurs at rest, not during exercise. Tends to occur at the same time each day, most often during the night and early morning.
Management of stable angina
Lifestyle advice:
- Stop smoking
- Weight loss
- Exercise
- Limit alcohol
Medication:
- Sublingual GTN
- Beta-blocker or calcium-channel blocker 1st line
- 2nd line= isosorbide mononitrate, nicorandil, ivabradine or ranolazine
-
Secondary prevention of CV events:
- Consider antiplatelet therapy (aspirin 75mg OD)
- Statin
- ACEi if co-existing HTN, heart failure, CKD or previous MI. Consider ACEi if diabetic
- Anti-hypertensive treatment if required as per NICE guidelines
In which type of angina are beta blockers contra-indicated? What is the alternative?
Prinzmetal’s angina
use rate-limiting calcium-channel blocker e.g. verapamil or diltiazem
Causes of cardiac failure
Myocardial disease e.g. CAD, HTN, cardiomyopathies
Valvular heart disease e.g. aortic stenosis
Pericarditis/pericardial effusion
Congenital heart disease
Arrythmias e.g. AF/other tachyarrythmias
High output states e.g. anaemia, thyrotoxicosis, phaeochromocytoma, sepsis, liver failure, AV shunts, Paget’s disease, thiamine deficiency
Volume overload
Obesity
Drugs incl. alcohol, cocaine, NSAIDs, beta blockers, calcium channel blockers
New York Heart Association classification of heart failure
(4 classes)
Class I- no limitation of physical activity
Class II- Slight limitation (ordinary activity results in breathlessness/fatigue/palpitations)
Class III- Marked limitation (less than ordinary physical activity results in breathlessness/fatigue/palpitations)
Class IV- unable to carry out any activity without discomfort. Symptoms at rest may be present.
Complications of chronic heart failure
Arrythmias (AF most common)
Depression
Cachexia
CKD
Sexual dysfunction
Sudden cardiac death
Typical symptoms of heart failure
- Breathlessness — on exertion, at rest, on lying flat (orthopnoea), nocturnal cough, or waking from sleep (paroxysmal nocturnal dyspnoea).
- Fluid retention (ankle swelling, bloated feeling, abdominal swelling, or weight gain).
- Fatigue, decreased exercise tolerance, or increased recovery time after exercise.
- Light headedness or history of syncope.
Clinical features of chronic heart failure
Tachycardia, abnormal rhythm
Laterally displaced apex beat, murmur, and 3rd/4th HS (gallop rhythym)
HTN
Raised JVP
Enlarged liver (due to engorgement)
Dependent oedema/ascites
Management of confirmed heart failure with reduced ejection fraction
Stop drugs which may cause/worsen heart failure
Loop diuretic e.g. bumetanide, furosemide, torasemide (to relieve sx of fluid overload)
Prescribe an ACEi and beta-blocker e.g. bisoprolol, carvedilol, nebivolol (but start one at a time)
- Consider antiplatelet if artherosclerotic disease*
- Consider statin if indicated*
Manage causes/comorbidites/precipating factors
Annual inflenza vaccine and once-only pneumococcal vaccines
Screen for depression and anxiety
Supervised exercise-based group rehab programme
Management of heart failure with preserved ejection fraction
Stop drugs which may cause/worsen heart failure
Loop diuretic- up to 80mg furosemide or equivalent (to relieve sx of fluid overload)
Consider antiplatelet if artherosclerotic disease
Consider statin if indicated
Manage causes/comorbidites/precipating factors
Annual influenza vaccine and once-only pneumococcal vaccine
Screen for depression and anxiety
Supervised exercise-based group rehab programme
Investigations for suspected chronic heart failure
Admit if severe symptoms/pregnant
If previous MI, refer urgently (seen within 2wks)
If has not had previous MI, measure BNP or NT-pro-BNP:
BNP >400pg/mL refer for ECHO + specialist assessment within 2 weeks
BNP 100-400 refer within 6 weeks
BNP <100
12-lead ECG
Consider tests for other conditions/aggravating factorse e.g. CXR, bloods (U&Es, eGFR, FBC, TFTs, LFTs, HbA1c, fasting lipids), urine dip (blood and protein), lung function tests
Investigations for new suspected acute heart failure
BNP
If BNP raised, do TTE
Treatment of acute heart failure
Initial treatment:
Pharmacological:
- IV diuretics (if already on diuretic then increase dose)
Non-pharmacological:
- Consider NIV if cardiogenic pulmonary oedema and severe dyspnoea and acidaemia
- Consider invasive ventilation if heart failure is (despite treatment) leading to respiratory failure, decreased consciousness or physical exhaustion
After stabilisation:
- Beta blocker if acute heart failure due to left ventricular systolic dysfunction, once IV diuretics are no longer needed
- ACEi and an aldosterone antagonist if acute heart failure and reduced ejection fraction
Long-term management:
- As per chronic heart failure
- Surgical aortic valve replacement if heart failure due to severe aortic stenosis (or transcatheter aortic valve implantation if unfit for surgery)
Causes of acute heart failure/decompensation of chronic heart failure
- Further/worsening ischaemia
- Myocardial infarction
- Additional valvular or diastolic dysfunction
- Infections
- Arrhythmias - commonly atrial fibrillation (AF).
- Electrolyte imbalance
- Worsening comorbidities - eg, anaemia, thyroid dysfunction, pulmonary disease, renal dysfunction, diabetes
- New medications
Ejection systolic murmur
Crescendo-decrescendo
Commonly heard in 2nd right intercostal space
Aortic stenosis
Slow rising pulse is associated with which murmur?
Aortic stenosis
Symptoms of aortic stenosis
May be asymptomatic
SOBOE
Dizziness
Chest pain/angina
Syncope
Swollen ankles
Diagnostic investigation for aortic stenosis
ECHO
Managament of aortic stenosis
Avoid heavy exertion
Modify atherosclerotic risk factors
Treat HTN
Maintain sinus rhythm
Surgery or transcatheter aortic valve implantation if symptomatic
Early diastolic murmur
Best heard in aortic area with patient sat forward in expiration
Soft S1
Collapsing pulse/wide pulse pressure
Aortic regurgitation
Causes of aortic regurgitation
Most common cause worldwide- rheumatic heart disease
Commonest cause in developed countries- congenital and degenerative valve abnormalities e.g. bicuspid aortic valve, endocarditis, collagen vascular diseases
Transcatheter aortic valve replacement
Management of aortic regurgitation
Surgery if symptomatic or asymptomatic with deteriorating left ventricular function (valve replacement or repair)
Pansystolic murmur
Heard loudest over tricuspid region
Loudest during inspiration
Large v waves in JVP
Hepatic pulsations
Signs of right sided heart failure
Tricuspid regurgitation
Ejection systolic murmur
Loudest over pulmonary area in inspiration
Radiates to left shoulder
“a waves” in JVP
Widely split S2
Pulmonary stenosis
Early decrescendo murmur
Loudest over left sternal edge during inspiration
Usually due to pulmonary hypertension
Pulmonary regurgitation
Mid-diastolic murmur (rarely audible)
Loudest at 3rd/4th intercostal space, left sternal edge, during inspiration
Signs of right atrial enlargment (raised JVP with giant a waves, peripheral oedema, ascites)
Tricuspid stenosis