Cardiovascular Flashcards
Pathophysiology of IHD
- primarily caused by atherosclerosis
- when 70-80% sclerosed → exertional symptoms → angina
What is the mechanism of atherosclerotic plaque formation?
- fatty streaks
- intermediate lesions
- fibrous plaques of advanced lesions
- plaque rupture → infarction
What is an atherosclerotic plaque?
complex lesion consisting of:
- lipid
- necrotic core
- connective tissue
- fibrous cap
What are the major cell types involved in atherogenesis?
- endothelium
- macrophages
- smooth muscle cells
- platelets
What arteries does atherogenesis affect most commonly?
- LAD
- circumflex
- RCA
Risk factors of IHD
- family history
- age
- South Asian
- smoking
- poor nutrition
- sedentary lifestyle
- alcohol
- stress
- HTN
- obesity
- DM
Presentation of angina
- constricting discomfort in front of chest, neck, shoulders, jaw or arms
- precipitated by physical exertion
- relieved by rest/GTN spray (5 mins)
normal exam
- typical angina = all 3
- atypical angina = 2
- non anginal pain = 1/none
Investigations for IHD
- ECG usually normal
- lipid profile → high LDL
- FBC
- HbA1c
GOLD STANDARD = CT coronary angiography
Treatment of IHD
- antiplatelet therapy → aspirin/clopidogrel
- lipid lowering thearpy → statin
- good hypertensive/glycaemic control
Treatment for angina
- symptomatic relief = GTN spray
- long term symptomatic relief = beta blocker/CCB
- secondary prevention = AAA
- PCI/CABG if extensive damage
What is the secondary prevention for angina?
AAA
- aspirin
- atorvastatin
- ACEi
What surgical interventions are available for angina?
- percutaneous coronary intervention
- coronary artery bypass graft → preferred in patients with diabetes, >65
What is ACS?
Acute Coronary Syndrome
- thrombus from an atherosclerotic plaque blocking a coronary artery
- unstable angina = ischaemia
- STEMI = complete occlusion
- NSTEMI = partial occlusion → subendocardial infarction
Presentation of ACS
- central constricting chest pain radiating to jaw/arms
- sweating
- SOB
- >20 mins
- unstable angina → pain not relieved by rest or GTN spray
- silent MI → in diabetics
ECG changes in ACS
STEMI
- ST segment elevation
NSTEMI/unstable angina
- ST depression
- deep T wave inversion
How do you differentiate between unstable angina and NSTEMI?
- unstable angina = troponin normal
- NSTEMI = troponin abnormal
Immediate management of ACS
MONAC
- morphine
- oxygen
- nitrate
- aspirin
- clopidogrel
Management of STEMI
PCI within 120mins
- clopidogrel/prasugrel and aspirin
Fibrinolysis if not PCI eg alteplase
- ticagrelor and aspirin
Management of NSTEMI/unstable angina
- GRACE score
- fondaparinux
low risk
- ticagrelor
- aspirin
medium/high risk
- angiography and PCI
- prasugrel and aspirin
What is the GRACE score?
- assess for PCI in NSTEMI
- gives 6 month risk of death and repeat MI after having a NSTEMI
Secondary prevention of ACS
ACAB
- ACEi
- clopidogrel
- aspirin and atorvastatin
- beta blocker
What are the post MI complications
DREAD
- death
- rupture of heart septum/papillary muscles
- edema (HF)
- arrhythmias and aneurysms
- Dressler’s syndrome
Definition of HTN
- >140/90 in clinic (be aware of white coat HTN)
- >135/85 with ABPM/home readings
Pathophysiology of HTN
95% idiopathic = essential HTN
rest = underlying cause → ROPE
- renal disease
- obesity
- pregnancy (pre-eclampsia)
- endocrine (Conns)
Risk factors for HTN
- >65
- family history
- Afro-caribbean
- alcohol intake
- DM
- sedentary lifestyle
- sleep apnoea
- smoking
Investigations for HTN
- clinic BP >140/90
- offer ABPM or home readings
- ABPM >135/95 = diagnosis confirmed
Stages of HTN
Further investigations for HTN
- urine ACR, dipstick, bloods
- ECG
- hypertensive retinopathy → fundus examination
- HbA1c
- lipids
What medications can be used to treat HTN?
ABCDA
- ACEi → ramipril
- beta blocker → bisoprolol
- CCB → amlodipine
- diuretic (thiazide like) → indapamide
- ARB → candesartan
ARB used instead of ACEi if
- not tolerated (dry cough)
- patient is black
When to offer medical management of HTN
- stage 2 HTN
- <80, stage 1 HTN, QRISK score 10%+, complications
NICE guideline treatment for HTN
- <55 and non-black = ACEi, >55 or black = CCB
- ACEi and CCB, alternative ACEi and D, CCB and D, if black use ARB not ACEi
- ACEi and CCB and D
- ACEi and CCB and D and additional
Definition of HF
- CO is inadequate for body’s requirement
- inability of heart to deliver blood and O2 at a rate the body needs to meet demand
- physiological changes occur to maintain CO
- eventually overwhelmed and become pathophysiological
Types of HF
- systolic = inability of ventricles to contract normally
- diastolic = inability of ventricles to relax and fill normally
- can be left or right ventricular failure
- acute or chronic HF
Causes of LHF
- coronary artery disease
- arrhythmias
- MI
- cardiomyopathy
- congenital heart defects
- valvular heart disease
Causes of RHF
- COPD
- pulmonary HTN
- right ventricular infarct
- cor pulmonale
- progression of LHF
- PE
Causes of systolic HF
- IHD
- MI
- cardiomyopathy
Causes of diastolic HF
- aortic stenosis
- chronic HTN
Pathophysiology of HF
- myocardium fails
- decreased volume of blood ejected, increased preload
- increased ventricular load causes hypertrophy of myocardium
- increase in muscle growth to compensate and pump more blood out
- increased myocardial demand for oxygen
- myocardium becomes ischaemic → patchy fibrosis → stiffness and reduced contractibility
- decreased contractibility = increased workload and amount of blood remaining
- more force needed to maintain cardiac output
- cells become tired → pathological
How does HF activate RAAS
- increased afterload and preload
- increased cardiac work
- damage to myocytes
- decreased cardiac output
- activates RAAS and adrenergic pathway
- Na+ and water retention
- increased HR and contraction force
- cardiotoxicity
Common clinical presentation of HF
- SOB
- fatigue
- peripheral oedema
Symptoms of LHF
- exertional dyspnoea
- orthopnoea
- nocturnal cough
- wheeze
- nocturia
- cold peripheries
Symptoms of RHF
- peripheral oedema
- ascites
- facial engorgement
- epistaxis
Signs of HF
- tachycardia
- elevated JVP
- cardiomegaly
- 3rd/4th heart sounds
- displaced apex beat
- bi-basal crackles
- pleural/peripheral effusion
Investigations for HF
- ECG → may indicate cause
- BNP
- chest xray
What is BNP
- brain natriuretic peptide
- marker of HF
- released when myocardial walls are under stress
- levels correlated to ventricular wall stress and HF severity
Chest xray findings in HF
ABCDE
- alveolar oedema
- B Kerley lines
- cardiomegaly
- dilated upper lobe vessels of lungs
- effusions (pleural)
Treatment of HF
- lifestyle changes
- diuretics reduce preload and pressure on ventricles → loop/thiazide/aldosterone antagonist
- ACEi for LV systolic dysfunction
- beta blocker and spironolactone to decrease mortality
- digoxin for symptom relief
What is cor pulmonale?
right sided HF caused by chronic pulmonary arterial HTN
Causes of cor pulmonale
- chronic lung disease
- pulmonary vascular disorders
- neuromuscular and skeletal diseases
Signs and symptoms of cor pulmonale
- cyanosis
- tachycardia
- raised JVP
- RV heave
- pan systolic murmur
- hepatomegaly
- oedema
- dyspnoea
- fatigue
- syncope
Investigations for cor pulmonale
- ABG → hypoxia +/- hypercapnia
Management of cor pulmonale
- treat underlying cause
- oxygen
- same treatment as HF
Pathophysiology of PVD
- commonly atherosclerosis → claudication of vessels
- other causes of claudication = aortic coarctation, temporal arteritis, Burger’s
- end stage PVD = critical limb ischaemia
Risk factors of PVD
- hyperlipidaemia
- history of CAD
- age >40
What are the signs of critical limb ischaemia
6 Ps
- pain
- paresthesia
- pulselessness
- pallor
- paralysis
- poikilothermia = perishingly cold
Presentation of PVD
- pain in lower limbs on excercise, relieved on rest = intermittent claudication
- severe = unremitting pain in foot
- legs may be pale, bold, loss of hair, skin changes
Investigation for PVD
- ankle brachial pressure index ≤0.90
- ABPI = doppler ultrasonography
- should be 1
Treatment for PVD
control risk factors - lifestyle changes
antiplatelet therapy
Treatment for critical limb ischaemia
as stated plus:
- revascularisation eg stenting, angioplasty, bypassing
- amputation if unsuitable
What is pericarditis?
inflammation of the pericardium +/- effusion
2 types
- fibrinous = dry
- effusive → purulent serous/haemorrhagic
Causes of acute pericarditis
- infection
- autoimmune → RA, sjogren’s, SLE
- secondary metastatic tumours
- traumatic and iatrogenic
- post cardiac injury
What infections can cause acute pericarditis?
- enteroviruses
- adenoviruses
- mycobacterium TB
Pathophysiology of pericarditis
- inflammation
- narrowing of pericardial space and scarring
- if untreated, build up of exudate and adhesions in pericardial space → pericardial effusion
Symptoms of pericarditis
- severe chest pain
- dyspnoea
- cough
- hiccups
- fever
- myalgia
Signs of pericarditis
- pericardial rub on auscultation
- tachycardia
- peripheral oedema
- increased JVP
Investigations for pericarditis
ECG = DIAGNOSTIC
- saddle shaped ST elevation
- diffuse ST elevation in all leads
- PR depression
chest xray → effusion may cause cardiomegaly
What is chest pain like in pericarditis
- sharp, pleuritic, rapid onset
- worse when laying flat, relieved sitting forwards
- radiates to trapezius ridge
Treatment for pericarditis
- reduce physical activity until symptoms resole
- NSAIDs with gastric protection → ibuprofen/aspirin
- colchicine 3 months
- treat cause
What is infective endocarditis
- an infection of the endocardium or vascular endothelium of the heart
- fever and new murmur = infective endocarditis until proven otherwise
What microorganisms cause infective endocarditis
- staph aureus
- streptococcus viridans
- strep bovis
- enterococci
- coxiella burnetii
Risk factors for infective endocarditis
- IVDU
- immunocompromised
- people with prosthetic valves
- aortic/mitral valve disease
- poor dental hygiene
- pacemakers
- IV cannula
Pathophysiology of infective endocarditis
- abnormal cardiac endothelium and organisms in bloodstream
- adherence and growth of organisms
- infective endocarditis
- LHS of heart = most common side effected
- RHS affected in IVDU
Symptoms of endocarditis
- fever
- rigors
- night sweats
- malaise
- weight loss
Signs of endocarditis
- anaemia
- splenomegaly
- clubbing
- new murmurs
- sepsis
- embolic events
Typical presentation of endocarditis
- embolic skin lesions
- petechiae
- splinter haemorrhages
- osler nodes
- janeway lesions
- roth spots
Investigations for endocarditis
- Duke criteria
- echo
- ECG → long PR interval, regular
transoesophageal echo = more sensitive, uncomfortable, better at diagnosing
Treatment for endocarditis
- antibiotics
- treat any complications
- surgery
What surgery can be used to treat endocarditis?
- replace valve if infection cannot be treated with Abs
- remove/replace infected devices
- remove large vegetations at risk of embolising
Prevention of endocarditis
- good oral health
- no IV drug use
- educate surgery patients on symptoms
What is pericardial effusion
- occurs if pericarditis is untreated
- buildup of exudate in pericardial space
- puts pressure on cardiac myocytes → cardiac dysfunction
Signs of pericardial effusion
- bronchial breathing at left base
- muffled heart sounds
Treatment for pericardial effusion
- treat the cause
- pericardiocentesis
complication = cardiac tamponade
What is cardiac tamponade
- life threatening
- accumulation of fluid in pericardial space
- compression of heart chambers
- decreased venous return and filling of heart
- reduces cardiac output
Symptoms and signs of cardiac tamponade
- Beck’s triad
- pulsus paradoxus = large decrease in stroke volume
What is Beck’s triad?
- falling BP
- rising JVP
- muffled heart sounds
Investigations for cardiac tamponade
GOLD STANDARD = echo
Treatment for cardiac tamponade
pericardiocentesis
Murmur in mitral stenosis
- mid-diastolic murmur with opening snap
Symptoms of mitral stenosis
- haemoptysis due to pulmonary oedema
- palpitations AF
Signs of mitral stenosis
- malar flush
- tapping apex beat
- low volume pulse
- loud S1
Causes of mitral stenosis
- rheumatic heart disease
- IE
Murmur in mitral regurgitation
pansystolic high pitched whistling murmur
Symptoms of mitral regurgitation
- palpitations
- exertional dyspnoea
- fatigue
- weakness
Signs of mitral regurgitation
- AF
- displaced, thrusting apex
- soft/absent S1
Causes of mitral regurgitation
- idiopathic
- IHD
- rheumatic heart disease
- EDS, Marfans
Complication of mitral regurgitation
congestive HF
Murmur in aortic stenosis
ejection systolic murmur
Symptoms of aortic stenosis
triad of
- syncope
- angina
- dyspnoea
Signs of aortic stenosis
- sustained heaving apex
- slow rising pulse
- narrow pulse pressure
- soft S2 if severe
Causes of aortic stenosis
- idiopathic
- rheumatic heart disease
AS = most common valve defect
Murmur in aortic regurgitation
- early diastolic murmur
- Austin flint murmur at apex
Symptoms of aortic regurgitation
- palpitation
- angina
- dyspnoea
Signs of aortic regurgitation
- water hammer pulse
- wide pulse pressure
- displaced apex
- Corrigan’s pulse → collapsing
Causes of aortic regurgitation
- idiopathic
- EDS, Marfans
Treatment for valve defects
- treat symptoms
- replace defective valve
What is VTE?
- venous thromboembolism
- blood clots develop in circulation
- due to stagnation of blood and hyper-cogulable states
What is a DVT?
- deep vein thrombosis
- thrombus that develops in the venous circulation
What is a PE?
- pulmonary embolism
- once thrombus develops, it can travel → embolise
- deep veins → through RHS of heart → lungs → PE
What is a complication of VTE?
- if patient has a hole in heart, clot can pass through LHS of heart into systemic circulation
- causes large stroke
Risk factors for VTE
- immobility, long haul travel
- recent surgery
- pregnancy
- hormone therapy with oestrogen → pill, HRT
- malignancy
- polycythaemia
- SLE
- thrombophilia → antiphospholipid syndrome
VTE prophylaxis
- hospital admission → risk assessment for VTE
- LMW heparin if high risk
contraindicated if active bleeding or existing coagulants
Presentation of DVT
- unilateral
- calf/leg swelling
- dilated superficial veins
- calf tenderness
- oedema
- colour changes in leg
What is a Wells score?
predicts risk of patients with symptoms having a DVT/PE
Diagnosis of VTE
D-dimer
DIAGNOSTIC FOR DVT = doppler US leg
GOLD STANDaRD FOR PE = CT pulmonary angiogram
- V/P scan if contraindicated
Initial management of VTE
- anticoagulation
- catheter directed thrombolysis
Long-term anticoagulation in VTE
DOAC, warfarin, LMW heparin
- 3 months if cause reversible
- 3-6 months if active cancer
What is an anuerysm?
weakening of vessel wall followed by dilation due to increased wall stress
What is the most common vessel aneursym
abdominal aortic aneurysm
Pathophysiology of aortic aneurysm
1 inflammation and degeneration of smooth muscle cells
- loss of structural integrity of aortic wall
- vessel widens
- mechanical stress acts on weakened wall tissue
- can lead to dilation or rupture
Complication of dilated aneurysm
peripheral thromboembolism
Risk factors of aortic aneurysm
- SMOKING
- family history
- connective tissue disorders
- age
- atherosclerosis
- male
Presentation of AAAs
- most are asymptomatic
- commonly found below renal arteries → infrarenal
- if big, pulsatile mass on palpation, bruit on auscultation
- lower back/abdominal pain if expanding rapidly
Diagnosis of aortic aneurysms
- ultrasonography
Management of aortic aneurysms
symptomatic → repair
asymptomatic
- surveillance
- if diameter >5.5cm (m) or >5cm (f) → repair
Complications of aortic aneurysms
- rupture of AAA
- thromboembolism
- fistula formation
Presentation of ruptured AAA
- acute onset of severe, tearing abdominal pain with radiation back, flank, groin
- painful pulsatile mass
- hypovolemic shock
- syncope
- nausea, vomiting
Diagnosis of ruptured AAA
clinical to save time
Treatment of ruptured AAA
- urgent surgery → endovascular aneurysmal repair
- maintain haemodynamic stability
What is an aortic dissection?
- teat in the intimal layer of aorta
- leads to collection of blood between intima and medial layers
- mainly in ascending aorta
Pathophysiology of aortic dissection
- tear in intimal layer
- blood passes through media propagating distally or proximally
- false lumen
- can occlude flow through branches of aorta
- ischaemia of affected regions
Risk factors of aortic dissection
- male
- 40-60
- HTN → most common
- trauma
- vasculitis
- cocaine use
- connective tissue disorders in younger adults
Clinical features of aortic dissection
- sudden and severe tearing pain in chest radiating to back
- hypotension
- asymmetrical BP
- syncope
Diagnosis of aortic dissection
- ECG
- chest xray
- CT
Management of aortic dissection
- maintain haemodynamic stability
- opioid analgesia
- endovascular stent-graft repair
- antihypertensives post surgery
How do you maintain haemodynamic stability
- fluid resuscitation
- ionotropes
- noradrenaline
What is tetralogy of Fallot?
- large ventricular septal defect
Features of tetralogy of Fallot
- overriding aorta
- RV outflow obstruction
- RV hypertrophy
Investigations for tetralogy of Fallot
echo
Treatment for tetralogy of Fallot
surgical repair
What is coarctation of aorta?
- narrowing of aortic arch around ductus arteriosus
- varied severity
- associated with Turners syndrome
- low BP in areas after narrowing
- high BP in areas before
Presentation of coarctation of aorta
- in neonates, weak femoral pulses
- grey and floppy baby
- poor feeding
- tachypnoea
- left ventricular heave
Management of coarctation of aorta
- if severe, prostaglandin E used to keep ductus arteriosus open
- surgery to correct coarctation and ligate ductus arteriosus
What is tachycardia?
- fast hear rate
- >100bpm
What is atrial tachycardia?
>150bpm
ECG
- abnormal P waves
- normal QRS
What is AV nodal re-entrant tachycardia?
- absent P wave
- normal QRS
What is ventricular tachycardia?
- no P waves
- regular wide QRS
- no T waves
What is bradycardia?
- slow heart rate
- <60pbm
What is atrial fibrillation?
- chaotic irregular rhythm
- irregular ventricular rate
ECG
- no P waves
- irregularly irregular QRS
Causes of a fib
- idiopathic
- HTN
- HF
- coronary artery disease
- vavlular heart disease
- cardiac surgery
- cardiomyopathy
- rheumatic heat disease
Pathophysiology of a fib
- continous rapid activation of atria
- no organised mechanical action
- 300-600bpm
Risk factors for a fib
- 60+
- diabetes
- high BP
- past MI
- structural heat disease
Presentation of a fib
- asymptomatic
- palpitations
- dyspnoea
- chest pain
- fatigue
- apical pulse>radial
Treatment of a fib
cardioversion
- LMW heparin
- shock with defib
What is atrial flutter?
- organised atrial rhythm
- rate of 250-250bpm
ECG → saw tooth pattern = DIAGNOSTIC
Causes of atrial flutter
- idiopathic
- coronary heart disease
- obesity
- HTN
- HF
- COPD
- pericarditis
Risk factors of atrial flutter
atrial fibrillation
Presentation of atrial flutter
- palpitations
- breathlessness
- chest pain
- dizziness
- syncope
- fatigue
Treatmen of atrial flutter
- cardioversion
- catheter ablation → creates conduction block
- IV amiodarone → restore sinus rhythm
What is bundle branch block
- block in conduction of one of the bundle branches
- ventricles don’t receive impulses at the same time
ECG changes in right BBB
- MaRRoW
- wide QRS
DIAGNOSTIC
Causes of right BBB
- PE
- IHD
- atrial ventricular septal defect
Pathophysiology of right BBB
- right bundle doesn’t conduct
- impulse spread from LV to RV
- late activation of RV
Presentation of right BBB
- asymptomatic
- syncope/presyncope
Treatment of right BBB
- pacemaker
- cardiac resynchronisation therapy
- reduce BP
ECG changes in left BBB
- WiLLiaM
- wide QTS and notched top
- T wave inversion in lateral leads
DIAGNOSTIC
Causes of left BBB
- IHD
- aortic valve disease
Pathophysiology of left BBB
- left bundle doesn’t conduct
- impulse spreads from RV to LV
- late activation of LV
Presentation of left BBB
same as right BBB
Treatment of left BBB
same as right BBB
What is heart block
a block at any level of the conduction system in which conduction seizes
What are the different types of heart block
1st degree
2nd degree
- Mobitz I
- Mobitz II
3rd degree
1st degree heart block
- PR interval >200ms
- asymptomatic
ECG changes 2nd degree Mobitz I
- progressive lengthening of PR interval
- one non-conducted P wave
- next PR interval is shorter
Presentation of 2nd degree Mobitz I
- light headedness
- dizziness
- syncope
ECG changes in 2nd degree Mobitz II
- constant PR
- occasional non-conducted P waves
- wide QRS
2: 1
- two waves per QRS
- normal consistent PR intervals
Presentation of 2nd degree Mobitz II
- SOB
- postural hypotension
- chest pain
ECG changes in 3rd degree heart block
- P waves and QRS at different rates → dissociation
- abnormally shaped QRS
Presentation of 3rd degree heart block
- dizziness
- blackouts
Treatment for 3rd degree heart block
- permanent pacemaker
- IV atropine
Causes of heart block
- athletes
- sick sinus rhythm
- MI
- drugs
- congenital
- aortic valve calcification
- cardiac surgery/trauma
Treatment for heart block
- cardioversion
- catheter ablation
- IV amiodarone
What is prolonged QT syndrome?
where the QT interval is greatly increased
ECG DIAGNOSTIC
Causes of prolonged QT syndrome
- congenital
- hypokalaemia
- hypocalcaemia
- drugs → amiodarone, tricyclic antidepressants
- bradycardia
- acute MI
- diabetes
Presentation of prolonged QT syndrome
- syncope
- palpitations
- may progress to VF
Treatment of prolonged QT syndrome
- cardioversion
- treat underlying cause
- if acquired → IV isoprenaline
What is Wolff-Parkinson-White syndrome?
- accessory pathway for conduction
- impulse can travel to AVN but also to ventricle quicker
ECG changes in WPW
pre-excitation
- short PR interval
- wide QRS complex that begins slurred
ECG DIAGNOSTIC
Causes of WPW
same as prolonged QT syndrome
Presentation of WPW
- palpitations
- severe dizziness
- dyspnoea
- syncope
Treatment of WPW
- vagal manoeuvre
- IV adenosine
- surgery → catheter ablation of pathway
What is the vagal manoeuvre?
- breath holding
- carotid massage
- valsalva manoeuvre
What is rheumatic fever?
- systemic infection common in developing countries
- from Lancefield group A B-haemolytic streptococci
- antibody from cell wall cross-reacts with valve tissue → permanent damage to heart valves
Symptoms of rheumatic fever
- fever
- arthritis
- chest pain
- SOB
- fatigue
- chorea → jerky movements
Signs of rheumatic fever
- tachycardia
- murmur → depends on valve
pericardial rub - erythema marginatum
- prolonged PR interval
Investigations for rheumatic fever
Jones criteria
Treatment for rheumatic fever
- rest until CRP is normal
- IV benzylpenicillin then phenoxymethylenicillin for 10 days
- analgesia
- haldoperidol/diazepam for chorea
Causes of cardiogenic shock
- pump failure
- MI
- cardiac arrest
Pathophysiology of cardiogenic shock
- decreased CO
- decreased MAP
Presentation of cardiogenic shock
- tachycardia
- tachypnoea
- decreased urine output, BP
- cold peripheries
- chest pain
Treatment for cardiogenic shock
- ABCDE
- rescucitation
Causes of hypovolaemic shock
- low fluid volume
- haemorrhage
- dehydration
Pathophysiology of hypovolaemic shock
- decreased MAP
- decreased CO
Presentation of hypovolaemic shock
- tachypnoea
- weak rapid pulse
- cyanosis
- increased CRT
Treatment of hypovolaemic shock
- ABCDE
- resuscitation
- fluids
- vasodilator GTN
Causes of septic shock
toxins. inblood
Pathophysiology of septic shock
- decreased MAP
- derangement in physiology
Presentation of septic shock
- tachycardia
- D&V
- decreased urine output, O2, BP
Treatment of septic shock
- broad spectrum IV Abs
- fluid
- O2
Causes of anaphylactic shock
severe allergic reaction
Pathophysiology of anaphylactic shock
- histamine release
- vasodilation
- hypoxia
Treatment for anaphylactic shock
- rescucitation
- adrenlaine
What does resuscitation entail in shock
- CPR
- fluids
- O2
What is cardiomyopathy?
a group of diseases of the myocardium that affect mechanical or electrical function
What are the types of cardiomyopathy?
- hypertrophic
- dilated
- restricted
What is dilated cardiomyopathy?
the left ventricle is dilated with thin muscle → contracts poorly
Causes of dilated cardiomyopathy
- ischaemia
- alcohol
- thyroid disorder
- genetic
Pathophysiology of dilated cardiomyopathy
- poorly generated contractile force → progressive dilation of the heart
- diffuse interstitial fibrosis
- systolic dysfunction of left or both ventricles
Signs of dilated cardiomyopathy
- HF
- arrhythmia
- thromboembolism
- increased JVP
- sudden death
Symptoms of dilated cardiomyopathy
- SOB
- fatigue
- dyspnoea
Investigations for dilated cardiomyopathy
- chest xray → cardiac enlargement
- ECG → tachycardia, arrhythmia, T wave changes
- echo → dilated ventricles
Treatment of dilated cardiomyopathy
treat cause
What is hypertrophic cardiomyopathy?
ventricular hypertrophy → obstruction of outflow tract
Causes of hypertrophic cardiomyopathy
- genetic → autosomal dominant
- 50% sporadic
Pathophysiology of hypertrophic cardiomyopathy
- gene mutation for sarcomere protein
- impaired diastolic filling
- reduced stroke volume
- reduced CO
Symptoms of hypertrophic cardiomyopathy
- sudden death may be first symptom
- chest pain/angina
- dyspnoea
- dizziness
- palpitations
- syncope
Signs of hypertrophic cardiomyopathy
- ejection-systolic murmur
- jerky carotid pulse
- left ventricular outflow obstruction
Investigations for hypertrophic cardiomyopathy
- ECG → T wave inversion, deep Q waves
- genetic analysis
Treatment for hypertrophic cardiomyopathy
- amiodarone → anti-arrhythmic
- CCB → verapamil
- beta blocker → atenolol
What is restrictive cardiomyopathy?
scar tissue replaces normal heart muscle and ventricles become rigid so don’t contract properly
Causes of restrictive cardiomyopathy
- amyloidosis
- idiopathic
- sarcoidosis
- end-myocardial fibrosis
Symptoms of restrictive cardiomyopathy
- dyspnoea
- fatigue
- embolic symptoms
Signs of restrictive cardiomyopathy
- increased JVP → diastolic collapse, elevated on inspiration
- hepatic enlargement
- ascites
- oedema
- 3rd and 4th heart sounds
Pathophysiology of restrictive cardiomyopathy
- normal/decreased volume in both ventricles
- bi-atrial enlargement
- impaired ventricle filling
- rigid myocardium restricts ventricular filling
Investigations for restrictive cardiomyopathy
DIAGNOSTIC = cardiac catheterisation
Treatment for restrictive cardiomyopathy
no treatment → poor prognosis
