CVS Flashcards
What is acute limb ischemia
blockage of peripheral artery
Pathophy of acute limb ischemia
blockage reduced perfusion causing ischemia
5 RF of acute limb ischemia
- Smoking
- Diabetes mellitus
- Obesity
- Hypertension
- Hypercholesterolaemia
The 6p’s (acute limb ischemia signs and symptoms)
Pulseless
Paraesthesia
Pain
Paralysis
Pallor
Perishing cold
Investigations for acute limb ischemia
clinical diagnosis
You can roughly localise the blockage by locating thebifurcation distal to the last palpable pulse.
doppler to confirm absence of pulse
Mangement of acute limb ischemia
EMERGENCY
Thrombolytic agent
angioplasty
2 complications of acute limb ischemia
amputation
death
What is acute pericarditis
Inflammation of the pericardium
90% idiopathic or due to viral infections
Associated with systemic autoimmune disorders too
Acute vs chronic: 4-6 weeks vs >3 months
SS of acute pericarditis
Pleuritic central chest pain, worse on lying down, better sitting forward, intermittent fevers
Investigations for acute pericarditis
Examination: pericardial friction rub, tachycardia
ECG shows global upwardly concave ST-segment (J-point) elevations with PR segment depressions in most leads with J-point depression and PR elevation in leads aVR and V1
Mangement of acute pericarditis
Management: NSAIDs, can add colchicine.
- Corticosteroids
What is acute rheumatic fever
Rare but common in developing countries (major cause of death and heart disease)
Improvement in developed countries due to penicillin and improved social conditions and reduction in virulence of the GpA BHS
Autoimmune disease following a group A streptococcal infection.
Can affect joints, heart, brain, skin
Effects on heart can lead to permanent illness: chronic changes to heart valves referred to as chronic rheumatic disease
SS of acute rheumatic fever
Symptoms appear 1-5 weeks after sore throat
- Arthritis and toxicity with mild carditis (chest pain, SOB if severe), fever
- Palpitations, heart murmur, signs of heart failure
- Subcutaneous nodules/ erythema nodosum (swollen fat under skin causing red bumps and patches), chorea (jerky involuntary movements)
Investigation for acute rheumatic fever
Diagnosis based on Jones 2015 criteria
- Throat swabs, ESR, CRP, FBC. ECHO
Management for acute rhematic fever
Management: eradicate streptococcal infection, suppress inflammation, provide supportive treatment especially if complications such as HF
- Penicillin, aspirin, HF treatment if necessary cardiac surgery if treatment fails), diazepam if chorea present
what is angina
Pain/constricting discomfort in the chest
Radiating to the neck/shoulders/jaw/arms
Difference between stable and unstable angina presentation
Stable:
Occurs predictably
Lasting less than 15 mins, relieved by rest
with physical exertion or emotional stress
relieved within minutes of rest or GTN
unstable:
New onset or abrupt
often occurring at rest
lasts longer than 15 minutes
RF of angina
- smoking
- hyperlipidaemia
- age
- common in men but increases for women after menopause
- hypertension
- diabetes
- obesity
- exercise
- ethnicity
Pathophysiology of angina
Caused by an insufficient blood supply to myocardium
Atherosclerotic plaque inadequate oxygen to myocardium at times when oxygen demand increases (exercise)
SS of angina
chest pain
pain radiating to jaw neck and left arm
SOB
Dizziness
Investigation for angina
clinical history
Physical examination
blood test- rule out anaemia
ECG
Q-RISK
Management for angina (first line)
First line- Beta blocker or CCB, if both contraindicated or not tolerated then monotherapy with one of the following: nitrate, ivabradine, nicorandil, ranolazine
Management for angina (2 line)
Second line: if on B-blocker then add CCB. if on CCB then add b-blocker
Other management for angina
Aspirin
GTN
lifestyle advice
Primary prevention -> statins
secondary prevention-aspirin/clopidogrel, acei, statin, anti HTN
Complications of angina
Stroke
MI
Unstable angina
sudden cardiac death
anxiety
depression
draw the diagram outlining MI/NSTEMI/UNDTABLE ANGINGA
chest pain……. Non -cardiac
:
:
ACS ……….. STEMI (ST elevation)
:
:
Unstable angina/NSTEMI (ecg shows no st elevation)
:
:
if normal troponin levels, then = unstable angina
if raised troponin levels then NSTEMI
What is the initial 2 medication offered to NSTEMI and unstable patients (early management)
Antiplatelet - 300mg aspirin
Anti-thrombin - fondaparinux
STEMI early management
offer 300 mg of aspirin
assess eligibility for reperfusion therapy:
if yes offer PCI or fibrinolysis
if no proceed with medical management, offer ticagrelor with aspirin
5 post MI medications
ACEi
Clopidogrel
B-blocker
statin
rivaroxaban
2 things to do post MI
cardiac rehab and secondary prevention
What is angina pectoris: prinzmetal’s /variant
Coronary artery spasm
Common in patients with underlying heart disease but can occur in healthy people as well
Pathophysiology of angina pectoris: prinzmetal’s/ variant
- Not fully clear but is thought to be linked with low nitric oxide (secondary to reduced acetylcholine release), increased adrenergic activities, vasoconstrictor mediators (thromboxane, serotonin etc)
- Acetylcholine normally results in the release of nitric oxide and also act directly as a vasodilator at rest
- Thromboxane/serotonin are involved in platelet activation/recruitment. There is more of these mediators in prinzmetal
- Increased adrenergic activities can cause an increase in heart rate and peripheral vasoconstriction
RF for angina pectoris: prinzmetal’s/ variant
- Heart disease
- Stress
- Drugs such as cocaine, sympathomimetics such as epinephrine
- Alcohol
- Smoking
SS for angina pectoris: prinzmetal’s/ variant
- Rest chest pain common at midnight/morning and lasting between 5-30 minutes
- Headache
- Patient may have a history of coronary heart disease
- Deranged vital signs such as tachycardia, tachypnoea, high BP
- There might not be any focal cardiac examination finding unless patient has underlying heart disease
- Raynaud phenomenon if severe
Ix for ngina pectoris: prinzmetal’s/ variant
Bloods
- Most important blood test is Troponin to rule out ACS.
- FBC, renal function, electrolytes, fasting blood glucose and lipid levels
X-ray/Imaging
- CXR to rule out alternative causes
ECG
- STAT ECG might show transient STE. 24 hour ECG tape can be used if symptoms have resolved
Special Tests
- Coronary angiography is the investigation of choice. Other options include stress echocardiography
Management for angina pectoris: prinzmetal’s/ variant
- Lifestyle management
- Manage co-existing disease
- GTN/Calcium channel blockers are mainstay of medical treatment (avoid beta blockers as may aggravate symptoms)
- Revascularization
- coronary artery stenting
Complication for angina pectoris: prinzmetal’s/ variant
- Arrhythmias
- MI
What is aortic coarctation
congenital narrowing of the aorta
RF for aortic coarctation
- Men > Women
- Turner’s syndrome
- Aortic valve is bicuspid in 80% of cases
- Patent ductus arteriosus
- Ventricular septal defect
- Mitral stenosis/regurgitation
- Circle of Willis aneurysms
SS of aortic coarctation
asymptomatic
headaches and nose bleed to due to HTN
Claudication and cold legs
HTN in upper limbs
Week delayed pulse in legs
radio femoral delay
Ix for aortic coarctation
CXR
ECG
LVH
aortagraphy
CT/MRI
Management for aortic coarctation
Surgery
What is aortic stenosis
- Narrowing of the aortic valve
- Progressive disease
Pathophysiology of aortic stenosis
- Calcification of the valve is most common cause.
- Congenital, history of rheumatic heart disease
SS of aortic stenosis
- Can be asymptomatic for many years
- Shortness of breath with exertion, angina, syncope
- Systolic murmur, mid-to-late peaking with a crescendo-decrescendo pattern, radiates to carotids
- Can cause left ventricular hypertrophy, heart failure. Can lead to sudden cardiac death. Damaged valve prone to endocarditis
Ix for aortic stenosis
ECHO
Management of aortic stenosis
avoid heavy exertion, surgical intervention
What is aortic regurgitation
- Diastolic leakage of blood from the aorta into the left ventricle
- Acute :caused by endocarditis or aortic dissection
- Chronic: asymptomatic for years until symptoms of heart failure develop
Pathophysiology of aortic regurgitation
Caused by disease of the aortic valve (bicuspid aortic valve, rheumatic fever, infective endocarditis, collagen vascular disease, degenerative aortic valve disease) or aortic root
Acute SS of aortic regurg
Acute presents with sudden onset pulmonary oedema and hypotension/cardiogenic shock. May also present as myocardial ischaemia or aortic root dissection
chronic SS for aortic regurg
Chronic: initial symptoms can include palpitations and uncomfortable awareness of pounding heart when lying on left side
Management for aortic regurg
- Acute severe AR – urgent surgical intervention
- Chronic severe AR – goals of treatment to prevent death, diminish symptoms, to prevent development of hear failure and avoid aortic root complications
- Valve replacement
What is aortic aneurysm
Aneurysm is a bulge in the aorta
it can be abdominal (common) or thoracic
dissection is a tear
Aortic dissection can either be Type A (Ascending aorta) or Type 2 (Descending aorta)
Pathophys of aortic aneurysm
- Arteries are made up of three layers from proximal to distal namely tunica intima, tunica media and tunica adventitia
- Aortic aneurysm occurs when there is an irreversible degradation of the elastic lamellae (outermost part of the tunica intima) and associated smooth muscle loss
- Aortic dissection occurs when there is a damage to the tunica intima and blood pulls inside the tunica media
RF for aortic aneurysm
- Advanced age
- Hypertension
- Marfan syndrome
- Smoking
- Trauma
SS for aortic aneurysm
- Sudden ripping/tearing chest pain radiating to the back
- Shortness of breath
- Abdominal/back pain
- Asymmetric pulse
- Abdominal pain/distension
- Unequal blood pressure in both arms
- Abdominal bruit
- Flank haemorrhage
Ix for aortic aneurysm
Bloods
- FBC (Anaemia-although not immediately)
- Cross match
- LFT/RFT (to look for end organ ischaemic damage)
Orifice Test
- PR test when indicated
X-ray/Imaging
- CXR (can initially show widened mediastinum if thoracic aneurysm/dissection)
- CT-aortogram (widely used) or MRI angiography for confirmation
ECG
- Might show ischaemic changes like STE/STD depending where the dissection occurs
Special Tests
- If aneurysm/dissection in the context of trauma, A FAST scan can be done
Management for aortic aneurysm
- Lifestyle/risk factor management (stop smoking etc)
- Statin/Aspirin when indicated
- Further Medical management depends on the size of the aneurysm (Refer to secondary care)
- If between 3-4.4cm (Annual ultrasound), If 4.5-5.4 (3 monthly ultrasound), if >5.5cm (Immediate referral for surgery and 3 monthly ultrasound)
- There is a one off screening program for over 65s in england which can rule out aneurysm for life if negative
Complication for aortic aneurysm
- Cardiac tamponade
- Cardiogenic shock
What are arrythmias
Arrhythmias are abnormalities of the heart rate or rhythm caused by disorders of impulse generation or conduction.
What is atrial fibrillation
A supraventricular tachyarrhythmia with uncoordinated atrial electrical activation and consequently ineffective atrial contraction.
What is ECG finding of AFib
- Irregularly irregular R-R intervals(when atrioventricular conduction is not impaired)
- Absence of distinct repeating P waves
- Irregular atrial activations.
3 different classifications of Afib
Paroxysmal AF – episodes lasting longer than 30 seconds but less than 7 days (often less than 48 hours), that are self-terminating and recurrent
Persistent AF – episodes lasting longer than 7 days (spontaneous termination of the arrhythmia is unlikely to occur after this time) or less than seven days but requiring pharmacological or electrical cardioversion
Permanent AF – AF that fails to terminate using cardioversion, AF that is terminated but relapses within 24 hours, or longstanding AF (usually longer than 1 year) in which cardioversion has not been indicated or attempted
What is atrial flutter and its ECG characteristics
Flutter wave (instead of P waves) organize atrial depolarisations of a rate around 300bpm producing a saw-tooth pattern in typical counterclockwise flutter.
Narrow QRS complex
ECG finding for ventricular tachyarrhythmia
Irregular R-R interval
Risk factors for arrythmia
Middle aged - older adults
Europe and North America
Comorbidities
RF for Afib
age
comorbidities - HTN, diabetes, HF, CHD ,CKD
Obesity
Obstructive sleep apnoea
Pathophysiology of arrythmia
ischemic
degeneration
mitral stenosis
metabolic
Pathophysiology of Afib
Left atrial arrhythmia
often in the form of rapidly firing ectopic foci located inside one or more pulmonary veins, and an abnormal atrial tissue substrate capable of maintaining the arrhythmia.
SS of arrythmias
Breathlessness
Palpitations
Syncope/dizziness
Chest discomfort
Reduced exercise tolerance
Ix for arrythmias
Patient Hx
ECG recording
Ambulatory ECG monitoring
External loop recorders
Implantable Loop Recorders (ILR)
Signal average ECG
Structural heart imaging – Chest x-ray/Echo/MRI
Electrophysiology study
‘Personal smart-tech’
Blood count, electrolyte levels, drug levels, thyroid study
Afib investigation
The diagnosis of AF requires rhythm documentation with an electrocardiogram (ECG) tracing showing AF. By convention, an episode lasting at least 30 seconds is diagnostic for clinical AF.
if pulse is irregular then 12 lead ECG , Ambulatory ECG monitoring
Management for afib and atrial flutter
Urgent referral
-If the onset of atrial fibrillation (AF) was within the last 48 hours urgently and haemodynamic instability/loss of consciousness/severe dizziness or syncope/ongoing chest pain/increasing breathlessness.
Comorbidities and lifestyle
-assess for signs and symptoms and do test to confirm or rule out underlying causes of AF
Rate control
-beta blocker
-rate limiting calcium channel blocker
-digoxin
Stroke risk
Asses CHA2DS2VASC and HAS-BLED score
anticoagulant option-
DOACS
Rhythm control
-Pharmacological - anti arrhythmic drugs
- Intervention- PVI ablatio, pharmacological cardioversion and DCCV
Ventricular tachyarrhythmia management
Emergency – 999
Urgent – transfer ASAP to A&E monitored by a defibrillator and all monitoring/IV line if possible.
Complications for arrythmias
stroke
TIA
HF
What is arterial embolism/thrombosis
occlusion of arteries
- Most commonly affected arteries include those in the heart, brain, kidneys & lower limbs.
Pathophysiology of arterial embolism/thrombosis
- A thrombus is a local formation of clot while an emboli is a clot that has broken off to lodge in another area of the body
- Embolism/thrombosis occurs due to risk factors like lipidemia, cigarettes etc. These risk factors damage the vascular endothelium and consequently lead to arterial occlusion manifesting as ischaemia.
RF for arterial embolism/thrombosis
- Smoking
- Lipidemia
- Sedentary lifestyle
- Recent surgery
- Hypertension
- Obesity
- Atrial fibrillation
- Hypercoagulability states e.g thrombocytosis
SS for arterial embolism/thrombosis
- Pain
- Numbness/Tingling
- Muscle spasm/weakness
- Change in colour
- Skin coldness
- Checking CRT, pulse, sensation. All of which would be absent or delayed in peripheral vascular disease
Ix for arterial embolism/thrombosis
Bloods
- Lipids. ESR. HBA1c. Renal/Liver function tests. Creatine kinase, Troponin, FBC
X-ray/Imaging
- CT/MRI angiography. Arterial doppler. Echocardiogram
ECG
- Can show ischaemic picture if heart involved
Special Tests
- Ankle brachial pressure index
Management for arterial embolism/thrombosis
- Urgent admission and anticoagulation should be started immediately.
- Surgical embolectomy or intra-arterial thrombolysis if occlusion is from embolus
- Angioplasty or bypass surgery or thrombolysis
- Managing risk factors/comorbidities e.g smoking, lipidemia
Complication for arterial embolism/thrombosis
- Necrosis/Gangrene
- Chronic pain syndrome
What is atrial septal defect
Communication between the left and right side of the heart
hole in the septum that divides the atrial wall chambers
SS for atrial septal defect
Asymptomatic in infants and children
Subtle SOBOE/palpitations in second decade of life
Adults with large defect → fatigue, exercise intolerance, palpitations, syncope, SOB, peripheral oedema, thromboembolic manifestations, and cyanosis
Ix for atrial septal defect
Widely split second heart sound. Soft systolic ejection murmur
ECHO
Management for atrial septal defect
Diuretics for those that develop heart failure. Surgical closure
What is AV block and what are 4 subtypes called
Atrioventricular (AV) block (often referred to as “heart block”) involves the partial or completeinterruption of impulse transmission from theatria to theventricles
sub-types of AV blockincluding:
- First-degree AV block
- Second-degree AV block (type 1)
- Second-degree AV block (type 2)
- Third-degree (complete) AV block
ECG finding for first degree heart block
- Rhythm: regular
- P wave: every P wave is present and followed by a QRS complex
- PR interval: prolonged >0.2 seconds (5 small squares)
- QRS complex: normal morphology and duration (<0.12 seconds)
ECG finding for second degree type 1 heart block
Second-degree AV block (type 1) is also known asMobitz type 1 AV block orWenckebach phenomenon
ECG:
- Rhythm: irregular
- P wave: every P wave is present, but not all are followed by a QRS complex
- PR interval: progressively lengthens before a QRS complex is dropped
- QRS complex: normal morphology and duration (<0.12 seconds), but are occasionally dropped
ECG finding for second degree type 2 heart block
Second-degree AV block (type 2) is also known asMobitz type 2 AV block
ECG:
- Rhythm: irregular (may be regularly irregular in 3:1 or 4:1 block)
- P wave: present but there are more P waves than QRS complexes
- PR interval: consistent normal PR interval duration with intermittently dropped QRS complexes
- QRS complex: normal (<0.12 seconds) or broad (>0.12 seconds)
- The QRS complex will be broad if the conduction failure is located distal to the bundle of His
ECG finding on a third-degree heart block
there isno electrical communication between the atria and ventricles due to acomplete failure of conduction
ECG:
- Rhythm: variable
- P wave: present but not associated with QRS complexes
- PR interval: absent (as there is atrioventricular dissociation)
- QRS complex: narrow (<0.12 seconds) or broad (>0.12 seconds) depending on the site of the escape rhythm (see introduction)
RF for 1 degree HB
often in athletes
post MI
Lyme disease
Congenital
RF for 2 degree t1 HB
- Increased vagal tone: often seen in athletes (non-pathological)
- Drugs: beta-blockers, calcium channel blockers, digoxin, amiodarone
- Inferior myocardial infarction
- Myocarditis
- Cardiac surgery (mitral valve repair, Tetralogy of Fallot repair)
RF doe 2 degree T2 HB
- Myocardial infarction
- Idiopathic fibrosis of the conducting system (Lenegre’s or Lev’s disease)
- Cardiac surgery (especially surgery occurring close to the septum such as mitral valve repair)
- Inflammatory conditions (rheumatic fever, myocarditis, Lyme disease)
- Autoimmune (SLE, systemic sclerosis)
- Infiltrative myocardial disease (amyloidosis, haemochromatosis, sarcoidosis)
- Hyperkalaemia
- Drugs (e.g. beta-blockers, calcium channel blockers, digoxin, amiodarone)
- Thyroid dysfunction
RF 3 degree HB
- Congenital: structural heart disease (e.g transposition of the great vessels), autoimmune (e.g maternal SLE)
- Idiopathic fibrosis: Lev’s disease (fibrosis of the distal His-Purkinje system in the elderly) and Lenegre’s disease (fibrosis of the proximal His-Purkinje system in younger individuals)
- Ischaemic heart disease: myocardial infarction, ischaemic cardiomyopathy
- Non-ischaemic heart disease: calcific aortic stenosis, idiopathic dilated cardiomyopathy, infiltrative disease (e.g. sarcoidosis, amyloidosis)
- Iatrogenic: post-ablative therapies and pacemaker implantation, post-cardiac surgery
- Drug-related: digoxin, beta-blockers, calcium channel blockers, amiodarone
- Infections: endocarditis, Lyme disease, Chagas disease
- Autoimmune conditions: SLE, rheumatoid arthritis
- Thyroid dysfunction
SS for 1 degree H block
asymptomatic
SS for 2 degree t1 H block
often asympto but can develop bradycardia and syncope, irregular pulse
SS for 2 degree t2 H block
Palpitations, Pre-syncope, Syncope, regular irregular pulse
SS for 3 degree H block
- Palpitations
- Pre-syncope/syncope
- Confusion
- Shortness of breath (due to heart failure)
- Chest pain
- Sudden cardiac death
Ix for AV block
ECG
Management for AV block
Stop any AV blocking drugs
if symptomatic then pacemaker
from second t2 onwards place on cardiac monitor as a result of risk of complete AV block
third degree: cardiac monitor, transcutaneous pacing/temporary pacing wire
orisoprenaline infusion, pacemaker
Complication for the different AV block subtype
First deg→ afib
Second deg T1 → haemodynamically compromised
second T2- complete AV block
third→ sudden cardiac death
What is bbb
A bundle branch block is a condition in which there is a delay or blockage along the pathway that electrical impulses travel to make a heartbeat.
The delay or blockage can occur on the pathway that sends electrical impulses either to the left or the right side of the bottom chambers (ventricles) of your heart.
Bifascicular → involves both right bundle branch block as well as blockade of one of the fascicles of the left bundle branch.
Trifasicular → is present when 3rd degree heart block exists along bifasicular block
Pathophysiology of BBB
A bundle branch block is a condition in which there is a delay or blockage along the pathway that electrical impulses travel to make a heartbeat.
The delay or blockage can occur on the pathway that sends electrical impulses either to the left or the right side of the bottom chambers (ventricles) of your heart.
Bifascicular → involves both right bundle branch block as well as blockade of one of the fascicles of the left bundle branch.
Trifasicular → is present when 3rd degree heart block exists along bifasicular block
RF FOR lbbb
Dilated Cardiomyopathy (the main cause of LBBB) Left ventricular hypertrophic cardiomyopathy (LBBB) HTN
MI myocarditis
RF for RBBB
RBBB Thin tall young people
MI myocarditis
SS for BBB
asymptomatic
underlying cause symptoms like MI with chest pain or SOB
ECG criteria for RBBB
- MarRoW
- QRS > 120 ms (3 small squares)
- RSR’ pattern in V1-V3
- Wide, slurred S wave in lateral leads – I, aVL, V5-V6
ECG criteria for LBBB
- WiLliaM
- QRS duration > 120ms (3 small squares)
- Dominant S wave in V1
- Broad, monophasic R wave in lateral leads – I, aVL, V5-V6
- Absence of Q waves in lateral leads
- Prolonged R wave > 60ms in leads V5-V6
Management for BBB
Patient based
treat any underlying cause
if hx of syncope due to it then pacemaker
Complication for BBB
- Complete heart block
- Ventricular tachycardia
- Ventricular fibrillation
What is cardiac tamponade
Accumulation of blood, fluid, pus, clots, or gas in pericardial space
Results in reduced ventricular filling and reducing cardiac output and subsequent haemodynamic compromise
Often: pericardial effusion cardiac tamponade
- Iatrogenic (cardiac surgery/intervention), trauma, malignancy, idiopathic effusion, viral, radiation, uraemia
SS of cardiac tamponade
Dyspnoea, tachycardia and tachypnoea cold and clammy extremities
Distended neck veins, hypotension tachycardia, tachypnoea and hepatomegaly
Mangement for cardiac tamponade
Medical emergency!
emergency. Managed in ITU. Pericardiocentesis is definitive treatment
What is cardiomyopathy
Myocardial disorder
Heart muscle is structurally and functionally abnormal
Without CAD, HTN, Valvular or congenital heart diseases.
Degree of dysfunction ranges from lifelong symptomless forms to major health problems, such as progressive heart failure, arrhythmia, thromboembolism and sudden cardiac death.
What are the 4 major types of cardiomyopathies
- Dilated cardiomyopathy
- Hypertrophic cardiomyopathy
- Restrictive cardiomyopathy
- Arrhythmogenic right ventricular cardiomyopathy (ARVC)
Primary vs secondary cardiomyopathy
Primary: Idiopathic. No specific cause.
Secondary: chronic kidney disease, cirrhosis, obesity, sarcoidosis, amyloidosis, SLE, diabetes, thyroid disease, thiamine deficiency, etc
Management for cardiomyopathy
- Symptomatic management
- Mainly directed towards treatment of heart failure and prevention of VTE and sudden death
- Implantable cardioverter defibrillators in high risk patients to prevent sudden death
- Surgical myectomy/ alcohol septal ablation
- Heart transplant
What is coronary artery disease
- Narrowing of the coronary arteries which leads to heart problem
- Narrowing can occur as a result of blood clot or atherosclerosis
- complete blockage leads to heart muscles dying leading to MI
- Coronary flow occurs during diastole
RF for CHD
- smoking
- unhealthy diet (hyperlipidaemia)
- age
- common in men but increases for women after menopause
- hypertension
- diabetes
- obesity
- exercise
- ethnicity
Pathophysiology of CHD
atherosclerosis
SS for CHD
angina
cold sweats
dizziness
neck pain
shortness of breath
Ix for CHD
ECG
Echocardiogram
stress test
Management for CHD
Immediate management - ABCDE
atorvastatin
Warfarin
beta blocker
ACEi
ARB
What does MONARCH stand for in CHD Management
Morphine
Oxygen
Nitrates
Aspirin 300mg
Reperfusion PCI
Clopidogrel/Ticagrelor
Heparin or LMWH
Complication for CHD
angina
MI
HF
Stroke
anxiety
reduced qualy
Pathophysiology of DVT
A clot develops at a site of damage to a vessel wall (e.g. an atherosclerotic plaque, or perhaps a site of trauma). This can impair venous drainage of the leg.
RF for DVT
- Stasis/immobility – e.g. hospital bed, long flight
- Dehydration
- Oestrogen (pregnancy, and to a lesser extent, theCOCpill)
- Genetic clotting defect (e.g. lack of protein C)
- Obesity (atherosclerosis)
- Age (old)
- Varicose veins
- Surgery
- Previous DVT/embolism
- Trauma
- Infection
- Malignancy
Virchow’s triadof risk factors:
- Stasis
- Hypercoagulability
- Vessel wall injury
SS for DVT
- Red, swollen leg (particularly calf)
- Tenderness
- Pitting oedema
- Fever
IX for DVT
WELLS score
- Venography
- D-dimer - negative test rules out dvt
- Leg measurement
WELLS score
- Score >3 –Treat as DVT –and also perform a compression USS to confirm
- Score 1-2 –Treat as DVT– and perform compression USS to confirm
- Score 0 –do a D-dimer test. If negative, then unlikely to be DVT. If positive,Treat as DVT,and perform compression USS.
Management for DVT
LMWH
Warfarin
Thrombolysis
Complication for DVT
PE
ODEMA
What is endocarditis
inflammation of the inner layer of the heart known as the endocardium
Difference between acute and subacute endocarditis
ACUTE
- Present as a rapidly progressive disease with high fevers, rigors, and sepsis
- Usually, staphylococcus aureus
- Mostly happens in healthy hearts
SUBACUTE
- Delayed and presents as non-specific symptoms such as weight loss, fatigue, low-grade fever dyspnoea over several weeks to months
- Usually, streptococcus viridans
- Mostly occurs in pre-existing heart disease
RF for endocarditis
- bacteria in other parts
- gum disease
- STI
- Damaged heart valves
SS for endocarditis
Murmurs
join aches
fever
SOB
Osler nodes
Ix for endocarditis
blood test
CT
MRI
X-ray
ECG
Management for endocarditis
ADMIT
Antibiotics
Complication for endocarditis
septic emboli
stroke
seizures
What are giant cell arteries
a type of chronic vasculitis characterized by granulomatous inflammation in the walls of medium and large arteries
RF for giant cell arteries
- It usually affects people over 50 years of age.
- European background
- Females
SS for giant cell arteries
Fever
Fatigue
anorexia
Weight loss
Depression
scalp tenderness
jaw claudication
visual disturbance
Investigation for Giant cell arteries
refer
temporal artery biopsy
ESR
CRP
FBC
LFT
What is HF
ability of the heart to maintain the circulation of blood is impaired as a result of structural or functional impairment of ventricular filling or ejection.
What is ejection fraction
- Heart failure with preserved ejection fraction (HF-PEF)
- heart failure with reduced ejection fraction
- LVEF less than or equal to 35-40%
symptomatic severity class types of heart failure
Class I — no limitation of physical activity. Ordinary physical activity does not cause undue fatigue, breathlessness, or palpitations.
Class II — slight limitation of physical activity. Comfortable at rest but ordinary physical activity results in undue breathlessness, fatigue, or palpitations.
Class III — marked limitation of physical activity. Comfortable at rest but less than ordinary physical activity results in undue breathlessness, fatigue, or palpitations.
Class IV — unable to carry out any physical activity without discomfort. Symptoms at rest can be present. If any physical activity is undertaken discomfort is increased
Pathophysiology of heart failure
factors that can increase myocardial work may aggravate existing HF or initiate
cardiac damage → decreases CO → neuroendocrine activation → increased peripheral resistance
Fluid retention can also decrease CO
RF for HF
CHD
AGE
Diabetes.
High blood pressure.
Obesity.
Other Conditions Related to Heart Disease.
Valvular Heart Disease.
Right sided HF symptoms
Fatigue
increased peripheral venous pressure
ascites
enlarge liver and spleen
distended jugular vein
anorexia or GI distress
weight gain
oedema
Left sided heart failure symptoms
Restlessness
confusion
orthopnoea
tachycardia
exertional dyspnoea
fatigue
cyanosis
PND
Pulmonary congestion
Ix for HF (what is sued to suspect HF)
BNP
What is the gold standard to confirm HF
ECHO
NICE guideline for Ix for HF pathway
measure NT-proBNP (can also perform ecg, CXR blood test urinalysis peak flow or spirometry at this point)
if bnp levels more than 2000 ng/l then refer urgently to be seen within 2 weeks
if bnp between 400-2000 then refer urgently to be seen within 6 weeks
if bnp below 400 then hf not confirmed and consider other causes
Management for HF
offer diuretics for fluid retention like furosemide
if HF with pr EF then manage comorbidities and cardiac rehab
if HF with red EF then offer aceI, BB and an MRA like spironolactone
Complication for HF
- depression
- cardiac arrhythmias
- chronic kidney disease
- sexual dysfunction
- sudden cardiac death
RF for HTN
- Age -increased risk with age
- sex-More common in male than female
- ethnicity
- genetic factor
- social deprivation
- lifestyle
- stress and anxiety
- Other things that can raise BPCocaine and other substance of abusecombine oral contraceptivecorticosteroidsNSAIDLiquoricesymptathomemtic
stage HTN reading
14/90 to 159/99
Stage 2 HTN reading
160/100 or higher but lower than 180/120
Stage 3 or severe HTN reading
higher than 180/120
diagnosis for HTN
see notes
nice guideline for HTN for treatment (diagram)
see notes
example of conditions that cause secondary HTN
- Renal artery stenosis
- Pheochromocytoma
- Aortic coarctation
- Cushing disease
- Conn’s syndrome
- Hyperparathyroidism
complications for HTN
increase risk of:
heart disease
stroke
chronic kidney disease
peripheral artery disease
What is isolated systolic HTN and what is caused by and what can increase the risk of
sys rises but diastolic remains in the normal range
diastolic less than 80 but systolic is 130 or higher
common in people older than 65
what is isolated systolic
HTN caused by
Caused by :
- Artery stiffness
- An overactive thyroid (hyperthyroidism)
- Diabetes
- Heart valve disease
- Obesity
Whts does isolated systolic HTN increase your risk of
increase your risk of strokes, heart disease or ckf
iatrogenic causes of HTN examples
HTN caused by a medication
sympathomimetics (amphetamine)
NSAIDS and COX inhibitor (ibuprofen)
Corticosteroids (prednisone)
CNS stimulants (caffeine)
Oestrogen and Progesterone (contraceptives and ERT)
Immunosuppressants (cyclosporine)
what is hypercholesterolaemia
- Hypercholesterolemia, an elevation of total cholesterol (TC) and/or low-density lipoprotein (LDL)-cholesterol or non-HDL-cholesterol in the blood(dyslipidaemia).
- increase in both cholesterol and triglycerides
- primary e.g. genetic
- secondary e.g. underactive thyroid
RF for hypercholesterolaemia
- Family history
- Diet- food high in saturated fats
- lack of physical activity
- obesity
Pathophysiology of hypercholesterolaemia
- Plaques of atheroma within inside lining of arteries
- Many constituents: white blood cells, lipids (cholesterol and fatty acids), calcium, fibrous connective tissue
- Over time gets larger and thicker → arterial narrowing → poor blood flow
- Sometimes atheroma develops a tiny crack (rupture) → blood clot
SS hypercholesterolaemia
- Hypercholesterolemia does not cause any symptoms but may eventually lead to heart attack, peripheral artery disease, or stroke due to atherosclerosis.
- Familial hypercholesterolemia is associated with:
- Xanthelasma palpebrarum (yellowish patches underneath the skin around the eyelids)
- Arcus senilis (white or gray discoloration of the peripheral cornea)
- Xanthomata (deposition of yellowish cholesterol-rich material) of the tendons
Ix hypercholesterolaemia
Health check programme
- Incidental finding on bloods
- Symptoms (angina/claudication)
- Risk factors
- Comorbidities
- QRISK
Management hypercholesterolaemia
Statins
lipid lowering therapies e.g ezetimibe
complications for hypercholesterolaemia
- atherosclerosis
- heart attack
- stroke
- any cvd
When to suspect FH hypercholesterolaemia
total cholesterol level greater than 7.4mmol/l and or
family history of premature CHD
Pathophysiology of hypertensive HF
- Cardiac failure is a clinical syndrome where due to ventricular dysfunction, the heart has an impaired ability to cope with the metabolic requirements of the body and can lead to fluid retention, fatigue and breathlessness. This is due to the heart being unable to provide the tissue with adequate perfusion, leading to elevated pulmonary or systemic venous pressure which could lead to organ congestion.
- Abnormalities can be with systolic or diastolic function, or both.
- In systolic failure there is left ventricle dysfunction, leading to an increased diastolic volume and pressure and decreased ejection fraction (<40%).
- In diastolic failure, there is a filling defect of the left ventricle, leading to an increased end-diastolic pressure and normal volume and a normal ejection fraction (>50%).
- In right ventricular failure systemic venous pressure increases which can lead to fluid extravasation and congestion in the peripheries leading to oedema in the ankles and feet, and congestion in the abdominal viscera leading to hepatic dysfunction, and malabsorption.
RF for Hypertensive heart failure
- Hypertension
- Advanced age
- Female gender
- Obesity
- Diabetes
- Chronic kidney disease
- Coronary artery disease
SS for hypertensive heart failure
- Fatigue
- Shortness of breath at rest
- Peripheral oedema (feet and ankles)
- Persistent cough or wheeze
- Reduced exercise tolerance
- Peripheral oedema in feet and ankles – deep visible palpable imprint on digital pressure.
- Enlarged liver - on palpation can be detected below right costal margin, may be able to illicit hepatojugular reflux.
- Abdominal distention, can have ascites
- Visibly raised JVP – large alpha or V waves may be seen, even at rest.
- Pulmonary crackles on auscultation
- S3 may be heard on auscultation
Ix for hypertensive heart failure
- Chest X-ray – enlarged cardiac silhouette, pleural effusion, fluid in major fissures, kerley B lines, upper lobe pulmonary venous congestion. ECG – may show previous MI, LVH, LBBB or any arrhythmia, such as AF, may indicate towards of cardiac failure Echocardiogram - to evaluate any structural abnormalities.
- Systolic heart failure: dilated left/right ventricle and low EF, left ventricular hypertrophy, abnormal diastolic filling patterns
- Diastolic: left ventricular diastolic dysfunction, left ventricle filling defect, normal EF. Cardiac MRI – can be used to further determine aetiology such as amyloidosis, sarcoidosis and myocarditis
Management for Hypertensive heart failure
Conservative
- Dietary and lifestyle changing advice. Dietary sodium intake reduction, daily weights, regular exercise.
Medical
- BP control (see management algorithm in hypertension)
- ACE inhibitors, beta blockers, ARBs can be used for long term management.
- Diuretics, nitrates and digoxin for any symptomatic relief.
- Implantable cardioverter-defibrillator (ICD) or cardiac resynchronization therapy (CRT) devices can be considered in some patients. ICDs should be considered in patients with good expected clinical outcomes with symptomatic SVT or VF. CRTs can be considered in patients with an EF <35%, on ECG widened QRS (>0.15s) and LBBB. A CRT can also have an ICD incorporated.
- In some patients (severe cardiorenal syndrome) venovenous filtration can be considered in an intensive care setting.
Surgical
- CABG can be considered in patients who have multivessel coronary artery disease
- Valvular replacement can be considered in patients, especially those with primary mitral regurgitation.
Complications for hypertensive heart failure
- Chronic renal insufficiency
- Pleural effusion
- Anaemia
- Acute decompensation of chronic heart failure
- Acute renal insufficiency
- Sudden cardiac death
What is innocent heart murmur
Young children have small, slim chests so heart is near to stethoscope
Blood travelling through heart and blood vessel can make a murmur like noise
RF for innocent heart murmur
Common in babies and young children
Heart is usually working fine
Ix for innocent heart murmur
Sometimes fevers can bring on heart murmurs in children. Get them back in in 1-2 weeks time for review
Management for innocent heart murmur
Obviously if symptomatic or other symptoms discuss with paediatrician / cardiology
What is mitral stenosis
Narrowing of the mitral valve
Pathophysiology of mitral stenosis
rheumatic fever. Degenerative calcification, congenital mitral
stenosis, infective endocarditis, etc.
SS of mitral stenosis
Progressive breathlessness is main symptom. Shortness of breath on
exertion, orthopnoea, paroxysmal nocturnal dyspnoea
Palpitations due to AF
Malar flush, raised JVP, laterally places apex beat, right ventricular heave, loud first heart-sound with an opening snap in early diastole
Mid-late diastolic murmur, best heard with the patient in the left lateral position, with the bell of the stethoscope
Ix for mitral stenosis
CXR: left atrial enlargement and interstitial oedema. Mitral valve calcification
ECG- AF, left atrial enlargement and right ventricular hypertrophy
ECHO
Management for mitral stenosis
Diuretics
long acting nitrates
beta blocker
percutaneous mitral commissurotomy
Valve replacement
What is mitral valve prolapse
Bulging of one or both of the mitral valve leaflets into the left atrium
During ventricular systole
Pathophysiology of mitral valve prolapse
Genetic?
Myxomatous Degenenration
Ix for mitral valve prolapse
Usually incidental finding on clinical examination or ECHO
Management for mitral valve prolapse
Low risk vs high risk
No treatment/ beta-blockers/surgical repair or replacement
What is mitral regurgitation
Mitral valve not closing properly, causing abnormal leaking from left ventricle through the mitral valve and back into the left atrium with the left ventricle contracts
Pathophysiology of mitral regurgitation
Causes: traumatic, mechanical, infectious, degenerative, congenital or metabolic
Acute caused by: infective endocarditis, ischaemic papillary muscle dysfunction or rupture
investigation for Mitral regurgitation
cxr, ECG,ECHO
what is patent ductus arteriosus
Should be closed after birth but remains open
- No umbilical cord: Increased oxygen levels and decreased prostaglandin from placenta help close PDA
- So poor oxygenation (born prematurely) or increased prostaglandins in foetal circulation or increased sensitivity to prostaglandins keep it open
- Rubella infection also keeps it open
SS for patent ductus arteriosus
Small PDA – asymptomatic
Large PDA – LRTI, feeding difficulties, poor growth, failure to thrive
Tachycardia, tachypnoea, wide pulse pressure, bounding peripheral pulses
Ix for patent ductus arteriosus
Continuous murmur. Described as machinery murmur or Gibsons’ murmur
- Accentuated in systole
- Best heard in left infraclavicular area
Management for patent Ductus arteriosus
- Diuretics in those with features of HF
- Non surgical or surgical closure
- In asymptomatic well infants: wait until 1 year of age with regular ECHO to check for spontaneous closure. If still open by 1 year of age close with surgery
What is pericardial effusion
Collection of fluid in pericardial space
Many causes. Local vs systemic
- Local e.g.: Acute/chronic pericarditis → effusion
- Systemic e.g.: kidney failure → rise in urea →uremic pericarditis → effusion
SS for pericardial effusion
Small to moderate formed over some time: asymptomatic
Quick forming → cardiac tamponade → symptoms
Chest pain similar to pericarditis, light headedness, palpitations
Management for pericardial effusion
Large effusions →drained if >1month
- Smaller effusions → followed up with regular ECHO clinical examination
- Oxygen therapy, treat underlying condition, surgery (pericardiocentesis?)
what is postural hypotension
Pathophysiology of postural hypotension
stand up→ blood shifts from chest to diaphragm → reduces venous return → reduces filling of vernicles → decrease preload → reduced CO
This gravity induced drop BP is detected by baroreceptors →triggers baroreflex → vasoconstriction and compensatory tachycardia, also increase total peripheral resistance
HOWEVER, postural hypotension occurs when this mechanism to regulate BP are impaired.
It can occur due to:
- Failure of baroreflexes (autonomic failure)
- Volume depletion
- End-organ dysfunction
RF postural hypotension
Pregnancy
Drugs
Age
Addison’s disease
Diabetes
Parkinsons disease
SS postural hypotension
Dizziness
weakness
confusion
Blurred vision
Nausea
Headache
syncope
Ix postural hypotension
Diagnosis is made by doing a lying and standing blood pressure. The patient lies down for 15 minutes, and the blood pressure is taken. The patient is then asked to stand for 2 minutes, and the blood pressure is taken again. A drop of >20mmHg along with symptoms is postural hypotension.
Management postural hypotension
Management mainly involvesavoiding exacerbating factors
- Heat
- Long periods of immobility
- Large meals
- Dehydration
- Sitting with crossed legs
Fludrocortisone
Midodrine
Pyridostigmine
complication of postural hypotension
increases falls
decrease ADL
What is phlebitis/Thrombophelbitis
Superficial veins become inflamed and blood clot can occur
- Phlebitisrefersto inflammation of a vein and it can be caused by any insult to the blood vessel wall, impaired venous flow, or coagulation abnormality
- Thrombophlebitisrefers to the formation of a blood clot associated with phlebitis
Pathophysiology of phlebitis/ thrombophlebitis
blood flow stasis
damage to the blood vessels walls
Hyper-coagulability of bloods
IV infusion, Obesity, Pregnancy, smoking, oral contraceptive
Rf for phlebitis/ thrombophlebitis
thrombophilia disorder
hx of thrombophlebitis
SS of phlebitis/ thrombophlebitis
- Localized redness & swelling of the vein affected
- Pain or burning along the length of the vein
- Vein feeling hard and cord-like
Ix of phlebitis/ thrombophlebitis
doppler ultrasonography
biopsy/screening
Management for phlebitis/ thrombophlebitis
compression socks
keep legs elevated
NDAIDS
Hirudoid cream
Fondaparinux
Complication for phlebitis/ thrombophlebitis
Suppurative thrombophlebitis (
a serious complication resulting in pus in the the vein, that can lead to the patient becoming septic)
What is peripheral vascular disease
chronic condition due to atherosclerosis of arteries
Pathophysiology of peripheral vascular disease
- High cholesterol, smoking, diabetes can cause arterial narrowing through inflammatory mediators
- Narrowing of the arteries cause tissue hypoperfusion/hypoxia to tissues downstream of infarct
- Signs/symptoms due to hypoperfusion
RF for peripheral vascular disease
- Diabetes
- Smoking
- Hypertension
- Lipidaemia
SS for peripheral vascular disease
pain
hx of cvd
weak/absent pulses
bruit
Ix for peripheral vascular disease
lipids
doppler
Management for peripheral vascular disease
Lifestyle advice
- e.g. smoking cessation, healthy diet, weight loss/exercise
Pharmacological treatment of identifiable cause
- e.g. Treating hypertension, diabetes, lipidemia
Symptomatic treatment with antiplatelets (aspirin, clopidogrel) and vasodilators (cilostazol-only effective in intermittent claudication)
Surgical management (revascularisation) only used when lifestyle/pharmacological management has failed
Revascularization also recommended for those with critical limb ischaemia (restpain/ABPI <0.3)
Complication for peripheral vascular disease
amputation
what is premature beats
Extra heartbeats that begin in the atria or ventricles. These extra beats disrupt the regular heart rhythm, sometimes causing patients to describe a fluttering or skipped beat in their chest
Pathophys of premature beats
- Premature beats are abnormal contractions that begin in the ventricles or atria
- These extra contractions usually beat sooner than the next expected regular heart beat and they often interrupt the normal order of pumping
- Certain triggers, heart diseases, scarring or changes in the body can make cells in the ventricles electrically unstable and electrical impulses to be misrouted
RF for premature beats
- Caffeine, tobacco, alcohol and illicit drugs
- Exercise - if you have certain types of PVCs
- Hypertension
- Anxiety
- Heart disease including CHD, CAD, previous MI, HF or cardiomyopathy
SS for premature beats
FHx
Palpitation
fluttering
Syncope
Fatigue
Atypical chest pain
Ix for premature beats
Bloods
- FBC, TFTs, Electrolytes, calcium, magnesium
ECG
- An ECG will detect extra beats and identify the pattern and source
- 24 hour ECG monitoring
Management premature beats
Conservative
- Lifestyle changes: Eliminating common triggers such as caffeine or tobacco
Medical
- Beta blockers
- Calcium channel blockers
- Antiarrhythmic drugs e.g amiodarone or flecainide
Surgical
- Radiofrequency catheter ablation (radiofrequency energy is used to destroy an area of heart tissue that is causing the irregular contractions)
Complication premature beats
- Increased risk of Arrhythmias
- Cardiomyopathy
- Sudden Cardiac death
What is paroxysmal supraventricular tachycardia
a type of abnormal heart Rythm
Pathophysiology of paroxysmal supraventricular tachycardia
- The cause is not known
- Underlying mechanism typically involves an accessory pathway that results in re-entry
RF for paroxysmal supraventricular tachycardia
- Alcohol intake
- Caffeine
- Nicotine
- Psychological stress
- Wolff-Parkinson-White syndrome
SS for paroxysmal supraventricular tachycardia
Often patients have no symptoms. Otherwise symptoms may include:
- Palpitations
- Feeling lightheaded
- Sweating
- SOB
- Chest Pain
- Episodes start and end suddenly
Ix for paroxysmal supraventricular tachycardia
ECG:
Narrow QRS and a fast rhythm typically between 150 and 240 bpm
Management for paroxysmal supraventricular tachycardia
- If patient has normal BP,
1) Adenosine
2) CCB or BB
3) Synchronized cardioversion
4) Catheter ablation
What is Pulmonary stenosis/insufficiency
Pulmonic valve diseases are rare
Pulmonary stenosis are usually congenital diseases when they happen. Pulmonary regurgitation commonly occur as a complication of surgical procedures e.g to relieve symptoms of pulmonic stenosis. Can also occur due to pulmonary hypertension or marfans
pathophysiology for Pulmonary stenosis/insufficiency
- Pulmonic valves have three cusps and they regulate blood flow from the right ventricle into the lungs
- Pulmonic stenosis causes an obstruction of blood flow to the lungs which lead to right ventricular dilation due to volume overload
- Pulmonary regurgitation also cause volume overload during diastole causing right ventricular dilation
RF for Pulmonary stenosis/insufficiency
- Rheumatic disease
- Congenital heart disease
SS for Pulmonary stenosis/insufficiency
- Sudden death
- SOB
- Exertional syncope
- Parasternal heaves/thrills
- Ascites/pedal oedema
- In pulmonic stenosis, Systolic murmur can be heard best lying down (can be physiological in healthy individuals). Ejection pulmonic click can also be heard
- Loud P2 (Pulmonic component may be heard in pulmonary regurgitation). Diastolic murmur also heard in pulmonary regurgitation
Ix for Pulmonary stenosis/insufficiency
Bloods
- FBC (Look for anaemia), Us and Es (Look for dilutional electrolyte problems), BNP (Might be raised in heart failure), LFTs (Might be deranged due to liver congestion)
X-ray/Imaging
- CXR might show cardiomegaly. Echocardiogram is useful in seeing valvular function
ECG
- Right ventricular hypertrophy. Right bundle branch block
Managment Pulmonary stenosis/insufficiency
- Manage cause as appropriate eg antibiotics for rheumatic fever
- Resuscitation if acutely unwell. In neonates with pulmonic stenosis, prostaglandin infusion can be used to dilate the ductus arteriosus
- Refer all symptomatic cases of pulmonic stenosis/regurgitation to cardiology. Mild Pulmonary regurgitation doesn’t require any specific intervention other than for cardiologist to monitor every 1-3 years
- If intervention required, patient might undergo valve replacement depending on severity
Complication Pulmonary stenosis/insufficiency
- Heart failure
- Arrhythmia
what is Shock
Hypoperfusion associated with low or declining blood pressure
3 types:
- cardiogenic - pump failure
- Hypovolemic - loss of intravascular volume
- failure of vasoregulation and obtruction to blood flow
pathophys of shock
cardiogenic:
MI, Cardiomyopathy, valve issue and arrythmias
Hypovolemic causes:
Haemorrhage, burns, heat stress, GI losses
Distributive causes:
Sepsis, anaphylaxis, poising, Addison’s disease
Obstructive causes:
Pulmonary embolus, cardiac tamponade, tension pneumothorax
SS for shock
cold, unwell, anxious, faint, SOB
Oliguria
Pale and sweaty
Tachypnoea
Cold peripheries
Tachycardia
postural hypotension
confusion
coma
Ix for shock
FBC, U&E, LFT, group and cross-match, coagulation, blood gasses, monitor urine output, CRP, ESR, lactate, blood glucose, pregnancy test?, CXR, ECG
Management for shock
- Remember ABC. Regular OBS
- Oxygen. Venous access. Resuscitation with fluid. Blood transfusion?
- Vasodilators? Analgesia? Surgery if needed (ectopic pregnancy), vasopressors?
What is stroke
Stroke is a sudden onset of brain dysfunction, caused byan alteration in cerebrovascular blood supply.It is characterised by:
- Rapid, acute onset – within a few minutes
- Focal neurological defect
Classification for stroke:
- Haemorrhage
- Brain ischaemia
- TIA
Pathophysiology of stroke
- Arterial embolism –from a distant site; e.g. carotids, vertebral or basilar arteries. The embolus will occlude an artery of the brain resulting in infarction. May also come fromheart valves in endocarditis.
- Haemorrhage –can be in the cerebrum itself, or also asubarachnoid haemorrhagemay cause a similar effect
RF for stroke
HTN
Smoking
Exercise and diet
Afib
Diabetes
Alcohol
Cholesterol
sleep apnoea
carotid artery stenosis
obesity
ethnicity
age
heart disease
Family Hx
sex-male
Anterior circulationstroke common presentation:
- Limb and/or facial weakness
- Paraesthesia or numbness
- Speech difficulty (aphasia/dysarthria/dysphasia)
- Headache
Investigation for stroke
- Non-contrast CT head on admission, can be followed by CT angiogram for vascular causes.
- MRI brain with diffusion weighted imaging to provide more accurate imaging about stroke lesion and/or haemorrhage.
Bloods
- FBC – to exclude anaemia or thrombocytopaenia prior to possible initiation of thrombolytic agents.
- U&Es – to exclude electrolyte disturbance and renal failure
- PT + PTT - coagulopathy
- INR
- Serum Glucose – to exclude hypoglycaemic cause
- Cholesterol HDL/LDL -
- Cardiac enzymes – concomitant MI
ECG
- To exclude cardiac arrhythmia or ischaemia, to identify AF/pAF
Special Tests
- ECHO – in subacute stage to investigate cardioembolic cause
- Carotid and/or Vertebral Dopplers – in subacute stage to investigate for carotid stenosis
Acute Management for stroke
Acute management of Ischaemic stroke:
- If patient presents within 4.5 hours of onset of neurological symptoms – r-tPA (alteplase 0.9mg/kg)
- Aspirin 300mg OD to be commenced 24 hours post administration of r-tPA
- Endovascular intervention (Thrombectomy) – patients must meet the following criteria:
- mRS 0
- occlusion of ICA or proximal M1
- Age ≥18 years old
- NIHSS ≥6
- ASPECTS ≥6
- Thrombectomy with stent retriever should be undertaken within 6 hours of onset.
- Admission to stroke unit for ongoing medical care, treatment of any complications and early initiation of rehabilitation therapy. Encourage VTE prophylaxis and early mobilisation
Complication for stroke
- Increased risk of further event (Stroke or TIA)
- Increased risk of haemorrhagic transformation of infarct
- Sepsis
- CKD
- Death
Posterior circulationstroke common presentation:
- Visual loss or double vision
- Confusion
- Dizziness
- Vertigo
- Nausea
Arterial dissectionscommon presentation:
- Neck or facial pain.
Lacunar strokescommon presentation:
- Limb and/or facial weakness (typically affects face, leg and arm)
- Speech difficulty
- Ataxia
- Paraesthesias or numbness (typically affects face, leg and arm).
SS for Anterior circulation infarct stroke
- Partial or total loss of tone in face and upper and/or lower limbs (usually unilateral)
- Expressive and/or receptive dysphasia (or aphasia)
- Decreased or loss of sensation in face and upper and/or lower limbs (associated sensory neglect if non-dominant hemisphere stroke)
- Gaze paresis (often horizontal and unidirectional).
- Gaze deviation (away from the side of lesion, towards the hemiparetic side) this should prompt consideration of seizure but can also occur infarcts in the pons or thalamus.
- Horner’s syndrome (suggests ipsilateral carotid dissection.)
SS of Posterior circulation infarct stroke
:
- Specific cranial nerve deficits (unilateral tongue weakness, diplopia)
- Horner’s syndrome (hemilateral triad of miosis, ptosis, and facial anhidrosis)
- Loss of visual fields
- Dysarthria
- Nausea and/or vomiting
- Difficulty with gait and fine motor co-ordination
- Altered level of consciousness
SS of Lacunar infarct stroke:
- Pure motor hemiparesis
- Pure sensory hemiparesis
- Ataxia
- Mixed motor and sensory signs
- Dysarthria.
SS of Haemorrhagic stroke:
- Headache of gradually increasing intensity
- Neck stiffness
- Visual changes
- Photophobia
- Sudden onset of symptoms with progression over time
- Aphaisa
- Dysarthria
- Ataxia
- Sensory loss
- Altered level of conciousness
- NIHSS to calculate severity of stroke
Long term Management for stroke
- Lifelong anticoagulation with warfarin in patients with aetiology of AF
- Antiplatelet therapy with clopidogrel is indicated in patients who do not have AF.
- Carotid endarterectomy should be considered for patients with symptomatic carotid artery stenosis – no evidence for benefit of CEA in patients with near-occlusion.
- Treat underlying aeitiology accordingly.
- In patients with an embolic stroke of undetermined source and a patent foramen ovale (PFO) and high ROPE score, closure of the PFO may be of benefit for secondary prevention.
Acute management of haemorrhagic strokes:
- Neurosurgical review for potential need for surgical intervention (craniectomy/craniotomy)
- Larger haemorrhages warrant ITU admission for intubation and invasive BP/ICP control
- Stable haemorrhages warrant HASU admission to monitor haemorrhage, blood pressure control, DVT prophylaxis and correction of coagulopathy
What is tetralogy of fallot
Common cyanotic congenital heart disease
Hole between ventricles → oxygen rich blood mixes with oxygen poor blood
Overriding aorta = aorta is deeper in heart overlying the hole = the oxygen poor blood flows into the aorta too
Pulmonary artery is narrowed = less blood reaches lungs = right ventricle works harder = hypertrophy
SS of tetralogy of Fallot
4 main anatomical features:
- Large ventricular septal defect
- Overriding aorta
- Right ventricular outflow obstruction
- Right ventricular hypertrophy
Baby is blue due to lack of oxygenated blood
Investigations for tetralogy of fallot
Foetal screening and ECHO have led to an increase in prenatal diagnosis
Squatting to rest whilst exercising is characteristic of a right-to-left shunt and presents in an older child
Management for tetralogy of fallot
Surgery
What is Tricuspid stenosis/insufficiency
Right heart valvular problems
Tricuspid stenosis is rare. Tricuspid regurgitation is more common
Pathophysiology of Tricuspid stenosis/insufficiency
- The tricuspid valve is in between the right atrium and ventricle
- Tricuspid stenosis is commonly caused by rheumatic fever. Other causes include SLE, right atrial myxoma
- In tricuspid stenosis the valves become thickened and narrow. This increases pressure in the right atrium causing dilation
- Tricuspid regurgitation commonly occurs due to infective endocarditis. This causes an incompetency of the valve causing blood to flow back into the right atrium during ventricular systole
- Tricuspid regurgitation may occur with mitral stenosis/regurgitation
RF Tricuspid stenosis/insufficiency
- Congenital heart disease
- Streptococcal infection
SS of Tricuspid stenosis/insufficiency
- Fever/history of previous untreated bacterial infection
- Fatigue
- SOB/exercise intolerance
- Pulmonary oedema/crackles (if biventricular heart failure)
- Hepatomegaly
- Ankle oedema
- Raised JVP
- Diastolic murmur in tricuspid stenosis. Pansystolic murmur in regurgitation (Accentuated by pressing the liver, inspiration or raising legs up)
- Split S1 or S2 only heard
- Ascites
- Chest Pain
Ix for Tricuspid stenosis/insufficiency
Bloods
- FBC-Might show leucocytosis/Anaemia
- LFT-Might show deranged LFTs
- BNP-Raised in heart failure
- Us and Es-might show dilutional electrolyte imbalance
X-ray/Imaging
- Echocardiogram to see valvular pathologies and pressure
- CXR-may show right atrial enlargement/cardiomegaly/pleural effusion
ECG
- Tall P waves due to right atrial hypertrophy
Special Tests
- Cardiac catheterisation might be used to determine severity and associated congenital defects
Management for Tricuspid stenosis/insufficiency
- Manage underlying conditions eg Bacteria infections with antibiotics
- Manage arrhythmias
- Manage heart failure (see heart failure matrix condition)
- Valve replacement in severe cases or if refractory to medical management (MIld cases of tricuspid stenosis/regurgitation does not need surgical input)
Complication Tricuspid stenosis/insufficiency
- Arrhythmia
- Heart failure
What is ventricular septal defect
One or more holes in the septum
Communication between left and right ventricles of the heart
ss ventricular septal defect
Symptoms depend on size of hole
Not obvious at birth
Exercise intolerance – impacts feeding poor weight gain
Ix ventricular septal defect
Splitting of second heart sound, harsh pansystolic murmur
ECHO
Management ventricular septal defect
No treatment/ medical management/ surgical management
What is varicose vein
dilated and tortuous veins mainly occurring in the superficial venous system of the legs
Pathophysiology of varicose vein
occurs due to incompetence of the one-way valve → leakage →pooling of blood
The weaker thinner walls make it more prone to the effects of high pressure build up leading to distension of the venous walls and tortuosity
RF of varicose vein
increase with age
pregnancy
long periods of standing
FHx
common in female
Hx DVT
SS of varicose vein
often asymptomatic
pain
leg fatigue
nocturnal leg cramps
discoloration
Ix of varicose vein
clinically diagnosed
doppler used to confirm diagnosis
Management of varicose vein
exercise and weight loss
refer to vascular Serivices
compression therapy - IMPORTANT to exclude arterial insufficiency
Endothermal ablation
(first line for surgery)
Complication of varicose vein
bleeding
DVT
What is venous thrombosis
Blood clot in the deep vein in the leg
Pathophysiology of venous thrombosis
DVT in leg, thighs, pelvis or abdomen → impaired venous flow and consequent oedema and pain
RF venous thrombosis
- Bedbound
- Hospitalisation within 2 months
- Major surgery within 3 months
- Active Ca
- History of trauma
- Age
- Pregnancy
- Factor V Leiden
- Obesity
- Recent long-distance air travel
- Family history
SS venous thrombosis
- On history taking note presence of risk factors and social history.
- History of DVT or PE
- Wells’ score <2 15% probability of DVT
- Wells’ score >2 40% probability of DVT
- unilateral swelling and difference in circumference more than 3 cm
- Pain
Ix venous thrombosis
- Wells’ Score - >2 = likely DVT
- D-Dimer – Consider in patients with a wells’ score of 2 or above.
- Elevated d-dimer: >500ng/mL – however d-dimer is non-specific and can be raised in patients who are older, acutely ill, have an underlying hepatic disease, have an infection, or are pregnant.
- USS Lower Limbs – whole leg or proximal USS performed to assess the presence of a thrombus by compressibility and venous flow, the presence of a thrombus prevents compression, reduced or absent spontaneous flow, lack of respiratory variation, intraluminal echoes, or colour flow patency abnormalities.
- CTPA – in patients with a confirmed DVT a CT pulmonary angiogram can be undertaken to exclude pulmonary emboli if clinically indicated.
Management venous thrombosis
Refer immediately for same day management for a woman who is pregnant or has given birth within past 6 weeks
For people who arelikelyto have DVT:
offer leg vein ultrasound
For people who areunlikelyto have DVT:
D-dimer
If interim therapeutic anticoagulation is required:
offer apixaban or rivaroxaban
carry out baseline blood test e.g. FBC eGFR LFT PT and APTT
Complication venous thrombosis
- Pulmonary Embolism (PE)
- Risk of bleeding
- Heparin-induced thrombocytopenia (HIT)
- Heparin resistance/aPTT confounding
- Post-thrombotic syndrome
- Osteoporosis (if being treated with unfractionated heparin)
What is ventricular tachycardia
VT is a type of regular and fast heart rate that arises from improper electrical activity in the ventricles of the heart
Pathophysiology of ventricular tachycardia
VT can occur due to
- CAD
- Aortic stenosis
- Cardiomyopathy
- Electrolyte problems
- Morphology of the VT depends on its cause and the origin of the re-entry electrical circuit in the heart
- Monomorphic VT - scarring of the heart muscle from previous MI. This scar cannot conduct electrical activity
- Polymorphic VT - abnormalities of ventricular muscle repolarization
RF ventricular tachycardia
- CAD
- Structural heart disease
- Electrolyte deficiencies e.g hypokalaemia, hypocalcaemia, hypomagnesaemia
- Sympathomimetic agents (e.g caffeine or cocaine) may stimulate VT in vulnerable hearts
SS ventricular tachycardia
- Lightheadedness
- Palpitations
- Chest Pain
- Dyspnoea
- Syncope
- Symptoms of HF
- Signs reflect degree of haemodynamic instability
- Basal fine lung crepitations
- raised JVP
- Hypotension
- anxiety
- Agitation
- lethargy
Ix ventricular tachycardia
Bloods
- electrolytes, including serum calcium, magnesium and phosphate levels. Serum troponin levels
X-ray/Imaging
- CXR if there is a possibility of CHF or other cardiopulmonary pathology as contributing factors
ECG
- showing a rate of greater than 120bpm and at least 3 wide QRS complexes in a row
Special Tests
- Levels of therapeutic drugs - e.g, digoxin
Management for ventricular tachycardia
- Address the ABCs of resuscitation and provide BLS and ALS
- VF or pulseless VT - unsynchronised defibrillation
- VT - synchronised cardioversion
- Defibrillation is followed by airway management if required, supplemental oxygen, vascular access
Complication ventricular tachycardia
- Ventricular fibrillation
- Cardiac Arrest
What is Ventricular fibrillation/flutter
Fibrillation: disorganised electrical impulses causing the heart to quiver rather than contract
Flutter: tachycardic arrhythmia affects the ventricles, considered as transition phase between ventricular tachycardia and ventricular fibrillation
Pathophysiology Ventricular fibrillation/flutter
- Ventricular Flutter is an arrhythmia characterised with a typical sinusoidal pattern on an ECG
- With a frequency of 250-300 bpm, Ventricular Flutter, due to its repolarisation, results in minimal cardiac output and subsequent ischaemia
- This can then lead to flutter becoming fibrillation
- Ventricular Fibrillation is a life threatening condition caused by the disorganised excitation replacing organised electrical activity to the ventricles
- The most common arrhythmia identified in cardiac arrest
- The inability of the ventricles to contract efficiently reducing the cardiac output is what leads to cardiac arrest and eventually death if not treated within the time frame
RF Ventricular fibrillation/flutter
- Previous ventricular fibrillation
- Previous myocardial infarction
- Cardiomyopathy
- Drug toxicity
- Electrocution
- Congenital heart diseases
- Sepsis
ss Ventricular fibrillation/flutter
- Nausea
- Vomiting
- Tachycardia
- Shortness of breath
- Chest pain
- Syncope
Ix Ventricular fibrillation/flutter
Bloods
- FBC
- U&E
- LFT
- CRP
- Troponin
- BNP
- Toxicology
X-ray/Imaging
- CXR, Echocardiogram, CT, Angiogram
ECG
- Ventricular Fibrillation: unsynchronised rapid irregular electrical activity between 400-500 bpm
- Ventricular Flutter: sinusoidal waves without clearly defined QRS and T waves, with a rate of 250-350 bpm
Special Tests
- Other comments: ECG will confirm the diagnosis of ventricular flutter/fibrillation. The rest of the work up is to determine possible cause of these arrhythmias and any damage caused as a result of the arrhythmias
Management Ventricular fibrillation/flutter
- Beta blockers and surgical treatment are considered after patient is stable
Medical
- Defibrillation, CPR, Beta Blockers
Surgical
- Angioplasty, Coronary Artery Bypass Graft, Implantable Cardioverter Defibrillator
Complication Ventricular fibrillation/flutter
Sudden Cardiac Death
what is Valvular cardiac failure
The heart is made up of 4 valves namely aortic, mitral, pulmonic, tricuspid
These valves ensure a unidirectional flow of blood normally during systole and diastole
Pathophysiology of Valvular cardiac failure
- Valvular heart failure can either be left or right sided depending on which valves are involved
- Aortic and mitral valve heart failure are the two types of left sided valvular heart failure
- Causes of left valvular heart failure includes idiopathic, SLE, Bicuspid aortic valve, rheumatic heart disease/infective endocarditis (can cause acute/chronic valvular heart failure)
- Tricuspid and Pulmonic valve heart failure are the two types of right side heart failure
- Pulmonic stenosis can cause valvular heart failure and they are usually congenital related heart failure caused by Tetralogy of fallot, congenital rubella syndrome
- Tricuspid valve heart failure can be caused by rheumatic fever and it results in dilation of the right ventricle
- Generally speaking, valvular heart failure results in either concentric or eccentric hypertrophy
RF of Valvular cardiac failure
- Rheumatic fever
- IV drug use
- Congenital heart disease
- Autoimmune conditions
SS of Valvular cardiac failure
- SOB/reduced exercise intolerance
- Orthopnea
- Dizziness/LOC
- Chest Pain
- Lethargy/’blue spells’ in children
- Haemoptysis-pressure in the bronchial veins
- Tachycardia/Tachypnea
- Raised JVP with hepatojugular reflux
- Bilateral pedal oedema
- Displaced apex beat
- Abdominal distension
- Heart murmurs (Can include Pansystolic, Mid systolic, Ejection systolic/Ejection clicks depending on which valves are involved)
- Cardiac wheeze/reduced air entry
- Framingham criteria is used to diagnose heart failure regardless of the cause. It uses full history, physical examination findings and CXR and it includes major and minor criteria
Ix of Valvular cardiac failure
Bloods
- FBC-For anaemia
- BNP-marker of heart failure, LFT-heart failure can mildly affect liver function, Renal function tests-Deranged electrolytes
- Thyroid function test
- Blood cultures
X-ray/Imaging
- CXR-Cardiomegaly/interstitial fluid
- Echocardiogram - (Urgency depends on BNP levels and history of MI (request echo within 2 weeks and no need for BNP). If no hx of MI and BNP between 100-400 request echocardiogram within 6 weeks and if >400 request echo within 2 weeks). Echocardiogram will then categorise heart failure into either reduced ejection fraction or preserved ejection fraction
ECG
- LVH. Arrhythmias. Bundle branch blocks depending on which valves are involved
Management for Valvular cardiac failure
- If acute presentation, use ABCDE
- Treatment will depend on cause e.g IV antibiotics for rheumatic fever
- Refer to cardiology-Symptomatic valvular problems might require TAVI or valvuloplasty depending which valves are involved
- Chronic but stable management will involve the stepwise ladder of ACEi and Beta blockers (1st line), ARB/Hydralazine with nitrate/Aldosterone antagonist (2nd Line), Digoxin or cardiac resynchronisation therapy (3rd line)
- See matrix condition on Aortic stenosis/Regurgitation, Mitral stenosis/regurgitation, Pulmonic stenosis/insufficiency, Tricuspid stenosis/insufficiency
Complications for Valvular cardiac failure
- Death
- Arrhythmias
