Cardiovascular Clinical Symposium

anatomical structures affected by pulmonary embolism

• all lobes in right and left lungs

• right and left pulmonary arteries with branches

physiology affected by PE

gaseous exchange in the alveoli of the lung

structural abnormalities associated with PE

• blockage of pulmonary arterial treedue to embolism (movement) of blood clot/fat/air/amniotic fluid

• blockage of deep veins of leg/abdomen by blood clot

physiological abnormalities associated with PE

• impaired perfusion of alveoli/lungs

  • results in low oxygen in blood

prior events leading to a pulmonary embolus

• usually source of thrombus that moves to the lungs→ deep veins of legs

• hospital admission for surgery and immobility may predispose

experienced symptoms of PE

• sudden onset dyspnoea

• tachypnoea

• pleuritic chest pain

• cough

• haemoptysis

clinical signs of PE

• sinus tachycardia

• collapse, circulatory instability due to decreased blood flow through lungs and left side of heart

• assessment for DVT if PE suspected

• raised jugular venous pressure

abnormal test results identified in PE

• low oxygen saturation

• low oxygen on blood gases

• elevated D-dimer

• VQ lung scan showing lack of blood flow to part of lung

• CT showing blood clot showing blood clot in artery

medical/surgical intervention for pulmonary embolism

• high flow rate oxygen

• thrombolytic drugs given by IV to dissolve blood clot

primary and secondary intervention for PE

• anticoagulants used immediately and for some moths

  • initially low molecular weight heparin

  • then direct oral anticoagulant e.g. apixaban, warfarin

anatomical structures affected by myocardial infarction

• left coronary artery with branches

physiology affected by myocardial infarction

delivery of blood to myocardial tissues

structural abnormalities associated with myocardial infarction

• narrowing of arteries due to coronary atheroma

• blockage of artery

physiological abnormalities associated with myocardial infarction

• ischaemia leading eventually to infarction→ necrosis of myocardium

• impaired contraction of myocardium

• abnormal electrical activity of heart cells

prior events causing myocardial infarction

• more common in men than women

• risk factors:

  • smoking

  • dyslipidaemia

  • diabetes

  • sedentary lifestyle

  • obesity

  • family history

symptoms experienced in a MI

• severe crushing central/generalised chest pain

• pain often spreads to arms/neck

• nausea, vomiting

• sweatiness, breathlessness

clinical signs of MI

• patient clearly distressed

• low BP

• fast heart rate

• breathlessness may be obvious with fluid heard on lungs during inspiration

abnormal test results associated with MI

• ECG showing ST elevation

• Blood test demonstrates raised troponin levels

• echocardiogram shows reduced contraction of affected area

• coronary angiogram shows blocked artery

medical/surgical intervention for MI

• medical emergency

• pain relief→ morphine, antiemetic, oral aspirin

• primary percutaneous coronary intervention:

  • through tube in arm/leg

  • metal stent inserted

primary and secondary intervention for MI

• avoidance of risk factors

• Key drugs used:

  • aspirin

  • clopidogrel

  • beta-blockers

  • statins

  • ACE inhibitors

anatomical structures affected by DVT

• deep veins of the leg and pelvis

physiology affected by DVT

• return of deox. blood to the right side of the heart and then on to the lungs

structural abnormalities associated with DVT

• blockage of the vein by blood clot

• usually first appears in calf but then extend above knee and into pelvis and abdomen

physiological abnormalities associated with DVT

• thrombophilia→ often expresses itself with recurrent thromboses

• prothrombotic states e.g. pregnancy, paraneoplastic factors can increase risk

prior events leading to DVT

• recent surgery/hospitalisation

  • LMWH helps reduce risk

• advanced age

• obesity

• infection

• immobilisation

• oestrogen containing contraceptives

• family history

symptoms experienced in DVT

• swelling of right/left calf

• pain in calf

• no symptoms related to the leg but sudden PE may occur

clinical signs of DVT

• swelling/redness of leg

• dilation of surface veins

• tenderness over veins when applying gentle pressure

abnormal test results associated with DVT

• ultrasound of leg demonstrates absence or reduction of venous flow and presence of thrombus

• low-probability situation→ D-dimer test

medical/surgical intervention associated with DVT

• immediate anticoagulation with LMWH

• 3-6 month anticoagulation with DOAC or warfarin

primary and secondary prevention of DVT

• early and regular walking

• hospitalised patients→ LMWH

• compression stockings for patients undergoing surgery

• long-term anticoagulation therapy

anatomical structures affected by cerebral infarction

• all parts of the brain

• arteries to the brain

• large and small arteries of the brain

physiology affected by cerebral infarction

• supply of oxygen and nutrients to the brain

• removal of CO₂ and waste products from the brain

structural abnormalities associated with cerebral infarction

• disease of the wall of arteries going to or within brain e.g. atherosclerosis

• dilated atria of the heart

physiological abnormalities associated with cerebral infarction

• ischaemia of brain tissue

• necrosis of brain tissue

• raised intercranial pressure due to brain swelling→ can risk further nerve damage

prior events leading to cerebral infarction

• CV risk factors→ smoking, hypertension, dyslipidaemia, diabetes etc

• atrial fibrillation

• TIA

symptoms experienced in cerebral infarction

• face→ drooping/weakness of one side of face

• arms→ weakness of one leg or arm

• speech→ slurred or incoherent

clinical signs of cerebral infarction

• possible evidence of atrial fibrillation

• possible high blood pressure

• possible bruit heard over carotid artery in the neck

abnormal test results associated with cerebral infarction

• brain CT or MRI shows changes of brain ischaemia, swelling and infarction

• ultrasound of carotid artery may show narrowing

• echocardiogram may show evidence of a blood clot in the atrial appendage

• ECG may show evidence of atrial fibrillation

medical/surgical intervention for cerebral infarction

• thrombolytic drugs→ dissolve blood clots from within artery

• thrombectomy

primary and secondary intervention for cerebral infarction

• treat patients with atrial fibrillation w DOAC/warfarin

• management of high blood pressure

anatomical structures associated with atrial fibrillation

• left and right atria of heart, left atrial appendage

• pulmonary veins and their junctions with the left atrium

physiology affected by atrial fibrillation

• pacemaker activity of the heart

• conduction of electrical depolarisation through the atrium

• stimulation of electrical activity in ventricles

structural abnormalities associated with atrial firbrillation

• dilated atria

• fibrosis (scarring) of atrial muscle

physiological abnormalities associated with atrial firbrillation

• arrhythmogenic environment e.g. electrolyte imbalance, sepsis

• ectopic activity from around pulmonary veins

prior events causing atrial fibrillation

• hypertension

• coronary artery disease

• excessive alcohol consumption

• hyperthyroidism

• heart failure

symptoms experienced in atrial fibrillation

• palpitations

• fatigue and/or breathlessness with exercise

• sometimes chest tightness or ankle swelling

clinical signs of atrial fibrillation

• pulse is irregularly irregular

• sings of underlying causes e.g. high BP, valve murmur, weight loss

abnormal test results associated with atrial fibrillation

medical/surgical intervention for atrial fibrillation

• rate control→ seeks to slow down heart rate to prevent palpitations

  • beta blockers, digoxin, Ca²⁺ channel blockers

• rhythm control→ seeks to convert heart rhythm back to normal, regular sinus rhythm

  • electrical shock (DIC cardioversion)

  • drugs e.g. amiodarone

• pulmonary veins can be electrically isolated/insulated→ from LA by surgery/catheter ablation

primary/secondary intervention for atrial fibrillation

• early and effective treatment of diseases that cause atrial fibrillation e.g. high blood pressure

• avoidance of excess alcohol and stimulants e.g. nicotine, caffeine

• prevent formation of blood clots in atrium by treatment w DOAC/warfarin

anatomical structures affected by aortic stenosis

aortic valve at outflow of left ventricle and origin of ascending aorta

physiology affected by aortic stenosis

aorta usually opens to allow blood to exit LV and closes to prevent blood from passing backwards from aorta to LV

structural abnormalities associated with aortic stenosis

• congenital→ bicuspid aorta

• valve becomes calcified gradually over many years

physiological abnormalities associated with aortic stenosis

• left ventricle has to generate more force to eject blood through narrowed aortic valve→ becomes hypertrophied

• ‘pressure overload’ in LV

prior events leading to aortic stenosis

• patients are most frequently male over 65

• aortic stenosis can cause no symptoms for many years

symptoms experienced in aortic stenosis

• angina type chest pain→ worsened with exercise

• breathlessness with exercise

• light-headedness or collapse with exercise

clinical signs of aortic stenosis

• harsh loud ‘ejection systolic’ heart murmur

• reduced pulse pressure

• forceful apex beat

abnormal test results associated with aortic stenosis

• ECG shows evidence of more muscular left ventricle→ QRS increased

• echocardiogram shows a narrowed aortic valve→ more muscular left ventricle

medical/surgical intervention for aortic

• if the pressure difference between left ventricle and aorta< 60→ patient kept under observation

• If LV starts to dilate or symptoms are present, surgery is considered

• aortic valve can be replaced by open chest surgery or using percutaneous approach

  • surgical valves either made of metal or plastic

primary and secondary intervention for aortic stenosis

• patients with metallic artificial aortic valves require life-long anticoag. treatment with warfarin

• patients with tissue valves do not require warfarin

anatomical structures affected by fallot’s tetralogy

• ventricular septum

• pulmonary valve

• aorta

• right ventricle

physiology affected by fallot’s tetralogy

sequential flow of deoxygenated blood through right heart to lungs and oxygenated blood through left heart body

structural abnormalities associated with tetralogy of fallot

• ventricular septal defect

• pulmonary stenosis

• overriding aorta

• right ventricular hypertrophy

prior events

patients are born with thus set of abnormalities with no recognisable prior events/ causes

experienced symptoms of fallots tetralogy

• primary symptom→ low blood oxygen with/without cyanosis

• congenital or developing in first year of life

• difficulty feeding and gaining weight

• delayed growth and physical development

• dyspnoea on exertion

clinical signs of fallots tetralogy

• heart murmur

• clubbing of fingernails and toenails

• hypercyanotic spells→ may result in brain injury and death

• older children may squat during hypercyanotic spell→ increases vascular resistance and allows for temporary reversal of a shunt

abnormal test results

echocardiogram demonstrates abnormal anatomy and can assess degree of shunting from left to right or from right to left

medical/surgical intervention

• oxygen is effective in treating hypercyanotic spells

• surgery designed to designed to relive right ventricular outflow tract stenosis by removal of muscle and repair of VSD

primary and secondary prevention

• despite surgery patient remain at increased risk of sudden cardiac death and heart failure

anatomical structures affected by systolic heart failure

• usually left ventricle

• right ventricle can be involved

physiology affected by systolic heart failure

• normal blood supply to lungs and body at the appropriate pressure to allow adequate blood flow

structural abnormalities associated with systolic heart failure

• ventricles may be dilated, thinned, thickened

• valve regurgitation

• mitral/tricuspid valve regurgitation may result from ventricular dilation due to stretching of valve ring

physiological abnormalities associated with systolic heart failure

• loses the ability to pump enough blood to meet body’s metabolic needs

• heart loses its pumping reserve

prior events leading to systolic heart failure

• MI

• viral myocarditis

• use of chemotherapy drugs

symptoms experienced in systolic heart failure

• fatigue

• dyspnoea

• breathlessness when lying flat

• paroxysmal nocturnal dyspnoea

• oedema

clinical signs of systolic heart failure

• tachypnoea

• oedema

• high jugular venous pressure

• tachycardia

• hypotension

• cachexia

abnormal test results associated with systolic heart failure

• echocardiogram shows red. pumping of heart

• dilation of ventricle may be seen and valved can be assessed

• ejection fraction

• blood test of NT-proBNP

• ECG often abnormal

medical surgical/intervention

• daily weight can help detect changes in fluid status

• standard drug therapy includes ACE inhibitor and beta-blocker

• other drugs e.g. mineralocorticoid receptor antagonists

• combination therapy with angiotensin II receptor blocker and neprilysin inhibitor

• loop diuretics such furosemide

primary and secondary interventions in systolic heart failure

• diagnose any underlying disease that might be treated directly

• secondary prevention may involve an implanted cardioverter defibrillator to reduce risk of sudden cardiac death

anatomical structures affected by complete heart block

• AVN

physiology affected by complete heart block

• transmission of wave of electrical depolarisation from atria to ventricles

structural abnormalities associated with complete heart block

• fibrosis of AVN

• necrosis/infarction of AVN

physiological abnormalities associated with complete heart block

• complete failure of AVN to transmit electrical impulse from atria to ventricles

• atria have electrical activity and contract independently of ventricles

• ventricles develop their own pacemaker activity→ much slower rate

prior events associated with complete heart block

• MI

• medications e.g. beta blockers or other rate lowering drugs that act to block AVN

symptoms associated with complete heart block

• light-headedness

• presyncope or syncope

• chest pain

• signs of heart failure

clinical signs associated with complete heart block

• pulse/ heart rate is slow (<60bpm)

• low bp

• sudden loss of concioussness

abnormal test results associated with complete heart block

medical/surgical intervention associated with complete heart block

• atropine→ blocks parasympathetic action w ACh= inc. HR

• temporary pacemaker on arrival at hospital

primary and secondary prevention associated with complete heart block

• permanent pacemaker needed if complete heart block persists

anatomical structures affected by ventricular fibrillation

• left and right ventricles

• septum

• free walls

• right outflow tract

physiology affected by VF

• ventricles pump blood to lungs for oxygenations and to the body to supply tissues with oxygen and nutrients

structural abnormalities associated with ventricular fibrillation

• heart COULD have normal structure→ Long QT-syndrome

• hypertrophied ventricles due to high bp or disease

• dilated/scarred ventricles

physiological abnormalities associated with ventricular fibrillation

• all electrical activity becomes disorganised and chaotic

• heart fibrillates (quivers) but does not beat

• no blood pumped to lungs or body

prior events associated with ventricular fibrillation

• no warning

• commonly occurs after myocardial infarction

symptoms associated with ventricular fibrillation

• may be some prior warning signs:

  • palpitations

  • light headedness

  • chest pain

• loss of consciousness within seconds of fibrillation

abnormal test results associated with ventricular fibrillation

medical/surgical intervention associated with ventricular fibrillation

• basic life support

• DC electrical shock→ defibrillation

primary and secondary intervention associated with ventricular fibrillation

• assessment of risk of VF in young adults requires knowledge of family history

• beta blockers are sometimes used

• implanted cardioverter defibrillators for high risk patients