Cardiovascular Clinical

Clinical Problems I – ECG Rate and Rhythm

• Features of a ECG:
- Regularity of rhythm
- Rate of depolarization (P wave and QRS wave)
- Shape of deflections
- Interval of deflection
- Sequence of events
• Breathing: irregular rhythm is observed with periods of faster rate and slower rates. This is due to stimulation of sympathetic nerves during inspiration to pump out the increased RV load.
• Sinus bradycardia: P waves are very far apart while everything else is normal.
• AV 2o block: p wave occurs regularly however a QRS interval does not precede immediately after a p wave, i.e. electrical conduction is blocked. The QRS occurs as a result of the intrinsic AV beat to keep the ventricle pumping.
• Wandering pacemaker: all features are normal except for the direction of deflection of the p wave which changes from beat to beat. This means activating of the SA node is in a different direction and most likely due to an ectopic pacemaker (sick myocytes fires AP before the SA).
• Wenckebach: some p waves do not trigger off a QRS instead they followed by a period of electrical inactivity. This is due to AV node getting “tired” and not repolarising fast enough to conduct another AP from the SA. The pattern of blockage is regular.
• Wolff-Parkinson-White syndrome: The P-R interval is short as the AP is not passing through the regular conduction system but instead an alternative pathway. Large QRS occurring for long duration due to the slow activation process from an independent location.
• Ventricular fibrillation: extremely disorientated ECG pattern with tachycardia.

Rheumatic Fever

• Case study progression:
- Sore joint and fever with mild MR
- Relapsed rheumatic fever, aortic regurgitation
- Stopped penicillin due to pain
- Recurrent rheumatic fever with severe MR and mild AR, restarted penicillin
- Fever and joint pain, confirmed vegetations on mitral valve (viridian strep)
- Left parietal mass, possibly abscess or mycotic aneurysm
- Death
• Complication of RHD and surgery
- Congestive heart failure
- Medication side effects
- Pneumonia
- Cardiac arrhythmias
- Endocarditis
- Strokes
- Death
• Events of rheumatic fever:
- Streptococcal pharyngitis colonization (group A)
- Post-disease complications of acute rheumatic fever
- Manifestations includes polyarthritis, chorea (nerve system damage – can’t control movement), carditis
- Valvular regurgitation (MR 60% and AR 5%)
• Diagnosis of Carditis: echocardiography picks up heart disease better than stethoscope and help diagnose ARF in polyarthritis
• Epidemiology:
- Decreased admission of ARF in NZ
- Increase admission of RHD in NZ
- Pacific and Maori suffer a great proportion of first attack of ARF
- Recurrence of RF occurs in younger age group
• Rheumatic fever risk factor:
- Social: crowding
- Economic: poverty
- Health: poor access to health care, smoking and gas
- Geographic
- Ethnic: Maori
• Treatment options:
- Penicillin: prevention of ARF and its recurrences, Benzethine penicillin is very effective in reducing recurrences but have severe allergic reactions anaphylaxis
- Aspirin/steroid
- Bed rest
- Intravenous immunoglobulin trial
• Effect of anti-inflammatory agents: does not affect severity of outcome. Strong response to aspirin indicates ARF while parecetamol and steroid may allow development of polyarthritis and control inflammatory oedema of mycocardium respectively
• Primary prevention of RF: IM penicillin
• Interventions:
- School based

Heart Failure

• Heart failure: condition when the heart is unable to pump sufficient blood to meet the requirement of the body. This is the end point of many progressive cardiovascular diseases.
- Epidemiology: the rate of heart failures have increased due to improved medical care that prolong morbidity of heart diseases whereas previously most would be encountered by mortality
• Cardiac causes:
- Systolic dysfunction: problems with myocardial contraction such as ischemic injury (coronary), pressure overload (hypertension), cardiomyopathy (pathogens), arrhythmias and others disease
- Diastolic dysfunction: problems of the heart chamber to relax, expand and fill during diastole such as myocardial fibrosis, deposition of amyloid, constrictive pericarditis and left ventricular hypertrophy
• Vascular causes: when normal heart is presented with a load that exceeds its capacity (pregnancy) or inadequate ventricular filling, such as septic shock in which vasodilatation of vessels from immune response cause loss of fluid into tissue space.
• Descriptions of heart failure:
- Forward: reduced cardiac output
- Backward: damming of blood from venous system
- Acute: rapid developing heart failure
- Chronic: slow developing
- Left sided: left heart chambers fails so blood accumulates in lungs
- Right sided: right heart chamber fails so blood builds up in the body
- Low output: intrinsic disease affecting the heart
- High output: increased bodily demand for pumping the blood
• Physiological adaptations: to maintain adequate perfusion to organs. Changes in heart muscles involve molecular, cellular and structural alterations.
- Frank-starling mechanism: with increased preload, cardiac dilation increases crossbridge within sacomeres and enhance Ca2+ sensitivity, enhance contractility.
- Myocardial structural change: hypertrophy due to increase size of individual muscles (through GF etc) in response to injury to increase contraction. Often called left ventricular remodelling.
- Neurohormonal: release of catecholamines by adrenergic cardiac nerves to increase heart rate, contractility and vascular resistance to fill the tissues. Activation of the renin-angiotensin-aldosterone system and release of ANP
• Cardiomegaly: dilation and hypertrophy of the heart as a result of heart failure
• Events of heart failure:
- Factors such as hypertension, valvular disease and MI’s all present pressure/volume overload stress on the heart as a result increasing cardiac work
- Increase cardiac work increase wall stress and initiate signalling cascades and protein synthesis that remodels the heart.
- Stress gene is turned on and fetal gene induce modelling of heart and vascular changes (however blood vessel usually do not growth fast enough to meet demand)
- Increased heart size and mass and fibrosis may occur
• Renin-angiotensin system:
- Decrease in blood pressure will decrease delivery of Na+ to the distal tubule. This is will initiate the angiotensin signal pathway
- Increased angiotensinogen is cleaved by renin to angiotensin I
- Angiotensin I is converted to II by ACE and it can act on periphery to raise blood pressure by vasoconstriction and increase sodium reabsorption in kidney to increase ECF and pressure.
• Cardiac decompensation: when the causes of the heart failure are progressive and prolonged eventually overwhelming the capacity of the adaptation to maintain cardiac function. At this point the adaptation itself becomes pathological as it forms a positive feedback system.
- Hypertrophic heart exceed coronary blood supply
- Excessive cardiac dilation becomes a mechanical disadvantage (lose efficiency)
- Increase circulating volume cause volume overload
• Consequences of cardiac failure:
- Organ hypoxia from lack of flow
- Left sided: back pressure on left atrium and pulmonary system cause congestion, haemorrhage (edematous lung) and heart cell in haemophysis. Breathlessness is due to not enough oxygen obtained with boggy lung.
- Right sided: back pressure on the systemic venous circulation will affect visceral organs, such as kidney and brain causing oedema.
• Tissue oedema: an increase of fluid within interstitial spaces. This can occur during inflammation and usually as a result of an imbalance of fluid movement homeostasis (i.e. excess intravascular pressure and high interstitial osmolarity)
- Pitting leg oedema: increase in venous pressure in right sided cardiac failure with raised jugular vein and boggy tissue.
- Pleura effusion
• Heart failure cells in lung: vessels burst and macrophages breaks down erythrocytes and release hemosiderin (deposits of iron)
• Overall pathogenesis of heart:
- Primary heart injury
- Ventricular dysfunction
- Heart remodelling and neuroendocrine response (produce symptoms)
- Pump failure
- Death
• Prevention and treatment:
- Reduce general CV risk factors
- Early detection and treatment of IHD such as weight control, smoking cessation
- Prompt intervention after MI to minimize loss of myocardial function, e.g. beta blockers
- Prompt treatment of remodelling and ventricular dysfunction, e.g. ACE inhibitors

Heart Failure/Transplant

• Epidemiology:
- death rate of heart disease has decreased due to prevention lifestyle factor
- heart failure has increased as patients are surviving with cardiac damage, i.e. living longer and surviving to get heart failure
• Symptoms of heart failure: fatigue, sweaty, breathlessness (major problem) and frequent hospital admission
- Heart failure develops before the symptoms
- As you treat breathlessness, the lethargy becomes major problem
• Classification: class I to IV. Categorizing conditions of increasing breathlessness with activities.
• Aims of treatment:
- Reduce symptoms and improve quality of life
- Improve exercise tolerance
- Improve left ventricular function
- Reduce hospital readmission
- Improve survival
• Treatment:
- Heart muscles damage leads to haemodynamic failure so treatment with inotropes helps increase force of contraction
- Remodelling of the heart causes cardiac dilation, changing from spherical to ellipse. The body compensate to increase afterload, i.e. vasoconstriction which can worsen the cycle (symptoms occurs a long time after vicious cycle). Vasodilators is given to overcome vasoconstriction, e.g. ACE inhibitors
- In long term setting, the heart should not be stimulated (no inotropic therapy) instead should be left to rest.
• Adverse effect of sympathetic stimulation:
- Arrhythmia
- Afterload increase
• Neurohormonal alterations chronic HF:
-
• ACE inhibitor: first line treatment that inhibits the effect of angiotensin-converting enzyme and hence prevents synthesis of angiotensin II molecules. This has the effect of reducing fluid retention and treat hypertension.
- However ACE inhibitors only block the secondary pathways to prevent worsening of conditions. The actual stimulus of the pathway itself is not addressed.
- Blocks only the RAA system for aldosterone stimulation
• Beta blockers: a standard treatment to block the sympathetic system and prevent death from sudden ventricular fibrillation. This is usually used after ACEi when afterload decrease and minimal congestion.
- Proven to increase survival and decrease hospital admission
- Don’t improve symptoms in the short term so poor response and compliance from patients (beta blockers may even worsen patient symptoms)
- Long term symptoms: dizziness, hypotension, bradycardia (heart block)
- Dosage: start on low dose and double, metaprolol and carvedilol
• Spiralactone: a diuretic aldosterone antagonist drug aimed to treat hypertension and ascites.
- Adverse effect of spiralactone is gynaecomastia as it also affect steroid receptors in the body
- Underwent rigorous trials in the context of best medical and it showed a clear improvement in survival
- Cheap and cost effective (NNT 9)
• Neutral agents: drug that improve symptoms of failure but not survival
- Digoxin
- Calcium channel blockers (amilodipine)
• Heart transplantation: effective treatment for only a minority of patients and means having to introduce long term immune-suppressant. Problem is limited number of donors
• Implantable defibrillators: small device pacemakers in the body and can send small electric shocks to prevent arrhythmias.

ECG II Signs of Abnormality

• Wolff-Parkinson White Syndrome: pre-excitation syndrome in which ventricles are electrically activated earlier than normal through accessory pathway called Bundle of Kent. The pathway is abnormal communication from atria to ventricle alternative to AV tract.
- ECG changes: shortened PR interval, wide QRS complex, delta wave
- Ventricular tachyarrhythmia: re-entry from atria to ventricles and rapid atrial rhythm where AV nodes can’t protect ventricles.
- Consequences: most WPW remain asymptomatic but with episodes of syncope, palpitations (irregular heartbeat) and small risk of death from tachyarrhythmia.
- Treatment: drugs to slow down rhythm and ablation of accessory pathway
• Long QT syndrome: disease with an abnormally long delay between electrical excitation and repolarisation of the ventricles.
- Drug induced LQTS: a result of treatment by anti-arrhythmic drugs such as amiodarone
- Genetic LQTS: mutations relating to ion channels and hence prolong action potential duration. Most common is LQT1 in which the channel conducting the delayed rectifier K+ current is mutated.
- Consequences: long QT results in abnormal repolarisation of ventricles causing a difference in refractoriness of myocytes. This can lead to abnormal activation of ventricles and thus arrhythmia, syncope and even sudden death.
- Treatment: arrhythmia prevention and termination
• Conduction disturbance: AV conduction blocks
• Electrolyte disturbances:
- Hyperkalaemia: K+ channels conduct faster when extracellular [K+] increases so faster repolarization. Effect is more pronounced at epicardium leading to tall peaked T waves.
- Hypokalemeia: flat T waves
- Hypercalcaemia: increased extracelluar [Ca2+] leads to a hyperpolarizing effect and inactivates the L-type calcium channels. As a result Ca current during the plateau is reduced and APD also decreased.
- Hypocalcaemia: prolonged QT interval
- Digitalis: ST segment depression and T wave inversion and also PR interval prolongation
• Ischaemic Heart disease: ECG changes depend on severity, extent and location and time since the onset of damage.
- MI leads to a characteristic and progressive series of ECG changes
- Ischemia affect T wave, injury associates with ST segments and infarction changes QRS complex
- Area of damage is shown by leads directly overlying them hence location can be determined
• Events of infarction: occurs in leads facing the area of damage while those facing away may observe reciprocal change.
- Tall T waves (similar to hyperkalaemia in leads over damaged area)
- ST segment elevation
- Reduced R waves amplitude
- T wave inversion (days)
- Pathological Q waves (days): these are the only residual ECG sings of MI and eventually disappear as scar replaces the damage tissue shrinks
- ST segment returns to normal (days)
- T waves returns to normal (weeks)
• T wave changes in ischaemia: not specific for MI and can occur in digitalis, pericarditis, myocarditis and temperature
- Tall T wave result from K+ leak from damages to myocytes
- T wave inversion is possibly due to repolarization differences.
• ST segment changes:
- Elevation often the earliest sign of acute MI and transmural MI, seeing in leads facing the infracted area.
- Shift must be greater than 1 mm to be considered significant
- Depression occur during angina pectoris due to inadequate subendocardial blood flow
- Mechanism: ischaemia lower resting membrane potential, shorten AP and change AP plateau. Consequently voltage gradient between normal and ischaemic zones are established and causing current flow. This is reflected by the ST segment change.
- Diastolic current of injury: injury current that occurs during diastole but effect is seen in the ST segment as a shift downwards (secondary)
- Systolic current of injury: current occurs during the AP plateau producing true ST shift (primary)
• QRS changes:
- Infarcted muscles become electrically inactive hence forming an electrical window in which activity of the distant opposite wall is detected, i.e. QRS becomes more negative.
- Wave fronts coming toward the electrode is reduced or absent while wave fronts moving away is emphasized
- QS complexes: when R wave is decreased/absent due to less/no incoming electrical activity
• Reciprocal leads: observe opposite changes, i.e. depression of ST and tall T wave.
• ECG criteria for MI:
- ST segment elevation > 1mm in 2 or more leads
- Q waves more than ¼ of R wave
- QS complexes present
- In appropriate R wave voltage in local area
• Downsides of MI diagnosis
- Variable changes
- Abnormal activation sequences (pacemaker) distorts normal ECG
- Not good at showing RV posterior and basal wall
- ECG abnormality
- Severe IHD shows no abnormality

Introduction to Acute Coronary Syndrome

• Features of atherosclerosis: not continuous process with phases of stability and periods of aggressive coronary plaque expansion and remodelling
- Plaque formation: around branching points
- Plaque cap rupture and erosion: small soft plaque rupture
- Clotting cascade (exposing of endothelium to plaque)
- Vasoconstriction
• Acute coronary syndrome: caused by atherosclerosis and leads to stable angina, non-ST elevated ACS and ST elevated MI.
- Risk factors: BP, diabetes and dyslipidaemia
- Vessel biology: occurs through interaction of the risk factors and shear points. Thrombo-emboli which are fragments of the thrombus can break off and lodge it self in a coronary artery completely occluding blood flow.
- Consequences: soft atherosclerotic plaque will obstruction flow causing stable angina but those that rupture and have thrombogenic potential will cause MI death.
• Myocardiac infarction: transmural scarring and death of heart muscles (large arteries are blocked)
- Direct muscle effects
- Remodelling
- LV dysfunction
- Arrhythmia
• Symptoms of ACS:
- Chest discomfort: (occurs 15-20% of times). Quality of pain will vary with different duration and trigger.
- Atypical symptoms: present in young and old patients, female and diabetic patients
• Prognosis:
- Decreasing left ventricular function, increase disease severity and ischaemia at rest and exercise
- Other factors: advanced age, congestive heart failure, diabetes, renal dysfunction and peripheral vascular disease
• Clinical presentation:
- Normal examination
- Haemodynamic status
- Valvular signs and complications
• Tests for ACS
- ECG
- Blood: check for troponin, WBC
- Chest X-ray
- Imaging
- Provocative tests
• ACS complications:
- Myocardial LV failure and rupture
- Percardial problems
- Abnormal rhythm in VT, VF and AF
- Valvular problems
- Psychological problems
• Therapy and treatment:
- Reperfusion
- Thrombolysis: antiplatelet agent and antithrombin agents
- Mechanical: PCI (percutaneous coronary intervention using balloon or stent is used to push plaque into the wall), CABG (coronary artery bypass graft where another artery from the aorta is redirect to the coronary artery to bypass atherosclerotic narrowing) and balloon pumps
- Medication: beta blockers, ACEi, statin and anti-arrhythmics
- Rehabilitation: exercise, work and driving
• Case scenario 1: 55 year old with chest pain and indigestion. Heart rate is 100
- ECG: ST segment elevation with injury, AV conduction lost due of damage to AV node
- Complete heart block (complication after infarction)
• Case scenario 2: 40 years old, collapse
- ECG: arrhythmia hence collapsed

Introduction to Chronic Stable Angina

• Vulnerable vessel: heart and carotids artery are most prone to atherosclerosis and thus being in danger of stroke and myocardial infarction.
• Effect of narrowing: 70% of the lumen must be narrowed to sufficiently cause symptoms and restrict blood flow
- After a long time, stimulus of angiogenesis will provide collateral blood supply
• Limitations of angiograms: only tell us the degree of narrowing but no information of the plaques
• Heart failure: this condition is brought after myocardial infarction (left ventricle damage) and scarring so loss of function. Sudden death is also likely.
• Symptom of angina:
- Heaviness across the chest
- Pain felt in jaw and shoulder and even across the back
- Shortness of breath
• Palpations:
- change in heart rhythm
- tachycardia and decreased diastolic volume and supply to the ventricles
• Syncope: blacking out
• Assessment and prevention: assess the risk factor for coronary disease.
- Extent of cardio function test such as treadmill exercise test
- symptoms
- changes in ECG: ST depression on ECG occurs during exercise
- Ischaemia is accepted during the exercise test but its more important to diagnose
• Direct muscle analysis: when ventricle becomes ischaemic, the cardiomyocte stop contract and die. Using echocardiograph, motion of the wall can be assessed.
- Hypokinesis
- Akinesis
• Perfusion: injection of dye into the artery and observe distribution of the dye before and after stress.

Clinical Hypertension

• Epidemiology:
- Importance of environmental effect (Japan to California)
• Blood pressure:
- Hypertension considered to be >90 (DBP) and >140 (SBP)
- Younger individual can tolerate high BP but old patients die within 3 years
• Causes of high blood pressure:
- 95% lifestyle factors: overweight, limited exercise, high salt intake, stress and alcohol intake
- Others include kidney disease, primary aldosteronism, Cushing’s syndrome, coarctation of aorta and drugs (NSAIDS)
• Complications of hypertension:
- cerebrovascular accidents
- ischemic stroke (blood clotting)
- haemorrhagic stroke (blood vessel burst)
- transient ischemia attack
- cardiovascular disease
- MI and angina
- Congestive heart failure
- Kidney damage
- Peripheral vascular disease (blockage in leg etc)
- Aortic aneurysm
- Retinopathy
- Malignant hypertension
• Variability of BP:
- During a day: blood pressure rises from morning and peak around noon. It then drops off and peak itself again during early night.
- During a year: in old people, blood pressure increase by up to 15mmHg in winter
• Trends of BP:
- Blood pressure is falling in spite of weight rising
- Developed country have high BP
- Above 75, 78% male and 75% females are hypertensive
- Maoris and PI have 5/6 and 4/6 greater proportion hypertensive than European. Asian is 1/5.
- Doxasosin is the most effective treatment. It is an alpha blockers.
• Measuring BP:
- GP screening provide most pick ups
- Repeated measuring needed if results varied substantially from last time (take average of 3 visits)
- White coat hypertension: increase in BP due to anxiety in a clinical setting
• Physical examinations:
- Coarctation of aorta: rushing sound with radio femoral delay
- Renal bruits
- Pulse for thyroids and arrhythmia
- BMI
- Organ damage: heart murmur for heart damage, fundi for retinal damage
• Investigations:
- Endocrine damage usually involved with elevated Na+ and K+
- Increased creatinine indicate kidney failure
- Urine albumin and casts for signs of proteinuria
- Level of thyroid-stimulating hormone for hypothyroidism
- Catecholamines and sodium for 24 hours urine
- Full blood count for large red cells and GGT in liver for signs of heavy alcohol intake (fatty liver)
- Fasting glucose and HBA1c for diabetes (prevention)
- Cholesterol level
- Chest X-ray, ECG
- Uric acid for gout
• Drugs:
- Diuretics: low dose thiazide. Adverse effect include gout
- Beta blocker: slows pulse. Good for angina and post myocardial infarct and heart failure. Adverse effect involve asthma, heart block
- ACE inhibitor: effective for diabetes and HF but adverse effect cause cough and hyperkaelemia
- Calcium channel blockers: good for angina and atrial arrhythmia but cause swollen ankle and decreased efficacy
- Alpha blocker: lipid lowering and treat prostatism. Adversely cause more CHF than thiazide diuretics
- AII blocker: used for heart failure with no cough but increase creatinine if renal artery is stenosed.
- Aldosterone blocker: good for heart failure but cause gynaecomastia and hyperkaelemia

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