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Cardiovascular, Drugs - Coggle Diagram

- - - - Rapid onset
      - Short duration
      - Inability to maintain postural tone
      - Spontaneous complete recovery
  - - - SYNCOPE
        
        Neurally-mediated reflex syndromes
        
        Orthostatic hypotension
        
        Cardiac arrhythmias
        
        Structural cardiovascular disease
      - DISORDERS MIMICKING SYNCOPE
        
        With loss of consciousness, i.e., seizure disorders, concussion
        
        Without loss of consciousness, i.e., psychogenic “pseudo-syncope”
  - - - Vasovagal
      - Carotid Sinus Syndrome
      - Situational
        
        Cough
        
        Post-Micturition
        
        Defecation
    - - Drug-Induced
      - Autonomic nervous system failure
        
        Primary
        
        Secondary
    - - Brady
        
        Sinus node dysfunction
        
        Atrioventricular Block
      - Tachy
        
        VT
        
        SVT
        
        WPW
      - Long QT Syndrome
      - Brugada syndrome
    - - Acute MI
      - Aortic Stenosis
      - Hypertrophic obstructive cardiomyopathy
      - Pulmonary Hypertension
      - Aortic Dissection
  - - - Distinguish TRUE syncope from syncope MIMICS
        
        Remember syncope can result in seizure-like activity.
        
        It is important to consider serious underlying causes
        
        Syncope vs. dizziness, presyncope, drop attacks, vertigo, & seizures.
      - Determine presence of cardiovascular disease
        
        Search for structural heart disease
        
        valvular stenosis, cardiomyopathy, or myocardial infarction.
        
        This may suggest more malignant causes such as ventricular tachycardia.
        
        Critical as most important factor in prognosis and risk stratification – cardiovascular causes of syncope have the highest mortality risk.
      - Establish the cause of syncope with sufficient certainty to:
        
        Assess prognosis confidently
        
        Initiate effective preventive treatment
    - - Meticulous patient history is vital
      - Collateral/witness history should be obtained where possible
      - Review patient’s medication list: note any recent changes in medications/doses
      - Physical exam: Full examination of all systems, with particular focus on cardiovascular and neurological systems
      - Supine and upright blood pressure
      - 12 lead ECG
      - Fingerprick glucose
    - - Circumstances of collapse
        
        Eyewitness account of event if available: What happened, appearamce of patient, breathing pattern, duration, abnormal movements, incontinence etc.
        
        Circumstances prior to episode e.g. position, activity, precipitating events, recent illnesses etc.
        
        Symptoms at onset of event e.g. headache, nausea, chest pain, palpitations, aura
      - Past medical history- especially history of similar episodes, cardiac and neurological conditions
      - Medications
        
        Proarrhythmic/antihypertensives/antianginal/QT prolonging agents
        
        Illicit drug use
      - Family history
        
        Sudden cardiac death
        
        Cardiac disease, particularly arrhythmogenic heart disease
        
        Syncope
    - - Vital signs
        
        Heart rate
        
        Orthostatic blood pressure change (drop in BP on standing)
      - Cardiac examination
        
        Tachycardia, bradycardia, irregular pulse, low volume pulse, pulsus parvus et tardus
        
        Cardiac murmurs
        
        Signs of cardiac failure
      - Neurological examination
        
        Focal neurological abnormalities e.g. weakness, signs of Parkinsonism
        
        Signs of raised intracranial pressure
    - - Should be guided by history and examination
      - Laboratory investigations: FBC, renal profile, glucose, D-dimer (if suspected PE), blood alcohol level or drug screen if indicated.
      - Cardiac investigations
        
        12 lead ECG
        
        Holter monitor
        
        Echocardiogram
        
        Event Recorder/Implantable Loop Recorder
      - CT brain if seizure or other neurological cause suspected
      - Special Investigations
        
        Pacemaker check if applicable
        
        Carotid sinus massage
        
        Method
        
        Massage, 5-10 seconds
        
        Don’t occlude
        
        Monitor cardiac rhythm and BP
        
        Outcome: Positive test is defined by cardiac asystole for 3 seconds or longer, or 50 mmHg fall in systolic BP, or 30 mmHg drop in SBP with reproduction of symptoms. (ESC guidelines). Reproduction of symptoms is necessary for Carotid Sinus Syndrome diagnosis
        
        Absolute contraindications
        
        Carotid bruit
        
        known significant carotid arterial disease
        
        previous TIA/stroke in last 3 months (unless recent carotid duplex study).
        
        Complications
        
        Primarily neurological
        
        Less than 0.2%3
        
        Usually transient
        
        Head-Up Tilt Test (HUTT)
        
        Protocols vary
        
        Useful as diagnostic adjunct in atypical syncope cases
        
        Useful in teaching patients to recognize prodromal symptoms
        
        Not useful in assessing treatment
        
        Electrophysiology study (EP study)
  - - - Syncope Due to Structural Cardiovascular Disease: Principal Mechanisms
        
        Acute MI/Ischemia: Neural reflex bradycardia – vasodilatation, arrhythmias
        
        Hypertrophic cardiomyopathy: Limited output during exertion (increased obstruction, greater demand), arrhythmias, neural reflex
        
        Acute aortic dissection: Neural reflex mechanism, pericardial tamponade
        
        Pulmonary embolus/pulmonary hypertension: Neural reflex, inadequate flow with exertion
        
        Valvular abnormalities
        
        Aortic stenosis – Limited output, neural reflex dilation in periphery
        
        Mitral stenosis, atrial myxoma – Obstruction to adequate flow
    - - Brady/Tachy
        
        Bradyarrhythmias
        
        Sinus arrest
        
        High grade or acute complete AV block
        
        Can be accompanied by vasodilatation (VVS, CSS)
        
        Tachyarrhythmias
        
        Atrial fibrillation/flutter with rapid ventricular rate (eg, pre-excitation syndrome, WPW)
        
        Paroxysmal SVT or VT
        
        Torsade de pointes
        
        Drug induced
      - Long QT syndrome
      - Torsade de pointes
      - Brugada
    - - Vasovagal Syncope (VVS)
      - Carotid Sinus Syndrome (CSS)
  - - - Reassure patients about the benign nature of the syncope
      - Avoid triggers
      - Identify warning symptoms
      - Lie supine, elevate legs when symptoms start
      - Treat any underlying conditions e.g. pulmonary disease in cough syncope
      - Good fluid intake
      - Support stockings
      - Physical counterpressure manoeuvres e.g. leg crossing
    - - Fludrocortisone
      - Midodrine
    - - A Symptom, Not a Diagnosis
      - Difficult diagnosis to make – detailed history and collateral history and exam
      - Many varied causes
      - Treatment varied and depends on proper diagnosis
- - - - Viruses – CMV, Coxsackie,
      - Bacteria - Neisseria
      - Fungi - Candida
      - Protozoa – Toxoplasmosis
    - - Post – Infectious
        
        viral
        
        streptococcal
      - SLE
      - Drug hypersensitivity – eg. chemo
      - Transplant rejection
    - - Sarcoidosis
      - Giant cell myocarditis
      - Idiopathic
    - - More evidence needed especially from autopsy studies
      - Direct v Indirect Injury ?
      - So far -->
        
        Myocardial infiltration by macrophages & CD4+ T lymphocytes
        
        Myocyte damage & lymphocytic myocarditis
        
        SARSCoV-2 viral particles identified in cardiac macrophages
        
        Long term consequence awaited – Troponin – Cardiac MRI
        
        Microthrombosis – small coronary vessels
        
        Consequence of Therapy in a few ??
        Cardiac dilatation & spotty necrosis,
  - - - Myocardium oedematous
      - Lymphocytic infiltrate, mononuclear cells
      - Non ischaemic necrosis
      - Viral inclusion rarely may be seen (eg. In CMV)
    - - Myocardial fibrosis
      - Ventricular dilatation
- - - - Rate
      - Contractility
      - Tension
    - - Oxygenated blood
      - Coronary Artery Flow
    - - Angina pectoris
        
        Stable
        
        Usually chest pain caused by exercise and relieved by rest and – often not clear-cut.
        
        Reflects “Significant” vessel narrowing → atheroma
        
        One vessel > 75% stenosis or 2 > 50% …usually
        
        Assessment via angiography. Often if autopsy done → microscopic myocardial fibrosis. Why?
        
        Angina may be worsened by anaemia or increased cardiac mass i.e. hypertrophy- may reflect important non-cardiac disease
        
        Unstable
        
        Stable angina with recent progressively increasing frequency
        
        Precipitated with progressively less effort- Often occurs at rest, and tends to be of more prolonged duration.
        
        Induced by disruption of an atherosclerotic plaque (plaque rupture) and secondary thrombus.
        
        Increased risk of subsequent acute MI
      - Myocardial infarction
        
        Myocardial necrosis due to reduced blood supply
        
        Usually reflects unrelieved coronary artery occlusion evolving to tissue death - Dynamic process and can be reduced by coronary reperfusion following “stenting”
        
        Certain plaques more likely to thrombose – lipid rich with fibrous cap cracks
        
        Of note statins stabilise plaques
        
        Clinical Presentation
        
        Crushing central chest pain, unrelieved by rest; accompanied by weakness, sweating, nausea & vomiting - Radiates commonly to left shoulder and jaw
        
        May be described as indigestion
        
        Can be painless [silent] – old / diabetes
        
        Pain may be atypical e.g. abdominal.
        
        May be “silent” present as heart failure (esp in elderly) arrhythmia – confusion – weakness.
        
        Need a high index of suspicion.
        
        Pathology
        
        Coronary atheroma --> plaque rupture and subsequent thrombosis initiates ischaemia – possibly reversible for 6 – 12 hours.
        
        Necrosis of myocardium begins 30 mins after occlusion and progresses from the subendocardial myocardium through the full thickness of the myocardium to the pericardial zone. (Transmural infarct)
        
        Why is it subendocardial?
        
        Most untreated episodes of ischaemia cause --> Transmural infarction.
        
        NB Subendocardial (AKA Non ST-elevation MI--NSTEMI) infarction more likely in incomplete artery occlusion or may develop in prolonged shock.
        
        Schematic representation of the progression of myocardial necrosis after coronary artery occlusion. Necrosis begins in a small zone of the myocardium beneath the endocardial surface in the center of the ischemic zone. This entire region of myocardium (shaded) depends on the occluded vessel for perfusion and is the area at risk. Note that a very narrow zone of myocardium immediately beneath the endocardium is spared from necrosis because it can be oxygenated by diffusion from the ventricle. The end result of the obstruction to blood flow is necrosis of the muscle that was dependent on perfusion from the coronary artery obstructed. Nearly the entire area at risk loses viability.
        
        Pathogenesis of Coronary Artery Occlusion
        
        Plaque rupture / fissure
        
        Exposure of lipid, smooth muscle foam cells
        
        Thrombin generation and fibrin platelet aggregates
        
        Thrombus in the atheromatous plaque with repair
        
        Plaque rupture with secondary thrombosis- can cause a myocardial failure or a fatal arrhythmia
        
        Diagnosis
        
        Clinical
        
        ECG (EKG): quick, easy and gives information about site and vessel involved as well as information about arrhythmias.
        
        Lab Evaluation : Troponin-I (TNI) and Troponin-T used most commonly. Also MB fraction of creatine kinase (enzyme) cardiac specific structural proteins
        
        Cardiac Troponins- Regulatory proteins of actin filaments in cardiac muscle – engage with calcium.
        
        Troponin Advantages
        
        Stays elevated for 7-14 days.
        
        Enzyme levels give some idea of extent of infarct, latter depending on location of obstruction, significance of vessel, degree of myocardial hypertrophy and presence of a collateral coronary circulation.
        
        More specific.
        
        Certain subtypes of troponin (I and T) are indicators of damage to the myocardium and can be measured in the blood by immunoassay techniques. Must be repeated to look for a rise
        
        Troponin levels are not specific Other conditions associated with raised troponins (any cause of myocardial necrosis)
        
        Cardiac surgery
        
        Cardiac contusion
        
        Myocarditis
        
        HOCM
        
        Cardiomyopathy
        
        Chemotherapy
        
        Renal disease
        
        Poly/dermatomyositis
        
        i.e. Troponins are a marker of all heart muscle cell necrosis
        
        - myocarditis
        
        Microscopic & Gross Pathology
        
        Up to 10 hours no microscopic change in myocardium
        
        Day 1: Myocardium. Coagulation necrosis with hypereosinophilia and wavy fibres. Dead vessels – haemorrhage.Macroscopically - Dark Red Firm
        
        Day 1 Coagulative necrosis on left characterised by non-nucleated wavy fibres with oedema causing widened space between fibres – rare neutrophils also present. Microscopic features of myocardial infarction and its repair. One-day-old infarct showing coagulative necrosis along with wavy fibers (elongated and narrow), compared with adjacent normal fibers (at right). Widened spaces between the dead fibers contain edema fluid and scattered neutrophils.
        
        Day 2 – 7: Beside necrotic area – inflammation – neutrophils and oedema. If marked can get fever and raised WCC (bad prognosis).Macroscopically – Soft yellowish/tan tissue.
        
        Day 2-7 Necrotic myocardium with polymorphs
        
        Day 7 Soft yellow Myocardium [Cross section of left ventricle]:
        
        Day 7 – 14: Ongoing repair process with resorption of dead tissue and granulation tissue at edges. Macroscopic – depressed area with red edges.
        
        Week 2-8: Evolving fibrosis and decreasing vascularity. Macroscopic – grey white tissue
        
        Week 8: Dense fibrosis. Macroscopic depressed thinned myocardium and scar.
      - Chronic ischaemic heart disease
  - - - Sudden large coronary thrombosis on a ruptured atheromatous plaque
      - Secondary to an arrhythmia in chronic ischaemic heart disease as defined above.
      - 50% dead before arrival in hospital
- - - - Decreased valvular diameter – i.e. Aortic stenosis
      - Inadequate valve seals – i.e. aortic or mitral regurgitation
  - - - Insult [Index Event] – Compensation – Decompensation
      - Index Event - Reduces contractility or compliance
      - Compensation
        
        May mask severity – disease advanced at presentation
        
        Adrenergic and Renin angiotensin aldosterone systems
      - Decompensation
        
        Characterised by remodelling
        
        Myocyte hypertrophy - contractility – desensitisation - loss – replacement
        
        Ventricular wall – perfusion – papillary muscle – AV ring
    - - Heart failure --> complex clinical syndrome resulting from: Impairment of :
        
        Ventricular filling- e.g. with poor venous return, poor volume, Starling’s law
        
        Ventricular ejection e.g. of blood from the left ventricle (pump function)
      - Heart failure occurs when the heart is unable to pump blood at a rate [cardiac output] sufficient to meet the metabolic demands of the tissue
    - - NB – Pathologists often use anatomical / morphological classifications e.g.
        
        Left ventricular failure V Right Ventricular Failure
        
        Lobar pneumonia V Bronchopneumonia
        
        Small cell carcinoma V Non-small cell carcinoma
      - Clinicians often use clinical classifications e.g.
        
        Reduced Ejection Fraction failure V Preserved EF failure
        
        Community acquired V Hospital acquired pneumonia
        
        Primary lung carcinoma V Metastatic lung carcinoma
    - - Left ventricular failure (LVF)
        
        Reduced ejection fraction (EF) (systolic HF) Vs Preserved EF (diastolic HF) filling
        
        Causes of The Index Event
        
        Ischaemic heart disease - Muscle failure and therefore pump failure
        
        Hypertension - Increased pressure to pump against [remember BP = CO x PR]
        
        Aortic & Mitral valve diseases
        
        Aort