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CVS Core Conditions
3+
Circulatory shock/hypotension
Cardiac failure…
CVS Core Conditions
3+
- Circulatory shock/hypotension
- Cardiac failure - ACS
- Ischaemic Heart Disease - ACS
- Essential Hypertension - leading to Hypertensive Heart Disease
- Arrhythmias and Conduction Defects
- Vascular Complications of Diabetes
2+
- Cardiac arrest - ACS
- Valvular Heart Disease
- Infective Endocarditis
- DVT
- Arterial Aneurysm
- Arterial Dissection
- Acute pulmonary Oedema
- Varicose Veins
Ischaemic Heart Disease
AETIOLOGY
Type 1 - Occlusive ischaemia
- Atherosclerosis
- Embolism - including atheroemboli, thromboemboli
- Thrombosis
Type 2 - Infarcted myocardium, in a patient with stable coronary artery disease, due to a non-occlusive event (i.e. tachyarrhythmia, significant anaemia etc)
- Hypotensive events - distributive, hypovolemia, obstructive shock
- Arrhythmia
- Exercise
- Increased Myocardium (cardiomyopathy, Hypertrophy)
- Aortic dissection
- Massive PE
Type 3: Cardiac Arrest + Death due to myocardial infarction without detection of biomarkers (death precedes circulation of biomarkers)
Types 4 and 5: Myocardial infarction associated with revascularisation procedures (stenting or bypass surgery)*-
Screening for Cardiovascular Wellbeing
- BEDSIDE
- LAB
- SPECIAL
- Absolute CVD 5-15% = Coronary Calcium score - indicated in patients without symptoms of IHD
- High Amount Ca = anti-platelet + functional tests
- Low Amount Ca = lifestyle changes
-
Heart Score (MD CALC)
Calculates risk of cardiovascular event in the next 6 weeks
- Useful for ED scenarios where pt. does not have classical features of IHD but it is still possible
Heart Failure
A constellation of signs and symptoms associated with impaired cardiac function, whereby the heart is unable to generate a cardiac output that can sufficiently meets the metabolic demands of the body
Pathophysiology
Compensated Heart Failure
- Obscured HF - In the initial stages of HF, the body is capable of employing homeostatic mechanisms which will accommodate for the impaired function. This renders HF relatively inconspicuous, and means that when it does present, it has an abrupt onset, yet truly this decline in cardiac function is insidious
Decompensated Heart Failure
- Decompensation - once the underlying disease causing heart failure progresses beyond the threshold of homeostatitic tolerance, heart failure begins to manifest
- What was compensated, becomes decompensated
AetioPathological Classification
Organise the aetiologies of heart failure in terms of diseases which either effect a) Stroke volume, b) Heart Rate.
Since heart failure is diminished cardiac output,
CO = SV x HR
LOW-OUTPUT HF
When cardiac output drops and failus to increase appropriately with exertion
- Impaired Contractility - systolic or diastolic heart failure, arrhythmia
- Excessive preload - dilational effect of increased ventricular filling exacerbates contractile issue
- fluid overload, mitral regurg
- Chronic excessive afteload - increased strain on ventricle with direct effect on SV
HIGH OUTPUT HF
Cardiac output increases in response to increase demand, yet in spite of this, fails to meet demands.
- Anaemia, pregnancy, infection, hyperthyroidism, hypoglycaemia, Paget's disease
Left Heart Failure
Impaired Stroke Volume
Impaired Systole (HF w/ reduced ejection fraction HFrEF<40%)
The phase of contraction and forceable ejection of blood from the heart
- WORSE PROGNOSIS - HFrEF prognosis < HFpEF prognosis
Disorders of Afterload
- Systemic Disease - hypertension (stenosis (atherogenic), sclerosis (atherogenic), coarctation of blood vessels (congenital) or calcification (reduced distensability))
- Cardiac Disease - Valvulopathy (aortic stenosis), aortic dissection
- Coarctation of the Aorta
Asymptomatic or otherwise presenting with symptoms of heart failure - SoB on exertion
TOP TIP
Clinical diagnosis of a valvular disease relies on the integration of examination findings rather than isolated interpretation of murmurs on auscultation
Examinaiton of Heart Heart Sounds
NORMAL
- S1
- Mitral and tricuspid valve closure
- Start of systole
- MV first but hard to hear separately
- S2
- Aortic and pulmonary valve closure
- End of systole
- AV before PV (lower pressure in pulmcircn; flow continues into pulmcircnafter end of LV systole)
ABNORMAL
- S3 - an added sound at mid-diastole
- noisy filling in reduced ventricular compliance
- S4 - an added sound at end-diastole
- atrial contraction against reduced ventricular compliance
-
-
-
-
Pathophysiology
- Obstruction
- Incompetence
- Diseased Leaflets
- Dilated aortic root - aortic dissection
Clinical Correlation
- Low Cardiac Output - SOBOE, fatigue angina, reduced end-organ blood flow,
- Left Heart failure - SOBOE, orthopnoea PND crackles bibasilar
- Right heart failure - SOBOE, JVP, Abdominal distension, peripheral oedema, reduced appetite
- Arrhythmia (palpitations, sudden death, decompensated heart failure
- Pulmonary HTN (SOBOE, RHF, RV angina)
- 2 more items...
Impaired Contractility
- Ischaemic Heart Disease - myocardial infarction
- Dilated cardiomyopathy - eccentric hypertrophy, discoordinated and ineffective contraction
- Acquired DCM - IHD, toxic (e.g. alcohol, haemochromatosis), myocarditis (coxsackie), peripartum, idiopathic
- Congenital DCM (20-50%) - genetic (e.g. connective tissue, or muscular dystrophic disorders)
- Arrhythmia - disorder of the cardiac conduction system
- atrial fibrillation with rapid ventricular response
- ventricular fibrillation
- Valvopathy - mitral, tricuspid regurgitation, aortic stenosis
- Myocarditis - infective (coxsackie), inflammatory, immune mediated
- Pericarditis - infective, immune mediated, inflammatory
-
Cardiomyopathy
- Diseased Heart Muscle =/= CAD, THN, Valv or Congenital - cardiomyopathies as disorders where heart muscle is structurally and functionally abnormal, in the absence of coronary artery disease, hypertension, valvular disease, and congenital heart disease, sufficient to explain the observed myocardial abnormality
- Four Pathological Subtypes - European Cardiology Society...
- *Hypertrophic
- Restrictive
- Dilated
- Arrhythmogenic.
- They may also be classified based on aetiology - American Heart Association
- Primary (those predominantly affecting the heart) and
- Secondary (those related to generalised systemic multiorgan disorders).
-
Dilated Cardiomyopathy
Dilation of all four chambers of the heart differentiates DCM from the single chamber dilatation seen in ischaemic heart disease
- 1 more item...
-
-
Impaired Diastole (HF w/ preserved ejection fraction HFpEF>40%)
The phase of relaxation and ventricular refill
- BETTER PROGNOSIS - HFpEF prognosis > HFrEF prognosis
Disorders of Preload
- CIRCULATORY SHOCK
- Hypovolaemia
- Hypotension - poor venous tone, or vasodilation of arterial circuitry
- Pulmonary Disease -
- Destruction of pulmonary vasculature (COPD),
- PTX - compression of vena cava (RIGHT heart reduced preload, compression if vasculature in affected lung (LEFT heart reduced preload) surface area
- Massive PE - reduced preload to left heart
- Tachyarrhythmia - reduce filling time
Impaired Distensability
- Acquired Ventricular Hypertrophy - secondary to increased afterload
- Longstanding Systemic Hypertension
- Aortic stenosis
- exposes to increased risk of ischaemic heart disease as vessels must supply more heart muscle
- Congential Hypertrophic Cradiomyopathy
- Restrictive Cardiomyopathy
- Pericardial effusion => Cardiac tamponade
-
Impaired Heart Rate
Braddyarrhyhtmia
- Inferior Myocardial infarction implicating the sino-atrial node
*1. Sick sinus Syndrome
- Tachy-Brady Syndrome
- Pacemaker malfunction
- AV block
Tachyarrhythmia
- Atrial fibrillation with rapid ventricular response
- accessory pathway, ectopic foci, re-entrant circuit
- Ventricular fibrillation - re-entrant circuit, ectopic foci
-
Clinical Presentation
SYMPTOMS
- Dyspnoea - exertional and positional shortness of breath worsened
- Orthopnoea
- Bendopnoea
- Paroxysmal Nocturnal Dyspnoea = Pathognomonic - gravity redistribution of fluid leads to accumulation in the lungs, acute pulmonary oedema
- Fatigue
- Leg swelling
SIGNS
- Fine late inspiratory crackles
- JVP
- Dependant oedema
- Causes
- Atherosclerosis - look for peripheral artery disease
- Valve Disease - cardiac murmurs
- VITALS
Investigation
- Diagnose HF
- ALL: ECG, BGL, FBC, UEC, LFT, CXR
- DIAGNOSTIC UNCERTAINTY: BNP/pro-BNP
- Assess Severity
- Determine Underlying cause
- BEDSIDE
- ECG
- BGL
- UA - exclude nephrotic
- VBG - prognostic value of blood gasses and informs pathway of treatment
- LAB
- H: FBC
- B: UEC (eGFR, ACR: impacts treatment options), Lipid profile, BGL (Hb1Ac), BNP (reserved for diagnostically ambiguous cases), good negative predictive value), LFT (congestive hepatopathy => deranged fxn), Iron studies (haemochromatosis cause of cardiomyopathy), TFT (hyperthyroidism)
- IMAGE
- CXR +/- CTpa, Angiogram (coronary)
- Cardiac MRI (structural changes, infiltration, scar/fibrosis)
- SPECIAL
- Echocardiogram
Diagnosis and Classification
- New York Classification of Heart Failure
- Dyspnoea on exertion (extra-ordinary activity)
- Dyspnoea with ordinary activities
- Dyspnoea on less than ordinary activities
- Dyspnoea at rest
- Radiographic Diagnosis
- A - alveolar oedema (calssically perihilar "BAT'S WINGS" shadow also lower lobe reticular opacification)
- B - Kerley B lines (septal lines)
- C - cardiomegaly (<50%) of horizontal lung field)
- D - dilated prominent upper lobe vessels
- E - effusion (pleural) - bluntening of costodiaphragmatic recess
Chronic Management - Principals
*PHARMACOLOGICAL
- SYMPTOM RELIEF
- ACUTE - vasodilators (NITRATES) + loop diuretics furosemide
- CHRONIC - loop diuretics furosemide
- CORRECT OVERLYING PATHOLOGY
- SNS Inhibition - beta blockers (reduce metabolic demand of the heart, reducing further ischaemia) - not immediately
- RAAS Inhibition - ACE-i/ARB - since RAAS incorrectly causes fluid retention
- Optimise plasma oncotic pressure - correct hypoproteinaemia
- Correct Anaemia, hyperthryoidism etc.
- REVERSE UNDELRYING CAUSE
- STATINS - to counteract atherosclerosis
- ANTI-PLATELETS - e.g. clopidogrel etc
- ANTI-ARRHYTHMICS - digoxin
- VALVULAR - TAVI
- CO-MORBID - treat co-morbidities*
NON-PHARMACOLOICAL
- RISK FACTOR MODIFICATION - cease smoking, alcohol, reduce salt, reduce fluids, optimise weight and nutrition
- CAUSE - dysrhythmias, (TAVI) valvular disease, IHD (stenting)
- EXACEBATORS - TREAT - anaemia, thyrotoxicosis, infection
- EXACEBATORS - AVOID - fluid retention (NSAIDs, corticosteroids), verapamil (-ve inotrope)
HFrEF < 40%
- ANTI-HYPERTENSIVE / IMPROVES CARDIAC REMODELLING
- PO Ramipril 2.5mg BD OR
- PO Candesartan 4mg daily
- CARDIAC SNS INHIBITION - wait until offloaded, cannot tolerate if fluid overloaded
- PO Bisoprolol 1.25mg daily OR
- PO metoprolol succinate 23.75mg daily
- MRA = MINERALOCORTICOID antagonists - careful with corticosteroids in HF patients
- PO Spironolactone 25mg daily
- PO eplerenone 25mg daily
- SGLT2 inhibitors
- Empagliflozin - Cardioprotective
- LOOP DIURETIC - symptom management
- PO frusemide 20-40mg - poorly absorbed when the patient has gut oedema
- PO bumetanide 0.5-1mg - not impacted by gut oedema and more effective in outpatient setting
- ACE/ARB => "ARNI (angiotensin receptor blocker an nisprelin inhibitor)" - cease ramipril wait 3 days and start on ARNI
- PO Sacubitril+valsartan 100mg (49+51)
- PO Hydralazine (opposite to metaraminal) 50-75mg + Isosorbide dinitrate 20-40mg -
Reverse Reversible Causes
- Arrythmia
- Cardiac pacemaker +/- implantable cardiac defibrillator
- Anti-lipid
- 1 more item...
Hyperkalaemia
- ACE-i (ramipril)+ MRA (spironolactone) - increases risk of hyperkalaemia
- Serial UEC to monitor - Once at baseline in the first week, monthly for first three months and then 3-6 monthly thereafter
Beware Coritcosteroids, these can cause fluid retention
HFpEF > 50%
Principles
- Identify and treat precipitating factors (eg arrhythmias such as atrial fibrillation)
- HTN - MRA - Spironolactone +/- ACE-i or ARB
- Treat the symptoms (eg diuretics to treat congestion)
- Recognise and treat comorbidities (eg hypertension, ischaemic heart disease, diabetes)
-
Pathophysiology of Acute Systolic vs Diastolic
Systolic heart failure = Primary pump failure
- Systolic heart failure is due to cardiac pump failure and results in decreased cardiac output. As the heart begins to weaken the body attempts to maintain cardiac output through the use of compensatory mechanisms.
- Systolic failure (in contrast to diastolic failure) is often associated with a 1 – 7 day history of gradually worsening dyspnoea on exertion, orthopnoea, paroxysmal nocturnal dyspnoea and marked peripheral oedema (eg pitting ankle oedema).
Diastolic heart failure = Failure of myocardial relaxation due to transient ischaemia
- The cardiac ventricle is required to relax between contractions (diastole) to fill adequately in preparation of next contraction (systole). Diastolic failure is failure of the cardiac muscle to relax normally resulting in decreased ventricular filling and increased (back) pressure behind the heart.
- Diastolic heart failure results from myocardial ischaemia. Relaxation of the left ventricle is an energy dependent process. Myocardial ischaemia especially in the endocardial portion to the left ventricle can cause the heart to remain contracted in diastole. As a consequence the ventricle becomes stiff and there is reduced ventricular filling.
Clinical Presentation Diastolic vs Systolic
When systolic failure is the cause for the APO the symptoms develop more gradually when compared to diastolic heart failure.The worsening systolic failure is often signaled by increasing orthopnoea, increasing shortness of breath with exertion and possibly episodes of paroxysmal nocturnal orthopnoea (PND) developing in the days immediately prior to presentation.The (pre-existing) systolic heart failure will frequently be well documented with poor ejection fraction, clinical findings indicating fluid retention and the use of ACE inhibitors and diuretics. Clinical features such as pitting ankle oedema, hepatomegaly, pleural effusion, and elevated jugular venous pressure will often be present and confirm fluid retention due to activation of the renin-angiotensin system.In contrast, patients with APO due primarily to diastolic heart failure present dramatically !Classically the patient reports being well the night before and then suddenly waking up with severe (life-threatening) breathlessness. Chest pain is often absent and cannot be used to rule in or exclude myocardial ischaemia. The associated clinical findings of fluid retention (pitting ankle oedema, pleural effusion) are absent and there is no history of gradually increasing orthopnoea or exertional dyspnoea.In clinical practice patients will often have features of chronic systolic failure and present acutely with sudden dramatic APO suggesting diastolic heart failure. The patient is severely dyspnoeic and on examination is severely tachypnoeic, tachycardic, hypertensive and hypoxic. They appear sweaty, “gray”, sitting up and are often drowsy. On auscultation bilateral moist crepitations are present. In some patients “wheezes” may be heard, a presentation referred to as cardiac asthma. This may result in misdiagnosis but is easily confirmed by a clinical picture indicating heart failure and a CXR showing interstitial and alveolar oedema.*
Acute Decompensation Heart Failure - Acute Pulmonary Oedema
GENERAL
Life threatening condition, adopt an emergency approach to management, investigation and treatment occur side by side. Low threshold for code blue, assemble MDT - cardiologist, experienced nurses. A-E approach
- A/B - Sit uprifght, SpO2 + RR - supplemental O2 via CPAP if SpO2 < 94
- CPAP increases intrathoracic pressure reducing cardiac preload and afterload
- CPAP maintains the patency of the fluid-filled alveoli preventing them from collapsing during exhalation. As a consequence, the patient saves the energy spent trying to reopen collapsed alveoli reducing workload and improving pulmonary air exchange, oxygenation and reducing respiratory distress
- CPAP results in a (beneficial) redistribution of lung fluid resulting in removal of fluid from alveoli and contributing to improved oxygenation*
- C - BP + HR 2 x IV access sites +/- invasive BP monitoring (in setting of post-MI)
- VBG/ABG, Troponins, FBC, UEC, LFT,
- IV GTN
- ?IV Frusemide - no if no perioheral oedema
- ?IV Morphine - not always because it may lead to deterioration
- Monitor CO via IDC, Artline, CVL
- Low threshold for IV Dobutamine in cardiogenic shock, with systolic failure
- D - GCS score. Documentation and Disposition (Tertiary Care centre, CCU/ICU/HDU
- E - Expose/Examine. History for symptoms of Haemodynamic compromise. Exam for haemodynamic compromise - APO, JVP, Confusion. Heart sounds, peripheral circulation ?cardiogenic shock)
Further Invx
SPECIFIC
- Revert the Pulmonary Oedema
- IV Frusemide 20-80 mg with repeat dose in 20 minutes if necessary
- Avoid if patient is in APO due to isolated diastolic failure (cold and dry), since CO in diastolic failure is highly volume dependant.
- GTN SL/PO if SBP > 90mmHg OR IV Glyceryl Trinitrate 10microgram/minute if SBP >100 - 30mg (6 ml) of GTN in 94 mls of 0.9% NaCl @ 2ml/hour (10 µg/min) increase by 2-4mL/hr every five minutes. SBP > 90mmHg
- Low doses => venodilatation and reduced preload (reduce pulmonary interstitial oedema)
- Higher doses => veno+vaso dilatation and reduced afterload
- Consider IV dobutamine 2.5-15 micrograms - if non-responsive pulmonary oedema with hypotension. It's an ionotropic medicine which increases cardiac output and serves to counter falling blood pressure due to heart failure
- Symptom Relief - SoB and pain
- CPAP starting at 5cm of water pressure -
- IV Morphine 1-2.5mg
- MONITOR
- Constant Vitals, SpO2 +/- invasive monitoring if blood pressure
- Urine Output
-
L.M.N.O.P
-
ANP & BNP: Prognosis
- *Myocardial Stretch Atrial natriuretic peptide is a hormone released by the atria when the myocardium is stretched. If homogenised and injected into rats, it promotes diuresis through sodium loss (natriuretic). BNP (brain natriuretic peptide - first isolated from pig brains), is released from the ventricles when stretched.
- eGFR, Sodium excretion, Smooth muscle relaxation - There role in homeostasis is to counteract fluid overload and prevent associated decompensation by increasing eGFR, increasing sodium secretion and venodilation. This collectively reduces both preload and afterload
- These natriuretic peptides are also released by tachycardia, glucocorticoid release and thyroid hormones
UTILITY
- Diagnosis - a reliable biomarker for heart failure (Sensitivity 90% Specificity 80-90%). BNP>100nd/L is consistent with heart failure, whilst BNP<50nd/L suggests dyspnoea due to another cause
- Less reliable as a measure to diagnose RHF or diastolic dysfunction. More reliable for LHF and systolic function
- Prognosis - the higher the BNP the higher the cardiovascular and all-cause mortality and the higher the likelhood of sudden death
- Independant of age, NYHA classification, or ejection fraction
- Pt with controlled symtpoms but high BNP would benefit from "aggressive treatment"
-
Obstetric History?
HTN conditions during pregnancy predispose to HF in adult life
- Check obstetric history for such events
Epidemiology
- 1-2% - of Adult population is effected in developed countries
- Elderly >10% - 1 in 10 are affected over the age of 70
- 1/6 Presentations amongst >65yo involved HF - breathlessness on exertion
- M>F - lifetime risk of 33% (M) vs 28% (W)
- 2-3 x commoner in Aboriginals
Peripheral Vascular Disease
Angiosomes
Temporal Classification
Chronic
- Slow/progressive onset of peripheral vasculopathy
Signs & Symptoms
Variable depending on underlying pathology
- Colour
- Dependant rubor
- Elevated Pallor
- Impaired Wound Healing
- Ischaemia - Intermittent claudication
- Cramping due to disparity in vascular perfusion and metabolic demand - release of anaerobic metabolites like adenosine = PAIN
- Pain on elevation - elevation increases challenges to perfusion => tissue hypoxia
Arterial
- Lower Limb - aortico-iliac, femoral popliteal, or calf vessel levels
- Singular or combinatorial vessel involvement
Contributing Mechanisms
- Dyslipidaemia - hypercholesterolaemia and dietary factors
- Inflammatory and Immunologic Factors
- Hypertension
- Haemodynamic Instability - points of abnormal flow, endothelial injury etc.
Lifestyle Factors
- Diabetes Mellitus
- +obesity,
- sedentary lifestyle
- Tobacco Smoking
- +FHx
Pathology
- Most Commonly - Progressive Vessel Occlusion due to atherogenesis
Classification
-
Fontaine Classification of Lower Limb Ischaemia
- Grade I- asymptomatic
- Grade II - Intermittent claudication\
- Grade III - Rest Pain
- Grade IV - Ulcers/Gangrene
III/IV = critical limb ichaemia
-
Pathology
- Neuroischaemic Pathology - Combination of Ischaemia and Neuropathy
Aortic Aneurysm
Defintion - 1.5xsize of undilated blood vessel
- Clinical Features - asymptomatic and 40% detected incidentally
Predisposing Factors
Protective Factors
Diabetes
- ?Diabetes - seems to be protective against AAA, though uncertain if this is because of;
- Pathogenesis of Diabetes itself
- The off-target effects of Diabetic Drugs
- Matrix Metalloporteinases - one of the two seem to influence the matrix metalloproteinases and protect against dilation
Anatomical Classification
AAA
- Infra-Renal (95%) - 1cm distal to renal arteries (leaves space for the neck)
- 15% extend down involving origins of iliac arteries
- Supra-Renal (5%) - slightly more complicated since they often involve renal arteries
Surgical Indications for AAA
- RATE OF EPXANSION >5mm in 6months or >10mm in 1 year
- DILATION > 5cm (or 1.5 x vessel size)
RoR - 1% risk of rupture each year if 4-5.4cm
Indications for Early Intervention?
- No indications - Intervening before 5cm in one group and then waiting to intervene at 5cm in the other, showed that neither option reduced long term mortality
Law of Laplace
As vessel increases in diameter, the force acting onwards reduces and the aneurysm continues to expand until rupture
Management
Aggressive risk factor modification
- Smoking cessation
- Blood pressure management - reduce systolic
- Treat underlying causes (M.I.C.T.) - mycotic infection, inflammatory process, congenital defect, trauma
Method of Surgical Intervention
- Endovascular Aneurysm Repair - using catheter to insert stent
- Open Endarterectomy - open surgery with inlay of synthetic graft
- 1 more item...
Thrombosis of Aorta
- Inflammatory - Sign of significant inflammatory processes, which may be systemic
Venous
- Symptomatic Chronic Venous Insufficiency = Post-phlebitic Syndrome
-
-
Acute
- Acute on Chronic - Most common seen in practice as an acute complication of a chronic condition
- Thromboembolism from Atherosclerotic plaque rupture
Venous
- Oedema
- Induration
- Post-phlebitic Syndrome
DVT
Aetiopathogenesis
Perturbances to Virchow's Triad
- Abnormalities in the Endothelium
- Abnormalities in Blood Flow
- Abnormalities of coagulation - namely hypercoagulable proclivity/propensity
-
-
Clinical Features
- Cramping Pain - worse on extension
- Oedematous Limb - visible swelling
- Discolouration
- Paralysis
Investigations
- ABCDE
- Hist+Exam -
- BEDSIDE
- LAB: Coag profile, U/E, FBC (exclude Cellulitis with WCC) CRP, +/- d-dimer
- IMAGE: Dopplersound USS
- if detected, requires follow up ultrasound
Management
PHARMACOLOGICAL
- Symptom Relief
- Reverse Reversible
- LMWH until resolved
- Presence of predisposing factors may warrant continued anti-coagulation, commence on DOAC
NON-PHARMACOLOGICAL
- Compression stockings (acute)
- Lifestyle modification - long journeys +8h then stand up and move legs
- Avoid HRT
- 1 more item...
Arterial
Pathogenesis
- Medial Degeneration + Hypertension
- CT disorder - marfan's, ehlers-danlos
- Elderly degenerartion
Clinical Features
- Excruciating Tearing Pain
- Hypotensive collapse
- Sudden Death - exsanguination, cardiac tamponade
Stanford Type A
"Ascending aorta
- Debakey I - ascending and descending
- Debakey II - ascending aorta only
Investigations
- LAB - Group and Hold, Coag Profile, FBC, U/E
- Imaging - CXR, CTAngiogram or transoesophageal Echo
Management
- Emergency Surgery - patient at risk of sudden death from cardiac tamponade
- Optimising Cardiovascular Physiology
- Obtain 10u of Cross-matched Blood
- SBP ~ 100-110 mmHg
- B-Blockers so HR<60 (Labetalol, esmolol) or Calcium Channels Blockers if BB's are contraindicated
- IV GTN infusion - once rate is controlled to HR<60 to ensure that vasodilation doesn't allow heart to pump more forcefully and extend the dissection
- Risk Factor Modification
- Lifelong Surveillance
Standord Type B
"Beyond ascending aorta
- Debakey III - descending aorta
Conservative Treatment
- treat underlying risk factors (hypertension)
Investigations
- LAB - Group and Hold, Coag Profile, FBC, U/E
- Imaging - CXR, CTAngiogram or transoesophageal Echo
Management
- Optimising Cardiovascular Physiology
- Obtain 10u of Cross-matched Blood
- SBP ~ 100-110 mmHg
- B-Blockers (Labetalol, esmolol) or Calcium Channels Blockers if BB's are contraindicated
- IV GTN infusion - once rate is controlled to HR<60 to ensure that vasodilation doesn't allow heart to pump more forcefully and extend the dissection
- Risk Factor Modification
- Lifelong Surveillance *
Clinical Correlation
Nature of pain - tearing pain, interscapular, migrating (suggests extension of dissection), diaphoresis, nausea, vomiting (SNS tone due to pain
Additional Symptoms dependant on which branches of the carotid ae compromised
- Syncope, AMS, focal neuro deficits, hemiplegia - involvement of the carotid arteries
- Paraplegia - ischaemia of spinal cord (compromised anterior spinal artery)
- Unequal Arm Pressures - if dissected after brachiocephalic
- Acute Limb Ischaemia
- Anuria - renal artery comrpomise
- Cardiac Tamponade - signs of cardiac tamponade (Beck's Triad - JVP, reduced heart sounds and hypotension)
Embolism
Pathophysiology
- ATRIAL FIBRILLATION - abnormal blood flow (turbulence) provoking thrombosis
- Thromboembolism - occludes distant blood vessel
- Acute Peripheral Vasculopathy - atheroembolism
-
Acute Compartment Syndrome
PATHOGENESIS
- Isovolumetric swelling - Swelling of a tissue within a fixed enclosed space (fascia/epimysium), leading to compression of supplying blood vessels
- Ischaemia, Infarction, Necrosis - Compromised perfusion will cause ishcaemia, infarction, necrosis
EFFECT OF SYSTEMIC BLOOD PRESSURE
- PRINCIPLE - Perfusion and Blood Pressure - tissues will continue to be perfused, so long as a pressure gradient exists, such that internal tissue pressure within the compartment is less than systemic circulating pressure
- Anoxia 10-30 mmHg of Diastolic - muscle tissue anoxia transpires when compartment pressure rises to within 10-30mmHG of diastolic pressure
- HYPOTENSIVE Pt.: Correlation - the hypotensive patient will therefore have poorer physiological tolerance and will succumb to infarction in the events of acute compartment syndrome sooner than a normotensive pt.
Clinical Presentation
- Symptoms
- Excruciating pain
- Signs
- Tense + Shiny
- Pulselessness
- Tender to passive movement
- Erythema
- Oedema
- P - arasthesia - present first since swelling causes compression of nerves
- P - ain
- P - allor
- P - aralysis (i.e. loss of function
- P - poikilothermia
- P - ulselessness*
Aetiology
Traumatic (w/o fracture)
- External Constriction - Constrictive bandages, splints, or casts (usually circumferential)
-
- Injection - High-pressure injection
- Vascular Injury - Injury to vascular structures
- Wound/Injury - Animal bites and stings
- Burns - Severe thermal burns
- Direct Trauma - Forceful direct trauma to a tissue compartment (eg, crush injury)
Non-Traumatic
- Hematologic: ischemia-reperfusion injury, thrombosis, bleeding disorders, vascular disease, spontaneous hemorrhage
-
- Nephrotic syndrome (or other conditions that decrease serum osmolarity)
- Toxic: animal envenomations and bites; injection of recreational drugs
- IV fluids - extravasation of fluid (transudate or exudate); massive fluid resuscitation (eg, severe thermal burns, sepsis)
- Revascularization procedures or treatments (eg, extremity bypass surgery, embolectomy, thrombolysis)
- Infection - Group A streptococcus infections of muscle; systemic inflammatory response
-
Severed/Ruptured Artery
Internal or External Bleeding
- Internal - ruptured aneurysm => haematoma formation
- External - injury sustained with clear evidence of laceration
-
-
-
Hypertension
- Hypertension >140/90 on two separate occasions - yet ideal if blood pressure is sweet is below 120/90
- At risk = vasculopathy, diabetics, connective tissue
- Hypertensive Urgency - severe blood pressure elevations (>180/110mmg)
- Hypertensive Emergency - occurs when blood pressure is exceedingly high (>220/140mmHg)
- with clinical and investigative findings of end-organ dysfunction,
- Myocardial Ishcaemi/APO - chest pain, shortness of breath, palpitations
- Hypertensive Encephalopathy/SAH - confusion sudden headache, nausea, vomiting, neurological deficits,
- Aortic Dissection - severe back/chest pain
Aetiolgical Classification
- In all HTN patients ask about snoring and possible symptoms of OSA
Primary (Idiopathic/Essential) Hypertension - 95%
- 20-50 - Onset between age 20 and 50.
- FHx - Positive family history.
- Nill Scndry - No features of secondary hypertension.
Features
- Longstanding - three readings before diagnosis
- Uncontrolled
- Drug-withdrawal
Secondary Hypertension - 5%
Triggers for investigation
- Precocious or <20 OR >50 - Onset age <20 or > 50 years.
- Nil FHx - No family history.
- Precipitous Increase - Hypertensive urgency.
- Refractory - Resistant hypertension.
Investigation
- ABCDE - vitals
- History + Exam
- Waist circumference (M<94, W<80)
- BEDISDE -
- BSL,
- ECG
- UA (kidney dysfunction
- Weight
- LAB
- H: FBC,
- B: UEC (ACR), lipid profile, hb1Ac, TFT, morning Cortisol, 24hr urine cortisol or dexamethasone suppresion, metanephrines (breakdown of catecholamines = NA/A for phaeochromocytoma), Renin:aldosterone ratio (investigating for specific Cons causes if suspected)
- IMAGE - looking for cause
- SPECIAL
- Echocardiogram
- Sleep studies for OSH/A
Causes - R.E.M.E. "Remy"
- Renal Parenchymal Disease
- Chronic Kidney Disease
- Glomerulonephritis
- AKI
- Macro-vascular Disease
- Congenital - Fibromuscular Dysplasia
- Atheromatous Stenosis - uni/bi-lateral renal artery stenosis
Examination
- Renal Artery Bruits - renal hypoperfusion can cause secondary hypertension as the R.A.A.S. interprets reduced kidney blood flow as a sign of systemic hypovolaemia. Retentin of salt and water will exacerbate hypertension
Exogenous
- CS - corticosteroids
- Pill - Oral contraceptive pill
- Stimulants - cocaine, meth
- Oddities - black licorice
- sodium and water retention, hypokalaemia, distrubed R.A.A.S. and resultant hypertension
- Meds - NSAID's, withdrawla of Betablocker, ACE =. hypertensive crisis
Endocrine
- Hypercortisolism (XS GC's - Cushing syndrome/disease
- UEC reveal Hyperkalemia with thiazode diuretics
- Hyperaldosteronism - Conn's syndrome/disease
- UEC reveal Hyperkalemia on thiazide diuretics
- Phaeochromocytoma - catecholamin XS
- Paroxysmal sweating, palpitations, anxiety
- Prior to surgery they want the patient to be completely adrenergic block, so much so that they check for nasal congestion
- Hyperthyroidism - systolic hypertension, thyrotoxicosis
- Hypothyroidism - diastolic hypertension
- Pregnancy - gestational hypertension and potential pre-eclampsia
Examination
- Striae - amongst other things, striae may indicate Cushing's syndrome/disease as a secondary cause for hypertension
Mechanical
- Obstructive Sleep Apnoea - relaxation and subsq. narrowing of the throat, interupting breathing, MORNING HEADACHES
- Nocturnal Hypertension - OSA episodes produce surges in systolic and diastolic pressure that keep mean blood pressure levels elevated at night and in some cases throughout day
- Aortic Coarctation - narrowing of the aorta with idiopathic causes
- Raised ICP evoking Cushing's Reflex - hypertension and bradycardia
Mislabelled Hypertension
Repeatedly normal blood pressure when taken at home/work/amubulatory monitor
Mislabelled
- White-coat Hypertension
- Masked Hypertension
Complications
Wherever/whenever you find hypertension, look for end organ damage (renal and cardiac changes - most sensitive organs)
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Retinopathy
- Haemorrhage and Oedema - small blood vessels prone to rupture => haemorrhage or intersitial oedema
Examination
- Arteriovenous nicking - indicates mild hypertensive retinopathy. Evidence of end organ damage secondary to hypertension. This microangipathic process will be occurring elsewhere
PATHOPHYSIOLOGY
- Hylani/Hyperplastic Arteioloscleoris
- Organ Ischaemi, Atrophyand Necrosis
- Glomeruloscleorosis and Tubulo/Interstitial sclerosis/fibrosis
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Anti-Hypotensive Agents (Vasopressors)
- Dopamine
- Adrenaline
- Noradrenaline
- Metaraminol
- Dobutamine
-
INVESTIGATIONS
- ABCDE - vitals
- History + Exam
- Waist circumference (M<94, W<80)
- BEDISDE -
- BSL,
- ECG
- UA (kidney dysfunction
- LAB
- H: FBC,
- B: UEC (ACR), lipid profile, hb1Ac, TFT, morning Cortisol, metanephrines (breakdown of NA/A), Renin & aldosterone (investigating for specific endocrine causes if suspected)
- IMAGE - looking for cause
- SPECIAL
CHRONIC Management
TARGETS
- 140/90 < e-HTN w/o comorbidities - aim for less than 140 in pts without cardiovascular disease
- 130/85 < e-HTN w/ comorbidities (e.g. T2DM) aim for less than 130 for essential hypertensive patients with concurrent cardiovascular conditions
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When to Prescribe Anti-hypertensives
OUTDATED, RECENTLY UPDATED 2023
CHRONIC Management
- Non-pharmacological for 3 months
- Mediterranean diet (included two vegetarian meals a week, those that they like)
- Vegetarians are right, vegans have gone too far, but take home is that pure meat eaters will die earlier than vegos
- Fruit and veg, high fibre, low saturated fats, reduce sugar and salt wherever can, nuts and avocados.
- weight loss (5%)
- Exercise (30 mins 5 per weekly) - develop the concept of athlete, any is better than none
- "I want you to do an extra 30 mins of cardio a week, what are the chances, out of 10 of that happening? - when they get to 7/10 you've won
- smoking cessation,
- alcohol reduction
- Pharmacological -
- <55yrs A or D - ACE-i/ARB or Thiazide
- RAAS system is more Active/Responsive
- >55yr C or D - Ca2+ or Thiazide
- DM - always ACE-i/ARB
- African Ethnicity - Ca2+ any age
BLOOD PRESSURE MONITORING
- Blood pressure measurement at home
- U/E tests at weeks 1+2 post starting pharmacotherapy - ACE-i + ARBs reduce kidney function, slightly, than it imporves
- Waist measurements
- Regular lipid profiling
- Check for postural hypotension
Pharmacotherapy for CHRONIC Management
Increase dose every three months
- A - start low and go slow to avoid encountering nasty side-effects
- A+C or A+D - Choose a second line that suits patient. I.e. Diabetes = calcium channel blockers, Fluid overloaded = thiazide diuretic
- A+C+D
- A+B+C+D
- If resistant to all four, load up the anti-hypertensives at night time (has best outcome for patient and prevents adverse outcomes)
Timing of pharmacotherapy
- Morning or night - get them to take it at the same time as their other medications (more likely to remember)
- Once or twice a day? - To increase effect rather than loading them up at once
- A = RAAS inhibitor ACE-i/ARB
- B = beta-blocker
- C = calcium channel blocker
- D = diuretic (thiazide or thiazide like diuretic)
Cardioselective Ca Channel Blocker (Verapamil) PLUS Betablocker (Metoprolol tartate) = Additive Myocardial Depressant
- Be cautious about using beta-blockers and cardioselective calcium channel blockers
ACE-i
S/E - skin rash, angioedema, irritating cough, allergies, hypotension, renal injury
ACUTE Management of Hypertension
The need for medical intervntion in cases of hypertension is determined by the threat of end-organ dysfunction, not the absolute BP level.
Priority is to exclude end-organ injury
Assessment
SUBJECTIVE
- BEFORE seeing patient
- Vitals - trending vitals - what is BP now and what has it been
- Reason for Admission + PMHx
- PREGNANT - Pre-eclampsia (3g >Urine, LFT, FBC, G+H)
- Medicines - MAOI antidepressrent? Missed anti-hypertensive
- WHEN seeing patient
- Symptoms of End Organ Dysfunction
- Myocardial Ischaemia/APO - chest pain, shortness of breath, palpitations
- Hypertensive Encephalopathy/SAH - sudden headache, confusion, nausea, vomiting
- Aortic Dissection - severe chest/back pain, focal motor/sensory deficits
- AKI - Acute oliguria
- PRIORITISATION
- Asymptomatic hypertension (i.e. hypertensive urgency, does not need to be assessed immediately, BP can be brought under control over hours. If symptomatic, needs urgent attention
OBJECTIVE
- A - maintaining airway
- B - RATES
- Auscultate the lung bases, check for acute pulomary oedema
- Supplemental O2 >94%
- C - BP (Botyh arms), HR (bradycardia - cushings reflec), ECG, Heart sounds, rhythm, CRT, peripheries, JVP
- 2 x IV cannulae (FBC, UEC, LFT, B-hCG
- D - GCS, PEARL, BSL
- E
- Neuro - clonus, hyperreflexia
- F - further investigations
- UA (protein, haem, B-hCG), CXR
Hypertensive Urgency
- Repeat BP in 10 minutes - allow time for spontaneous resolution before instituting medical management
- Resume prescribed anti-hypertensive - reasonable if they usually take anti-HTN but had a dose withheld - provided there are no contraindications
MEDICAL PTS
For patients w/o regular BP lowering medicines, or who have had a missed/withheld dose and are still hypertensive
- ANTI-HYPERTENSIVE - Slow drop
- PO Amlodopine 5mg 2hrly max 15mg - amlodopine has a delayed onset of action, do not give repeated doses
- Top GTN Patch 5mg/24hr or 10mg/24hr - if NBM
- ANTI-HYPERTENSIVE - Rapid (2-3hr drop). Useful if patient is symptomatic or at risk of hypertensive emergency (coagulopathy, kidney impairment, pregnancy)
- PO Nifedipine 10mg - pregnancy
- PO Clonidine 25micrograms-50 - central acting anti-hypertensive (alpha2-adrenergic receptors)
- PO Captopril 12.5mg - AVOID ACE-i ARB unless Renal Fxn known to be adequeate
Also option of just resuming their prescribed medications, especially if the reason for hypertension is due to poor adherence
ICU PTS
SBP, not MAP increases risk of bleeding at surgical site
- <24hrs - IV Anti-Hypertensive - no reliable PO absorption in first 24hrs
- HEARTS < 120-130mmHg: IVI GTN infusion (
- Remaining < 140-150mmHG: IV Hydralazine Bolus (5mg per 15min up to 30mg, half dose if elderly and frail) OR If hypertensive and agitated IV Clonidine Bolus 25mcg-50mcg per 15min up to 300micg, avoidif HR<50), OR if tachycardic and hypertensive IV Metoprolol Bolus (2.5mg-5mg, up to 20mg)
- >24hr - PO Anti-hypertensive, unless C/I
- HEARTS < 130-140mmHg
- REMAINING < 160mmHg
- PO Amlodopine 5mg 2hrly max 15mg - SLOW drop OR
- PO Prazocin 1mg 2hrly Max 6mg - FAST drop
Hypertensive Emergency - Initiated by Senior
- ANTI-HYPERTENSIVE - BOLUS
- IV bolus hydralazine 5mg - repeat every minute as required, maximum of30mg
- IV bolus metoprolol tartrate 1mg
- ANTI-HYPERTENSIVE - Infusion
- IV sodium nitroprusside 0.3microgram
- IV esmolol 500micrograms
- IV GTN 10 micrograms
Targeted Investigations
- Diagnosis
- Serial BP measurements in clinic (>3)
- Home blood pressure measurements
- Assess overal risk
- Fasting BSL
- Serum cholesterol
- Severity of Disease - end organ dysfunction
- ECG/Echo - ?LVH
- UA - protein/blood
- Optometry - posterior segment examination for retinopathy
- Secondary Causes
- UEC (hypokalaemia in Conn's) CMP (Hypercalcaemia in hyperparathyroidism)
- Renal artery USS - renal artery stenosis
- Urinary free cortisol (Cushing), 24hr urinary meta-adnrenaline (phaeochromocytoma)
- Renin:aldogsterone
- MRI aorta (coarctation)
Calcium Score
- Low-Risk - Measure if pt posses CD risk factors but doesn't clear yet have CVD
- Some evidence to suggest that calcium score above 100 warrants primary prevention with antiplatelet (PO 100mg OD) + further investigatoin with stress test
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SCREENING
NAHF - recommend screening for AF in all individuals aged over 65 via palpation of radial pulse + ECG
TACHYCARDIA
- Sinus Tachycardia
- Supraventricular Tachycardia - atrial Fibrillation, Atrial flutter AVRT, AVNRT
(Regularly Irregular) TachyArrhythmias
- Sinus Tachycardia
- Supraventricular Tachycardia - atrial tachycardia (e.g. atrial ectopics, AVNRT, AVRT)
- Atrial flutter - once diagnosed managed as per AFib.
Investigations
- ABCDE - vital obs
- History - Ask them to tap it out (regular, irregular,, fast, slow)
- EXAM
- BEDSIDE: ECG (WPW short pr interval; long QT), Blood glucose
- LAB: FBC, TFT's, U&E's (Ca2+, Mg2+,
- IMAGE:
- SPECIAL
- Echocardiogram (TOE, TTE)
- Electrophysiologicla studies
Management of Acute Palpitations/Tachycardia
A-E Assessment
- A - speaking in full sentences, check airway, sit up
- B: HR, SpO2 + Supplemental O2 to saturate circulating blood
- C: HR, BP +12ECG (provide diagnosis), though also feel pulse
- 2 x IV access - +/- VBG, Troponin, FBC, UEC, CRP, LFT, TFT
- D: GCS - document, consider disposition
- E: T - expose for secondary survey, history, examine + further investigation and specific management
Cardiovascular Compromise/Haemodynamic Instability
- Chest Pain
- Hypotension <90mmHg
- Signs of Heart Failure
- syncope, altered mental state, pulmonary oedema, peripheral oedema
DC Cardioversion
- IF TIME - can give anxiolytic (IM midazolam <5mg, 40microg Fentanyl) prior to reduce anxiety and sedate (amnestic)
Kids 1-4 joules per kg-
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Bradyarrhthmias
Investigate Causes
Heart rate stuck in a DICH it's low
- Drugs - cardio selective calcium channel blockers + beta-blockers
- Glucagon + High dose insulin (1u/kg/hr) + High concentration IVI dextrose + IVI potassium + electrolytes*
- ICP - rasied intracranial pressure
- CAD - ischaemic heart disease
- Other infiltrative myocardial disease
- H - hypothyroidism
- Hypothermia -
- E - yperkalaemia - elongated PR interval and other electrolyte disturbances
- S - Neurogenic Shock
Management
Haemodynamically Stable
TREATMENT OR NOT
- Asymptomatic + (BP > 90 & HR >40) = Prepare but seek confirmation from Consultant before treating
- Asymptomatic + (BP < 90 & HR < 40) = Prepare and administer
Acute Management
Asymptomatic Bradyarrhythmia is a potentially life threatening condition, an emergency approach to management whereby investigation of an underlying cause and treatment occurs concurrently. Request review by cardiologist. A-E approach to management
- A - maintain a patent airway
- B assist with breathing, oxygen if required (Monitor with SpO2%)
- C - monitor heart with 12 lead ECG, monitor BP, establish IV, prepare for transcutaneous pacing
- 2 x IV access - VBG, Trop, FBC, UEC, TFT
- If symptomatic, whilst IV access is being acquired - Passive Leg Raise -(PLR) - Raise legs returns 200-300mL of blood
- Prepare transcutaneous pacing
- D - GCS, PEARL, BSL/Ketones, Document (R/V medicines), Dispositions
R/V medications
CHRONOTROPIC PHARMACOTHERAPIES
PREPARE
- Transcutaneous Pacing - whil awaiting transvenous pacing, use sedation
- Rapid Bolus Atropine (One vial IV 0.5 mg) - able to repeat 3 times, typically used if increased parasympathetic drive thought to be the cause
- Useful for sinus bradycardia, AV node block
- Adrenaline (IV 2-10 mcg/min) - may be used if atropine ineffective and as an alternative to isoprenaline if BP is < 80
- Alternative: IV Isoprenaline 5mcg/min
Complications
- Prolonged QT interval => Torsades de Pointes => Malignant Arrythmia
DEFINITIVE Management
- Reverse Reversible
- Permanent implantable pacemaker
Haemodynamically Unstable
- Symptoms: chest pain, syncope, shortness of breath
- Signs: hypotensive, stigmata of M/I, syncope/AMS, acute pulmonary oedema
Acute management
- A - maintain a patent airway
- B assist with breathing, oxygen if required (Monitor with SpO2%)
- C - monitor heart with 12 lead ECG, monitor BP, establish IV, prepare for transcutaneous pacing
- D - GCS, PEARL, BSL/Ketones, Document (R/V medicines), Dispositions
R/V medications
INTERVENE
- Pacemaker - transcutaneous (PADS) => transvenous
- INDICATIONS: (1) Stigmata of 2nd Degree + History of Syncope OR (2) Third degree Heart Block
- Rapid Bolus Atropine (IV 0.5mg) - reduces PSNS tone
- Chemical Pacing - Isoprenaline (IV 5mcg/min) - titrated to effect
- Adrenaline 2-10mcg/min - as an alternative to isoprenaline if BP is < 80
Complications
- Prolonged QT interval => Torsades de Pointes => Malignant Arrythmia
DEFINITIVE Management
- Reverse Reversible
- Permanent implantable pacemaker
Adrenaline Infusion
- Preparation: 6 mg (6 ampoules of 1:1000 Adrenaline) in 100 ml Normal Saline
- Concentration : The above mixture gives a concentration of 60 microgram / ml
- Infusion rate : 2 – 20 microgram / min (equivalent to an infusion rate of 2 – 20 ml/hr)
(Irregularly Irregular) Atrial Fibrillation
OR(Regularly Irregular) Atrial Flutter (Managed as SVT with valsalva to help diagnose, then treated similarly to AFib.)
Typically caused by atrial dilatation, disturbing conduction pathways, leading to ectopics and then full blown fibrillation
Atrial flutter maximum heart rate is 150BPM, rate does not go wuicker then this because the AV node slows down electricla transmission. If the rate is 300BPM, then it's 1:1 Atrial flutter with an accessory pathway present
Stable
ACUTE Management
- Rate control - indicated if over 110, aim for 80 bpm. -VE Ionotropy, avoid give if symptoms or signs of haemodynamic instability
- Rate Control - Beta-blockers: metoprolol (PO) OR atenolol (PO) | Ca-blockers: Diltiazem (PO) Verapamil (PO) | amiodarone (lipophilic, high load with long half life)
- IV Magnesium Sulphate - possible alleviation of symptoms
- Rhythm Control = Cardioversion - pursue for highly symptomatic and young individuals
- AC 3/52 - Requires anticoagulant for 3/52 pre/post cardioversion
- AF<48hrs candidate for conversion (pharm/electric) as thromboembolic risk is low.
- AF>48hrs requires TOE to exclude atrial thrombus or anticoagulant for 3 weeks
- DC CARDIOVERSION
- Defibrillator with sedation and enoxaparin/clexane AC
- Pharmacological cardioversion
- Flecainide - sodium channel blockers
- Amiodarone 300mg loading dose (leave for a cardiologist) + 900mg over next 24h
- Sotolol - higher risk of long QT
- Anti-coagulation (AF/thromboembolic stroke >>>>bleeding stroke) - reduces risk of stroke by 66%
- DOAC - for non-valvular (non-mitral stenosis or prosthetic valve
- Dabigatran, Rivoroxiban
- REQUIRES at LEAST ANNUAL UEC, LFT - and follow up 7 days post commence to check for signs of bleeding
- Valvular = Warfarin - mod-severe mitral stenosis or valve replacement requires warfarin
- Mitigate Risk in perceived high risk - educate bleeding reduce alcohol related falls, avoid NSAIDs, treat GORD etc with PPI
CHRONIC Management
- Rate Control (HR <90 though tolerate <110 if asymptomatic and rate is limiting discharge - older people beta blocker | calcium channel
- Rhythm Control - more appropriate for SYMPTOMATIC and young patients (40yo) without structural heart disease since older people more likely to have structural defects and less likely to remain in sinus rhythm
- Chemical rhythm control or electrophysiological ablation
- Anti-coagulation - weigh CHADS2 VASC vs HAS-BLED. If CHADS2 VASC > 0, AC should be strongly considered
- Risk of ischaemic stroke is an order of magnitude greater than haemorrhagic stroke. Anti-coagulation saves more lives through prevention of ischaemic stroke than non coagulation has saved from haemorrhagic stroke.
- Look at HAS-BLED as modifiable risk factors that should be acted upon in order to reduced risk of anti-coagulation
Lifestyle
SNAPI + OSA - associated with paroxysmal AF
Further Investigaition
- Consider Catheter Ablation - The National Heart Foundation of Australia has four recommendations regarding catheter ablation for AF:
- The primary indication for catheter ablation of AF is the presence of symptomatic AF that is refractory or intolerant to at least one Class 1 or Class 3 anti-arrhythmic medicine.
- In selecting patients for catheter ablation of AF, consideration should be given to the patient's age, duration of AF, left atrial size and the presence of significant structural heart disease. Best results are obtained in younger patients with paroxysmal AF and without structural heart disease or marked atrial enlargement.
- Discontinuation of warfarin or equivalent therapies is not considered a sole indication for this procedure.
- After ablation of AF, anticoagulation therapy is generally recommended for all patients for at least 1 to 3 months. Discontinuation of warfarin or equivalent therapies after ablation is generally not recommended in patients who have a CHADS2 score of ≥ 2.
- Most patients will manage their AF with pharmacological intervention. Patients who undergo catheter ablation require anticoagulation before and after the procedure. Repeat ablation is required in about 20%-30% of patients within the first 12 months, as it is hard to achieve full-thickness, complete and permanent lesions.*
Pacemaker & Implantable Defibrillator
- Pacemaker - Pacemaker for brady AF patients
- Defibrillator - Reserved for malignant ventricular arrhythmia* - dc defibrillation is unpleasant therefore we would only offer it to a patient if they were unconscious
- VF patients - implantable cardiac defibrillator
- Unstable AF - implantable cardiac defibrillator
Unstable
Consider immediate Electric cardioversion
- Rate Control - to buy time
- Digoxin - if patient is hypotensive
- Metoprolol or verapimil if patient is normotensive? avoid if hypotensive since these are -ve ionotropes and they will reduced cardiac output
- Enoxaparin/Clexane - anticoagulated prior to procedure
- May require sedation
- DC Cardioversion
-
Inbvestigations
- BEDSIDE
- LAB
- FBC
- UEC (Mg, Ca), Metanephrines, BHcG
- IMAGE
- SPECIAL
- Echocardiogram
Counselling patients
- Heart has four chambers, the atria sit above the ventricles
- AF is when the atria don't contract in a coordinated fashion, instead of contracting in the same way you'd squeeze a tube of toothpast, they "quiver" and don't propel blood properly into ventricles
-
Circulatory Shock
Distributive Shock
Anaphylaxis
Differentials
- Vasovagal - difference being heart rate
- Asthma attack - difference being singular system involvement
- SEPSIS - difference being absence of fever in anaphylaxis
Weird and Wacky DDx
- Carcinoid Carcinomatosis
- Phaeochromocytoma
- Hereditary Angioedema
- Systemic mastocytosis
Aetiopathogenesis
- Type 1 Hypersensitivity reaction - release of histamines and other inflammatory mediators (Histamine, Bradykinin, Platelet Activating factor, Heparin, Protease and Leukotrienes) in response to non-pathogenic allergen
- Anaphylactoid Reaction - inflammatory mediators causing shock, not involving allergen
- Non-Immune Anaphylaxis / Anaphylactoid Reactions - non-immunologically mediated anaphylaxis certain drugs, contrasts, exercise, cold temperatures which cause direct activation of effector cells (Mast Cells, Neutrophils, Basophils, Platelets) without allergen
- Summation Anaphylaxis - combination of allergen and indirect anaphylactoid element are both needed to cause anaphylaxis (e.g. peanuts alone not causative, exercise alone not causative, peanuts PLUS exercise = anaphylaxis)
Clinical Presentations
- Skin Features + Severe System Features - Acute onset illness with typical skin features PLUS either +/- respiratory symptoms +/- cardiovascular symptoms, +/- severe gastrointestinal symptoms
- Swelling of mouth to lungs => Difficulty breathing, speaking
- Systemic Features +/- Skin Features - Acute onset of hypotension, bronchospasm or URT obstruction where anaphylaxis is possible, +/- typical skin features
Differential Diagnosis
- Idiopathic urticaria/angioedema
- Sepsis
- Flushing syndromes - alcohol, red-man syndrome, carcinoid syndrome
Assessment
- A - stridor, oropharyngeal oedema, hoarsness of voice (laryngeal oedema)
- Early Intubation - low-threshold for early intubation if evidence of threatened airway
- Stridor +/- Adrenaline Neb (5mg of 1:1000) - if stridor post IM adrenaline, consider nebulised adrenaline
- B - RATES - RR (tachypnoea), Ascul (wheeze). trach, effort (resp distress), saturation (hypoxic)
- Sit up
- Supplemental O2 - 10-15L non-rebreather
- Wheeze +/- Salbutamol Neb 2 x 5mg
- C - peripheral temp, pulse (R,C,V), c-CRT, HR, BP, 12LECG
- Reduced cerebral perfusion - lie down, passive leg raise
- 2 x IVA large bore (VBG, FBC, UEC, LFT, CRP, 3 x Mast Cell tryptase (ASAP, 1-2hr post, 24hr post)
- 500mL Boluses CSL/Colloid
- IM Adrenaline 0.5mg - 5 minutely - consider IVI after 2 doses without adequate response
- <6yrs = 0.15mg
- 6-12yrs = 0.3mg
- +12yrs = 0.5mg
- PO Pred 50mg or IV Hydrocortisone 100-200mg - prevents/shortens protracted reaction
- SPEC CVC +/- IVI inotrope, vasopressors - IVI Adrenaline (1) 1mg/1000mL at 5mL/k/hr or if IVI pump 2) 6mg/100mL at 2-20mL/hr)IV / IM Glucagon (1 - 2 mg) should be considered if patient is on ß-Blockers. Selective vasoconstrictors : Metaraminol (2 - 10 mg) or Vasopressin (10 - 40 units) may be used in adults with persistent hypotensio*
- D - GCS/AVPU, BSL, Doc, Disp
- 4hr monitoring last adren
- Biphasic possible
- E - Temp, expose
SubAcute
- Monitor 4hrs post last adrenaline of symptoms, provided asymptomatic
- Admit for >12hr monitoring if; concerned for rebound symptom
- Evidence of Biphasic - Further treatment is required within 4 hours of last adrenaline administration (biphasic or prolonged reaction)
- Thought to be due to re-exposure of the immune system to residual allergen (Gut, Airway, Skin etc)
- Hx Biphasic - Previous history of biphasic reaction
- RF for Biphasic - Poorly controlled asthma
- Isolated/Inaccessbile - The child lives in an isolated location with delay to emergency services
- Anaphylaxis to monoclonal antibody
Consider
- Chlorphenamine (10mg IV) - antihistamine (avoid in acute setting, since 1st gen antihistamines (IV prep) can worsen hypotension, and 2nd Gen are only available PO, which is inappropriate.
- PO Prednisone/Dexamethasone - immunosuppressant
Discharge
- Arrange specialist review
- Determine likely trigger and wear bracelet
- Patient Education + Communication of issue to family, work/school
- Anaphylaxis action plan (ASCIA) - EPIPEN use, sit down, need for ambulance
- Avoidance of triggers
-
Adrenaline Infusion
- Preparation: 6 mg (6 ampoules of 1:1000 Adrenaline) in 100 ml Normal Saline
- Concentration : The above mixture gives a concentration of 60 microgram / ml
- Infusion rate : 2 – 20 microgram / min (equivalent to an infusion rate of 2 – 20 ml/hr)
Heart Inflammation
Inflammation of the pericardium (outermosts layer of the heart)
Aetiology
- Vascular - Recent M/I (Dressler's syndrome)
- Infecion/Iatrogenic - Viral Illness or Vaccination
- Trauma
- A/Inflammatory Disease - RA, Immune related event from immunotherapy
- Metabolic - uraemia
- Idiopathic
- Neoplasia - Malignancy
Clinical Features
- Chest pain
- Radiates to back, alleviated by leaning forwards, sharp and worse with deep inspiration
- Healthy Individual
- Recent viral illness/vaccination
- Recent M/I - Dressler's syndrome
Investigation
- BEDSIDE
- ECG - supportive in 60% of cases
- Widespread ST segment changes due to involvement of the epicardium or of the myocardium in myopericarditis
- IMAGE
- SPECIAL
- Echocardiogram - exclude effusion, tamponade
Management
- Managed by Cardiologist
Medical
- Up to 3/12 of PO Colchicine 500micrograms OD or BD - PLUS 2/52 either of;
- PO Ibuprofen 600mg TDS
- PO Aspirin 750-1000mg
- PO Pantoprazole 40mg OD for duration of NSAID
- Non-Pharm - no physical exertion or significant exercise for 3-6 months
Factors for Admission
F, R, E, T, IS - Anti-coagulation
- Fever > 38
- Sub-acute onset
- Refractory ymptoms after 1 week of thereapy
- Effusion - Evidence of a large effusion or tamponade
- Evidence of Myopericarditis - myocardial inflammation and pericardial infllamtion
- Trauma
- ImmunoSuppresion
- Oral Anti-coagulant therapy
Dianostic Criteria
Requires at least two of the following
- Chest pain - sharp, pleuritic, improved in sitting up/leaning forward
- Pericardial rub
- ECG changes - mild sinus tachycardia, widespread concave ST elevation (not in blood vessel distribution), widespread PR depression (esp Lead II)
- Pericardial effusion - usually small (Echo, CXR, CT
Beck's Triad => Cardiac Tamponade Complication
- Low blood pressure
- Distended jugular veins
- Muffled or diminished heart sounds on auscultation
Clinical Definition: Fever + New murmur = Infective Endocarditis
Classification
- ACUTE - rapid development of infective + heart failure symptoms. Tends to occur on "normal valves". Common culprits are S.aureus
- CHRONIC - subacute development of heart failure symptoms. Tends to be on "abnormal" or prosthetic valves
Aetiology
RISK FACTORS
- Nosocomial: IVC, Haemodialysis Skin breaches, immunosuppression
- Community: IVDU, renal failure, diabetes, valvulopathy, especially Right Heart, any anatomical deformity/vulnerability of the heart (VSD, PDA)
MICROBIOLOGY
Transient bacteraemia occurs all the time. ABx prophylaxis during dental procedures is therefore unhelpful
- Common: Strep. viridans, S.aureus and Strep bovis (colonoscopy), CRC?)
- Uncommon: HACEK gram -ve bacteria (haemophilus, actinobacillus, cardiobacterium, eigniella, kingella), diptheroids, chlamydia,
INFLAMMATORY
- SLE (Libmann-Sacks endocarditis)
Pathophysiology
Clinical Features
- INFECTIVE FEATURES
- Fevers, rigours
- Malaise, anorexia
- Weight loss
- Splenomegaly
- Clubbing
- CARDIAC LESION
- New murmur
- LHF/RHF
- Prolonged PR interval
- IMMUNE COMPLEX DEPSOITION
- Vasculitis
- Glomerulonephritis (Microscopic Haematuria)
- Acute Kidney Injury
- Splinter haemorrhages
- Osler nodes (painful pulp infarcts in extremitis)
- EMBOLIC PHENOMENA
- End-organ abscess
- Skin embolisms = Janeway Lesions: non-painful palmar/plantar macules
Investigation
- BEDSIDE
- LAB
- Blood cultures x 3 (different sites, different times)
- VBG, FBC, CRP, UEC, Mg, LFT, ?Procalcitonin
- IMAGE
- SPECIAL
Management
Involve ID, Cardiology and Cardiothoracics
- Non-Operative
- Treat SEPSIS: IV ABx, IVH, IDC, Supp O2, Inotropes, Vasopressors
- Operative (Source control): intractable heart failure, valvular obstruction, unstable prosthesis, myocardial abscess
Diagnosis
2 major criteria or 1 major and 3 minor criteria or all 5 minor criteria
MAJOR
- Positive Blood Culture
- Typical organisms in 2 separate blood culture
- Persistently positive blood cultures 3>12hrs apart
- Positive culture for Coxiella burnetii
- Endocardium Involvement
- Positive echocardiogram
- Abnormal activity of PET/CT
- Abnormal valvular anaotmy on cardiac CT
MINOR
- Predisposition (Valve prosthesis, IVDU)
- Infective Features: Fever > 38C
- Immunological Phenomena (Glomerulonephritis, Osler Nodes etc)
- Embolic Phenomena (end-organ abscess, janeway lesions)
- Positive blood cultures that do not meet major criteria
Aetiology
- Idiopathic (50%)
- Infectious -
- Viral - enteroviruses, adenovirus, EBV, CMV, Hepatitis, HSV, HIV, Influenza, mumps
- Bacterial - staph, strep, clostridia, diptheria, TB, meningococcous, psittococis, brucellosis
- Spirochaetes - leptospirosis, lyme's disease, syphillis
- Protozoa - Chagas', leishmania, toxoplasmosis
- Toxins - cocaine, lithium, lead, alcohol arsenic
- Immunological - SLE, Kawasaki's, Scleroderma, heart transplant rejection
Clinical Features
- ACS-like
- Heart failure syndrome
- Palpitations
- Features of underlying aetiology
Investigations
- BEDSIDE
- ECG
- LAB
- Troponin, FBC, UEC, CRP, ESR, +/- LFT,
- Viral serology, bacterial serolgy
- Image
- SPECIAL
- Echo: Regional wall abnormalities
- Endomyocardial wall bipsy
Management
- Supportive
- Treat Arrythmia
- Treat Heart Failure
3. Anti-coagulate, reperfuse, reduce cardiac effort
ACUTE MANAGEMENT
- Anti-coagulation - 30 mins post reperfusion
- Anticoagulants + anti-platelets - aspirin (330mg) + ADP-R antagonist (clopidogrel (300mg), ticagrelor (180mg))
- Hold off on DAPT until after they've been to cath lab
- Speak with Cardiologist WHETHER Enoxaparin (30mg)/Heparin (5000IU) - protect against further thrombosis
- Cardiologist Chooses - if for PCI promptly then heparin (shortern half life, easier to reverse, though more difficult to reach therapeutic window (needs 6hrly APTT, if delay then enoxiparin (quicker therapeutic, though longer half life and more difficult to reverse0
- Analgaesia
- Morphine - analgesia + cardiosuppression
- Pain increases heart rate and therefore increases metabolic demands of strained heart. Take away pain prevents raised HR
- Also has beneficial SE of cardiosuppresion
- Reperfusion
- Nitrates - SL GTN vs IVI GTN infusion (30mg/6mL GTN in 94mL 0.9% NaCl at 1mL/hr - induce vasodilation and improve perfusion also offers effective analgaesia
- C/I in RHF - since nitrates are a powerful venodilator. This will diminish preload, thereby reducing perfusion and exacerbating ishcaemia
- Optimise Physiology
- PO Atorvostatin 80mg STAT - modulates inflammatory response, improve lipid profile (which is elevated by cardiac injury). stabilises thrombolytic plaque and improves endothelial function
- Oxygen - only if required to maintain at saturation at 94%. Caution is recommended
Further Investigation
- BEDSIDE
- Serial ECGs
- Serial troponins
- LAB
- IMAGE
- CXR - assess complications and exclude other diagnoses (aortic dissection)
- Echocardiogram - looking for dyskinesis, akinesis
- Coronary CTa - Conduct invasive Angiography for Risk Stratification
Secondary Management
Post reperfusion
- CCU ~ 2 days
- Step down cardio ward - for further monitoring
- Can't Drive w/ private licensed for 2 weeks after STEMI - check fitness to drive
PHARMACOTHERAPY
- Anti-platelet therapy
- Aspirin (Life)
- Dual Antiplatelet Therapy (12 months) - ticagrelor/clopidogrel
- ACE-i/ARB (Life)
- Statin (Life) - (anti-cholesterol + anti-inflammatory)
- Beta-Blocker (12 months)
- GTN Infusion - Recurrent Pain - these patients are very high risk for recurrent ACS and complications
- 30mg (6mL) GTN to 94mL/100mL NS. Give at 1mL/hr and titrate up every 3-5 minutes until pain relieved.
NON-PHARMACOTHERAPY
- Cardiac Action Plan
- Echocardiogram - 3 months post + annual thereafter
- Cardiac rehabilitation Program - comprehensive program that improves life outcomes
- Dietary Lifestyle changes - food, physical exercise, smoking cessation
- Seasonal immunisations
- Psychotherapy at 3 months - most people are in depressive episode
SURGICAL
- Angioplasty and stent insertion
- Coronary artery bypass graft
Complications (80-85%)
DARTH VADER
- Death - 15%
- Arrhythmia - Malignant Arrythmia
- Rupture of Cardiac tissue
- Tamponade
- Heart Failure
- Valvular Disease
- Aneurysm
- Dressler's Syndrome - autoimmune pericarditis (2-10 weeks post ACS)
- Simple pericarditis (2-4 days post ACS) is more common than DS
- Embolism pulmonary - site of infarcted heart creates a nidus for thrombosis, embolism and pulmonary embolism
- Reinfarction
5 Most Important (Ma.R.Cs Pe.Ct), In order of occurrence
- Malignant Arrhythmia - ventricular fibrillation, ventricular tachycardia
- Rupture of cardiac tissue - papillary muscle rupture, ventricular septum rupture
- Cardiogenic Shock - Failure - reduced cardiac outpute
- Pulmonary Embolism - site of infarction becomes a nidus for thrombosis and subsequent embolism owing to the resulting endothelial injury
- Cardiac Tamponade - rupture of the ventricles with blood haemorrhaging into the pericardial sac
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Aetiology
- HF = 2ry to underlying cardiopathology - heart failure is not diagnosis. It represents the final event of a diseases' pathological timeline
- Cause?? - One needs to deduce what the underlying cause of HF is
Ischaemic Causes
Angina
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Acute Coronary Syndrom
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Myocardial Infarction
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Of course, these diseases are linked
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Non-Ischaemic Causes
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Functional
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Extra Cardiac
Chronic Obstructive Pulmonary Disorder
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