Foundations - Module 1 PDF

**[Foundations]** **[MODULE 1]** **[Hypertension]** **[Definition]** - BP \> 140/90 mmHg - **[White coat hypertension]** = BP reading at healthcare setting is higher than at home - **[Isolated systolic hypertension]** = reflects high pulse pressure (with relatively low DBP) -...

**[Foundations]** **[MODULE 1]** **[Hypertension]** **[Definition]** - BP \> 140/90 mmHg - **[White coat hypertension]** = BP reading at healthcare setting is higher than at home - **[Isolated systolic hypertension]** = reflects high pulse pressure (with relatively low DBP) - Seen in aged + stiff arteries **[Predispositions]** - Coronary heart disease - Stroke - Cardiac hypertrophy - Heart failure - Kidney failure **[Group of factors leading to high BP]** - Primary hypertension - Polygenic - Sympathetic hyperactivity - Renin activation - Susceptibility to salt - Multi-environmental - Obesity - Excess salt (especially in elderly) - Alcohol - Secondary hypertension - In 5% specific cause is identified - Renal disease - Renal artery stenosis - Adrenal tumours secreting - Aldosterone - Cortisol - Catecholamines - Sleep apnoea **[History]** - Family history - Past coronary or cerebrovascular events - HF symptoms - Renal disease symptoms - Smoking - Diabetes - High cholesterol **[Examination]** - BP - Pulse rate/rhythm - Weight + height (BMI) - Cardiovascular exam - Fundal inspection - Renal mass or bruits - Stigmata of secondary causes **[Routine tests]** - Plasma K+ and creatinine - High in renal disease - Low K in aldosteronism - Fasting glucose - Associated glucose tolerance - Fasting lipids - Associated CV risk - UEC (urea, electrolytes, creatinine) = good test for kidney things - FBE - Associated anaemia of CKD - LFTs - Fatty liver disease - Drug reaction - Urine albumin/creatinine ratio - Renal damage - MSU (midstream urine) - Renal disease - ECG + echocardiogram - Coronary disease - Cardiac hypertrophy **[When to treat BP]** - SBP \> 160 mmHg - DBP \> 100 mmHg - SBP ? 160 mmHg + DBP \< 70 mmHg **[High CV risk]** - \>15% CV event risk over 5y (NHF) - Standard risk factors: - Age - Systolic BP - Total:HDL cholesterol ratio - Smoking - Diabetes **[High CV risk by end organ damage]** - Microalbuminuria (increase in albumin in urine) or low eGFR - Renal damage - LV hypertrophy - Cardiac damage - High pulse wave velocity (measurement of **[arterial stiffness]**) - Stiff large arteries - Increased **[intima-media thickness]** - Atherosclerosis **[Non-pharmalogical treatment]** - Lose weight - Improve fitness - Avoid excess salt - Moderate alcohol - Stop smoking **[Drug treatment ("A B C D")]** - ACEi, ARBs - Beta blockers - Ca antagonists - Diuretics **[Drug treatment algorithm]** - Step 1 = A + C + D - Step 2 = (A + C), (A + D) - Step 3 = A + C + D **[Step 1 considerations]** - A = Preferred step 1 if \< 55 years - B = Not preferred because of side effects of increased weight and insulin resistance - Beta-blockers, particularly non-selective ones (e.g., propranolol), can block beta-2 adrenergic receptors in the pancreas, which are involved in the regulation of insulin release - ↓ insulin release ↑ higher blood glucose insulin resistance - C = preferred step 1 if \> 55 years or black - D = useful step if there is fluid retention **[General considerations]** - A = useful in coronary disease and HF + renoprotective in diabetes + **[contraindicated in pregnancy]** - B = useful in coronary disease + HF - C = avoid **verapamil** + **diltiazem** in HF - D = **[Thiazide]**-like drugs have less metabolic side effects - NOTE: most important cause of "resistant HTN" = poor compliance - **Resistant HTN** = higher BP despite taking multiple medications **[Step 4]** - **"Resistant HTN"** - Consider adding: - **Spironolactone** - **Beta blocker** - **Centrally-acting agent** - **Alpha-blocker** - **Vasodilator** - Question compliance - Check for use of [NSAIDs, cold remedies, antidepressants, etc.] - Consider secondary causes **[IHD]** **[Definition]** - Symptoms of acute myocardial ischemia - New ischemic ECG changes - Development of **[pathological Q waves]** - Loss of viable myocardium or new regional wall motion abnormality - Identification of coronary thrombus by **angiography** (medical imaging) including intracoronary imaging or by autopsy 1. Spontaneous MI 2. Supply/demand mismatch 3. Suspected MI-related death 4. **[PCI]** related MI - **[Percutaneous Coronary Intervention (PCI)]** is a [non-surgical procedure] used to treat narrowing or blockage of the coronary arteries of the heart - PCI is commonly known as angioplasty, often involving the placement of a stent to keep the artery open - While PCI is effective in restoring blood flow and alleviating symptoms of coronary artery disease, it carries risks, including the possibility of myocardial infarction (MI) induced by the procedure (via plaque or thrombus disruption) 5. Stent thrombosis 6. **[CABGS-related]** (coronary bypass to restore bloody supply) **[Definition of acute coronary syndrome]** - Caused by coronary thrombosis in association with ruptured atherosclerotic plaque - Causes acute narrowing or occlusion of coronary artery (pain due to acute decreased myocardial O2 supply) - Clinically this presents as either: - ST elevation MI (STEMI) - Non-ST elevation MI (NSTEMI) - Unstable angina - Sudden cardiac death - **Troponin = very sensitive** **[Subendocardial infarct]**  - 1^st^ area affected = inner 1/3 of myocardium (since it's the farthest coronary artery + last area to receive blood) subject to higher pressure inside heart - If blockage suddenly lysis or break down and blood flow returns, sometimes patient's damage will be limited to inner 1/3 **subendocardial infarct** - Can be caused by: - Hypotension - Atherosclerosis - **ECG = ST segment depression [NSTEMI] (non-ST segment elevation MI)** **[Transmural infarct]** - After about 3-6 hours however, zone of necrosis extends through entire wall thickness **transmural infarct** - **ECG = ST-segment elevation STEMI (ST segment elevation MI)** **[Risk factors]** - Age - Family history of IHD - Obesity - Sedentary lifestyle - Smoking history - Hypercholesterolaemia - Hypertension - Diabetes **[Symptoms]** - Ischaemic chest pain - Non-typical from shoulder and neck also possible - SOB - Palpitations - Syncope - Lethargy  **[Gender]** - Female sex more common - More women to experience non-chest pain symptoms - Women x2 as likely to experience microvascular angina as men - Women more likely to experience non-obstructive causes of acute coronary syndrome than men - E.g. spontaneous coronary artery dissection or Takotsubo cardiomyopathy **[Treatments]**   **[Preferred strategy]** - **[Primary percutaneous intervention (PCI)] generally preferred to [fibrinolysis ]**   **[Adjunctive therapies in acute MI]** - O2 - IV morphine (**pain relief)** - Aspirin - IV heparin or s/c clexane (**anti-platelet**) - IV GTN (nitrate) - Additional antiplatelet agents - Clopidogrel (P2Y12 antagonist) - Prasugrel (P2Y12 antagonist) - Ticagrelor (P2Y12 antagonist) **[Beta blockers + ACEi]** - Beta blockers administered following acute MI reduces mortality - Most effective in those patients with reduced LV function acute coronary syndrome or when administered in 1^st^ 12 months following acute coronary syndrome - **[ACEi]** started within 24 hours to 16 days following acute MI improves left ventricular EJ fraction and reduces mortality - EXTRA: **[CK (creatine kinase)]** rise may indicate there is early reperfusion if CK rise is small - DO NOT rely on CK - **Half-life is shorter than troponin which is better if a pt is getting another AMI**     **[Post-hospital management of AMI]** - Modify lifestyle - No regular exercise: aim to walk daily for \>20 mins - Smoking history: aim to cut down/cut out smoking - Unhealthy diet: aim to eat fresh fruit and vegetables - Overweight/obese: target weight +- waist circumference goals - Alcohol excess: cut down/cut out alcohol - Life stressors: identify and reduce if possible - Modify cardiac risk factors - Diabetes: management plan - Hypercholesterolemia: aim total cholesterol \< 4.0 mmol/l + LDL \< 1.8 mmol/l for secondary prevention - HTN: salt restriction + weight reduction - Medications - Ensure range of medications used for IHD are instituted and tolerated - Ensure role of each drug is explained to patient to improve compliance - Review medication chart at each review  **[Cardiac failure]** **[Definition]** - CO less than body needs - Due to reduced CO - Rarely due to increased body needs - High output HF e.g. due to thyrotoxicosis and fistula - Usually due to reduced systolic function - Low ejection fraction (HFrEF) - May be due to stiff diastolic function - Normal ejection fraction (HFpEF)   **[Forces across capillaries]** - Fluid leaks in or out according to balance of forces - Tends [out] at **arterial** end - Tends [in] at **venous** end - Excess fluid removed by lymphatics - Increases in VENOUS pressure causes fluid to leak out and oedema **[Causes of oedema]** - Increased **[venous]** pressure - HF - Decreased osmotic pressure - Plasma protein loss: renal or liver failure (hypoalbuminaemia) - Increased capillary permeability - Infection - Blocked lymphatics - Cancer **[Oedema]** - Increased **[pulmonary]** venous pressure (LA) - Causes pulmonary "congestion" and oedema - Left HF - Increased **[systemic]** venous pressure (RA) - Causes peripheral "congestion" and oedema - Right HF - NOTE: high **venous** pressures, not arterial pressures  - With systolic HF, the curve shift downwards - For the same ventricular end diastolic pressure, there is decreased CO - To maintain same CO, a **[high EDP]** is required which may be achieved by fluid-retention pulmonary oedema  **[Cardiac failure fluid retention]** - Decreased CO Decreased renal blood flow activation of RAAS - Aldosterone - Fluid - Na+ retention - K+ loss - Vasoconstriction **[Cardiac failure (SNS)]** - SNS stimulated - Increased NA and HR - Initial increased contractility - Long-term deleterious effect - Vasoconstriction (RAAS-induced) - Ventricular arrhythmias - Direct toxic effect - Hence use **[beta blockers]** **[Does this patient have cardiac failure?]** - History - SOB - On exertion - On lying down orthopnoea - Swollen ankles **[SOB]** - Can be due to: - Cardiac - Respiratory - Anaemia - Poor fitness - Orthopnoea is more specific for cardiac failure, though not entirely - Why? - Fluid shifts from extra thoracic regions like lower extremities causing **[increased venous return]** - Heart cannot cope and back pressure - May also occur in: - Asthma - Ascites - GORD **[Examination]** - Crackles (creps) on chest examination - Could be cardiac failure or respiratory cause - JVP elevated - Indicates high RA (and so RVED) pressure - Often correlates with high LA (and LVED) pressure - Oedema - With high JVP causes other than cardiac failure are unlikely (e.g. low protein) **[Investigations]** - Chest x-ray - Heart size - Lung fields - Cardiomegaly - Interstitial oedema - Pleural effusion - Echocardiogram - Chamber size, function - Valves - Structure - Wall thickness - Systolic and diastolic function - Septal defects **[Cardiac failure causes]** - Ischemic heart disease: - MI infarct - Ischemic cardiomyopathy - Valvular heart disease - Hypertensive heart disease - Congenital heart disease - Cardiomyopathy - Cor pulmonale (right heart) - **Pericardial disease** **[What is the cause of this patient's HF?]** - History - Previous myocardial infarct(s) or angina, PCI, CABG - PHx rheumatic fever valve defect - Known murmur valve defect - PHx hypertension degree of control - PHx congenital heart defect - Possible causes of cardiomyopathy - Alcohol, meth - Cytotoxic drugs (especially chemotherapy) - PHx lung disease - Asthma - COPD - Cystic fibrosis - Pulmonary fibrosis - Examination - BP - Pulse -- rate, rhythm - Rapid AF may cause HF or be result of HF - JVP - Cardiac murmurs - Chest - Oedema - DVT - PE **[JVP and HF]** - Usually increased JVP correlates with increased pulmonary venous pressure - i.e. left + right HF - Can the JVP be elevated but the pulmonary venous pressure be normal? - **i.e. pure right HF** **[Right HF causes]** - Pulmonary HTN - Cor pulmonale: HF due to lung disease - E.g. COPD, cystic fibrosis, pulmonary fibrosis - Pulmonary embolism - Right sided structural disease - **Pulmonary or tricuspid valves** - R ventricular cardiomyopathy - Pericardial disease - Affects right before left because the right operates at lower pressure and therefore is more affected by intrapericardial pressure **[Left HF]** - SOB is cardinal symptom - Lung creps are cardinal sign - CXR will show fluid overload - Echo is diagnostic showing reduced left ventricular function - Low ejection fraction - 40-50% mild - 30-40% moderate - \ - Infarct-related scar - Chronic HTN - Ventricular hypertrophy - Infiltrative cardiomyopathies - Mechanism is still high LVEDP -- high LA and PV pressures **[Why is this patient more SOB now?]** - New myocardial infarct or ischemia - New arrhythmia especially AF - Fluid overload - Drinking more or renal failure - Change in drugs - Reduced diuretic dose - Started a new drug causing fluid retention - Poor BP control - Anaemia - Thyrotoxicosis - Infection esp. pneumonia - Pulmonary embolus **[Patient diagnosis (4 key parts) ]** - Is it HF? What type? - What is the underlying cause? - What is the precipitating cause of this episode? - What other problems are there? - Cardiac: ischemia, arrhythmias - Other: anaemia, iron deficiency, renal failure, electrolytes, liver **[Principles of treatment of HF]** - Reduce venous pressure - Relieves congestion and oedema - But without reducing CO too much - Block RAAS - Produces long-term fluid loss and vasodilation - Block SNS (beta) - Block direct toxic effect of beta stimulation - Treat underlying and precipitating causes  **[Treatment of cardiac failure]** - Diuretics -- furosemide - Aldosterone antagonists -- spironolactone - ACE inhibitors -- ramipril - Angiotensin receptor antagonists -- irbesartan - Beta blockers -- carvedilol - Angiotensin receptor -- neprilysin inhibitors (ARNi) - Sacubitril/valsartan (Entresto) **[Additional treatment]** - Biventricular pacing -- cardiac resynchronisation - Improves cardiac function - Synchronises left and right ventricles - Implantable cardioverter defibrillator - Because **[ventricular arrhythmias and sudden death are common in HF]** - Cardiac assist devices and transplantation - For a small group who do not respond to other treatment