Cardiovascular system Flashcards

Question

atrial flutter,

Answer 1

A supraventricular tachyarrhythmia usually caused by a single macroreentrant rhythm within the atria that is classically characterized on ECG by the sawtooth appearance of P waves, also known as "flutter waves", with narrow QRS complexes. Atrial flutter is another type of commonly seen supraventricular tachyarrhythmia that is usually caused by a single macroreentrant rhythm within the atria. The risk factors for atrial flutter are similar to those of Afib. In atrial flutter, the atrial rate is slower than in Afib and the ventricular rhythm is usually regular. Treatment is similar to that of Afib, consisting of anticoagulation and strategies to control heart rate and rhythm. Atrial flutter frequently degenerates into atrial fibrillation. Epidemiology Incidence: 88 per 100,000 person-years (increases with age) Sex: ♂ > ♀ (5:2) Etiology: similar to atrial fibrillation (see “Etiology” above) Pathophysiology Type I (common; typical or isthmus-dependent flutter): caused by a counterclockwise (more common) or clockwise (less common) macroreentrant activation of cardiac muscle fibers in the right atrium that travels along the tricuspid annulus and passes through the cavotricuspid isthmus Type II (rare, atypical atrial flutter): various reentrant rhythms that do not involve the cardio-tricuspid isthmus, are not well defined, and/or occur in the left atrium Clinical features Most patients are asymptomatic Less commonly, symptoms of arrhythmias such as palpitations, dizziness, syncope, fatigue, and or dyspnea Symptoms of the underlying disease (e.g., murmurs of mitral stenosis) Tachycardia with a regular pulse Diagnostics: similar to atrial fibrillation; see “Diagnostics” above Sawtooth appearance of P waves: identical flutter waves (F waves) that occur in sequence at a rate of ∼ 300 bpm Regular, narrow QRS complexes The rhythm may be: Regularly irregular if atrial flutter occurs with a variable AV block occurring in a fixed pattern (2:1 or 4:1) Irregularly irregular with a variable block occurring in a nonfixed pattern Treatment: similar to atrial fibrillation (see “Therapy” below) Complications Frequently degenerates into atrial fibrillation (see “Clinical features” above) 1:1 conduction leading to life-threatening ventricular tachycardia.

Answer 2

Atrioventricular (AV) block (often referred to as “heart block) involves the partial or complete interruption of impulse transmission from the atria to the ventricles. This interruption of impulse transmission results in characteristic ECG findings that different depending on the sub-type of AV block. The commonest cause of AV block overall is idiopathic fibrosis and sclerosis of the conduction system. Any patient presenting with possible AV block would require a number of investigations to identify possible underlying causes including: ``` ECG – to help determine the subtype of AV block Blood tests (e.g. FBC, U&Es, TSH, Troponin) – to rule out underlying causes Echocardiogram – to rule out structural heart disease. Some forms of AV block can be managed conservatively, whereas other sub-types require intervention. ``` ``` Different types of blocks include: First-degree AV block Second-degree AV block (type 1) Second-degree AV block (type 2) Third-degree (complete) AV block ```

Answer 3

Third-degree (complete) AV block occurs when there is no electrical communication between the atria and ventricles due to a complete failure of conduction.4 Typical ECG findings include the presence of P waves and QRS complexes that have no association with each other, due to the atria and ventricles functioning independently. Cardiac function is maintained by a junctional or ventricular pacemaker.4 Narrow-complex escape rhythms (QRS complexes of <0.12 seconds duration) originate above the bifurcation of the bundle of His. A typical heart rate would be >40bpm. Broad-complex escape rhythms (QRS complexes >0.12 seconds duration) originate from below the bifurcation of the bundle of His. These escape rhythms produce slower, less reliable heart rates and more significant clinical features (e.g. heart failure, syncope).

Answer 4

``` Congenital: Structural heart disease (e.g transposition of the great vessels) Autoimmune (e.g maternal SLE) Idiopathic fibrosis: Lev’s disease (fibrosis of the distal His-Purkinje system in the elderly) Lenegre’s disease (fibrosis of the proximal His-Purkinje system in younger individuals) Ischaemic heart disease: Myocardial infarction Ischaemic cardiomyopathy Non-ischaemic heart disease: Calcific aortic stenosis Idiopathic dilated cardiomyopathy Infiltrative disease (e.g sarcoidosis, amyloidosis) Iatrogenic: Post ablative therapies and pacemaker implantation Post cardiac surgery Drug-related: Digoxin Beta-blockers Calcium channel blockers Amiodarone Infections: Endocarditis Lyme disease Chagas’ disease Autoimmune conditions: SLE Rheumatoid arthritis Thyroid dysfunction ```

Answer 5

Rhythm: variable P wave: present but not associated with QRS complexes PR interval: absent (as there is atrioventricular dissociation) QRS complex: narrow (<0.12 seconds) or broad (>0.12 seconds) Depending on the site of the escape rhythm (see introduction). Clinical features History Palpitations Pre-syncope/syncope Confusion Shortness of breath (due to heart failure) Chest pain Sudden cardiac death Clinical examination Irregular pulse Profound bradycardia Haemodynamic compromise (e.g. prolonged capillary refill time and hypotension) Management Patients should be placed on a cardiac monitor Transcutaneous pacing/temporary pacing wire or isoprenaline infusion may be required Some rhythms (particularly narrow-complex escape rhythms) may respond to atropine A permanent pacemaker is generally required Complications Ventricular arrhythmias leading to sudden cardiac death.

Answer 6

``` Definition: Ventricular tachycardia (VT) is a potentially life-threatening arrhythmia originating in the cardiac ventricles. Usually, VT results from underlying cardiac diseases such as myocardial infarction or cardiomyopathy, but it can also be idiopathic or iatrogenic. Clinical manifestations range from palpitations and syncope to cardiogenic shock and sudden cardiac death. The characteristic ECG findings of VT are broad QRS complexes (> 120 ms) and tachycardia (> 120 bpm). In the acute setting, management of VT may require immediate cardioversion, defibrillation, or administration of antiarrhythmic drugs. Most patients who develop symptomatic, sustained VT require long-term antiarrhythmic therapy involving medication, intracardiac devices, or catheter ablation. ``` Aetiology: Cardiac scars (usually due to infarction; also iatrogenic, e.g., postoperative) Conduction disorders Drugs (e.g., digitalis, antiarrhythmics) Long-QT syndrome Congenital long-QT syndrome Acquired long-QT syndrome Drugs Antiarrhythmics Class Ia (e.g., quinidine, disopyramide) Class III (e.g., sotalol, amiodarone) Antibiotics (e.g., macrolides, fluoroquinolones) Antidepressants (most tricyclic and tetracyclic antidepressants, lithium) Antipsychotics (e.g., haloperidol) Anticonvulsants (fosphenytoin, felbamate) Electrolyte imbalances (hypokalemia, hypomagnesemia, hypocalcemia) Ischemic stroke or intracranial hemorrhage Endocrine disorders (e.g., hypothyroidism) Nutritional disorders (e.g., anorexia nervosa) In rare cases, VT can occur in healthy individuals. Pathophysiology: Monomorphic VT (all QRS complexes look similar) Increased automaticity Re-entry circuit Polymorphic VT (dissimilar QRS complexes): caused by abnormal ventricular repolarization (e.g., long QT syndrome, drug toxicity, electrolyte abnormalities) Decreased cardiac output: asynchronous atrial and ventricular beats + rapid ventricular rhythm → ↓ blood flow into the ventricle during diastole → ↓ CO → hemodynamic compromise → symptoms of syncope, MI, angina. ``` Clinical features: Often asymptomatic, especially if nonsustained Common symptoms of sustained VT include: Palpitations Hypotension Syncope In more severe cases: Chest pain/pressure (often in conjunction with MI) Cardiogenic shock Loss of consciousness Progression to ventricular fibrillation Sudden cardiac death. ``` Investigations: 3 or more consecutive premature ventricular beats (i.e., widened QRS) Heart rate > 120 bpm Duration Nonsustained: < 30 s Sustained: > 30 s Morphology Monomorphic: all QRS complexes look similar (identical origin) Polymorphic: QRS complexes are different (multiple origins) Other possible ECG findings AV-dissociation: no relationship between P waves and QRS complexes (in VT, ventricular rhythm is often faster than atrial rhythm) Fusion complex: atrial and ventricular impulses occur simultaneously Capture beats: Occasionally, a supraventricular impulse may reach AV node and produce a subsequent ventricular beat (similar to a beat in sinus rhythm). Other diagnostic tests Holter monitor: useful for diagnosing intermittent VT which may not be present on a single ECG Patient-activated (manual) event recorder Echocardiography: provides information about possible etiologies of VT (e.g. structural heart disease, prior MI) and is thus a useful tool for evaluation of VT. Differential diagnosis: Confirming the diagnosis of VT can be challenging and, in some cases, impossible. However, VT accounts for nearly 80% of wide-complex tachycardias. Supraventricular tachycardia with aberrancy (RBBB, LBBB, Wolff-Parkinson-White) It is important to make the distinction between SVT with aberrancy and VT because treatment of the two conditions differs and sometimes the wrong treatment can lead to hemodynamic instability (e.g., using AV-nodal blocking drugs in patient with VT). Signs and symptoms that suggest VT rather than SVT are: Age > 35 (high PPV) History of structural heart defects or past MI AV dissociation, fusion beats, and capture beats Signs and symptoms that suggest SVT with aberrancy rather than VT are: Bundle branch block on prior ECG History of SVT Evidence of WPW (e.g., delta wave) If there is any doubt regarding the diagnosis, assume VT rhythm and treat accordingly. Treatment: Initial therapy If patient is hemodynamically unstable (hypotension, loss of consciousness): VT with pulse → cardioversion VT without pulse → defibrillation See “Advanced cardiac life support” If patient is hemodynamically stable: Antiarrhythmics (typically lidocaine, procainamide, amiodarone) Cardioversion if medical therapy fails In all patients, look for and address possible causes of VT such as: Electrolyte abnormalities (e.g., hypokalemia) → correct any electrolyte imbalances Medication-induced QT prolongation → remove any offending medication, digoxin immune fab (fragment antigen-binding) for digoxin toxicity Long-term therapy Intracardiac devices (ICD) (most effective treatment for reducing mortality): indicated in case of VT that does not respond to therapy Catheter ablation Antiarrhythmics (usually class I or III).

Answer 7

Pulmonary oedema occurs when fluid accumulates in the parenchyma and air spaces in the lungs. It is most commonly caused by heart failure or fluid overload. ``` Clinical features: Symptoms MAIN SYMPTOM: SEVERE DYSPNEA Shortness of breath Respiratory distress Production of pink frothy sputum (haemoptysis) Signs Pallor Tachypnoea Decreased oxygen saturations Raised jugular venous pressure (JVP) Peripheral oedema. -their tactile fremitus is possibly increased, percussion dull, auscultation: fine or coarse crackles, depending on severity, no tracheal deviation. ``` You will come across acute left ventricular failure often during your medical jobs. This occurs when the left ventricle is unable to adequately move blood through the left side of the heart and out into the body. This causes a backlog of blood (like too many buses waiting to pick up people at a bus stop) that increases the amount of blood stuck in the left atrium, pulmonary veins and lungs. As the vessels in these areas are engorged with blood due to the increased volume and pressure they leak fluid and are unable to reabsorb fluid from the surrounding tissues. This causes pulmonary oedema, which is where the lung tissues and alveoli become full of interstitial fluid. This interferes with the normal gas exchange in the lungs, causing shortness of breath, oxygen desaturation and the other signs and symptoms. ``` Risk factors/triggers: Iatrogenic (e.g. aggressive IV fluids in frail elderly patient with impaired left ventricular function) Sepsis Myocardial Infarction Arrhythmias ``` ``` Management: Intravenous opiates (opiates such as morphine act as vasodilators but are not routinely recommended). ``` Non-Invasive Ventilation (NIV). Continuous Positive Airway Pressure (CPAP) involves using a tight fitting mask to forcefully blow air into their lungs. This helps to open the airways and alveoli to improve gas exchange. If NIV does not work they may need full intubation and ventilation. “Inotropes”, for example an infusion of noradrenalin. Inotropes strengthen the force of heart contractions and improve heart failure, however they need close titration and monitoring, so by this point you would need to send the patient to the local coronary care unit / high dependency unit / intensive care unit.

Answer 8

Pulmonary oedema: build up of fluid in lungs and airways e.g alveoli, and interstitium. Space is mostly filled with proteins, when it fills up with fluid, it can make it hard for oxygen to cross over from the alveoli into the capillary. This leaves the body hypoxic/deprived of oxygen. The two factors hydrostatic pressure and oncotic pressure oppose each other. Capillary permeability of pulmonary arteries also a factor. All 3 of these factors keep the lungs free of excess fluid,. The underlying cause of pulmonary oedema can be cardiogenic: it develops as a result of heart disease, or it can be non-cardiogenic: damage is to the pulmonary capillaries or alveoli. The most common cardiogenic cause is left sided heart failure. In this, the left ventricle becomes unhealthy and can't pump effectively. This means that blood starts to back up into the left atrium, and then the pulmonary veins and pulmonary capillaries. The extra blood in the pulmonary capillaries causes pulmonary hypertension which is an increase in the hydrostatic pressure of the pulmonary blood vessels. This pushes more fluid into the interstitial space of the lungs which leads to pulmonary oedema. Another cardiogenic cause is severe systemic hypertension, this is greater than 180 systolic and 110 diastolic. In this situation the left ventricle is healthy but can't effectively pump blood in a system with such a high afterload. Or under conditions with such high systemic pressures. This means that blood starts to back up in the left atrium, pulmonary veins and pulmonary capillaries.This ultimately then leads to pulmonary hypertension and pulmonary oedema. Non cardiogenic causes of pulmonary oedema include pulomnary infections, inhalation of toxic substances, and trauma to the chest. All of these can cause direct injury to the alveoli. If this happens there is usually an inflammatory process that makes nearby capillaries more permeable. As a result, proteins and fluid enter the interstitial space. Another cause is sepsis, A key difference is that sepsis is when inflammation happens throughout the body, rather than just in the lungs. So in addition to pulmonary oedema, sepsis can cause extra fluid in the interstitial space of fluids throughout the body. Another cause is having low oncotic pressure, this can result from not making enough proteins, such as albumin, due to malnutrition or from liver failure. Alternatively it can be due to losing protein too quickly, as in nephrotic syndrome. Regardless of the cause, low oncotic pressure causes fluid from capilliary to enter into the interstitial space of the body. In the lungs this results in pulmonary oedema. Pulmonary oedema now makes gas exchange difficult because oxygen and carbon dioxide have to diffuse through a wide layer of interstitial fluidm to get from alveoli to pulmonary capillary and vice versa. That journey CAN also take too long relative to blood moving through the lungs. tHIS MAKES IT hard to fully oxygenate the blood. Pulmonary oedema can lead to severe shortness of breath, and in left sided heart failure it can lead to orthopnea, which is when there is worse shortness of breath when lying flat. this happens because there is increased pulmonary congestion when lying down. In left sided ventricular heart failure, the pulmonary circulation is already overloaded, as a result the extrablood can't be pumped out efficiently, and it causes shortness of breath. This pumonary congestion and shortness of breath decrease when a person sits up. Diagnosis: made with a chest x-ray or a chest CT scan. This shows fluid in the interstitial space. Treatment for pulmonary oedema involves giving supplemental oxygen, other treatments are dependent on the underlying cause. If the cause is cardiogenic in nature then medications aimed at boosting hearts performance or lowering blood pressure can be helpful. If the cause is related to inflammation or low oncotic pressure, then managing that illness will help resolve the pulmonary oedema.

Answer 9

D: Hypertension is a common condition that affects one in every three adults in the United States. The AHA/ACC guidelines define it as a blood pressure of ≥ 130/80 mm Hg and by JNC 8 criteria as ≥ 140/90 mm Hg. Hypertension can be classified as either primary (essential) or secondary. Primary hypertension accounts for approx. 95% of cases of hypertension and has no detectable cause, whereas secondary hypertension is due to a specific underlying condition. R: Ddx: Typical underlying conditions include renal, endocrine, or vascular diseases (e.g., renal failure, primary hyperaldosteronism, or coarctation of the aorta). Hypertension: Diagnostic findings and underlying conditions: -Hypokalemia--> underlying condition: Conn syndrome, renal artery stenosis. -Metabolic alkalosis and increase aldosterone to renin ratio--> underlying condition Conn syndrome. -Difference in blood pressure: 1. In both arms: takayasu arteritis, aortic dissection, aortic arch syndrome, subclavian steal syndrome. 2. Of upper and lower limbs: coarctation of the aorta distal to the left subclavian artery. -Daytime sleepiness (Epworth scale, Berlin questionnaire), Nondipping (“Nondipping” is a term used to describe the failure of blood pressure to fall by 10% or more during sleep. Patients who show this pattern are often referred to as “nondippers.”) in 24-hour blood pressure monitoring: obstructive sleep apnea. -Increased 24-hour urinary metanephrines: pheochromocytoma. -Increase serum calcium, increase PTH level, decrease serum phosphates: hyperparathyroidism. -increase serum cortisol: excess of glucocorticoids (e.g Cushing syndrome). -Decrease TSH, increase free T4. E: Prevalence One in three adults in the US is affected. Prevalence increases with age (∼ 65% among those ≥ 60 years of age). African Americans are more commonly affected than Asian American or white individuals. 60–75% of obese and overweight patients are affected. Sex: ♂ > ♀ below age of 45; the sex ratio is almost balanced at > 45 years of age (i.e., after menopause) Most common risk factor for cardiovascular disease A: Primary (essential) hypertension No specific cause; multifactorial etiology including epigenetic/genetic and environmental factors Accounts for 85–95% of cases of hypertension in adults Accounts for 15–20% of cases of hypertension in children < 12 years of age Age at onset: 25–55 years (prevalence is increasing in adolescents) Risk factors Nonmodifiable risk factors Positive family history Ethnicity Advanced age Modifiable risk factors Obesity Diabetes Smoking, excessive alcohol or caffeine intake Diet high in sodium, low in potassium Physical inactivity Psychological stress Secondary hypertension Caused by an identifiable underlying condition Accounts for 5–15% of cases of hypertension in adults Accounts for 70–85% of cases of hypertension in children < 12 years of age Age at onset < 25 years or > 55 years Causes Endocrine hypertension Primary hyperaldosteronism (Conn syndrome): most common cause of secondary hypertension in adults Hypercortisolism (Cushing syndrome) Hyperthyroidism Pheochromocytoma Primary hyperparathyroidism Acromegaly Congenital adrenal hyperplasia Renal hypertension Renovascular hypertension (e.g., due to renal artery stenosis) Polycystic kidney disease (ADPKD) Renal failure (renal parenchymal hypertension) Glomerulonephritis Systemic lupus erythematosus Renal tumors Coarctation of the aorta Obstructive sleep apnea Medication: sympathomimetic drugs, corticosteroids, NSAIDs, oral contraceptives Recreational drug use: amphetamines, cocaine, phencyclidine Isolated systolic hypertension: See “subtypes and variants” below for details. RECENT can help you remember the causes of secondary hypertension: R = Renal (e.g., renal artery stenosis, glomerulonephritis), E = Endocrine (e.g., Cushing syndrome, hyperthyroidism, Conn syndrome), C = Coarctation of aorta, E = Estrogen (oral contraceptives), N = Neurologic (raised intracranial pressure, psychostimulants use), T = Treatment (e.g., glucocorticoids, NSAIDs). C: Clinically, hypertension is usually asymptomatic until organ damage occurs, which then commonly affects the brain, heart, kidneys, or eyes (e.g., retinopathy, myocardial infarction, stroke). Common early symptoms of hypertension include headache, dizziness, tinnitus, and chest discomfort. Hypertension is usually asymptomatic until: Complications of end-organ damage arise (see “Complications” below) Or an acute increase in blood pressure occurs (see hypertensive crisis below) Secondary hypertension usually manifests with symptoms of the underlying disease (e.g., abdominal bruit in renovascular disease, edema in CKD, daytime sleepiness in obstructive sleep apnea). Nonspecific symptoms of hypertension Headaches, esp. early morning or waking headache Dizziness, tinnitus, blurred vision Flushed appearance Epistaxis Chest discomfort, palpitations; strong, bounding pulse on palpation Nervousness Fatigue, sleep disturbances. P: I: Hypertension is diagnosed if blood pressure is persistently elevated on two or more separate measurements. Further diagnostic measures include evaluation of possible organ damage (e.g., kidney function tests) and additional tests if an underlying disease is suspected. General approach Blood pressure monitoring Repeated measurements on both arms : Hypertension is diagnosed if the average blood pressure on at least two readings obtained on at least two separate visits is elevated. Long-term measurement of blood pressure (24 hours) See “Blood pressure measurement” for the basic approach to measurement. Initial evaluation of newly diagnosed hypertensive patients Stratification of cardiovascular risk: fasting blood glucose, lipid profile (HDL, LDL, and triglycerides levels) Evaluation of end-organ damage and underlying causes Complete blood count Renal function tests: serum creatinine and eGFR Serum Na+, K+, and Ca2+ Urinalysis TSH Electrocardiogram (ECG) Approach to diagnosing secondary hypertension General indicators of secondary hypertension Young age (< 30 years) at onset of hypertension Onset of diastolic hypertension at an older age (> 55 years) Abrupt onset of hypertension End-organ damage that is disproportionate to the degree of hypertension Recurrent hypertensive crises Resistant hypertension: hypertension that is resistant to treatment with at least three antihypertensives of different classes including a diuretic Specific indicators (For details regarding individual diagnostic procedures, see the individual articles.) Screening for hypertension (USPSTF recommendations) [36] Individuals 18–39 years of age with normal blood pressure (< 130/85 mm Hg) and without other risk factors: Screen every 3–5 years. Individuals > 40 years of age or who are at increased risk for high blood pressure : Screen every year. M: Treatment of primary hypertension includes lifestyle changes (e.g., diet, weight loss, exercise) and pharmacotherapy. Commonly prescribed antihypertensive medications include ACE inhibitors, angiotensin receptor blockers, thiazide diuretics, and calcium channel blockers. Management of pediatric patients and pregnant women differs from that of nonpregnant adults because some of these drugs are contraindicated in these patient groups. To treat secondary hypertension, the underlying cause needs to be addressed. Initiation of treatment Number of antihypertensives Newly diagnosed hypertension with BP < 150/90 mm Hg: Begin therapy with one primary antihypertensive. Newly diagnosed hypertension with BP > 150/90 mm Hg: Begin therapy with two primary antihypertensives. Choice of antihypertensive drug Non-African American patients (including individuals with diabetes): thiazide-type diuretic, calcium channel blocker (CCB), angiotensin-converting enzyme inhibitor (ACE-I), or angiotensin receptor blocker (ARB) African American patients (including individuals with diabetes): thiazide-type diuretic or CCB In adults with chronic kidney disease: initial (or add-on) treatment should include an ACE inhibitor or ARB to improve kidney outcome. Follow-up Reassess within one month of initiating or changing pharmacological therapy. If the treatment goal is not reached with one drug, increase the dose of the initial drug or add a second drug. If the treatment goal cannot be reached with two drugs: Add a third drug. Evaluate for secondary causes of hypertension. If blood pressure is controlled: Reassess after 3–6 months and annually thereafter. Overview of antihypertensive drugs: First-line drugs: -ACE inhibitors (e.g lisinopril, captopril, enalapril) and Angiotensin-receptor blockers (e.g losartan, valsartan) -Preferred as a first-line drug in patients with diabetes mellitus, renal disease (nephroprotective), ischemic heart disease, and heart failure ACEi and ARBs should not be used in combination. -Angiotensin-receptor blockers (ARB)(e.g, losartan, valsartan). -Thiazide diuretics (e.g hydrochlorothiazide, chlorthalidone) -Calcium channel blockers. Treatment of hypertension in pregnancy: Treatment of hypertension in pregnancy First-line treatment: methyldopa , labetalol, hydralazine (vasodilator), and nifedipine (CCB) Second-line treatment: thiazides, clonidine (alpha-2 agonist) Contraindicated: furosemide, ACE-I, ARB, renin inhibitors (aliskiren) For details, see treatment of gestational hypertension. Treatment of hypertension in children Treat the underlying cause (e.g., surgical correction of coarctation of the aorta) Lifestyle changes in children with elevated BP (see nonpharmacologic measures in the treatment section below) Pharmacologic management is indicated for symptomatic hypertension, diabetes mellitus, CKD, and end-organ damage, as well as if there is an insufficient response or no response to lifestyle changes. Goal: BP < 90th percentile (BP < 50th percentile in children with DM or CKD) Drugs: ACE inhibitor, ARB, or calcium channel blocker In children with CKD or diabetes mellitus, ACE inhibitors or ARBs are preferable. Hypertensive emergency: labetalol, nicardipine, or sodium nitroprusside. Beta blockers are not recommended for initial treatment of hypertension in children due to their metabolic side effects (e.g., impaired glucose tolerance) and the fact that they exacerbate asthma! ``` P/C: -Arterial hypertension leads to changes in the vascular endothelium, particularly of the small vessels, and can therefore affect any organ system. See also hypertensive crises. Cardiovascular system Congestive heart failure, dilated cardiomyopathy, hypertrophic cardiomyopathy Coronary artery disease and myocardial infarction Atrial fibrillation Aortic aneurysm Aortic dissection Carotid artery stenosis Peripheral artery disease Atherosclerosis ``` Brain: Stroke , TIA Cognitive changes such as memory loss. Kidneys Hypertensive nephrosclerosis Pathophysiology: chronic hypertension → narrowing of afferent arterioles and efferent arterioles → reduction of glomerular blood flow → glomerular and tubular ischemia → arteriolonephrosclerosis and fibrosis (focal segmental glomerulosclerosis) → end-stage renal disease Typical findings Initially microalbuminuria and microhematuria With disease progression, nephrosclerosis with macroalbuminuria (usually < 1 g/day) and progressive renal failure occur. Biopsy: sclerosis in capillary tufts, arterial hyalinosis Eyes Hypertensive retinopathy Arteriosclerotic and hypertension-related changes of the retinal vessels Fundoscopic examination: Cotton-wool spots Retinal hemorrhages (i.e., flame-shaped hemorrhages) Microaneurysms Macular star (results from exudation into the macula) Arteriovenous nicking Marked swelling and prominence of the optic disk with indistinct borders due to papilledema and optic atrophy (end-stage disease) Presence of papilledema in a hypertensive patient may indicate a hypertensive crisis and warrants urgent lowering of the blood pressure (see hypertensive crises). Local treatment of the eye is not possible; therefore, systemic reduction of blood pressure is critical!

Answer 10

White coat hypertension: Definition: arterial hypertension detected only in clinical settings or during blood pressure measurement at a physician's practice Etiology: anxiety experienced by the patient Clinical features: consistently normal blood pressure measurements and normalization of elevated blood pressure outside of a clinical setting Diagnostics: 24-hour blood pressure monitoring. Isolated systolic hypertension (ISH) Definition: increase in systolic blood pressure (≥ 140 mm Hg) with diastolic BP within normal limits (≤ 90 mm Hg) Etiology ISH in elderly: decreased arterial elasticity and increased stiffness → decreased arterial compliance ISH secondary to increased cardiac output Anemia Hyperthyroidism Chronic aortic regurgitation AV fistula Clinical features: Often asymptomatic Signs of increased pulse pressure: e.g., head pounding, rhythmic nodding, or bobbing of the head in synchrony with heartbeats Symptoms of hypertension (see “clinical features” above) Diagnostics: See “diagnosis of hypertension” below. Treatment: thiazide diuretics or dihydropyridine calcium antagonists Prognosis: high risk of cardiovascular events (MI, stroke, renal dysfunction).

Answer 11

D: Congestive heart failure (CHF) is a clinical condition in which the heart is unable to pump enough blood to meet the metabolic needs of the body because of pathological changes in the myocardium. Congestive heart failure (CHF): a clinical syndrome in which the heart is unable to pump enough blood to meet the metabolic needs of the body; characterized by ventricular dysfunction that results in low cardiac output Systolic dysfunction: CHF with reduced stroke volume and ejection fraction (EF) Diastolic dysfunction: CHF with reduced stroke volume and preserved ejection fraction Right heart failure (RHF): CHF due to right ventricular dysfunction; characterized by backward heart failure Left heart failure (LHF): CHF due to left ventricular dysfunction; characterized by forward heart failure Biventricular (global) CHF: CHF in which both the left and right ventricle are affected, resulting in simultaneous backward and forward CHF Chronic compensated CHF: clinically compensated CHF; the patient has signs of CHF on echocardiography but is asymptomatic or symptomatic and stable (see “Diagnostics” below) Acute decompensated CHF: sudden deterioration of CHF or new onset of severe CHF due to an acute cardiac condition (e.g., myocardial infarction) R: Obesity Smoking COPD Heavy drug (recreational and prescription) and alcohol abuse D: E: revalence 1–2% of the population (∼ 5.7 million individuals) in the US has CHF. The incidence is higher among African Americans, Hispanics, and Native Americans. Increases with age: ∼ 10% of individuals > 60 years old are affected. Systolic heart disease is the most common form of CHF overall. A: The three main causes of CHF are coronary heart disease, diabetes mellitus, and hypertension. These conditions cause ventricular dysfunction with low cardiac output, which results in blood congestion (backward failure) and poor systemic perfusion (forward failure). General causes: -systolic dysfunction (reduced EF) & Diastolic dysfunction (preserved EF): Coronary artery disease, myocardial infarction Arterial hypertension Valvular heart disease Diabetes mellitus (diabetic cardiomyopathy) Renal disease Infiltrative diseases (e.g., hemochromatosis, amyloidosis). Specific causes: -systolic dysfunction (reduced EF) Cardiac arrhythmias Dilated cardiomyopathy (e.g., Chagas disease, chronic alcohol use, idiopathic) Myocarditis -diastolic dysfunction (Constrictive pericarditis Restrictive or hypertrophic cardiomyopathy Pericardial tamponade). C: CHF is classified as either left heart failure (LHF) or right heart failure (RHF), although biventricular (global) CHF is most commonly seen in clinical practice. LHF leads to pulmonary edema and resulting dyspnea, while RHF induces systemic venous congestion that causes symptoms such as pitting edema, jugular venous distension, and hepatomegaly. Biventricular CHF manifests with clinical features of both RHF and LHF, as well as general symptoms such as tachycardia, fatigue, and nocturia. In rare cases, high-output CHF may occur as a result of conditions that increase cardiac output and thereby overwhelm the heart. Acute decompensated heart failure (ADHF) may occur as an exacerbation of CHF or be caused by an acute cardiac condition such as myocardial infarction. CHF is diagnosed based on clinical presentation and requires an initial workup to assess disease severity and possible causes. Initial workup includes measurement of brain natriuretic peptide levels, chest x-ray, and an ECG. P: Cardiac output, which is stroke volume times heart rate, is determined by three factors: preload, afterload, and ventricular contractility. Underlying mechanism of reduced cardiac output Systolic ventricular dysfunction (most common) due to: Reduced contractility: Damage and loss of myocytes reduce ventricular contractility and stroke volume. Increased afterload: increase in mean aortic pressure, outflow obstruction Increased preload: ventricular volume overload Cardiac arrhythmias High-output conditions (see “High-output heart failure” below) Diastolic ventricular dysfunction due to: Decreased ventricular compliance: increased stiffness or impaired relaxation of the ventricle → reduced ventricular filling and increased diastolic pressure → decreased cardiac output Increased afterload: increase in pulmonary artery pressure Increased preload: ventricular volume overload Consequences of systolic and diastolic dysfunction Forward failure: reduced cardiac output → poor organ perfusion → organ dysfunction (e.g., hypotension, renal dysfunction) Backward failure Increased left-ventricular volume and pressure → backup of blood into lungs → increased pulmonary capillary pressure → cardiogenic pulmonary edema Reduced cardiac output → systemic venous congestion → edema and progressive congestion of internal organs Resulting macroscopic findings: nutmeg liver Compensation mechanisms Aim: maintain cardiac output if stroke volume is reduced ↑ Adrenergic activity → increase in heart rate, blood pressure, and ventricular contractility Increase of renin-angiotensin-aldosterone system activity (RAAS): activated following decrease in renal perfusion secondary to reduction of stroke volume and cardiac output ↑ Angiotensin II secretion → vasoconstriction → ↑ systemic blood pressure → ↑ afterload Kidney: vasoconstriction of the efferent arterioles and, to a lesser degree, the afferent arterioles → ↓ net renal blood flow and ↑ intraglomerular pressure to maintain GFR ↑ Aldosterone secretion → ↑ renal Na+ and H2O resorption → ↑ preload Brain natriuretic peptide (BNP): ventricular myocyte hormone released in response to increased ventricular filling and stretching ↑ Intracellular smooth muscle cGMP → vasodilation → hypotension and decreased pulmonary capillary wedge pressure. I: Heart failure is primarily a clinical diagnosis. Laboratory tests and imaging tests, including a chest x-ray and echocardiogram, are useful for evaluating the severity and cause of the condition. Diagnostic approach [22] Medical history, including preexisting conditions and history of alcohol and recreational or prescribed drug use Initial evaluation involves a range of routine laboratory tests and a test for BNP level, ECG, and chest x-ray. Echocardiography is the gold standard tool for assessing cardiac morphology and function, as well as investigating the underlying cause of CHF. Other procedures (exercise testing, angiography) may be required for further investigation. Initial evaluation [22] Laboratory analysis Elevated BNP and NT-pro BNP High levels of BNP in patients with classic symptoms of CHF confirm the diagnosis (high predictive index). Elevated atrial natriuretic peptide (ANP): Complete blood count: may show anemia Serum electrolyte levels: hyponatremia → indicates a poor prognosis Kidney function tests: ↑ creatinine, ↓ sodium Urine analysis: rule out concurrent renal impairment Fasting glucose: to screen for diabetes mellitus, which is a common comorbidity Fasting lipid profile: to detect dyslipidemia associated with a higher cardiovascular risk Electrocardiogram (ECG) ECG abnormalities in CHF are common, but are mostly nonspecific and nondiagnostic. Signs of left ventricular hypertrophy ↑ QRS voltage (in the left chest leads and limb leads I and aVL) → positive Sokolow-Lyon index ↑ QRS duration (incomplete or complete left bundle branch block) Left axis deviation Assessment of prior or concurrent heart conditions Previous or acute MI: see ECG changes in STEMI Arrhythmias (e.g., atrial fibrillation, ventricular arrhythmias, sinus tachycardia or bradycardia, AV block) Signs of pericardial effusion and tamponade: low voltage ECG Chest x-ray Useful diagnostic tool to evaluate a patient with dyspnea and differentiate CHF from pulmonary disease Signs of cardiomegaly Cardiac-to-thoracic width ratio > 0.5 Boot-shaped heart on PA view (due to right ventricular enlargement) Assess pulmonary congestion (see x-ray findings in pulmonary congestion). Transthoracic echocardiogram Gold standard for evaluating patients with heart failure Assess ventricular function and hemodynamics Atrial and ventricular size Interventricular septum thickness: > 11 mm (normal 6–11 mm) indicates cardiac hypertrophy Systolic function: left ventricular ejection fraction Normal EF: > 55% Reduced EF: 30–44% Extremely reduced EF: < 30% Diastolic function (diastolic filling, ventricle dilation) Investigate etiology Valvular heart disease Wall motion abnormalities (indicate prior or acute MI) Right ventricular strain Tissue Doppler: ↑ PCWP in left-sided heart failureTransthoracic echocardiogram Gold standard for evaluating patients with heart failure Assess ventricular function and hemodynamics Atrial and ventricular size Interventricular septum thickness: > 11 mm (normal 6–11 mm) indicates cardiac hypertrophy Systolic function: left ventricular ejection fraction Normal EF: > 55% Reduced EF: 30–44% Extremely reduced EF: < 30% Diastolic function (diastolic filling, ventricle dilation) Investigate etiology Valvular heart disease Wall motion abnormalities (indicate prior or acute MI) Right ventricular strain Tissue Doppler: ↑ PCWP in left-sided heart failure. Further tests Cardiac stress test (exercise tolerance test): to assess the functional impairment due to CHF or other conditions (particularly CHD!) Radionuclide ventriculography : indicated to assess left ventricular volume and ejection fraction (LVEF) Cardiac MRI: particularly useful for assessing cardiac morphology and function Cardiac size and volumes, wall thickness, valvular defects, wall motion abnormalities Coronary angiography (left heart catheterization): indicated to detect/confirm CHD and possible percutaneous coronary intervention Right heart catheterization: if pulmonary hypertension is suspected, to assess the severity of systolic dysfunction, and/or to differentiate between types of shock SvO2: will be low in decompensated heart failure Endomyocardial biopsy: may be performed if a specific diagnosis is suspected in patients with rapidly progressive clinical CHF or in case the results would alter the management of the patient, e.g., in amyloidosis. M: Management of CHF includes lifestyle modifications and treatment of associated conditions (e.g., hypertension) and comorbidities (e.g., anemia), along with pharmacologic agents that reduce the workload of the heart. ADHF requires hospitalization and more intensive measures, such as hemodialysis. General measures [22] Lifestyle modifications Salt restriction (< 3 g/day) Fluid restriction in patients with edema and/or hyponatremia Weight loss and exercise Cessation of smoking and alcohol consumption Immunization: pneumococcal vaccine and seasonal influenza vaccine Patient education Self-monitoring and symptom recognition Daily weight check Weight gain > 2 kg within 3 days: consult the doctor Monitoring of potential side effects (e.g., hypotension caused by ACE inhibitors, hyperkalemia caused by aldosterone-antagonists, sensitivity to sunlight caused by amiodarone) Treat any underlying conditions and contributing comorbidities. Pharmacologic treatment algorithm Drugs that improve prognosis: beta blockers, ACE inhibitors, and aldosterone antagonists! Drugs that improve symptoms: diuretics and digoxin (significantly reduce the number of hospitalizations)! Conducting regular blood tests to assess electrolyte levels (potassium and sodium) is mandatory if the patient is on diuretics! Contraindicated drugs NSAIDs Worsen renal perfusion (see “Side effects” of NSAIDs) Reduce the effect of diuretics May trigger acute cardiac decompensation Calcium channel blockers (verapamil and diltiazem): negative inotropic effect; worsen symptoms and prognosis Thiazolidinediones: promote the progression of CHF (↑ fluid retention and edema) and increase the hospitalization rate Moxonidine: increases mortality in CHF with reduced ejection fraction (systolic dysfunction) Invasive procedures Implantable cardiac defibrillator (ICD): prevents sudden cardiac death Primary prophylaxis indications CHF with EF < 35% and prior myocardial infarction/CHD Increased risk of life-threatening cardiac arrhythmias Secondary prophylaxis indications: history of sudden cardiac arrest, ventricular flutter, or ventricular fibrillation Cardiac resynchronization therapy (biventricular pacemaker): improves cardiac function Indications: CHF with EF < 35%, dilated cardiomyopathy, and left bundle branch block Can be combined with an ICD Coronary revascularization with PCTA or bypass surgery may be indicated if CAD is present. Valvular surgery if valvular heart defects are present Ventricular assist devices: may be implanted to support ventricular function; may be indicated for temporary or long-term support (e.g., to bridge time until transplantation) of decompensated CHF Cardiac transplantation: for patients with end-stage CHF (NYHA class IV), ejection fraction < 20%, and no other viable treatment options. P: The prognosis depends on the patient, type and severity of heart disease, medication regimens, and lifestyle changes. The prognosis for patients with preserved EF is similar to or better than for patients with decreased EF Risk stratification scales may be used to evaluate the prognosis (e.g., CHARM and CORONA risk scores). Factors associated with worse prognosis Elevated BNP Hyponatremia Systolic BP < 120 mm Hg Diabetes Anemia Weight loss or underweight S3 heart sound Implantable cardioverter-defibrillator use Frequent hospitalizations due to CHF 1-year survival according to NYHA stage Stage I: ∼ 95% Stage II: ∼ 85% Stage III: ∼ 85% Stage IV: ∼ 35%. Complications include: acute decompensated heart failure. Cardiorenal syndrome.

Answer 12

Angina Typically retrosternal chest pain or pressure Pain can also radiate to left arm, neck, jaw, epigastric region, or back. Pain does not depend on body position or respiration No chest wall tenderness Angina may be absent, particularly in younger patients Often gradual progression Can also present as gastrointestinal discomfort Dyspnea Dizziness, palpitations Restlessness, anxiety Autonomic symptoms (e.g., diaphoresis, nausea, vomiting, syncope) Stable angina Symptoms are reproducible/predictable Complaints often subside within minutes , with rest or after administration of nitroglycerin Common triggers Mental or physical stress Exposure to cold Unstable angina Symptoms are not reproducible/predictable Usually occurs at rest or with minimal exertion and is usually not relieved by rest or nitroglycerin Every new-onset angina Severe, persistent, and/or worsening angina (crescendo angina) Increasing intensity, frequency, or duration in a patient with a known stable angina Unstable angina is a form of acute coronary syndrome and may progress to myocardial infarction. Most patients with CHD first become symptomatic with acute myocardial infarction or sudden cardiac death!

Answer 13

``` D: A narrowing of the coronary arteries reduces blood flow to the myocardium (heart muscle). During times of high demand such as exercise there is insufficient supply of blood to meet demand. This causes symptoms the symptoms of angina, typically constricting chest pain with or without radiation to jaw or arms. Angina is “stable” when symptoms are always relieved by rest or glyceryl trinitrate (GTN). It is “unstable” when the symptoms come on randomly whilst at rest, and this is considered as an Acute Coronary Syndrome. Stable angina (aka Angina Pectoris) is a common presentation of Coronary Heart disease – CHD(aka Ischaemic Heart disease – IHD) ``` Stable angina, (aka ‘Angina pectoris’, and colloquially “Angina“) is a syndrome which causes exertional chest pain, relieved by either rest or the use of nitrates Stable angina is a clinical syndrome rather than a disease – and represents a clinical manifestation of underlying coronary artery disease It occurs when there is insufficient oxygen supply to the heart to meet demand i.e. when there is myocardial ischaemia without infarct This inability typically occurs as a result of narrowing of the coronary arteries. This narrowing can be due to: Atherosclerosis Arterial spasm (Blood clot – which is the mechanism seen in acute coronary syndromes. R: The risk factors are the same as for all manifestations of cardiovascular disease: ``` Hypertension Dyslipidaemia High LDL and low LDL levels Diabetes Obesity FHx of arterial disease Significant if a first degree relative had MI before the age of 55 Smoking Age Male gender ``` D: It is extremely important to differentiate stable angina from ACS – acute coronary syndrome (unstable angina, NSTEMI and STEMI) – whereby there is an acute narrowing or complete occlusion of the coronary artery due to blood clot – as the treatment is very different. Acute coronary syndrome results in infarction (and death) of myocardial tissue, not just ischaemia. However, the presenting symptom – chest pain – often feels identical to that of ACS – as the mechanism of the pain is essentially the same – lack of oxygen to the heart muscle. If the pain doesn’t resolve within 5 minutes of cessation of activity, and/or with use of GTN spray, treat as ACS Angina is typically exertional Suspicion of ACS should be increased if the symptoms have occurred at rest MI causes permanent heart muscle damage (infarct), stable angina does not. They have similar symptoms, although the pain of MI is often greater than angina. Any diagnosis of sudden onset chest pain should be treated as ACS until proven otherwise (unless the pain does resolve as above and the patient already has a diagnosis of stable angina). E: Prevalence of about 3% This is lower than some other manifestations of cardiovascular disease – such as peripheral vascular disease – which is about 10% A: Atheroma seen in coronary artery disease – this accounts for the vast majority of cases Aortic valve disease Hypertrophic cardiomyopathy Classifying causes by oxygen supply and demand Oxygen demand factors – heart rate, blood pressure, left ventricular hypertrophy (more muscle to supply!), valve disease – e.g. aortic stenosis – so the heart has to work harder to pump Oxygen supply – duration of diastole (needs to be long enough to allow sufficient blood to flow to the heart), coronary vasomotor tone, haemoglobin levels, oxygen saturation. People normally experience angina as exertional chest pain that is relieved by rest. People may also experience myocardial ischaemia as shortness of breath or without symptoms (silent ischaemia). Other precipitating factors Cold weather Heavy meals Intense emotion C: Angina typically presents as central or left sided chest pain, with or without radiation to the neck, arm or jaw, and is generally transient, most commonly occurring on exertion, but can also be triggered by emotion Acute attacks are treated with nitrites (e.g. sublingual GTN spray) It is diagnosed with a combination of history, ECG and myocardial imagining – typically an angiogram Long-term management involves the use of beta-blockers, calcium-channel blockers, long-acting nitrates, aspirin and statins Central or left sided chest discomfort May radiate to the jaw, arm epigastrium – like ACS pain Can vary from mild to severe Usually described as a “tight” or “crushing” sensation Dyspnoea may or may not be present Usually results from exertion Symptoms relieved by rest Symptoms typically of several minutes duration – shorter acting symptoms of a few seconds only are unlikely to be ischaemia related Patient may get frequent symptoms (several times daily) or only rarely (months between episodes) This does not necessarily correspond to the severity of the disease Crescendo angina is said to occur when attacks are increasing in frequency and / or severity and is correlated to high risk of severe ACS Any changes to a patient’s usual pattern of symptoms should be considered a significant risk for ACS and investigated as such. P: I: Diagnosing Stable Angina Diagnosing stable angina can be quite tricky. There are several aspects: Ruling out other causes of chest pain – particularly ACS Assessing the history as being “typical” for stable angina, with ECG ECG might be normal, but changes can include: Pathological Q waves ST depression LBBB T-wave flattening or inversion Confirming the diagnosis with imaging Usually CT coronary angiogram (CTCA) is the first line investigation Consider stress echo or myocardial perfusion scan if this is not available or appropriate Depending on the severity of the disease detected, patients may be offered angiogram If very high clinical suspicion you can refer to cardiology without imaging – start treatment first If low clinical suspicion – consider stress test (ECG or Echo) +/- other cardiac imaging (e.g. CTCA, myocardial perfusion scan) to confirm the diagnosis before referral Typical History Chest Pain – is ‘tight’, heavy’, or ‘gripping’. The pain is usually felt behind the sternum and can radiate to the neck, jaw, arms, and sometimes back. Shortness of breath (SOB) Both pain and SOB brought on by exertion, and relieved by rest Symptoms typically last several minutes after the precipitating event has stopped (e.g. exercise or stress) Classically relieved by GTN The likelihood of a diagnosis of angina increases when there are risk factors for cardiovascular disease present: ``` Smoking Hypertension Diabetes FHx of cardiovascular disease under the age of 55 Raised cholesterol. ``` Investigations CT Coronary Angiography is the Gold Standard diagnostic investigation. This involves injecting contrast and taking CT images timed with the heart beat to give a detailed view of the coronary arteries, highlighting any narrowing. All patients should have to following as baseline investigations: Physical Examination (heart sounds, signs of heart failure, BMI) ECG FBC (check for anaemia) U&Es (prior to ACEi and other meds) LFTs (prior to statins) Lipid profile Thyroid function tests (check for hypo / hyper thyroid) HbA1C and fasting glucose (for diabetes). M: -First thing is to refer to cardiology, and do this urgently if they are having unstable angina, or routinely if stable. Advise about diagnosis and management and when to call an ambulance. Treat medically, then do procedures and surgical interventions to treat the underlying stenosis of the coronary arteries. Medical Management There are three aims to medical management: Immediate Symptomatic Relief Long Term Symptomatic Relief Secondary prevention of cardiovascular disease Immediate Symptomatic Relief Their GTN spray is used required. It causes vasodilation and helps relieves the symptoms. Take GTN, then repeat after 5 minutes. If there is still pain 5 minutes after the repeat dose – call an ambulance. Long Term Symptomatic Relief is with either (or used in combination if symptoms are not controlled on one): ``` Beta blocker (e.g. bisoprolol 5mg once daily) or; Calcium channel blocker (e.g. amlodipine 5mg once daily) Other options (not first line): ``` Long acting nitrates (e.g. isosorbide mononitrate) Ivabradine Nicorandil Ranolazine Secondary Prevention Aspirin (i.e. 75mg once daily) Atorvastatin 80mg once daily ACE inhibitor Already on a beta-blocker for symptomatic relief. Procedural / Surgical Interventions Percutaneous Coronary Intervention (PCI) with coronary angioplasty (dilating the blood vessel with a balloon and/or inserting a stent) is offered to patients with “proximal or extensive disease” on CT coronary angiography. This involves putting a catheter into the patient’s brachial or femoral artery, feeding that up to the coronary arteries under xray guidance and injecting contrast so that the coronary arteries and any areas of stenosis are highlighted on the xray images. This can then be treated with balloon dilatation followed by insertion of a stent. Coronary Artery Bypass Graft (CABG) surgery may be offered to patients with severe stenosis. This involves opening the chest along the sternum (causing a midline sternotomy scar), taking a graft vein from the patient’s leg (usually the great saphenous vein) and sewing it on to the affected coronary artery to bypass the stenosis. The recovery is slower and the complication rate is higher than PCI. TOM TIP: When examining a patient that you think may have coronary artery disease, check for a midline sternotomy scar (previous CABG), scars around the brachial and femoral arteries (previous PCI) and along the inner calves (saphenous vein harvesting scar) to see what procedures they may have had done and to impress your examiners. P: If stable angina is present, without history of MI, and with normal resting ECG and normal BP, then annual mortality is about 1.5% If risk factors are present, then annual mortality greatly increases: Abnormal ECG – 8.4% Hypertension – 7.5% Both – 12% T2DM – quoted risks (above) – doubled

Answer 14

Below is an outline of the investigations that may be used in the work-up of stable angina. ECG – will often be normal – a normal ECG does not exclude a diagnosis of angina or ACS! If performed during an episode of angina (e.g. during an exercise tolerance test – aka stress test) then typical changes on an ECG might include: ST-depression Ventricular ectopic beats Bundle branch abnormalities – mainly LBBB CXR Useful to look for other causes of chest pain (e.g. pneumonia, pneumothorax) May shown signs of heart failure, which may be associated with severe coronary artery disease ETT – Exercise tolerance test – aka exersize stress test. Can be ECG or echo after exercise stress. Assess for symptoms and ECG changes when the heart is stressed Exercise increases cardiac load and can provoke myocardial ischaemia – which manifests as chest pain, dyspnoea and ECG changes Has sensitivity of about 90% but a specificity of only about 70% ECG based ETT should not be used for a diagnosis of stable angina, and is more commonly used after a single acute episode of chest pain to rule out coronary artery disease Stress echo is a variation of the stress test which can be used to diagnose stable angina (see below) CTCA Recommended by NICE is the primary diagnostic investigation A type of high resolution CT scan, with contrast – injected through a peripheral cannula A non-invasive test Typically takes about 10-15 seconds. Scan conducted whilst patient holds their breath The contrast fills the coronary arteries and can indicate where they are narrowed Has a very good negative predictive value for cardiovascular disease Not as sensitive as coronary angiogram – (see below) – whereby the contrast is injected directly into the coronary vessels through a cardiac catheter. MPS – myocardial perfusion scan An alternative to CTCA Is a type of stress test – shows blood flow to different areas of the heart during exercise Reduced blood flow to any given area can indicate vessel blockage in the vessel associated with that particular area of the heart Does NOT directly visualise the arteries It is a nuclear medicine scan – typically using technetium Results are reported as a “risk stratification” – coronary artery disease, normal, or equivocal If equivocal – will need other form of imaging to assess if CAD is present Echocardiograph – may be considered to establish the level of left ventricular function Can either be performed at rest, or as a stress test Echo gives information about left ventricular function and ventricular and atrial wall motion defects Wall motion defects at rest are due to previous MI On stress test, stress-induced ischaemia may show similar, reversible changes Stress echo is an echo performed immediately after exercise stress (i.e. within seconds). It can assess for “dynamic” (i.e. they ‘come-and-go’) contraction changes. Particularly useful in stable angina, when a resting echo may be normal, but a stress echo shows changes of ischaemia. Stress echo provides similar risk stratification to MPS – i.e. it can tell if coronary artery disease is “present” or “absent” but not the location and degree of the abnormality Pharmacological stress testing can be performed in individuals who cannot exercise. In this instance, medication is given to increase cardiac output – placing similar stresses on the heart as exercise. Left-ventricular ejection fraction (LVEF) (at rest) is a strong predictor of long-term outcome LVEF >50% – 12 year survival = 75% LVEF 35-49% – 12 year survival = 55% LVEF <35% – 12 year survival = 21% Angiogram – is the most accurate diagnostic test for coronary artery disease (and therefore for stable angina), But it is relatively expensive, and not without risk, and not necessary for the diagnosis. An invasive test – requires the insertion of a cardiac catheter This gives exact information on the level of narrowing of the coronary arteries, and which vessels are affected. It is particularly useful to help determine if revascularisation is necessary. With medical treatment only (without revascularisation), 12-year survival rates are: Single vessel disease – 75% Two vessel disease – 59% Triple vessel disease – 50% Its main indication is to assess the extent of coronary artery lesions when revascularisation therapies (e.g. stenting (PCI) or bypass) are being considered. As such it is typically reserved for the most symptomatic patients, although its use is increasing. Coronary artery narrowing is considered significant when the luminal diameter is reduced by >70% In particular, proximal narrowing of the left main coronary artery and the left anterior descending artery is associated with a poor prognosis. The preferred test when the patient already has known coronary artery disease and the clinician wants to assess the extent of the disease Blood tests – for screening of risk factors – cholesterol, fasting glucose

Answer 15

The presence of angina indicates underlying coronary artery disease. The next step is to evaluate the severity of this underlying cardiac disease, for the purposes of assessing future risk of myocardial infarction – and in particular whether or not revascularisation (e.g. coronary artery stenting, or coronary artery bypass graft – CABG) is indicated. Prognostic indicators include: ``` Left ventricular function Stress testing (e.g. treadmill or pharmacological stress test) Coronary artery disease extent as seen on angiogram Age Diabetes Hypertension Hypercholesterolaemia Heart failure ```

Answer 16

This can be divided into lifestyle modifications, pharmacological interventions, and revascularisation. Lifestyle Diet advice – plant-based whole foods diet (e.g. mediterranean diet) has been shown to improve long term outcomes Smoking cessation After 2 years, risk of MI is same as for those who have never smoked Control hypertension Treat hyperlipidaemia – start statin regardless of cholesterol levels Alcohol – within safe drinking limits No more than 2 standard drinks on any single day, and two days per week with no alcohol intake Weight – aim for BMI <=25 Regular exercise – 150 minutes per week of moderate intensity exercise – reduces cardiovascular risk regardless of weight loss, by up to 30% Pharmacological There are two main mechanisms used to relieve the symptoms of angina: Increasing blood flow to the heart muscle (by dilating coronary arteries) – e.g. wth GTN (Glycerytrinitrate) Decreasing the workload on the heart (e.g. with beta-blocker or calcium channel blocker long term) First line treatment Beta-blocker (e.g. atenolol or metoprolol) Proven to reduce MI and sudden death risk Decreases heart rate, contractility, and cardiac output – which reduces cardiac O2 demand e.g. metoprolol 25mg BD Calcium channel blocker (e.g. verapamil, diltiazem) These two agents are preferred due to their negative chronotropic events Typically reserved for patients who are unable to tolerate beta-blockers or whose symptoms are incompletely controlled with beta-blockers e.g. verapamil 120mg OD Nitrates Patients will also likely carry GTN spray or pills with them at all times to relieve acute episodes. Nitrates cause vasodilation Can cause hypotension Provide quick relief – within a couple of minutes, and lasts for up to 30 minutes e.g. GTN sublingual spray 400mcg – repeat every 5 minutes as required GTN sublingual tablets 300mcg are also available Aspirin (or another anti platelet drug – such as clopidogrel or ticagrelor) Reduced the risk of thrombus formation and thus ACS e.g. aspirin 100mg daily Second line treatment Consider adding… ``` Long acting nitrate e.g. isosorbide mononitritae 30mg PO OD – up to a max of 120mg daily Typically effect lasts for 4-6 hours Nicorandil Ivabradine Ranolazine Third line treatment ``` Consider PCI (cardiac stent, balloon angioplasty) Typically both balloon angioplasty and stenting are performed simultaneously The procedure carries a 1-3% mortality, and 5% risk of MI There is no evidence that angioplasty (+/- stent) improves survival or reduces risk of ACS. It may however reduce symptoms of stable angina CABG – Coronary arty bypass graft Similar risks as PCI (above) Completely eliminates symptoms in about 85% of patients Does not appear to improve survival for those with class I or II disease (see above) Modest improvement in survival for those with left main coronary artery disease or triple vessel disease Patients with T2DM have better outcomes with CABG than PCI

Answer 17

D: Cardiac arrest is an ‘arrest’ in the activity of the heart – the heart has stopped beating. There will be no contraction of the heart muscle, but there may still be electrical activity in the heart (we call this PEA = pulse-less electrical activity). Irreversible brain damage can occur after <5 minutes of cardiac arrest. When you carry out CPR, you are trying to reverse the affects of cardiac arrest by proving a cardiac output – at first manually with chest compression, and hopefully later with ROSC – Return of Spontaneous Circulation – when the heart starts beating again. R: D: E: ``` A: In some cases, cardiac arrest may be reversible. The causes of reversible cardiac arrest are the 5H’s and the 4T’s. H's: -Hypoxia -Hypovolaemia -Hypokalaemia -Hyperka;aemia -Hypothermia. T's: -Tension pneumothorax -Tamponade (cardiac) -Toxins -Thrombosis. ``` M: Defibrillation and cardioversion When you pass a large current through the heart, you can completely depolarise it. After this time, there will be a period of asystole, hopefully after which normal sinus mechanisms will restore sinus rhythm to the heart. Defibrillators deliver a high-voltage, short duration DC shock, via two metal pads (coated in conducting gel or jelly) placed on the chest. These should be placed over the upper right sternal edge and the apex. You can also deliver a shock right to the heart during open surgery! Defibrillation vs cardioversion – defibrillation is a general term often used to describe the shock given to the heart, and more specifically it describes an ‘unsynchronised ‘shock. Cardioversion refers to this shock when it is applied at a specific time in the ECG cycle (a ‘synchronised’ shock). Before attempting to shock the heart, you need to establish what the current rhythm is. Determining the rhythm determines further treatment options. All this will also take place in the context of CPR. Beware! – if you give a shock at around the peak of the T wave, you can induce unusual and dangerous rhythms such as atrial fibrillation or ventricular tachycardia. Thus the current is usually synchronised with the ECG so that the pulse is given about 0.02s after the peak of the R wave. In ventricular fibrillation, the timing of the impulse is not important. Shockable rhythms: - Ventricular fibrillation - Pulseless ventricular tachycardia. Non-shockable rhythms: PEA – pulseless electrical activity – this means any electrical activity that appears on an ECG like it should be producing a pulse, but it is not. The most common cause is hypovolaemia. Asystole – no rhythm present Cardioversion therapy is often pre-planned, and used to treat significant, although not immediately life-threatening arrhythmias, such as narrow complex tachycardias, atrial fibrillation and atrial flutter. Sedation or no sedation? in an emergency situation, the patient is often unconscious as a result of cardiogenic shock, and in such cases, there is no anaesthesia given. In cases where the patient is awake (most commonly elective cardioversion), then the patient may receive sedation to make the treatment more tolerable. Contraindications and complications Digoxin – this increases the risk of arrhythmias after cardioversion, and thus in cases of elective cardioversion, the drug is usually withheld for 24 hours before treatment. Risk of systemic embolus – is increased in patients with long standing atrial arrhythmias who undergo elective cardioversion. Thus, these patients should be given 4 weeks anticoagulant therapy for at least 4 weeks either side of the treatment. P: Cardiac arrest is a medical emergency, and has extremely poor prognosis. Out of hospital arrest has a survival rate of 2-8% In hospital cardiac arrest has a 1-year survival rate of about 15%. The best centres in the world have a ‘survival to discharge’ of up to 50% Prognosis is particularly dependent on the electrical rhythm of the heart during the arrest.

Answer 18

Tear in tunica intima. The tear only occurs in the tunica intima and this causes a separation of the tunica intima and tunica media layers.

Answer 19

Bendroflumethiazide - inhibits sodium reabsorption by blocking the Na+-Cl− symporter at the beginning of the distal convoluted tubule

Answer 20

Ankle swelling is a common side-effect of amlodipine. According to NICE guidelines thiazide diuretics can be used instead of calcium channel blockers in the initial management of hypertension in patients over 55. Mannitol is an osmotic diuretic that is used to lower intracranial pressure following a head injury. Spironolactone is an aldosterone antagonist. Furosemide acts on the thick ascending loop of Henle to prevent reabsorption of potassium, sodium, and chloride. Acetazolamide is a carbonic anhydrase inhibitor that is used to treat acute angle closure glaucoma.

Answer 21

Bosentan - endothelin-1 receptor antagonist

Answer 22

Aortic regurgitation. Aortic regurgitation typically causes an early diastolic murmur The murmur heard in aortic regurgitation occurs early in diastole due to the backflow of blood from the aorta into the left ventricle through an incompetent aortic valve. The carotid pulse rises rapidly due to the vigorous ejection of blood from an overloaded left ventricle. It then falls rapidly due to the backflow of blood into the left ventricle. Patients with aortic regurgitation may also have an ejection murmur, caused by the turbulent ejection of blood from the overloaded left ventricle. Aortic regurgitation due to aortic root dilation can be associated with ankylosing spondylitis, Marfan syndrome or aortic dissection. Causes of aortic regurgitation due to aortic valve leaflet disease are calcific degeneration, congenital bicuspid aortic valve, rheumatic heart disease and infective endocarditis.

Answer 23

Hoarse voice. All innervation for speech originates from the vagus (X) nerve so injuries to the vagus will cause speech problems. Remember that the vagus nerve has both autonomic and somatic effects; the most important somatic pathway being motor supply to the larynx via the recurrent laryngeal nerves, which are branches of the vagus. Damage to one vagus nerve would therefore result in the same effect as damage to a single recurrent laryngeal which is a hoarse voice. Anal tone, erections and urination are all controlled by the sacral parasympathetics and would not be affected by loss of the vagus. Pupillary constriction is controlled by parasympathetics on the oculomotor nerve and so would also not be affected by loss of the vagus.

Answer 24

Angina pectoris may be defined as: Signs and Symptoms: An acute pain in the thorax lasting seconds to minutes (according to WHO < 20 min). Typically, the pain radiates out into the left shoulder/arm or neck region. May be a vague, barely troublesome ache, or it may rapidly become a severe, intense precordial crushing sensation. Aetiology: The cause is usually critical coronary artery obstruction due to atherosclerosis. Pathogenesis: Angina pectoris occurs when the myocardial oxygen demand exceeds the ability of the coronary arteries to supply oxygenated blood. Treatment: Glyceyl nitrate is a potent smooth-muscle relaxer and vasodilator. It lowers systolic BP and dilates systemic veins, thus reducing myocardial wall tension, a major determinant of oxygen demand. Beta-blockers block sympathetic stimulation of the heart and reduce systolic pressure, heart rate, contractility, and cardiac output, thus decreasing myocardial oxygen demand and increasing excercise tolerance. Calcium channel blockers are vasodilators useful in the treatment of angina with hypertension. They are also used in the treatment of variant or Prinzmetal's angina where they prevent coronary artery spasm. Usually non dihydropiridin derived calcium antagonists are used when beta-blockers are contraindicated or not clinically effective.

Answer 25

The ST elevation can be clearly seen on the ECG; this is common in the early stages of a heart attack. Since these changes are observed in leads II, III, AVL, AVF, and V4-6 he has an inferolateral STEMI. A diagnosis of MI is confirmed by 2 out of 3 of the following findings: Clinical picture (typical chest pain) Appropriate laboratory evidence showing elevated enzymes (troponin, CK,) ECG changes So now that you are quite certain of the diagnosis, how would you treat Mr.

Answer 26

Lignocaine is only necessary if the patient developes a ventricular arrythmia. This is a common complication within the first 24 hours.

Answer 27

If the patient is very anxious, benzodiazepines may improve this problem and indirectly lower the heart rate. However, the patient must not be given intramuscular injections (any medication) as this will make a treatment with plasminogen activators impossible! If benzodiazepines are essential, they should be given orally or iv.

Answer 28

sTATIN Heparin: This could be given iv (unfractionated heparin) or sc (low molecular weight heparin). LMWH is usually given as it is easier and does not require monitoring. It should not be given to patients with renal impairment or those at high risk of bleeding (as it cannot easily be reversed). This will ease the patient's pain and reduce his anxiety. Also B-blocker, indication: bradycardia. aspirin also needed for treatment

Answer 29

ST elevation 1.5mm in leads II and III--> Acute onset of at least 1mm ST elevation in 2 adjacent limb leads or at least 1mm ST elevation in 2 adjacent precordial leads. New Left Bundle Branch Block Symptoms began less than 12 hours ago

Answer 30

ST depression generally means that there is an area of ischaemia in the cardiac muscle and therefore this indicates that thrombolysis will not definitely reverse this.

Answer 31

Active internal bleeding Aortic dissection Previous history of a hemorrhagic stroke Ischaemic stroke 3 months ago--> relative contraindications, not absolute. The age of a patient is a relative contraindication, as older patients tend to have a higher risk of developing bleeding complications. One must weigh the risks of thrombolysis on a case by case basis.

Answer 32

Absolute contraindications: ``` Aortic dissection Acute pericarditis Active bleeding Cerebral haemorrhage or known intracerebral vascular disease Relative contraindications: ``` GI or GU haemorrhage within past 6 months Stroke within past 6 months Major surgery Organ biopsy Non-compressible vessel puncture within past 2-4 weeks Prolonged CPR with chest trauma or remaining unconscious Diabetic proliferative retinopathy Severe uncontrolled hypertension (SBP>200 or DBP>120) History of bleeding diathesis or hepatic dysfunction or cancer Pregnancy

Answer 33

Pain started less than 12 hours ago. Angioplasty can take place within first 90 mins after symptoms onset An Interventional cardiologist should be available to perform the procedure. He should also be linked to an experienced department with a coronary care unit.

Answer 34

1 in 100 risk of complete occlusion of coronary artery 1 in 200 risk of damage to coronary artery, both which may require an emergency CABG Puncture site haematoma, infection or false aneurysm.

Answer 35

(Possible, but unlikely. In a hypovolemic shock, the patient would have cold peripheries, but also a low CVP.)

Answer 36

``` Early reocclusion and proagation of the infarction area. Pericardial tamponade (this is possible and is a recognised complication of angioplasty. The absence of pulsus paradox makes it less likely.) -Right ventricular infarct: This could well be the case since he is quite breathless ```

Answer 37

This will be useful in excluding pericardial tamponade. It will also assess LV and RV function and look for regional wall abnormalities

Answer 38

to assess myocardial infarction. To diagnose extension of myocardial ischemia, an ECG with additional right-ventricular leads (V1R-V6R) would be helpful. An ECG would also help to determine if there is regional damage in the contraction of the right or left ventricle and also give an indication of the presence of a pericardial effusion (low ECG voltage).

Answer 39

CVP normal/low | Patient is warm (hyperdynamic form)

Answer 40

The most important disgnostic factors in this instance are: CVP low Patient is warm History

Answer 41

The most important diagnostic factors in this instance are: CVP mostly high Patient is cold. Treated with dobutamine

Answer 42

The most important disgnostic factors in this instance are: Low CVP Patient is cold

Answer 43

Dopamine is an intermediate in tyrosine metabloism and precursor of norepinephrine and epinephrine; it accounts for 90% of the catecholamines. Dopamine affects dopamine receptors at low doses and raises the perfusion in the splanchnic and renal areas. At intermediate levels, dopamine works on beta-receptors causing a positive inotropic effect with minimal peripheral vasoconstriction. At high doses, dopamine works on alpha-receptors and causes distinct peripheral vasoconstriction. Since there is a clear elevation of the afterload, dopamine appears to have a negative effect on the heart.

Answer 44

Dobutamine is a synthetic derivative of dopamine. It is a direct acting inotropic agent which causes stimulation of the beta receptors of the heart while producing less marked chronotropic, hypertensive, arrhythmogenic or vasodilatory effects. It does not cause the release of endogenous noradrenaline as does dopamine and it has no specific effect on the renal vasculature. In both animal and human studies, dobutamine produces a reduced increase in heart rate and a reduced decrease in peripheral vascular resistance for a given inotropic effect than does isoproterenol.

Answer 45

1. Mechanical methods (graduated compression stockings and intermittent pneumatic compression devices) 2. Pharmacological agents 3. Conservative: early mobilisation, stay hydrated.

Answer 46

NSTEMI is usually diagnosed on the basis of: A suggestive history Elevated troponin levels Be aware that any condition that causes myocardial damage can result in an elevated troponin. Examples of other causes of elevated troponin include PE, myocarditis, renal failure (chronically raised). What is particularly important is the pattern of the troponin result (see below) ECG changes An absence of ST evevation ECG may be normal There may be other changes on ECG to suggest MI. These might include: ST depression Hyperacute T wave (tall pointy T waves) – often an early sign which resolve but the time the patient is seen in hospital TWI (T-wave inversion) – a late sign, often indicates previous MI Non-specific ST changes

Answer 47

Unstable angina is distinguishable from NSTEMI only through troponin results. Troponin – negative ECG changes – as for NSTEMI above

Answer 48

Dressler’s Syndrome This is also called post-myocardial infarction syndrome. It usually occurs around 2-3 weeks after an MI. It is caused by a localised immune response and causes pericarditis (inflammation of the pericardium around the heart). It is less common as the management of ACS becomes more advanced. It presents with pleuritic chest pain, low grade fever and a pericardial rub on auscultation. It can cause a pericardial effusion and rarely a pericardial tamponade (where the fluid constricts the heart and prevents function). A diagnosis can be made with an ECG (global ST elevation and T wave inversion), echocardiogram (pericardial effusion) and raised inflammatory markers (CRP and ESR). Management is with NSAIDs (aspirin / ibuprofen) and in more severe cases steroids (prednisolone). They may need pericardiocentesis to remove fluid from around the heart.

Answer 49

Secondary Prevention Medical Management (6 As) Aspirin 75mg once daily Another antiplatelet: e.g. clopidogrel or ticagrelor for up to 12 months Atorvastatin 80mg once daily ACE inhibitors (e.g. ramipril titrated as tolerated to 10mg once daily) Atenolol (or other beta blocker titrated as high as tolerated) Aldosterone antagonist for those with clinical heart failure (i.e. eplerenone titrated to 50mg once daily) Dual antiplatelet duration will vary following PCI procedures depending on the type of stent that was inserted. This is due to a higher risk of thrombus formation in different stents. Secondary Prevention Lifestyle: Stop smoking Reduce alcohol consumption Mediterranean diet Cardiac rehabilitation (a specific exercise regime for patients post MI) Optimise treatment of other medical conditions (e.g. diabetes and hypertension)

Answer 50

Atherosclerosis is a chronic inflammatory process affecEng the in&ma of arteries. It is characterised by the formaEon of lipid-rich plaques in the vessel wall.

Answer 51

For pracEcal purposes the inEma equates to the endothelium (the layer of cells that lines the interior surface of the circulatory system). The important *modifiable risk factors for developing atherosclerosis are: • smoking • hypertension • diabetes mellitus • dyslipidaemia (abnormal lipoprotein levels ie. high raEo of LDL:HDL) All four of these risk factors damage the endothelium. The damaged endothelial cells become dysfunc&onal: • there is increased permeability. • they produce adhesion molecules and cytokines which aSract inflammatory cells and prothromboEc molecules. eg. VCAM-1 (vascular cell adhesion molecule-1) binds monocytes and T cells. Consequently, there is recruitment of inflammatory cells to the site of injury: monocytes and T cells adhere to the endothelium and migrate into the inEma. The monocytes differenEate into macrophages. The macrophages have a number of effects: • they produce free radicals that drive LDL oxidaEon to form oxidised LDL. [Remember: naEve LDL is not atherogenic. oxidised LDL is highly atherogenic.] • they engulf oxidised LDL and cholesterol crystals, becoming foam cells. [A foam cell is a macrophage containing abundant lipid in its cytoplasm, giving the cytoplasm a ‘foamy’ appearance microscopically - hence the name]. • foam cells produce growth factors what sEmulate migraEon of smooth muscle cells from the media to the inEma. The migraEon and acEvaEon of smooth muscle cells is also driven by factors released by acEvated platelets and endothelial cells. *Do not forget the most important non-modifiable risk factors for developing atherosclerosis: family history and male gender. Other modifiable risk factors include obesity, diet and exercise. Endothelial Injury Atherosclerosis is a chronic inflammatory process affecEng the in&ma of arteries. It is characterised by the formaEon of lipid-rich plaques in the vessel wall. turn over

Answer 52

Oxidised LDL accumulates within macrophages and smooth muscle cells just underneath the endothelial cells. CollecEons of lipid-laden macrophages siyng in the inEmal layer may be visible as yellow elevaEons called faSy streaks. The faSy streak has no clinical significance but it is important because it may progress to an atheroscleroEc plaque.

Answer 53

A core of lipid debris forms as the foamy macrophages die and the lipid in their cytoplasm is released. Smooth muscle cells proliferate and change their behaviour: they secrete collagen and other extracellular matrix proteins (rather than being contracEle), resulEng in the formaEon of a fibrous cap over the core. The core is composed of oxidised lipid and inflammatory cells. The cap represents the body’s aSempt to repair by scarring (see InflammaEon lecture notes pg 5).

Answer 54

- persistent injury (endothelial damage due to the previously described risk factors). - on-going inflammaEon (macrophages and lymphocytes). - repair with scarring (the fibrous cap of the plaque).

Answer 55

Four Cardiac Arrest Rhythms These are the four possible rhythms that you will see in a pulseless unresponsive patient. They can be categorised into shockable (meaning defibrillation may be effective) and non-shockable (meaning defibrillation will not be effective and should not be used). Shockable rhythms: Ventricular tachycardia Ventricular fibrillation Non-shockable rhythms: Pulseless electrical activity (all electrical activity except VF/VT, including sinus rhythm without a pulse) Asystole (no significant electrical activity)

Answer 56

Supraventricular tachycardia (SVT) is caused by the electrical signal re-entering the atria from the ventricles. Normally the electrical signal in the heart can only go from the atria to the ventricles. In SVT the electrical signal finds a way from the ventricles back into the atria. Once the signal is back in the atria it travels back through the AV node and causes another ventricular contraction. This causes a self-perpetuating electrical loop without an end point and results in fast narrow complex tachycardia (QRS < 0.12). It looks like a QRS complex followed immediately by a T wave, QRS complex, T wave and so on. Paroxysmal SVT describes a situation where SVT reoccurs and remits in the same patient over time. There are three main types of SVT based on the source of the electrical signal: “Atrioventricular nodal re-entrant tachycardia” is when the re-entry point is back through the AV node. “Atrioventricular re-entrant tachycardia” is when the re-entry point is an accessory pathway (Wolff-Parkinson-White syndrome). “Atrial tachycardia” is where the electrical signal originates in the atria somewhere other than the sinoatrial node. This is not caused by a signal re-entering from the ventricles but instead from abnormally generated electrical activity in the atria. This ectopic electrical activity causes an atrial rate of >100bpm. Acute Management of Stable patients with SVT When managing SVT take a stepwise approach trying each step to see whether it works before moving on. Make sure they are on continuous ECG monitoring. Valsalva manoeuvre. Ask the patient to blow hard against resistance, for example into a plastic syringe. Carotid sinus massage. Massage the carotid on one side gently with two fingers. Adenosine (see below) An alternative to adenosine is verapamil (calcium channel blocker) Direct current cardioversion may be required if the above treatment fails Adenosine Adenosine works by slowing cardiac conduction primarily though the AV node. It interrupts the AV node / accessory pathway during SVT and “resets” it back to sinus rhythm. It needs to be given as a rapid bolus to ensure it reaches the heart with enough impact to interrupt the pathway. It will often cause a brief period of asystole or bradycardia that can be scary for the patient and doctor, however it is quickly metabolised and sinus rhythm should return. A few key points on administering adenosine: Avoid if patient has asthma / COPD / heart failure / heart block / severe hypotension Warn patient about the scary feeling of dying / impending doom when injected Give as a fast IV bolus into a large proximal cannula (e.g. grey cannula in the antecubital fossa) Initially 6mg, then 12mg and further 12mg if no improvement between doses Long Term Management of patients with paroxysmal SVT When patients develops recurrent episodes of SVT then measures can be taken to prevent these episodes. The options are: Medication (beta blockers, calcium channel blockers or amiodarone) Radiofrequency ablation

Answer 57

Wolff-Parkinson White Syndrome is caused by an extra electrical pathway connecting the atria and ventricles. Normally there is only one pathway connecting the atria and ventricles called the atrio-ventricular node. The extra pathway that is present in Wolff-Parkinson White Syndrome is often called the Bundle of Kent. The definitive treatment for Wolff-Parkinson White syndrome is radiofrequency ablation of the accessory pathway. ECG Changes: Short PR interval (< 0.12 seconds) Wide QRS complex (> 0.12 seconds) “Delta wave” which is a slurred upstroke on the QRS complex Note: If the person has a combination of atrial fibrillation or atrial flutter and WPW there is a risk that the chaotic atrial electrical activity can pass through the accessory pathway into the ventricles causing a polymorphic wide complex tachycardia. Most antiarrhythmic medications (beta blockers, calcium channel blockers, adenosine etc) increase the risk of this by reducing conduction through the AV node and therefore promoting conduction through the accessory pathway – therefore they are contraindicated in patients with WPW that develop atrial fibrillation or flutter.

Answer 58

``` Radiofrequency Ablation (RFA) Catheter ablation is performed in a electrophysiology laboratory, often called a “cath lab”. It involves local or general anaesthetic, inserting a catheter in to the femoral veins and feeding a wire through the venous system under xray guidance to the heart. Once in the heart it is placed against different areas to test the electrical signals at that point. This way the operator can hopefully find the location of any abnormal electrical pathways. The operator may try to induce the arrhythmia to make the abnormal pathways easier to find. Once identified, radiofrequency ablation (heat) is applied to burn the abnormal area of electrical activity. This leaves scar tissue that does not conduct the electrical activity. The aim is to remove the source of the arrhythmia. ``` This can be curative for certain cases of arrhythmia caused by abnormal electrical pathways, including: Atrial Fibrillation Atrial Flutter Supraventricular Tachycardias Wolff-Parkinson-White Syndrome

Answer 59

Ventricular ectopics are premature ventricular beats caused by random electrical discharges from outside the atria. Patients often present complaining of random, brief palpitations (“an abnormal beat”). They are relatively common at all ages and in healthy patients however they are more common in patients with pre-existing heart conditions (e.g. ischaemic heart disease or heart failure). They can be diagnosed by ECG and appear as individual random, abnormal, broad QRS complexes on a background of a normal ECG. Bigeminy This is where the ventricular ectopics are occurring so frequently that they happen after every sinus beat. The ECG looks like a normal sinus beat followed immediately by an ectopic, then a normal beat, then ectopic and so on. Management Check bloods for anaemia, electrolyte disturbance and thyroid abnormalities Reassurance and no treatment in otherwise healthy people Seek expert advice in patients with background heart conditions or other concerning features or findings (e.g. chest pain, syncope, murmur, family history of sudden death)

Answer 60

Torsades de pointes is a type of polymorphic (multiple shape) ventricular tachycardia. It translates from French as “twisting of the tips”, describing the ECG characteristics. It looks like normal ventricular tachycardia on an ECG however there is an appearance that the QRS complex is twisting around the baseline. The height of the QRS complexes progressively get smaller, then larger then smaller and so on. It occurs in patients with a prolonged QT interval. A prolonged QT interval is the ECG finding of prolonged repolarisation of the muscle cells in the heart after a contraction. Depolarisation is the electrical process that leads to the heart contraction. Repolarisation is a period of recovery before the heart muscle cells (myocytes) are ready to depolarise again. Waiting a longer time for repolarisation can result in random spontaneous depolarisation in some areas of heart myocytes. These abnormal spontaneous depolarisations prior to repolarisation are known as “afterdepolarisations”. These depolarisations spread throughout the ventricle, leading to a ventricular contraction prior to proper repolarisation occurring. When this occurs and the ventricles continue to stimulate recurrent contractions without normal repolarisation it is called Torsades de pointes. When a patient develops Torsades de pointes it will either terminate spontaneously and revert back to sinus rhythm or progress in to ventricular tachycardia. Usually they are self limiting but if they progress to VT it can lead to a cardiac arrest. Causes of Prolonged QT Long QT Syndrome (inherited) Medications (antipsychotics, citalopram, flecainide, sotalol, amiodarone, macrolide antibiotics) Electrolyte Disturbance (hypokalaemia, hypomagnesaemia, hypocalcaemia) Acute Management of Torsades de pointes Correct the cause (electrolyte disturbances or medications) Magnesium infusion (even if they have a normal serum magnesium) Defibrillation if VT occurs Long Term Management of Prolonged QT Syndrome ``` Avoid medications that prolong the QT interval Correct electrolyte disturbances Beta blockers (not sotalol) Pacemaker or implantable defibrillator ```

Answer 61

- ST segment depression. - Deep T wave inversion. - Pathological Q waves: suggests a deep infarct and is a late sign.

Answer 62

1. Look for ST elevation greater than or equal to 0.2 millimeters and leads v1 to v3 or greater than or equal to 0.1mm, which is a small square on the ECG charts in any other leads. 2. left bundle branch block. If someone comes in with new LBBB, and they have a convincing history of MI, that convinces you that they are having a STEMI.

Answer 63

A number of studies over the past 10 years have provided an evidence for the management of ST-elevation myocardial infarction (STEMI) In the absence of contraindications, all patients should be given aspirin P2Y12-receptor antagonist. Clopidogrel was the first P2Y12-receptor antagonist to be widely used but now ticagrelor is often favoured as studies have shown improved outcomes compared to clopidogrel, but at the expense of slightly higher rates of bleeding. This approached is supported in SIGN's 2016 guidelines. They also recommend that prasugrel (another P2Y12-receptor antagonist) could be considered if the patient is going to have a percutaneous coronary intervention unfractionated heparin is usually given for patients who're are going to have a PCI. Alternatives include low-molecular weight heparin NICE suggest the following in terms of oxygen therapy: do not routinely administer oxygen, but monitor oxygen saturation using pulse oximetry as soon as possible, ideally before hospital admission. Only offer supplemental oxygen to: people with oxygen saturation (SpO2) of less than 94% who are not at risk of hypercapnic respiratory failure, aiming for SpO2 of 94-98% people with chronic obstructive pulmonary disease who are at risk of hypercapnic respiratory failure, to achieve a target SpO2 of 88-92% until blood gas analysis is available. Primary percutaneous coronary intervention (PCI) has emerged as the gold-standard treatment for STEMI but is not available in all centres. Thrombolysis should be performed in patients without access to primary PCI With regards to thrombolysis: tissue plasminogen activator (tPA) has been shown to offer clear mortality benefits over streptokinase tenecteplase is easier to administer and has been shown to have non-inferior efficacy to alteplase with a similar adverse effect profile

Answer 64

This patient has severe, symptomatic mitral stenosis. P Mitrale represents left atrial hypertrophy/strain e.g. in mitral stenosis The bifid P wave is termed P Mitrale since mitral valve stenosis is the commonest cause of its appearance on EC

Answer 65

The bifid P wave is termed P Mitrale since mitral valve stenosis is the commonest cause of its appearance on ECG. Right bundle branch block is often a sign of problems on the right side of the heart such as right ventricular hypertrophy, cor pulmonale, pulmonary embolism, and is not a common ECG finding in mitral stenosis. Left bundle branch block is also not a common finding in mitral stenosis, with common causes including ischaemic heart disease, hypertension, aortic stenosis, and cardiomyopathy. Tall Tented T waves are seen in hyperkalaemia, and P Pulmonale (which looks like a peaked P wave) reflects any process causing the right atrium to become hypertrophied such as tricuspid regurgitation and pulmonary hypertension.