Heart Arrhythmias: Tachycardia & Bradycardia

Taquiarrythmias

• Re-entry is the most common mechanism for tachyarrhythmias.
• Atrial fibrillation has a disorganized atrial rhythm with multiple re-entry circuits.
• Extreme bradycardia is not a trigger for sinus tachycardia.
• The sinoatrial (SA) node acts as the primary pacemaker of the heart in normal conditions.
• Paroxysmal supraventricular tachycardia is associated with Wolff-Parkinson-White syndrome.
• Atrial flutter type I is characterized by "sawtooth" waves on the ECG.
• Ventricular fibrillation increases the risk of sudden death and requires immediate defibrillation.
• Vagal maneuvers and adenosine are appropriate treatments for paroxysmal supraventricular tachycardia in a stable patient.
• Thromboembolism and stroke are important complications of atrial fibrillation.
• Sustained ventricular tachycardia is characterized by a duration longer than 30 seconds.

Bradyarrhythmias

• Bradyarrhythmia is defined as a heart rate slower than 60 bpm.
• Beta-blocker use is a frequent cause of sinus bradycardia.
• First-degree AV block on an ECG shows a prolonged PR interval without impeding conduction.
• Third-degree AV block is the most severe type of AV block and frequently requires a pacemaker.
• A characteristic ECG pattern of right bundle branch block is rSR' in V1-V2.
• Left anterior hemiblock is associated with left axis deviation.
• Trifascicular block is a combination of RBBB, LAHB/LPHB, and first-degree AV block.
• Brugada syndrome is a hereditary arrhythmia that can cause sudden death due to ventricular tachycardia.
• A prolonged QT interval on an ECG suggests long QT syndrome.
• Emotional stress or exercise can precipitate a crisis in long QT syndrome.

Antiarrhythmic Drugs

• Quinidine is a Class I antiarrhythmic that prolongs the action potential duration.
• Amiodarone carries a high risk of inducing pulmonary fibrosis.
• Beta-adrenergic blockers (Class II) reduce sympathetic stimulation of the heart.
• Procainamide use can lead to a lupus-like syndrome.
• Verapamil is a calcium channel blocker (Class IV).
• Esmolol, due to its short half-life, is frequently used in emergencies.
• Adenosine is used to treat paroxysmal supraventricular tachycardia because of its ability to induce transient AV block.
• Dronedarone is contraindicated in patients with heart failure due to its negative inotropic effect.
• Magnesium is useful for treating arrhythmias induced by hypokalemia or digitalis toxicity.
• Ivabradine blocks the If current in the SA node and treats inappropriate sinus tachycardia.

Hypertension

• The minimum value to define arterial hypertension, according to current guidelines, is ≥130/80 mmHg.
• Primary hypertension is the most common form of hypertension.
• Hepatic insufficiency is not a common cause of secondary hypertension.
• Excessive salt consumption is a modifiable risk factor for hypertension.
• The kidneys can be affected by long-term arterial hypertension.
• Left ventricular hypertrophy is common in patients with chronic arterial hypertension.
• Arterial pressure values of 180/120 mmHg indicate a hypertensive emergency.
• Lifestyle modification is the first-line treatment for primary hypertension.
• Enalapril is an angiotensin-converting enzyme (ACE) inhibitor.
• The eye suffers hypertensive retinopathy as a complication of uncontrolled hypertension.

Hypertension in Specific Cases

• Chronic hypertension in pregnancy is characterized by elevated blood pressure before pregnancy or before the 20th week of gestation, with or without proteinuria.
• Gestational hypertension is considered when blood pressure elevates after the 20th week of gestation, without proteinuria or clinical signs.
• Non-severe preeclampsia is defined by BP ≥ 140 mmHg systolic and ≥ 90 mmHg diastolic, with proteinuria of 300 mg/24 h.
• Severe preeclampsia signs include BP ≥ 160 mmHg systolic, ≥ 100 mmHg diastolic, with end-organ damage and risks like pulmonary edema, infarction, stroke, ARDS, and coagulopathies.
• The key factor in preeclampsia's pathogenesis is placental dysfunction, releasing toxic mediators that affect maternal blood vessels.
• Eclampsia's main clinical manifestations are tonic-clonic seizures, hyperreflexia, headache, and visual disturbances.
• Aging-related factors increasing blood pressure include arterial stiffness, reduced baroreceptor sensitivity, decreased renal flow, and increased peripheral vascular resistance.
• Women develop coronary artery disease later than men due to the protective effect of estrogen on the cardiovascular system.
• Chronic kidney disease affects between 10% and 15% of the world's population.
• Markers of kidney damage must persist for more than 3 months to diagnose chronic kidney disease.
• The glomerular filtration rate (GFR) indicates chronic kidney disease if it's under 60 ml/min/1.73 m².
• A healthy adult eliminates less than 150 mg of protein and less than 30 mg of albumin in urine per day.
• Target blood pressure in patients with chronic kidney disease without proteinuria is 140/90 mmHg.
• Target blood pressure in patients with chronic kidney disease with proteinuria is 130/80 mmHg.
• Management objectives for chronic kidney disease include avoiding exacerbating factors, slowing progression, treating complications like anemia, and adjusting medications based on renal function.

Antihypertensives

• The main anatomical sites where antihypertensives act are the heart, kidney, blood vessels, and brain.
• Diuretics reduce blood pressure by promoting sodium and water excretion, reducing blood volume.
• Renin activates the conversion of angiotensinogen to angiotensin I.
• ACE inhibitors work by inhibiting the conversion of angiotensin I to angiotensin II.
• Angiotensin II receptor antagonists (ARBs) do not cause a dry cough, unlike ACE inhibitors.
• ACE inhibitors are contraindicated in pregnancy because they can cause kidney damage to the fetus.
• Dihydropyridine calcium channel blockers act more on blood vessels, while non-dihydropyridines affect the heart more.
• Common adverse effects of direct vasodilators like hydralazine and minoxidil include reflex hypotension, tachycardia, and fluid retention.
• Sodium nitroprusside requires strict monitoring due to the risk of cyanide toxicity.
• When administering fenoldopam to patients with glaucoma, adjust the dose, as it can increase intraocular pressure.

Mechanism of action of calcium channel blockers (CCB)

• CCBs inhibit Ca2+ flow through L-type channels, causing smooth muscle relaxation & reduced peripheral resistance.
• A characteristic adverse effect of dihydropyridines is reflex tachycardia and peripheral edema.
• Verapamil and diltiazem have an antiarrhythmic effect as calcium channel blockers.
• Methyldopa is used to treat hypertension during pregnancy.
• An important adverse effect of sodium-glucose cotransporter 2 (SGLT2) inhibitors is an increased risk of genital mycotic infections.
• Furosemide can cause Ototoxicity.
• Thiazide diuretics are used for nephrolithiasis due to idiopathic hypercalciuria.
• Hyperkalemia is a characteristic adverse effect of potassium-sparing diuretics.
• Spironolactone, aldosterone antagonist cause gynecomastia as adverse effect.
• Mannitol is osmotic diuretic.

Atherosclerosis and Thrombi

• Atherosclerosis involves the formation of plaques in the arteries due to the accumulation of lipids and inflammatory cells.
• Age is a non-modifiable risk factor for atherosclerosis.
• LDL cholesterol contributes to atherosclerosis by transporting cholesterol to peripheral tissues and promoting plaque formation in the arteries.
• Hypertension increases mechanical stress on the arterial wall, fostering plaque formation.
• Smoking damages the vascular endothelium and encourages inflammation.
• Hypercholesterolemia increases the risk of diabetes and favors atherosclerosis
• C-reactive protein (CRP) is an inflammatory marker linked to atherosclerosis.
• Vulnerable atherosclerotic plaques have a thin fibrous cap and a higher risk of rupture.
• When an atherosclerotic plaque ruptures, it can trigger the activation of blood coagulation, leading to a heart attack or stroke.
• A thrombus that blocks an artery is the primary consequence when an atherosclerotic plaque ruptures.

Dyslipidemia

• The primary function of LDL is to transport cholesterol to the tissues.
• A high LDL level increases the risk of developing clogged arteries.
• Statins are the first-line treatment for dyslipidemia.
• Statins Lower cholesterol by inhibiting HMG-CoA reductase.
• A common adverse effect of statins is myopathy and the risk of rhabdomyolysis.
• Fibrates are most commonly used to reduce triglycerides.
• Niacin reduces LDL synthesis and increases HDL levels.
• Ionic exchange resins reduce cholesterol absorption.
• Ezetimibe reduces the amount of cholesterol absorbed in the intestine.
• The main therapeutic use for PCSK9 inhibitors is for the treatment of familial hypercholesterolemia.
• Anticoagulants mainly inhibit the coagulation cascade.
• Heparin functions mainly through inhibiting factor Xa and thrombin via antithrombin.

Anticoagulants

• Unfractionated heparin's therapeutic activity is monitored using the activated partial thromboplastin time (aPTT).
• Rivaroxaban is a direct factor Xa inhibitor.
• Heparin use has a common adverse effect of Heparin-induced thrombocytopenia (HIT).
• Fondaparinux is an anticoagulant administered subcutaneously once daily for treating venous thromboembolism.
• A major risk of warfarin use is major bleeding.
• Rivaroxaban does not require INR monitoring.
• Direct thrombin inhibitors like Dabigatran block the active site of thrombin.
• Bivalirudin is commonly used in cardiac procedures and is administered intravenously.
• Antiplatelet agents are intended to prevent blood clots by preventing platelet aggregation.
• Aspirin (Acetylsalicylic Acid - AAS) inhibits COX-1.

Antiplatelet Agents

• An adverse effect of aspirin is gastrointestinal bleeding risk
• Ticlopidine is a medicine used in brain procedures & based to ADP P2Y12
• Clopidogrel action mechanism has a blockade to the ADP P2Y receptors
• Abciximab is mainly used to block GP IIb/IIIa & has a anti thromboses effect mostly
• Cilostazol is a vasodilator with use with aspririn used against brain ischemia
• Cilostazol blocks phosphodiesterase and improves circulation with claudication
• Streptokinase promotes indirectly plasminogen, in thrombosis or pulmanory emobolism
• Alteplasa (t-PA recombinante) use is for severe IAM miocardium attacks.

Heart Failure

• Coronary artery disease is a common cause of heart failure.
• In stage B heart failure, structural heart disease is present without symptoms of heart failure.
• Reduced myocardial contractility primarily contributes to systolic dysfunction in heart failure.
• Left ventricular dysfunction is associated with pulmonary congestion and reduced cardiac output.
• Ineffective compensatory mechanisms found in heart failure , but not the Frank-Starling mechanism.
• Fluid overload and increased pressure are common to be seen in Congestive heart failiure.
• The main respiratory symptom of is acute pulmanory edemas.
• Natriuretic peptides are elevated diagnostic in heart failure.
• High-output failure can happen from severe anemia.
• Atrial fibrillation is the most frequent arrythmia with heart falliures.
• Heart failiure drugs use for cardiac arrest the action is on a positive inotropic drugs.
• Digoxin in severe heart arrest action, the main action its caused by inhibitors Na+ / K+ ATPase, with calcium increasing.
• Gynecomastia is a rare side efect that causes the digoxin drug.
• Acute heart failure often needs the Levosimendan.
• Spironolactone (aldosterone antagonist) often used in heart failure.
• IECAs benifits for heart failiure are to lower periphical or aftercharge resistence.

Heart Failure Classes

• Heart Failiure classes mainly inatopic are in case of heart sistolic failiure.
• Hidralazina drug reduce pre and aftercharge in heart arrest & vasodilation.
• Betablockers effects on heart arrest, helps to reduce Cardiac Frecuency / remodelling.
• Valsartan combined with Sucabrilo uses is mostly when less Ejecttion.
• The aneurisms main effect can see all layers of the Arteria & its True (Verdadero).
• Risk factos of aortic anyeurisms are High arterial Pressures, Smokes & deficiency of Vitamine C.
• DIssections its due to Gentical connectios issues, or High arterial Pressures.
• The age to have desiction problems is 40~60 Years.
• The chests & intense pain is the Desicttion main sytomps
• The main diagnostic for aneurysm is TAC scanner or ecocardio transmural.
• Anyerisma Complications its by breakage or ruputres.

Cardiomyopathies & Valve Conditions

• Anyerasm genetically conditions are due to Marfan Sindrome
• Cardiac dessecion & aneurisms uses TAC / ecocardio transofagica
• ichemec conditions the coronaries problems cause Descendent Ant. & Izq
• The Noo way to solve those damages are mostly by smoking / high blood pressures.
• BioMarker helps to diagnosers the myocardial is to analyse theTroponinas
• Infarcts due to myocardium caused due to Transmoral transmural
• Angins Variant / Prinzmetal its presented with coronaries spasm usually.
• Angina that doesnt respond to vasodialters but infects the microcirculating is cause by Síndrome X
• The main miocardium effect its due to Arteriosclerosis
• Most common symptoms during an heart failure its high chest pains.
• Pericarditis is connected with dilations of ventriculous.
• High tropminas distinguish a higher segmet compared with lesser in the ST during heart failliures.

Drugs / treatments

• Nitriglicerina Its mainly action mechanisim its by releasing an NOx to dilate the vasculation system.
• Ranolazina drugs is mainly helps with hygh pressures problems.
• Calcium blocker drugs does effects in most heart patients but can cause high pressures / edeams.
• labradina drugs is mainly for angina stabilies & to lower the frequencys.
• Beta Blockers are mainl contraindicates for Asthma.
• Ranalozine helps to with high blood pressure & the calcium overload.
• The drugs with 6~8hr action helps to make profilaxis the heart stabilising action.
• High headaches and most common for nitrate drug effects.
• Sildefanil is to not have hypotension effect
• Caused by sarcomere protein with mutations & caused by genetics . Heart high pressure is common.
• Genetics mutations problems with Heart & protient C problems cause a heart faliure.
• The cause of young athelties heart arrrests its due ventriculous A

I hope these notes are helpful for your studies!