Exam 4 - Notes Week 1 to 5 Flashcards

Question

Topic 1: An Introduction to the ECG * TLO 4.1.1: Identify components of the normal ECG (P wave, QRS complex, T wave) and their intervals.

Answer 1

o P wave: Atrial depolarization. o QRS complex: Ventricular depolarization. o T wave: Ventricular repolarization. o PR interval: Time from the start of atrial depolarization to the start of ventricular depolarization. o QT interval: Time from the start of ventricular depolarization to the end of ventricular repolarization.

Answer 2

o P wave: Electrical activity during atrial depolarization (atrial contraction). o QRS complex: Reflects electrical activity during ventricular depolarization (ventricular contraction). o T wave: Represents ventricular repolarization.

Answer 3

o Lead placement and represented cardiac structures:  Limb leads (I, II, III): Bipolar; record differences in electrical potential between limbs.  Augmented limb leads (aVR, aVL, aVF): Unipolar; record potential between one limb and the average of the other two.  Chest leads (V1-V6): Unipolar; record potential between the chest electrode and a central reference point. Each lead views the heart from a different angle to provide comprehensive electrical information.

Answer 4

 Represents the overall direction of ventricular depolarization in the frontal plane.  Provides information about the heart's orientation and can indicate conditions like hypertrophy or bundle branch blocks.

Answer 5

 The direction of deflection (upward or downward) depends on the direction of the electrical vector relative to the lead axis.  A wave moving towards a positive electrode produces an upward deflection, and vice versa.

Answer 6

o Rate: Determine heart rate (e.g., by counting large squares between R waves and dividing 300 by that number). o Rhythm: Assess regularity of R-R intervals (e.g., sinus rhythm vs. irregular rhythm). o Axis: Evaluate the general direction of ventricular depolarization. o Hypertrophy: Look for signs of atrial or ventricular enlargement (e.g., tall R waves, wide P waves). o Ischemia: Identify changes indicating reduced blood flow to the heart muscle (e.g., ST-segment depression or elevation, T wave inversion).

Answer 7

o Sinus rhythm: Normal P wave preceding each QRS complex, regular R-R intervals, rate 60-100 bpm. o Sinus bradycardia: Sinus rhythm with a heart rate <60 bpm. o Sinus tachycardia: Sinus rhythm with a heart rate >100 bpm. o Left axis deviation: Axis between -30° and -90°. o Right axis deviation: Axis between +90° and +180°.

Answer 8

o Tachyarrhythmia: An arrhythmia with a heart rate greater than 100 bpm. o Clinical manifestations: Palpitations, presyncope, syncope, chest pain, dyspnea.

Answer 9

 Risk factors/etiology: Ischemic heart disease, cardiomyopathy, electrolyte imbalances.  ECG: Wide QRS complexes, rate >100 bpm, often regular rhythm.  Pathophysiology: Rapid firing of one or more ventricular ectopic foci.

Answer 10

 Risk factors/etiology: Severe cardiac disease, myocardial infarction.  ECG: Chaotic, irregular deflections; no distinct waves or complexes.  Pathophysiology: Uncoordinated ventricular electrical activity leading to ineffective contraction.

Answer 11

 Risk factors/etiology: Severe cardiac disease, myocardial infarction.  ECG: Chaotic, irregular deflections; no distinct waves or complexes.  Pathophysiology: Uncoordinated ventricular electrical activity leading to ineffective contraction.

Answer 12

 Risk factors/etiology: Similar to AF; often associated with structural heart disease.  ECG: Sawtooth pattern of flutter waves, usually regular ventricular response (but can be irregular).  Pathophysiology: A re-entrant circuit in the atria.

Answer 13

 Risk factors/etiology: Often occurs in young individuals; can be triggered by stress, caffeine.  ECG: Narrow QRS complex tachycardia, often with absent or hidden P waves.  Pathophysiology: Re-entrant circuit involving the AV node or an accessory pathway.

Answer 14

o Bradyarrhythmia: An arrhythmia with a heart rate less than 60 bpm. o Clinical manifestations: Lethargy, syncope, palpitations, heart failure

Answer 15

 ECG: Prolonged PR interval (>200 ms).  Risk factors/etiology: Medications, increased vagal tone, conduction system disease.  Pathophysiology: Delay in AV node conduction.

Answer 16

 ECG: Progressive PR interval lengthening until a QRS complex is dropped.  Risk factors/etiology: Medications, increased vagal tone, inferior wall MI.  Pathophysiology: Progressive AV node conduction delay.

Answer 17

 ECG: Consistent PR intervals with intermittent dropped QRS complexes.  Risk factors/etiology: Conduction system disease, anterior wall MI.  Pathophysiology: Abrupt, intermittent block in the His-Purkinje system.

Answer 18

o ECG (12-lead). o Holter monitor (24-hour ECG). o Loop recorder (long-term ECG monitoring). o Pacemaker interrogation.

Answer 19

 Hemodynamic instability (e.g., hypotension, shock).  Thromboembolism (especially AF).  Heart failure.

Answer 20

o Na+ channel blockers. o β-blockers. o K+ channel blockers. o Ca2+ channel blockers.

Answer 21

 Syncope.  Heart failure.  Asystole (cardiac arrest).

Answer 22

o Na+ channel blockers: Slow conduction velocity by blocking sodium channels. o β-blockers: Decrease heart rate and contractility by blocking β-adrenergic receptors. o K+ channel blockers: Prolong repolarization by blocking potassium channels. o Ca2+ channel blockers: Reduce contractility and conduction by blocking calcium channels.

Answer 23

o Defibrillation: Electrical shock to terminate life-threatening arrhythmias (VF, VT). o Pacemakers:  Transcutaneous pacing: Temporary pacing via skin electrodes.  Permanent pacing: Implanted device to regulate heart rhythm. o Ablation: Procedure to destroy arrhythmogenic tissue.

Answer 24

o Address underlying conditions (e.g., hypertension, heart disease). o Avoid triggers (e.g., caffeine, alcohol). o Maintain a healthy lifestyle (diet, exercise). 1

Answer 25

Amiodarone  Amiodarone is not a calcium channel blocker. It is an antiarrhythmic which works by prolonging the action potential duration, prolonging there fractory period by acting at potassium channels, and affecting the flow of ions across the membrane.

Answer 26

a. 0.06–0.10secs  ventricular depolarization represented by QRS complex is normally 0.06-0.10 secs

Answer 27

b. Ventricular fibrillation  In ventricular fibrillation, the electrocardiogram is bizarre and ordinarily shows no tendency toward a regular rhythm of any type

Answer 28

d. Depolarization of the area of the heart near the base  The QRS complex shows the depolarization of the ventricles, which also masks the repolarization of the atria. The S wave represents the depolarization of the area of the heart near the base

Answer 29

e. It may be due to multiple re-entrant excitation waves in the atria Atrial fibrillation is due to multiple circulating re-entrant excitation in theatria. This results in an irregular and fast atrial rate (up to 500 per minute).Hence the AV node also discharges at an irregular, but slower rate (about90–150 beats per minutes). P waves cannot usually be detected on theECG

Answer 30

a. Conduction through theatrioventricular node takeslonger than normal,prolonging the PR interval  First-degree atrioventricular (AV) block occurs whenconduction through the AV node takes longer thannormal.

Answer 31

b. PRinterval  The PR interval is the time from the onset of the P wave to the start of the QRScomplex. It reflects conduction through the AV node

Answer 32

a. Atropine  Atropine is a muscarinic receptor antagonist, producing an initial bradycardiabecause of central stimulation, followed by tachycardia (the vagus is blockedso that sympathetic effect is unopposed)

Answer 33

atrial fibrillation ECG Rate control What is the most likely diagnosis? Answer = Paroxysmal atrial fibrillation What is the next diagnostic step? Answer = Electrocardiogram What is the next step in therapy? Answer = Anticoagulation and rate control Considerations: This 54-year-old patient has several risk factors for the development of atrial fibrillation. Hypertension,obesity, sleep apnea, and heavy alcohol consumption–especially binge drinking–are all associated with agreater risk for atrial fibrillation. Thus, while other supraventricular tachycardias are possible, atrialfibrillation or atrial flutter is the most likely diagnosis. The irregularly irregular pulse is also verysuggestive. An ECG should confirm the diagnosis and differentiate between atrial fibrillation and atrialflutter. The first priority should be prevention of thromboembolic stroke, which is perhaps the directconsequence of atrial fibrillation or flutter. For most patients and for patients in whom an early rhythmcontrol strategy is planned, stroke prevention requires systemic anticoagulation with warfarin or a noveloral anticoagulant (NOAC). Control of the ventricular rate is also important to limit symptoms and toavoid the deleterious effects of persistent tachycardia on left ventricular function. Rate control isgenerally achieved with negatively chronotropic drugs such as beta-blockers and nondihydropyridinecalcium channel blockers such as diltiazem. Acute cardioversion of atrial fibrillation or atrial flutter episodes with a definite onset within the last 48hours can be considered, although in this case the onset of symptoms is outside this timeframe. Ifspontaneous conversion to sinus rhythm does not occur, cardioversion can be undertaken after either atleast 3 weeks of therapeutic anticoagulation or a transesophageal echocardiogram demonstrating theabsence of left atrial appendage thrombus. Underlying potentially reversible causes of atrial fibrillation such as hyperthyroidism should beexcluded, and an echocardiogram to assess for structural heart disease– especially mitral valve diseaseand left ventricular dysfunction–should be ordered. Patients with symptoms or signs suggestive ofcoronary artery disease may require noninvasive testing to exclude active ischemia. TLO 4.3.4: Describe the pathophysiological process - Focus conditions: atrial fibrillation Topic 6: Management of Arrhythmias and Lifestyle Modifications TLO 4.6.1: Identify appropriate pharmacological management options for the treatment of arrhythmias * Na+ channel blockers * β-blockers * K+ blockers * Ca2+ channel blockers TLO 4.6.2: Describe the mechanism of action for each of the options identified in TLO 4.6.1 TLO 4.6.3: Identify and describe appropriate interventional approaches to arrhythmias: * defibrillation * pacemakers –transcutaneous and permanent pacing * ablation TLO 4.6.4: Identify the lifestyle modifications required for secondary

Answer 34

Capillaries are the smallest blood vessels in the body, designed to facilitate the exchange of substances between blood and tissues. Their key features include: * Single endothelial cell layer: Very thin walls (one cell thick) to allow for efficient exchange. * No smooth muscle: Unlike arterioles or venules, capillaries lack smooth muscle in their walls. * Basement membrane: Surrounds the endothelium and supports the capillary structure. * Pores or fenestrations: Depending on type (continuous, fenestrated, or sinusoidal), capillaries can have tight or leaky junctions for selective permeability

Answer 35

Diffusion * Movement of solutes (e.g., oxygen, carbon dioxide, glucose) down their concentration gradient. * Most important mechanism for exchange across capillaries. * Lipid-soluble substances (e.g., O₂, CO₂) pass directly through endothelial cells; water-soluble substances pass through intercellular clefts or pores. 2. Osmosis * Movement of water across a semi-permeable membrane from a region of lower solute concentration to one of higher solute concentration. * Driven by osmotic gradients created mainly by plasma proteins (especially albumin). 3. Bulk Flow * Movement of large volumes of fluid (and some solutes) in or out of capillaries due to pressure differences. * Two types: o Filtration: Fluid moves out of the capillary into the interstitial space (usually at the arterial end). o Reabsorption: Fluid moves back into the capillary (usually at the venous end).

Answer 36

Four pressures determine the direction of fluid movement (Starling forces): 1. Capillary Hydrostatic Pressure (CHP) * Pushes fluid out of the capillary. * Higher at the arterial end, lower at the venous end. * Promotes filtration. 2. Interstitial Fluid Hydrostatic Pressure (IFHP) * Pressure exerted by fluid in the interstitial space. * Usually low or slightly negative, so it may assist filtration. 3. Blood Colloid Osmotic Pressure (BCOP or πc) * Created by plasma proteins, primarily albumin. * Pulls fluid into the capillary. * Promotes reabsorption. 4. Interstitial Fluid Colloid Osmotic Pressure (IFCOP or πi) * Caused by proteins in the interstitial fluid. * Pulls fluid out of the capillary. * Promotes filtration, but normally this pressure is low. Net Filtration Pressure (NFP) = (CHP + IFCOP) − (BCOP + IFHP) Starling's forces explain how fluid moves in and out of tiny blood vessels (capillaries). Two main forces are at play: - Hydrostatic pressure: This pushes fluid out of the capillaries into surrounding tissues. - Oncotic pressure: This pulls fluid back into the capillaries, thanks to proteins like albumin in the blood. The balance between these forces determines whether fluid stays in the blood vessels or leaks into tissues. If this balance is disrupted, it can lead to swelling (oedema). - Capillary Hydrostatic Pressure: Pushes fluid out of the capillaries into surrounding tissues. - Interstitial Hydrostatic Pressure: Pushes fluid back into the capillaries from the surrounding tissues. - Capillary Oncotic Pressure: Pulls fluid into the capillaries due to plasma proteins like albumin. - Interstitial Oncotic Pressure: Pulls fluid out of the capillaries into the surrounding tissues due to proteins in the interstitial space.

Answer 37

The lymphatic system: * Collects excess fluid and proteins from the interstitial space that are not reabsorbed by capillaries (~10% of filtered fluid). * Returns this fluid to the venous circulation, maintaining fluid balance. * Helps prevent edema (swelling due to fluid accumulation). * Also plays roles in immune defense and fat absorption (via lacteals in the intestine).

Answer 38

Arterial End Venous End (Filtration) (Reabsorption) --------------------------------------------------------------- Blood Flow → → → → → → → → → → → → → → → → → → → → → ↑ ↑ ↑ [CHP high] [CHP lower] [BCOP constant] (push fluid out) (less push out) (pulls fluid back in) ← Interstitial Space ← ← ← ← ← ← ← ← ← ← ← ← ← ← ← ← ← Net Movement: ➤ Filtration at arterial end (fluid leaves capillary) ➤ Reabsorption at venous end (fluid returns) ➤ Excess fluid goes to lymphatic system

Answer 39

Force Symbol Direction Effect Capillary Hydrostatic Pressure CHP Out of capillary Promotes filtration Interstitial Fluid Hydrostatic Pressure IFHP Into capillary (usually) Opposes filtration Blood Colloid Osmotic Pressure BCOP Into capillary Promotes reabsorption Interstitial Fluid Colloid Osmotic Pressure IFCOP Out of capillary Promotes filtration

Answer 40

* Picks up ~10% of fluid not reabsorbed. * Prevents swelling (edema). * Returns fluid/proteins to blood. * Supports immune and fat transport functions.

Answer 41

Oedema is the accumulation of excess fluid in the interstitial (extracellular) space, leading to swelling of tissues. It occurs when fluid filtration exceeds reabsorption and lymphatic drainage.

Answer 42

There are four main mechanisms of oedema: 1. ↑ Capillary Hydrostatic Pressure (CHP) o Too much pressure pushes fluid out of the capillaries into tissues. o Common in heart failure, venous obstruction, or fluid overload. 2. ↓ Plasma Oncotic Pressure (↓BCOP) o Less protein (esp. albumin) in blood means less fluid is pulled back into the capillary. o Seen in liver failure, nephrotic syndrome, malnutrition. 3. ↑ Capillary Permeability o Leaky capillaries let proteins and fluid escape into interstitial space. o Occurs in inflammation, allergic reactions, burns. 4. Lymphatic Obstruction (↓Drainage) o Lymph system fails to remove excess interstitial fluid. o Can be caused by tumors, infections (e.g. filariasis), or surgery.

Answer 43

Mechanism Common Causes ↑ Capillary Hydrostatic Pressure - Congestive heart failure - Deep vein thrombosis - Pregnancy (compression of venous return) - Excess IV fluids ↓ Plasma Oncotic Pressure - Liver disease (↓ albumin production) - Nephrotic syndrome (protein loss in urine) - Malnutrition (low protein intake) ↑ Capillary Permeability - Sepsis - Burns - Trauma - Allergic reactions Lymphatic Obstruction - Cancer (e.g. lymph node invasion) - Lymph node removal (post-surgery) - Parasitic infection (e.g. filariasis)

Answer 44

General Symptoms (what patients feel): * Swelling (feet, legs, hands, face) * Weight gain * Abdominal discomfort/distention (due to ascites) * Breathlessness (if pulmonary oedema) Physical Signs (what you find on exam): Site Manifestation Legs/Ankles Pitting oedema (indentation when pressed) Lungs Pulmonary oedema → breathlessness, crackles, pulmonary infiltrates on X-ray Neck veins Raised Jugular Venous Pressure (JVP) in right heart failure Liver Hepatomegaly (enlarged liver from congestion) Abdomen Ascites (fluid in peritoneal cavity; tense, distended abdomen)

Answer 45

↓↓↓ Oedema (Tissue Swelling) ↓↓↓ ↓ ┌─────────────────────────────────────────────────────┐ │ Causes of Oedema (4 Mechanisms) │ └─────────────────────────────────────────────────────┘ ↓ ┌────────────────────┬────────────────────┬────────────────────┬─────────────────────┐ │ ↑ Capillary │ ↓ Plasma │ ↑ Capillary │ ↓ Lymphatic │ │ Hydrostatic │ Oncotic Pressure │ Permeability │ Drainage │ │ Pressure (CHP) │ (↓BCOP) │ │ │ ├────────────────────┼────────────────────┼────────────────────┼─────────────────────┤ │ - Heart failure │ - Liver disease │ - Inflammation │ - Tumors │ │ - DVT │ - Nephrotic │ - Allergic rxns │ - Filariasis │ │ - IV overload │ - Malnutrition │ - Burns, trauma │ - Surgery (lymph │ │ │ │ │ node removal) │ └────────────────────┴────────────────────┴────────────────────┴─────────────────────┘

Answer 46

Q1: What is oedema? A1: Oedema is the excess accumulation of fluid in the interstitial space, causing tissue swelling. ________________________________________ Q2: Name the 4 main mechanisms of oedema. A2: 1. ↑ Capillary hydrostatic pressure 2. ↓ Plasma oncotic pressure 3. ↑ Capillary permeability 4. ↓ Lymphatic drainage ________________________________________ Q3: What are 2 conditions that lower plasma oncotic pressure? A3: * Liver disease (↓ albumin production) * Nephrotic syndrome (protein loss in urine) ________________________________________ Q4: What are common signs of pulmonary oedema? A4: * Breathlessness * Crackles on auscultation * Pulmonary infiltrates on chest X-ray ________________________________________ Q5: What causes pitting oedema? A5: Increased interstitial fluid compresses tissue when pressed, leaving a visible dent. ________________________________________ Q6: What is ascites, and what can cause it? A6: Ascites is fluid buildup in the abdominal cavity; causes include liver cirrhosis and right heart failure.

Answer 47

Heart failure (HF) is a clinical syndrome where the heart is unable to pump blood effectively to meet the metabolic demands of the body, or it can only do so at the cost of increased filling pressures. * May involve systolic dysfunction (↓ contractility) or diastolic dysfunction (↓ filling). * Also known as congestive heart failure (CHF) when fluid accumulation is prominent.

Answer 48

Major Risk Factors: * Hypertension * Coronary artery disease (CAD) * Diabetes mellitus * Valvular heart disease * Obesity * Smoking * Sedentary lifestyle * Family history of cardiomyopathy Common Aetiologies: Cause Mechanism Ischemic heart disease MI leads to scarred myocardium → systolic failure Hypertension Chronic ↑ afterload → LV hypertrophy → dysfunction Valvular disease Volume/pressure overload (e.g., aortic stenosis) Cardiomyopathies Dilated, hypertrophic, or restrictive types Arrhythmias Impaired cardiac output (e.g., AF) Infections (e.g., viral myocarditis) Direct myocardial damage

Answer 49

A. AHA/ACC Stages of HF (focuses on disease progression): Stage Description A At risk (e.g., HTN, diabetes), no structural disease B Structural heart disease, no symptoms C Structural disease + prior/current symptoms D Refractory HF needing advanced interventions B. NYHA Functional Classification (focuses on symptoms): Class Symptoms I No limitation of physical activity II Slight limitation (comfortable at rest) III Marked limitation (less than ordinary activity causes symptoms) IV Symptoms at rest

Answer 50

Pathophysiology: * Left ventricle can't effectively pump blood → blood backs up into lungs → pulmonary congestion. * Decreased cardiac output → ↓ perfusion to tissues. Clinical Features: Symptoms (what patient feels): * Dyspnoea (especially on exertion) * Orthopnoea (needs to sit up to breathe) * Paroxysmal nocturnal dyspnoea (wakes up gasping) * Fatigue * Exercise intolerance Signs (what you find on exam/investigations): * Pulmonary crackles * Tachypnoea * S3 gallop * Pulmonary oedema on chest X-ray * Elevated BNP or NT-proBNP

Answer 51

Pathophysiology: * Right ventricle fails → blood backs up into systemic circulation * Often secondary to left-sided failure or pulmonary disease (cor pulmonale) Clinical Features: Symptoms: * Swelling of feet/ankles * Abdominal discomfort (due to ascites or hepatomegaly) * Fatigue * Weight gain (fluid retention) Signs: * Raised jugular venous pressure (JVP) * Pitting peripheral oedema * Hepatomegaly * Ascites * Right ventricular heave

Answer 52

Cardiac remodeling is the structural and functional change in the size, shape, and function of the heart after stress or injury, such as myocardial infarction, hypertension, or volume overload. * It involves changes at the cellular and molecular level (e.g., hypertrophy, fibrosis). * Remodeling can be adaptive at first but becomes maladaptive over time, leading to heart failure.

Answer 53

Cause Mechanism Hypertension Pressure overload → LV hypertrophy Myocardial infarction (MI) Loss of contractile tissue → dilation Valvular heart disease Pressure or volume overload (e.g., AS, MR) Cardiomyopathies Genetic or acquired changes in heart muscle Chronic sympathetic stimulation ↑ Catecholamines → hypertrophy, fibrosis Neurohormonal activation RAAS, natriuretic peptides → volume changes Inflammation or infection Viral myocarditis or autoimmune responses

Answer 54

What is Concentric Remodeling? * Occurs in pressure overload states (e.g., chronic hypertension, aortic stenosis). * Characterized by: o Increased wall thickness o No change or reduction in chamber size o ↑ Relative wall thickness o Sarcomeres added in parallel ⚠️ Complications: * ↓ Diastolic compliance → diastolic heart failure (HFpEF) * Increased risk of arrhythmias * Myocardial ischemia (due to impaired coronary perfusion) * Progression to eccentric hypertrophy if pressure overload persists

Answer 55

What is Eccentric Remodeling? * Occurs in volume overload states (e.g., mitral or aortic regurgitation, post-MI) * Characterized by: o Dilated chamber o Thinner walls relative to chamber size o Sarcomeres added in series ⚠️ Complications: * Systolic dysfunction → HFrEF (Heart Failure with Reduced Ejection Fraction) * Progressive ventricular dilation * Functional mitral regurgitation * ↑ Wall stress and oxygen demand * Ventricular arrhythmias, especially in dilated ventricles ________________________________________ 🧠 Mnemonic Tip: “C” for Concentric = “Contracted walls” “E” for Eccentric = “Enlarged chamber”

Answer 56

TLO 3.5.1: Steps to Diagnose Heart Failure 1. History Look for symptoms suggestive of heart failure: * Dyspnoea (especially on exertion, orthopnoea, PND) * Fatigue, weakness * Swelling in ankles/legs * Weight gain (fluid retention) * Nocturia, palpitations, or chest discomfort 2. Clinical Examination Look for signs: * Raised JVP * Pulmonary crackles (basal) * S3 gallop * Peripheral oedema * Hepatomegaly, ascites * Tachycardia, hypotension, or cool peripheries 3. Diagnostic Tests

Answer 57

Test Use/Findings ECG May show LVH, past MI, atrial fibrillation, bundle branch blocks BNP / NT-proBNP Elevated in heart failure due to ventricular stretch (helps differentiate dyspnoea causes) Troponin Rules out/ischaemia or myocardial infarction Chest X-ray (CXR) Detects signs of pulmonary congestion or cardiomegaly Echocardiogram Gold standard to assess EF (ejection fraction), wall motion, valve function Bloods U&Es, LFTs, FBC, TSH – check for contributing causes or complications (e.g., anaemia, CKD)

Answer 58

CXR Feature Interpretation Alveolar oedema “Batwing” perihilar pattern – indicates pulmonary oedema Upper lobe diversion Redistribution of blood flow to upper lobes (CHF sign) Cardiomegaly Cardiothoracic ratio >50% Pleural effusions Usually bilateral, more on the right Kerley B lines Short horizontal lines at lung bases – indicate interstitial oedema

Answer 59

Acute Complications * Acute pulmonary oedema * Cardiogenic shock * Arrhythmias (e.g., AF, VT/VF) * Renal dysfunction Chronic Complications * Progressive decline in EF * Thromboembolism * Liver congestion → cardiac cirrhosis * Cachexia and muscle wasting * Anemia and hyponatraemia

Answer 60

Initial Management of ADHF: 1. Oxygen Therapy: o Administer oxygen if hypoxemia is present. o Non-invasive ventilation (NIV), such as CPAP (Continuous Positive Airway Pressure) or BiPAP (Bilevel Positive Airway Pressure), is often used in acute pulmonary oedema to improve oxygenation and reduce preload. 2. Diuretics: o Frusemide (Furosemide) – Loop diuretic:  Mechanism: Inhibits sodium and chloride reabsorption in the loop of Henle, leading to increased urine output.  Indication: Relieves pulmonary congestion and peripheral oedema.  Dose: Initial bolus, followed by continuous infusion or repeated bolus, depending on severity.  Monitor: Electrolytes, renal function, and fluid status. 3. Vasodilators: o Nitrates (e.g., nitroglycerin):  Mechanism: Venodilation (reduces preload) and arterial dilation (reduces afterload), leading to reduced myocardial oxygen demand.  Indication: Severe pulmonary oedema and when BP allows for vasodilation.  Administration: Sublingual or IV. 4. Inotropic Support (if necessary): o Dobutamine (Beta-1 agonist):  Mechanism: Increases myocardial contractility and cardiac output.  Indication: Used in cases of cardiogenic shock with severe hypotension. o Milrinone (Phosphodiesterase inhibitor):  Mechanism: Increases cardiac contractility and vasodilation.  Indication: Often used when dobutamine is ineffective or contraindicated. 5. Monitoring: o Regular assessment: Monitor vital signs, oxygenation, urine output, electrolytes, and acid-base status.

Answer 61

Pharmacologic Management of Chronic Heart Failure: 1. ACE Inhibitors (e.g., Enalapril, Lisinopril): o Mechanism: Inhibits conversion of angiotensin I to angiotensin II → vasodilation, reduced preload/afterload, and improved renal perfusion. o Indication: Standard treatment for systolic heart failure to reduce symptoms and mortality. o Monitor: Renal function, potassium levels (risk of hyperkalemia), blood pressure. 2. Angiotensin Receptor Blockers (ARBs) (e.g., Losartan, Valsartan): o Mechanism: Block angiotensin II receptors, providing similar benefits as ACE inhibitors with less risk of cough. o Indication: For patients intolerant to ACE inhibitors. 3. Angiotensin Receptor-Neprilysin Inhibitors (ARNI) (e.g., Sacubitril/Valsartan): o Mechanism: Combines ARB (Valsartan) with neprilysin inhibitor (Sacubitril) to reduce vasoconstriction, sodium retention, and myocardial fibrosis. o Indication: Standard therapy for patients with HFrEF (Heart Failure with Reduced Ejection Fraction). 4. Beta-blockers (e.g., Metoprolol, Carvedilol, Bisoprolol): o Mechanism: Reduce sympathetic nervous system activation, decreasing heart rate, blood pressure, and myocardial oxygen demand. o Indication: First-line for chronic heart failure to improve symptoms, prevent hospitalization, and prolong survival. o Monitor: Heart rate, blood pressure, and signs of fluid retention. 5. Mineralocorticoid Receptor Antagonists (MRAs) (e.g., Spironolactone, Eplerenone): o Mechanism: Block aldosterone effects → reduces sodium and water retention, and prevents myocardial fibrosis. o Indication: Beneficial in HFrEF, improves survival, and reduces hospitalizations. o Monitor: Renal function, potassium levels (risk of hyperkalemia). 6. SGLT2 Inhibitors (e.g., Dapagliflozin, Empagliflozin): o Mechanism: Inhibit sodium-glucose co-transporter 2, reducing glucose reabsorption in the kidneys and promoting natriuresis. o Indication: Shown to improve outcomes in both diabetic and non-diabetic patients with heart failure. o Monitor: Renal function, electrolytes, and risk of dehydration. 7. Digoxin: o Mechanism: Increases myocardial contractility and decreases heart rate through inhibition of Na+/K+ ATPase. o Indication: Used for rate control in atrial fibrillation and in severe heart failure for symptom relief. o Monitor: Serum digoxin levels, renal function, and electrolytes (especially potassium).

Answer 62

* Lifestyle modification: Weight management, low-sodium diet, fluid restriction. * Exercise: Regular, moderate activity as tolerated. * Device therapy: o Implantable cardioverter-defibrillator (ICD) for prevention of sudden cardiac death in high-risk patients. o Cardiac resynchronization therapy (CRT) for patients with intraventricular conduction delay (e.g., wide QRS).

Answer 63

Shock is a syndrome characterized by impaired tissue perfusion, resulting in cellular hypoxia and potential organ failure. It is usually classified based on its etiology:

Answer 64

Types of Shock: 1. Hypovolemic Shock: o Caused by decreased blood volume (e.g., hemorrhage, dehydration, fluid loss). 2. Cardiogenic Shock: o Caused by impaired cardiac function leading to inadequate cardiac output (e.g., acute myocardial infarction, heart failure). 3. Distributive Shock (e.g., septic shock, neurogenic shock, anaphylactic shock): o Caused by vasodilation and abnormal distribution of blood flow. 4. Obstructive Shock: o Caused by physical obstruction of blood flow (e.g., massive pulmonary embolism, cardiac tamponade, tension pneumothorax).

Answer 65

There are typically four stages of shock based on severity and clinical progression: 1. Compensated Shock (Non-progressive stage): * Body compensates for reduced perfusion using mechanisms like vasoconstriction, tachycardia, and fluid retention to maintain blood pressure and perfusion. * Clinical signs: Cold extremities, mild tachycardia, low-normal blood pressure, increased respiratory rate. 2. Progressive Shock: * The compensatory mechanisms begin to fail as the body is unable to maintain adequate perfusion. * Clinical signs: Hypotension, marked tachycardia, oliguria, altered mental status (confusion, lethargy). 3. Irreversible Shock: * Organ damage becomes irreversible; cells undergo necrosis, leading to multi-organ failure. * Clinical signs: Severe hypotension, bradycardia, severe metabolic acidosis, loss of consciousness, and multi-organ failure.

Answer 66

Pathophysiology: 1. Reduced Cardiac Output: o A fall in stroke volume (SV) and heart rate results in decreased cardiac output. 2. Compensatory Mechanisms: o Activation of sympathetic nervous system (SNS) and renin-angiotensin-aldosterone system (RAAS) to increase heart rate and vasoconstrict. 3. Increased Preload: o Venous congestion occurs due to backward failure (blood accumulates in the venous system), causing pulmonary edema or systemic edema. 4. Impaired Oxygen Delivery: o Decreased cardiac output leads to tissue hypoxia, organ dysfunction, and metabolic acidosis. 5. Metabolic Derangements: o Lactate accumulation and acidosis occur as cells switch to anaerobic metabolism.

Answer 67

1. Stage 1 (Initial Stage): o Clinical Manifestations: Mild hypotension, increased heart rate, mild tachypnea. o Compensatory Mechanisms: SNS and RAAS activation maintain blood pressure. 2. Stage 2 (Progressive Stage): o Clinical Manifestations: Severe hypotension (< 90 mmHg), rapid tachycardia, cold extremities, oliguria, restlessness. o Pathophysiology: Decreased perfusion to organs, worsening metabolic acidosis, and impaired oxygen delivery. 3. Stage 3 (Irreversible Stage): o Clinical Manifestations: Severe hypotension, bradycardia, altered consciousness, multi-organ failure. o Pathophysiology: Extensive tissue damage, irreversible cell death, and failure of compensatory mechanisms.

Answer 68

General Measures: * Oxygen therapy: To improve tissue oxygenation. * Monitoring: Continuous monitoring of vital signs, urine output, and central venous pressure (CVP). * Intensive care: Most patients require ICU admission. 2. Pharmacologic Treatment: * Inotropes (e.g., dobutamine, milrinone): o Mechanism: Increase myocardial contractility and cardiac output. * Vasopressors (e.g., norepinephrine, dopamine): o Mechanism: Vasoconstriction to improve systemic vascular resistance and raise blood pressure. * Diuretics (e.g., furosemide): o Mechanism: Reduce pulmonary edema and venous congestion by promoting fluid excretion. 3. Mechanical Support: * Intra-aortic balloon pump (IABP): o Mechanism: Increases coronary perfusion and reduces afterload by inflating during diastole and deflating during systole. * Left ventricular assist device (LVAD): o Used in refractory cases of cardiogenic shock when other treatments are ineffective. 4. Treatment of Underlying Cause: * Revascularization: Percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG) in cases of acute myocardial infarction. * Valve repair/replacement: In cases of valvular heart disease. 5. Fluid Management: * Careful fluid resuscitation: Use judiciously to avoid fluid overload, which can worsen pulmonary congestion.

Answer 69

Summary of Key Management Points for Cardiogenic Shock: * Inotropes and vasopressors to maintain cardiac output and blood pressure. * Oxygen therapy to prevent tissue hypoxia. * Diuretics for fluid management, avoiding volume overload. * Mechanical support devices (IABP, LVAD) in refractory cases. * Revascularization or surgery to treat the underlying cardiac condition.

Answer 70

A:Major Arteries : Aorta/ carotid arteries/ subclavian arteries/ renal arteries/ femoral arteries. [cite: 1/ 2/ 3] Major Veins : Superior vena cava (SVC)/ inferior vena cava (IVC)/ jugular veins/ femoral veins/ renal veins. [cite: 1/ 2/ 3] Lymphatics : Thoracic duct/ lymph nodes near major vessels. [cite: 1/ 2/ 3/ 4]

Answer 71

A:Conducting Arteries : Large elastic arteries (e.g./ aorta); expand and recoil to maintain blood flow during diastole. [cite: 4/ 5/ 6] Distributing Arteries : Medium muscular arteries; regulate blood flow to specific organs. [cite: 4/ 5/ 6] Small Arteries/Arterioles : Smooth muscle regulates resistance; critical for blood pressure control. [cite: 4/ 6/ 7]

Answer 72

A:Venules : Small/ collect blood from capillaries. [cite: 7/ 8] Medium Veins : Contain valves to prevent backflow. [cite: 7/ 8/ 9] Large Veins : Thick walls/ large lumen (e.g./ IVC/ SVC). [cite: 7/ 9]

Answer 73

A:Arteries : Thick tunica media with elastic fibers; narrow lumen. [cite: 10/ 11] Veins : Thin tunica media; wider lumen; valves present. [cite: 10/ 11]

Answer 74

A:Flow = Pressure difference ÷ Resistance. [cite: 12/ 13] High pressure or low resistance increases flow. [cite: 12/ 13]

Answer 75

A:Preload : Volume of blood in ventricles at end-diastole; affected by venous return and ventricular compliance. [cite: 14/ 15] Afterload : Resistance the ventricles must overcome; determined by arterial pressure and vascular resistance. [cite: 15/ 16]

Answer 76

A:Cardiac Output (CO) = Heart Rate (HR) × Stroke Volume (SV). [cite: 17] Influenced by preload/ contractility/ afterload/ and heart rate. [cite: 17]

Answer 77

A:MAP = Diastolic Pressure + (1/3 × Pulse Pressure). [cite: 18/ 19]

Answer 78

A:Cardiac Output (CO) : Heart rate × Stroke volume. [cite: 19/ 20/ 21] Total Peripheral Resistance (TPR) : Resistance in systemic vasculature. [cite: 19/ 20/ 21] Stroke Volume (SV) : Volume of blood pumped per heartbeat. [cite: 20/ 21] Heart Rate (HR) : Beats per minute. [cite: 20/ 21]

Answer 79

A:↑ CO or TPR → ↑ MAP. [cite: 22] ↓ CO or TPR → ↓ MAP. [cite: 22/ 23]

Answer 80

A:Factors: Autonomic regulation/ blood volume/ vascular tone. [cite: 23/ 24] Effect: Adjusted MAP (↑ or ↓). [cite: 23/ 24]

Answer 81

A:Continuous partial contraction of smooth muscle; influenced by sympathetic nervous system and local factors. [cite: 24/ 25]

Answer 82

A:Control vascular tone to regulate blood flow and blood pressure. [cite: 26/ 27]

Answer 83

A:Sympathetic Nervous System : Vasoconstriction → ↑ BP. [cite: 28/ 29] Adrenaline/Noradrenaline : Vasoconstriction; ↑ BP. [cite: 28/ 29] Histamine : Vasodilation; ↓ BP. [cite: 28/ 29] Angiotensin II : Vasoconstriction; ↑ BP. [cite: 29/ 30] Vasopressin : Vasoconstriction; ↑ BP. [cite: 29/ 30] Vasodilator Nerves : Relaxation; ↓ BP. [cite: 30/ 31] ANP : Vasodilation; ↓ BP. [cite: 30/ 31]

Answer 84

A:Regulate local blood flow based on tissue needs. [cite: 31/ 32]

Answer 85

A:O2 : Vasoconstriction in systemic circulation; vasodilation in lungs. [cite: 33/ 34] CO2 : Vasodilation → ↑ local blood flow. [cite: 33/ 34] Lactic Acid : Vasodilation → ↑ local blood flow. [cite: 34/ 35] Adenosine : Vasodilation → ↑ local blood flow. [cite: 34/ 35] Nitric Oxide : Vasodilation; ↓ BP. [cite: 35/ 36] Endothelin-1 : Vasoconstriction; ↑ BP. [cite: 35/ 36]

Answer 86

A:Heart : Maintains flow during pressure changes. [cite: 36/ 37] Brain : Regulates flow based on CO2 levels. [cite: 36/ 37] Kidneys : Adjusts based on filtration needs. [cite: 37/ 38] Lungs : Responds to O2 levels. [cite: 37/ 38] Skeletal Muscle : Adjusts based on demand. [cite: 38/ 39] Skin : Responds to temperature. [cite: 38/ 39]

Answer 87

A:Locations: Carotid sinus/ aortic arch. [cite: 39/ 40] Function: Detect pressure changes and adjust autonomic output. [cite: 39/ 40]

Answer 88

A:Sympathetic activation: ↑ BP. [cite: 41/ 42] Parasympathetic activation: ↓ BP. [cite: 41/ 42]

Answer 89

A:Pressure change detected → Signal to medulla → Adjusts HR/ vascular tone. [cite: 42/ 43]

Answer 90

A:Kidneys : Release renin. [cite: 44/ 45] Liver : Produces angiotensinogen. [cite: 44/ 45] Lungs : Contain ACE (angiotensin-converting enzyme). [cite: 44/ 45] Adrenal Cortex : Releases aldosterone. [cite: 44/ 45]

Answer 91

A:Maintains blood pressure and fluid balance by regulating vasoconstriction and sodium retention. [cite: 46/ 47]

Answer 92

A:Renin converts angiotensinogen to angiotensin I. [cite: 47/ 48/ 49] ACE converts angiotensin I to angiotensin II. [cite: 47/ 48/ 49] Angiotensin II causes vasoconstriction and stimulates aldosterone release. [cite: 47/ 48/ 49] Aldosterone promotes sodium and water retention. [cite: 48/ 49]

Answer 93

A:Overactive RAAS → Hypertension due to increased vasoconstriction and fluid retention. [cite: 49/ 50/ 51] Underactive RAAS → Hypotension due to decreased vascular resistance and fluid loss. [cite: 49/ 50/ 51]

Answer 94

A:High salt intake suppresses renin release. [cite: 51/ 52] Low salt intake stimulates renin release. [cite: 51/ 52]

Answer 95

A:Definition : Persistent systolic BP ≥140 mmHg or diastolic BP ≥90 mmHg. [cite: 53/ 54] Types : Primary (essential) hypertension: No identifiable cause (~90–95% of cases). [cite: 55/ 56] Secondary hypertension: Due to an underlying condition (e.g./ renal disease/ endocrine disorders). [cite: 55/ 56]

Answer 96

A:Epidemiology : Common in adults/ higher prevalence with age. [cite: 57/ 58] Risk factors : Obesity/ sedentary lifestyle/ high salt intake/ stress/ genetics. [cite: 57/ 58]

Answer 97

A:Increased vascular resistance due to endothelial dysfunction/ reduced nitric oxide/ and increased sympathetic tone. [cite: 58/ 59]

Answer 98

A:Definition : Severe BP elevation (≥180/120 mmHg) with potential end-organ damage. [cite: 60/ 61] Pathogenesis : Sudden vasoconstriction/ arterial injury/ and ischemia. [cite: 60/ 61]

Answer 99

A:Normal : <120/80 mmHg. [cite: 61/ 62/ 63] Elevated : Systolic 120–129 mmHg/ diastolic <80 mmHg. [cite: 61/ 62/ 63] Stage 1 : Systolic 130–139 mmHg or diastolic 80–89 mmHg. [cite: 62/ 63] Stage 2 : Systolic ≥140 mmHg or diastolic ≥90 mmHg. [cite: 62/ 63/ 64]

Answer 100

A:Often asymptomatic ("silent killer"). [cite: 64/ 65] Symptoms: Headache/ dizziness/ visual changes/ chest pain in advanced cases. [cite: 64/ 65]

Answer 101

A:Multiple BP measurements over time. [cite: 65/ 66/ 67] Ambulatory BP monitoring. [cite: 65/ 66/ 67] Assessment for end-organ damage (e.g./ ECG/ urine analysis). [cite: 65/ 66/ 67]

Answer 102

A:Lifestyle modifications. [cite: 67/ 68] First-line medications: ACE inhibitors/ ARBs/ β-blockers/ calcium channel blockers/ thiazide diuretics. [cite: 67/ 68]

Answer 103

A:ACE Inhibitors : Block conversion of angiotensin I to angiotensin II. [cite: 68/ 69/ 70/ 71] ARBs : Block angiotensin II receptors. [cite: 68/ 69/ 70/ 71] β-blockers : Reduce heart rate and contractility. [cite: 68/ 69/ 70/ 71] Calcium Channel Blockers : Reduce vascular smooth muscle contraction. [cite: 68/ 69/ 70/ 71] Thiazide Diuretics : Increase sodium and water excretion. [cite: 68/ 69/ 70/ 71]

Answer 104

A:IV antihypertensives (e.g./ nitroprusside/ labetalol). [cite: 71/ 72] Gradual BP reduction to prevent ischemia. [cite: 71/ 72]

Answer 105

A:Cardiovascular: Left ventricular hypertrophy/ heart failure/ atherosclerosis. [cite: 72/ 73/ 74] Cerebral: Stroke/ hypertensive encephalopathy. [cite: 72/ 73/ 74] Renal: Chronic kidney disease. [cite: 73/ 74] Ocular: Hypertensive retinopathy. [cite: 73/ 74]

Answer 106

A:Atherosclerosis : Endothelial damage → plaque formation. [cite: 74/ 75/ 76/ 77/ 78] Aortic Dissection : Weakening of arterial walls. [cite: 74/ 75/ 76/ 77/ 78] Left Ventricular Hypertrophy : Increased workload → myocardial thickening. [cite: 74/ 75/ 76/ 77/ 78] Heart Failure : Chronic pressure overload → pump failure. [cite: 74/ 75/ 76/ 77/ 78] Stroke : Vessel rupture or occlusion. [cite: 74/ 75/ 76/ 77/ 78] Nephropathy : Glomerular damage → proteinuria. [cite: 74/ 75/ 76/ 77/ 78] Retinopathy : Vascular damage → vision loss. [cite: 74/ 75/ 76/ 77/ 78]

Answer 107

A:Weight loss/ reduced salt intake/ regular exercise/ DASH diet/ stress reduction/ smoking cessation. [cite: 78]

Answer 108

c. Antidiuretic hormone is released when arise in osmolarity is detected. Increased plasma osmolarity will stimulate antidiuretic hormone release.

Answer 109

d. Constriction of cutaneous arterioles brought about by the baroreceptor reflex can be overcome by thermoregulatory changes in vascular tone. The baroreceptor reflex is important in the cutaneous circulation if the temperature is neutral but can be overcome if there is peripheral vasodilation due to high temperature

Answer 110

Arteries typically have higher blood pressure, necessitating thicker, more elastic walls than veins Arteries have thicker, more elastic walls than veins to handle the higher pressure of blood flow

Answer 111

e. Emergency hypertension Acute, severe elevation of blood pressure (>220/130) most likely associated with objective findings of acute end-organ damage

Answer 112

e. ACE inhibitors —angio-oedema, cough, postural hypotension, hyperkalaemia, progression of renal failure and first-dose hypotension

Answer 113

e. There is evidence of rapidly progressive end organ damage Malignant hypertension is often associated with acute end-organ damage, including the eyes

Answer 114

c. Venous compliance Baroreceptor reflex after bleeding will lead to sympathetic stimulation resulting in venous constriction as a result of decreased venous compliance to allow for increased venous return

Answer 115

e. Angiotensin I toAngiotensin II ACE inhibitors stop action of ACE to convert Angiotensin I to angiotensin II

Answer 116

e. Thiazide diuretics —hypercholesterolaemia, hyperglycaemia, thrombocytopenia and gout Your concern is the risk factor of hyperglycaemia from a thiazide diuretic with a patient who already had hyperglycaemia from uncontrolled diabetes

Answer 117

d. Hematocrit Hematocrit reflect blood viscosity, if it decreases resistance is decreased and allow to increase blood flow to the organ

Answer 118

c. Angiotensin II Angiotensin II is a potent vasoconstrictor

Answer 119

d. Capillaries The capillaries have the lowest velocity of flow in the systemic circuit. This reduced flow rate is essential for allowing sufficient time for the exchange of gases, nutrients, and waste products between blood and tissues

Answer 120

e. Obesity Obesity is a modifiable risk factor for hypertension

Answer 121

e. binds to β1-adrenergicreceptors on cardiac myocytes this is one of the responses to positive inotropic effects of sympathetic stimulation on the heart and how it increases cardiac output

Answer 122

b. Increases aldosterone secretion and increases vasoconstriction It is a powerful vasoconstrictor and stimulates adrenal glands to produce aldosterone

Answer 123

A: Mediastinum: Contains the heart, thymus, trachea, esophagus, and major vessels. Pleural Cavities: Contain the lungs and pleural membranes. [cite: 1, 2]

Answer 124

A: Boundaries : Superior: Thoracic inlet. Inferior: Diaphragm. Anterior: Sternum. Posterior: Vertebral column. Lateral: Pleural cavities. Divisions : Superior mediastinum, and inferior mediastinum (further divided into anterior, middle, and posterior). [cite: 3, 4]

Answer 125

A: Superior Mediastinum: Thymus, great vessels, trachea, esophagus, thoracic duct, vagus and phrenic nerves. Inferior Mediastinum: Anterior : Fat, lymph nodes, thymic remnants. Middle : Heart, pericardium, roots of great vessels, phrenic nerves. Posterior : Esophagus, descending aorta, azygos veins, thoracic duct, sympathetic trunks. [cite: 5, 6, 7, 8]

Answer 126

A: Structure : Fibrous Pericardium: Outer layer that protects and anchors the heart. [cite: 9, 10] Serous Pericardium: Divided into parietal and visceral layers with a pericardial cavity containing lubricating fluid. [cite: 11] Blood Supply : Pericardiophrenic artery, branches of bronchial and esophageal arteries. [cite: 12] Innervation : Phrenic nerve, vagus nerve, and sympathetic trunks. [cite: 12]

Answer 127

,A: Protects the heart. Reduces friction with pericardial fluid. [cite: 13, 14] Prevents overdistension of the heart. Anchors the heart in place. [cite: 14]

Answer 128

A: Structure : Four chambers (right atrium, right ventricle, left atrium, left ventricle), valves (tricuspid, mitral, pulmonary, aortic), and layers (endocardium, myocardium, epicardium). [cite: 15] Great Vessels : Superior and inferior vena cava. Pulmonary arteries and veins. Aorta. [cite: 15, 16]

Answer 129

A: Right Coronary Artery : Branches into right marginal artery and posterior interventricular artery, supplying the right atrium, right ventricle, and parts of the left ventricle and interventricular septum. [cite: 17, 18] Left Coronary Artery : Branches into the circumflex artery and anterior interventricular artery (LAD), supplying the left atrium, left ventricle, and anterior interventricular septum. [cite: 19]

Answer 130

,A: Deoxygenated blood: Body → Right atrium → Right ventricle → Lungs. [cite: 20, 21, 22] Oxygenated blood: Lungs → Left atrium → Left ventricle → Body. [cite: 21, 22]

Answer 131

A: Right Side: Thinner walls, pumps deoxygenated blood to the lungs (low pressure). [cite: 23, 24, 25] Left Side: Thicker walls, pumps oxygenated blood to the body (high pressure). [cite: 24, 25]

Answer 132

A: Location : In the thoracic cavity, within the mediastinum, posterior to the sternum and resting on the diaphragm. [cite: 26, 27] Orientation : Apex points downward, forward, and to the left (at 5th intercostal space). [cite: 28]

Answer 133

A: Aorta: Ascends, arches over the heart, descends into the thorax and abdomen. [cite: 29, 30, 31] Pulmonary Trunk: Exits the right ventricle and splits into pulmonary arteries. [cite: 31] Superior/Inferior Vena Cava: Drain blood into the right atrium. [cite: 31]

Answer 134

A: Carotid artery (neck). Radial/ulnar arteries (wrist). [cite: 32, 33] Apical impulse (5th intercostal space). Femoral and popliteal arteries. [cite: 33]

Answer 135

A: Aortic valve: Right 2nd intercostal space. Pulmonary valve: Left 2nd intercostal space. Tricuspid valve: Left 4th intercostal space near sternum. [cite: 34, 35] Mitral valve: Left 5th intercostal space, midclavicular line. [cite: 35]

Answer 136

A: Atrial Systole : Atria contract, filling the ventricles. [cite: 36] Ventricular Systole : Isovolumetric contraction (pressure builds, valves closed). [cite: 36, 37] Ventricular ejection (blood exits via semilunar valves). [cite: 37] Diastole : Isovolumetric relaxation (pressure drops). Ventricular filling (passive flow). [cite: 37]

Answer 137

A: Blood moves from high-pressure to low-pressure areas. Valves prevent backflow (AV valves into atria; semilunar valves into ventricles). [cite: 38, 39]

Answer 138

A: Composed of cardiac muscle cells (cardiomyocytes) . [cite: 40, 41, 42] Arranged in spiral or circular bundles for contraction efficiency. [cite: 41, 42] Contains intercalated discs (gap junctions and desmosomes) for synchronized contraction. [cite: 42]

Answer 139

A: Cylindrical, striated muscle cells with a central nucleus. Rich in mitochondria for high energy demands. [cite: 43, 44] Interconnected by intercalated discs, allowing electrical and mechanical continuity. [cite: 44]

Answer 140

A: Cardiac Output (CO) = Heart Rate (HR) × Stroke Volume (SV). [cite: 45] Determinants: Heart rate (sympathetic and parasympathetic regulation). [cite: 45, 46] Stroke volume (preload, afterload, and contractility). [cite: 46]

Answer 141

A: Muscle pump action. Intrathoracic pressure changes (respiration). [cite: 46, 47] Venous valve function. Blood volume and venous tone. [cite: 47]

Answer 142

A: Atrioventricular (AV) Valves : Tricuspid (right), Mitral (left). [cite: 47, 48, 49] Supported by chordae tendineae and papillary muscles . [cite: 48, 49] Semilunar Valves : Pulmonary (right ventricle), Aortic (left ventricle). [cite: 49] Pocket-like cusps prevent backflow. [cite: 49]

Answer 143

A: AV valves: Prevent backflow from ventricles to atria during systole. [cite: 50, 51] Semilunar valves: Prevent backflow from arteries into ventricles during diastole. [cite: 51]

Answer 144

A: S1 ("lub"): Closure of AV valves at the start of systole. [cite: 52, 53] S2 ("dub"): Closure of semilunar valves at the start of diastole. [cite: 53]

Answer 145

A: Regurgitation: Backflow of blood due to incomplete valve closure. Stenosis: Narrowing of valve, increasing resistance to flow. [cite: 54]

Answer 146

A: Sinoatrial (SA) node. Atrioventricular (AV) node. [cite: 54, 55, 56] Bundle of His. Right and Left Bundle Branches. Purkinje fibers. [cite: 56]

Answer 147

A: SA node initiates impulse → spreads to atria → AV node delays conduction → travels via Bundle of His and bundle branches → Purkinje fibers stimulate ventricles. [cite: 56, 57]

Answer 148

A: SA node: Pacemaker, initiates electrical impulses (~60–100 bpm). [cite: 58, 59] AV node: Delays conduction to allow atrial contraction. [cite: 59] Purkinje fibers: Ensure rapid conduction for coordinated ventricular contraction. [cite: 60]

Answer 149

A: Resting Membrane Potential: Stable potential before excitation. Depolarization: Sodium influx rapidly increases voltage. Plateau Phase: Calcium influx sustains contraction. [cite: 60, 61, 62] Repolarization: Potassium efflux restores resting potential. [cite: 62]

Answer 150

A: Depolarization triggers contraction. [cite: 62, 63] Plateau phase corresponds to sustained contraction for blood ejection. [cite: 63] Repolarization allows relaxation and filling. [cite: 63]

Answer 151

A: Action potential opens voltage-gated calcium channels → calcium influx triggers sarcoplasmic reticulum calcium release → actin-myosin interaction → contraction. [cite: 63, 64]

Answer 152

A: Longer duration (~200 ms). [cite: 65, 66] Plateau phase due to calcium influx, important for sustained contraction. [cite: 66]

Answer 153

A: Spontaneous depolarization (automaticity). [cite: 66, 67] No true resting potential. Key ions: Sodium, potassium, calcium. [cite: 67]

Answer 154

A: Sympathetic nerves: Increase heart rate and contractility. Parasympathetic (vagus) nerves: Decrease heart rate. Autonomic control influences conduction speed and rhythm. [cite: 68, 69]

Answer 155

A: Releases noradrenaline . [cite: 70, 71] Increases SA node firing rate, conduction velocity, and force of contraction. [cite: 71]

Answer 156

A: Releases acetylcholine . [cite: 72, 73] Slows SA node firing, reduces heart rate, and prolongs conduction time. [cite: 73]

Answer 157

A: Autonomic nervous system activity. Hormones (e.g., adrenaline). Electrolyte levels (potassium, calcium). Drugs (e.g., beta-blockers, calcium channel blockers). [cite: 74, 75] Ischemia or infarction affecting conduction tissue. [cite: 75]

Answer 158

SA node -> AV node -> Bundle if his -> Bundle branches -> Purkinje fibers

Answer 159

QRS prolongation

Answer 160

b. Isovolumetric relaxation

Answer 161

d. Rostral ventrolateral medulla (RVLM)

Answer 162

e. Phase 0

Answer 163

b. Striated muscle tissue arranged in a branching pattern

Answer 164

b. Potassium channels

Answer 165

c. The apex of the heart is anterior to its base

Answer 166

a. The coronary sulcus

Answer 167

d. Composed of three parts: collagen with some elastic fibres leaflets; fine, strong fibrous ligaments and papillary muscles

Answer 168

d. Reduced ventricular ejection ECG Wave Cardiac Cycle Phase Event P wave Atrial systole Atrial depolarization QRS complex Isovolumetric contraction & rapid ventricular ejection Ventricular depolarization & onset of systole T wave Reduced ventricular ejection Ventricular repolarization End of T wave Isovolumetric relaxation Completion of repolarization, onset of diastole

Answer 169

a. AP Cardiac muscle can occur in cardiac muscles other than SA & AV AP SA Node -AP Cardiac muscle Occur in pacemaker cells -Occur in cardiac muscles other than SA and AV Driven by funny current Na channels -Driven by stimulus, no funny current Unstable RMP (-50 to -90 mV) -Stable RMP -90 mV Only 3 phases -4 phases Automaticity is possible -No automaticity Feature Pacemaker AP (SA, AV Nodes) Non-Pacemaker AP (Cardiac Muscle) Location SA node, AV node Atria, ventricles, Purkinje fibers Resting Membrane Potential Unstable (~-60mV, drifts up) Stable (~-90mV) Phase 4 (Initiation) Driven by funny current (If, Na⁺) Maintains resting potential Depolarization (Phase 0) Ca²⁺ influx (L-type channels) Na⁺ influx (fast sodium channels) Phases Three phases (4, 0, 3) Five phases (4, 0, 1, 2, 3) Repolarization (Phase 3) K⁺ efflux K⁺ efflux Automaticity Present (spontaneous depolarization) Absent (requires stimulus)

Answer 170

d. The right coronary artery supplies part of left ventricle

Answer 171

d. 3.2 Litres/minute Cardiac output= SV X HR. 40 x 80= 3.2 L/min

Answer 172

1. Definition: Murmurs are abnormal heart sounds caused by turbulent blood flow. 2. Causes: Narrowed or leaky valves, high blood flow states, or heart defects. 3. Inspiration Effect: Right-sided murmurs get louder. 4. Expiration Effect: Left-sided murmurs get louder. 5. Valsalva Effect: Straining makes most murmurs quieter, except HCM and MVP. 6. Handgrip Effect: Louder murmurs from leaky valves, quieter murmurs from narrow valves.

Answer 173

1. S3 Sound: Happens after S2; normal in young people but abnormal in heart failure. 2. S4 Sound: Happens before S1; always abnormal, linked to stiff ventricles.

Answer 174

1. Aortic Stenosis: Systolic murmur, harsh sound heard at the right chest, radiates to neck. 2. Aortic Regurgitation: Diastolic blowing sound, heard at left chest, radiates down. 3. Mitral Stenosis: Diastolic rumble with snap, heard at heart apex. 4. Mitral Regurgitation: Constant, high-pitched murmur at heart apex, radiates to armpit.

Answer 175

1. What is it: Narrow valve stops blood from leaving the heart. 2. Symptoms: Chest pain, fainting, shortness of breath. 3. Treatment: Surgery for severe cases.

Answer 176

1. What is it: Narrow valve blocks blood from the atrium to the ventricle. 2. Symptoms: Difficulty breathing, fatigue, and coughing blood. 3. Treatment: Balloon procedure or surgery.

Answer 177

1. What is it: Valve doesn’t close properly, letting blood flow backward. 2. Symptoms: Pounding heartbeat, tiredness, and breathlessness. 3. Treatment: Medications or valve surgery.

Answer 178

1. What is it: Blood flows backward from the ventricle to the atrium. 2. Symptoms: Fatigue, heart palpitations, and breathing problems. 3. Treatment: Valve repair or replacement.

Answer 179

1. Intervals: o PR Interval: Start of atrial contraction to start of ventricular contraction. o QT Interval: Start of ventricular contraction to end of ventricular relaxation.

Answer 180

1. ECG Components: o P Wave: Atrial contraction. o QRS Complex: Ventricular contraction. o T Wave: Ventricular relaxation.

Answer 181

1. Key Steps: o Rate: Measure heartbeats per minute. o Rhythm: Check if beats are regular or irregular. o Axis: See the heart’s electrical direction. o Hypertrophy: Look for bigger chambers (e.g., tall waves). o Ischemia: Spot signs of poor blood flow (e.g., ST changes).

Answer 182

1. How is a 12-lead ECG set up? o Limb Leads (I, II, III): Compare electrical signals between limbs. o Augmented Leads (aVR, aVL, aVF): Measure one limb's signal compared to others. o Chest Leads (V1-V6): Detect heart's electrical signals from chest views.

Answer 183

1. Sinus Rhythms: o Normal Rhythm: Regular beats, rate 60–100 bpm. o Bradycardia: Beats slower than 60 bpm. o Tachycardia: Beats faster than 100 bpm.

Answer 184

1. What are they? o Heart rate above 100 bpm; symptoms include palpitations and fainting.

Answer 185

1. Ventricular Tachycardia (VT): o ECG: Wide QRS, fast and regular. o Cause: Heart disease, low electrolytes.

Answer 186

1. Ventricular Fibrillation (VF): o ECG: Chaotic, no clear waves. o Cause: Serious heart damage.

Answer 187

1. Atrial Fibrillation (AF): o ECG: No P waves, irregular beats. o Cause: Age, high blood pressure.

Answer 188

1. Atrial Flutter: o ECG: Sawtooth pattern. o Cause: Heart structure issues.

Answer 189

1. What are they? o Heart rate below 60 bpm; symptoms include fainting, tiredness.

Answer 190

1. Supraventricular Tachycardia (SVT): o ECG: Narrow QRS. o Cause: Stress, caffeine.

Answer 191

1. Heart Blocks: o 1st Degree Block: Long PR interval; slow signal through AV node. o 2nd Degree Type I (Wenckebach): PR gets longer until one beat drops. o 2nd Degree Type II: Dropped beats without warning. o 3rd Degree Block: No connection between atrial and ventricular beats.

Answer 192

1. How to diagnose arrhythmias: o ECG, Holter monitor, or long-term devices (e.g., loop recorder).

Answer 193

1. Complications: o Fast rhythms: Can cause low blood pressure or clots. o Slow rhythms: Can lead to fainting or cardiac arrest.

Answer 194

1. Medications: o Sodium blockers: Slow conduction. o Potassium blockers: Slow relaxation. o Calcium blockers: Reduce heart muscle strength. o Beta blockers: Lower heart rate.

Answer 195

1. Procedures: o Defibrillation: Shock to restart normal rhythm. o Pacemaker: Controls heartbeats. o Ablation: Removes faulty tissue.

Answer 196

What are capillaries? * Smallest blood vessels, allowing exchange of substances between blood and tissues.

Answer 197

1. Lifestyle Tips: o Fix heart risks (e.g., high blood pressure). o Avoid triggers like alcohol. o Stay healthy with good diet and exercise.

Answer 198

Key features: * Single thin cell layer for exchange. * No smooth muscle in walls. * Basement membrane supports the structure. * Pores or fenestrations for selective permeability.

Answer 199

3. Processes across capillary walls: * Diffusion: Moves solutes (e.g., O₂, glucose) down concentration gradients. * Osmosis: Water moves toward higher solute concentrations.

Answer 200

5. Lymphatic system role: * Collects extra fluid (~10%) from interstitial space. * Prevents swelling (edema) and maintains fluid balance.

Answer 201

CAPILLARIES * Bulk Flow: o Filtration: Fluid out of capillaries (arterial end). o Reabsorption: Fluid back into capillaries (venous end).

Answer 202

Signs and symptoms of edema: * Swollen limbs, pitting (press leaves a dent). * Pulmonary edema: Shortness of breath. * Ascites: Fluid in abdomen (distended belly).

Answer 203

4. Factors affecting exchange: * Capillary hydrostatic pressure (CHP): Pushes fluid out. * Blood colloid osmotic pressure (BCOP): Pulls fluid in. * Interstitial pressures (IFHP, IFCOP): Affect outward/inward movement.

Answer 204

1. What is edema? * Fluid buildup in interstitial spaces causing swelling.

Answer 205

2. Causes of edema: * ↑ Hydrostatic Pressure: E.g., heart failure, venous blockage. * ↓ Oncotic Pressure: Low proteins (e.g., albumin) from malnutrition or liver/kidney issues. * ↑ Capillary Permeability: From trauma, inflammation. * Lymph Obstruction: E.g., cancer, infections, post-surgery.

Answer 206

Definition: * Heart can’t pump blood effectively to meet the body’s demands.

Answer 207

2. Types of dysfunction: * Systolic failure (reduced contraction). * Diastolic failure (reduced filling).

Answer 208

3. Risk factors: * High blood pressure, coronary artery disease, diabetes. * Obesity, smoking, sedentary lifestyle.

Answer 209

Symptoms: * Breathlessness, fatigue, swollen limbs, chest discomfort.

Answer 210

5. Stages (AHA/ACC): * A: Risk only (e.g., diabetes, no disease). * B: Structural issues, no symptoms. * C: Symptoms + structural issues. * D: Severe disease, needing advanced care.

Answer 211

1. What is cardiac remodeling? * Changes in heart size, shape, or function after stress (e.g., MI, hypertension).

Answer 212

2. Types of remodeling: * Concentric: Thick walls due to pressure overload (e.g., hypertension). * Eccentric: Dilated chambers due to volume overload (e.g., valve regurgitation).

Answer 213

3. Complications: * Concentric: Stiff heart (diastolic heart failure), arrhythmias. * Eccentric: Weak heart (systolic failure), progressive dilation.

Answer 214

1. What is shock? * Poor tissue perfusion causing cellular and organ failure.

Answer 215

2. Types of shock: * Hypovolemic: Low blood volume (e.g., bleeding, dehydration). * Cardiogenic: Heart pump failure (e.g., MI). * Distributive: Poor blood flow distribution (e.g., sepsis). * Obstructive: Blood flow blockage (e.g., pulmonary embolism).

Answer 216

3. Stages of shock: * Compensated: Body tries to adjust (cold hands, faster pulse). * Progressive: BP drops; confusion, less urine output. * Irreversible: Severe damage and multi-organ failure.

Answer 217

1. Acute heart failure: * Oxygen therapy, diuretics for fluid removal. * Vasodilators or inotropes for better heart function.

Answer 218

2. Chronic heart failure: * Medications: ACE inhibitors, beta blockers, SGLT2 inhibitors. * Lifestyle: Low salt, regular activity, weight control.

Answer 219

Thoracic Cavity 1. Contents: Includes lungs, heart, esophagus, thymus, major blood vessels, lymph nodes.

Answer 220

MANAGING CONDITIONS 3. Cardiogenic shock: * Oxygen, inotropes, fluids (carefully), mechanical support if needed.

Answer 221

Mediastinum 1. Boundaries: Central space of the thoracic cavity, bordered by lungs. Divided into superior, anterior, middle, and posterior mediastinum. 2. Contents: o Superior: Thymus, major vessels like aorta and SVC, trachea, esophagus. o Middle: Heart, pericardium, main bronchi. o Posterior: Esophagus, thoracic duct, descending aorta.

Answer 222

1. Key terms: o Stroke Volume (SV): Amount of blood pumped per beat. o End-Diastolic Volume (EDV): Blood in ventricle before contraction. o Ejection Fraction: Percentage of EDV pumped out.

Answer 223

Pericardium 1. Structure: Double-layered sac; fibrous (outer) and serous (inner). 2. Functions: Protects the heart, reduces friction during heartbeats, prevents over-distension. 3. Blood supply and innervation: o Arteries: Pericardiacophrenic and coronary arteries. o Innervation: Phrenic nerve and vagus nerve.

Answer 224

Palpation 1. Key areas: Apex beat felt at left mid-clavicular line (5th intercostal space).

Answer 225

Heart 1. Structure: Four chambers (right atrium/ventricle, left atrium/ventricle); surrounded by pericardium. 2. Great vessels: Aorta, pulmonary arteries/veins, venae cavae. 3. Blood flow: Right side pumps blood to lungs; left side pumps to body. 4. Coronary arteries: Supply blood to heart muscle, branching into circumflex and LAD. 5. Comparison: Left heart thicker (pumps to body), right heart thinner (pumps to lungs).

Answer 226

Positioning 1. Heart Position: Located centrally in thorax, tilted slightly left. 2. Major vessels: Aorta, venae cavae, pulmonary arteries/veins near heart.

Answer 227

Auscultation 1. Sites: o Aortic valve: Right 2nd intercostal space. o Pulmonary valve: Left 2nd intercostal space. o Tricuspid valve: Lower left sternum. o Mitral valve: Heart apex.

Answer 228

Myocardium and Cardiomyocytes 1. Structure: Thick heart muscle; individual cells connected by gap junctions. 2. Function: Contracts in coordination for pumping blood.

Answer 229

1. Phases: o Systole: Heart contracts, pumping blood out. o Diastole: Heart relaxes, chambers fill with blood.

Answer 230

Cardiac Output 1. Definition: Blood volume pumped by heart per minute. 2. Determinants: Heart rate and stroke volume.

Answer 231

Graph showing pressure, volume, and heart sounds during the cardiac cycle.

Answer 232

Venous Return 1. Factors: Blood pressure, muscle contractions, respiratory movements, valve function.

Answer 233

1. Valves: o Atrioventricular: Mitral and tricuspid. o Semilunar: Aortic and pulmonary. 2. Functions: Prevent blood backflow during heartbeats. 3. Heart sounds: First sound (S1): AV valves closing; second sound (S2): Semilunar valves closing. 4. Valvular dysfunction: Leads to regurgitation or stenosis.

Answer 234

Cardiac Conduction Pathway 1. Key Structures: SA node, AV node, bundle of His, Purkinje fibers. 2. Electrical Spread: Begins in SA node, stimulates atria, reaches AV node, and spreads through ventricles.

Answer 235

Electrical Phases 1. Action Potential: o Resting membrane potential → depolarization → repolarization → refractory period. 2. Mechanical Link: Electrical activity triggers muscle contraction (e.g., repolarization → ventricular relaxation).

Answer 236

Ventricular Action Potential Phases: Includes plateau phase for sustained contraction

Answer 237

Pacemaker Action Potential 1. SA Node: Automatic firing regulates heartbeat.

Answer 238

Autonomic Control of Cardiac Conduction 1. Sympathetic Effects: Speeds up heart rate; uses noradrenaline to enhance conduction. 2. Parasympathetic Effects: Slows down heart rate; uses acetylcholine. 3. Factors Influencing Conduction: Electrolyte levels, medications, autonomic balance.

Answer 239

Types of Arteries: * Conducting arteries (elastic): Large; include the aorta and carotid arteries. Function: Absorb pressure changes with elastic recoil. * Distributing arteries (muscular): Medium; regulate blood flow to organs. * Small arteries/arterioles: Control blood flow into capillary beds; major role in resistance.

Answer 240

Types of Veins: * Venules: Small, collect blood from capillaries. * Medium veins: Contain valves to prevent backflow. * Large veins: E.g., IVC, SVC; return blood to the heart.

Answer 241

Arterial vs. Venous Walls: * Arteries: Thick walls, more elastic tissue and smooth muscle. * Veins: Thin walls, larger lumens, and valves.

Answer 242

Relationships in Blood Flow: * Blood flow = Pressure / Resistance. * ↑ Pressure = ↑ Flow (if resistance unchanged).

Answer 243

Preload & Afterload: * Preload: Blood volume filling ventricles before contraction. * Afterload: Pressure ventricles must work against to eject blood.

Answer 244

3. Cardiac Output (CO): * CO = Stroke Volume (SV) × Heart Rate (HR). * Determinants: Contractility, preload, afterload, HR.

Answer 245

1. Formula: MAP = CO × Total Peripheral Resistance (TPR). 2. Parameters: * CO (HR × SV), TPR, stroke volume, and HR. 3. Basal Vascular Tone: Constant partial contraction of blood vessels.

Answer 246

1. Main Roles: Regulate blood pressure and blood flow. 2. Effects on Smooth Muscle: * Sympathetic System: Constricts vessels via noradrenaline. * Adrenaline: Can dilate (beta-2 receptors) or constrict (alpha receptors). * Vasodilators: E.g., atrial natriuretic peptide reduces blood pressure.

Answer 247

1. Key Factors: * Oxygen (O₂): Low levels dilate vessels. * Carbon dioxide (CO₂): High levels dilate vessels (e.g., in brain). * Nitric Oxide (NO): Vasodilation; lowers BP. * Endothelin-1: Vasoconstriction; raises BP. 2. Autoregulation: * Local tissue adjusts blood flow based on needs (e.g., brain, kidneys).

Answer 248

1. RAAS: * Key structures: Kidneys (renin), lungs (ACE), adrenal glands (aldosterone). * Renin converts angiotensinogen to angiotensin I → ACE converts to angiotensin II → increases BP by constricting vessels and retaining sodium. 2. Salt Intake Effect: High salt → Increases blood volume → Raises BP.

Answer 249

1. Baroreceptors: * Found in carotid sinus and aortic arch; sense changes in BP. 2. Reflex Pathway: Baroreceptors → Brainstem → Autonomic adjustments (sympathetic/parasympathetic systems).

Answer 250

1. Types of Hypertension: * Primary (essential): No clear cause. * Secondary: Due to other conditions (e.g., kidney disease). 2. Risk Factors: Age, obesity, smoking, sedentary lifestyle, family history. 3. Diagnosis: BP > 140/90 mmHg on multiple occasions.

Answer 251

1. Complications: * Heart: LV hypertrophy, heart failure. * Kidneys: Nephropathy. * Brain: Stroke. * Eyes: Retinopathy. 2. Lifestyle Modifications: * Reduce salt, quit smoking, regular exercise, maintain healthy weight.

Answer 252

1. Main Drugs: * ACE Inhibitors: Block angiotensin II production. * Beta Blockers: Lower HR and contractility. * Calcium Channel Blockers: Relax arteries. * Thiazide Diuretics: Remove excess fluid to lower BP.

Exam 4 - Notes Week 1 to 5 Flashcards

(277 cards)