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Summary

This on-demand teaching session, presented by Dom Jarvissurfaceanatomy, will explore the main structures of the thorax in relation to their surface anatomy and radiologic images, including key landmarks such as the jugular notch, clavicles, sternal angle and xiphoid process, as well as the regions of the thorax, cardiac surface markings, pericardium, costophrenic angle, diaphragm and the inner heart (chambers, atrioventricular and pulmonic/aortic valves). It will also cover the lungs, lateral pleurae and pulmonary hila. Medical professionals will be able to gain an enhanced understanding of the anatomy and pathological conditions related to the thorax, in order to better diagnose and treat patients.

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Learning objectives

Learning Objectives

  1. Identify key landmarks of the thorax and their associated radiological and surface anatomy
  2. Describe the anatomical features of the mediastinum, sternum, ribs, costal cartilages, cardiac surface markings, and pericardium
  3. Relate specific landmarks such as the jugular notch and xiphoid process to their anatomical reference points
  4. Explain the physiology of the diaphragm, costophrenic angle, pulmonary pleurae, lungs, hilae of the lungs, and inner heart
  5. Analyze radiographic images and clinical scenarios to diagnose common thoracic pathologies
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LEARNING OUTCOME: RELATETHE MAIN STRUCTURES OFTHETHORAXTOTHEIR SURFACE ANATOMYAND RADIOLOGICAL IMAGES LO PRESENTED BY DOM JARVISSURFACEANATOMY Key Landmarks Jugular Notch Clavicles SternalAngle (Angle of Louis) Xiphoid Process Costal MarginREGIONS OFTHETHORAX SuperiorThoracicAperture Superior Mediastinum Left Lung + Right Lung Inferior Mediastinum Pleura + Pleura - Anterior - Middle - Posterior InferiorThoracicAperture (Diaphragm) Mediastinum is the central compartment of the thoracic cavity and contains the viscera between the pleural cavities STERNUM,RIBSAND COSTAL CARTILAGES Sternum ¡ True Ribs (1- 7) - attach directly to sternum via their costal cartilages Flat Bone Manubrium (vertebrosternal) ¡ Jugular Notch ¡ SternalAngle-T4/T5 ¡ False Ribs (8-10) – attach indirectly to the sternum via the 7 costal Body ¡ Demi-facet & Facets cartilage (vertebrochondral) Xiphoid Process ¡ Tip atT10 ¡ Floating Ribs (11-12) – do not attach to the sternum (free) CARDIAC SURFACE MARKINGS ¡ Behind the Sternum ¡ Between Ribs 2- 6 ¡ BetweenT5-T8 ¡ Apex – 5 intercostal space,midclavicular line. ¡ Position of heart can be marked out using the costal cartilages on the right. R3,6,L 2,5PERICARDIUM ¡ Loose fitting sac surrounding the heart and the roots of the great vessels. ¡ Fibrous = tough,non-distensible ¡ Serous - Parietal = mesothelium - Pericardial Space à serous fluid - Visceral = epithelium ¡ Innervation = Phrenic Nerves (C3,4,5)INNER HEART 4 Chambers:TwoAtria andTwoVentricles Atria andVentricles are separated by atrioventricular valves: - Tricuspid = Right Side - Mitral = Left Side PulmonaryTrunk (Right) andAorta (Left) also have Semilunar valves (Pulmonary andAorticValves)RIGHTATRIUM VENTRICLESAUSCULTATORY POINTS ¡ AORTIC – right second intercostal space ¡ PULMONARY – left second intercostal space ¡ TRICUSPID - left,4 /5 intercostal spaces ¡ MITRAL – apex beat PULMONARY PLEURAE ¡ Visceral Pleurae – lines the lung surface ¡ Pleural space containing pleural fluid. - Reduces friction between the membranes when breathing. - Produces surface tension which ensures the lungs remain adhered to the thoracic wall ¡ Parietal Pleurae – lines the thoracic cavity.Sensitive to… … pain … pressure … temperatureLUNGS Right Lung = 3 lobes - Superior - Middle - Inferior 2 fissures – oblique horizontal ----------------------------- Left Lung = 2 lobes - Superior - Inferior 1 Fissure - obliqueHILA OFTHE LUNGS Royal Bank of Scotland – RBS ¡ R ight ¡ B ronchus ¡ S uperiorDIAPHRAGM ¡ Fills the inferior thoracic aperture ¡ Acts as a floor to the thoracic cavity ¡ Left and Right Dome ¡ Right Dome higher at rest because of Liver ¡ ------- ¡ VENA CAVA – 8 letters –T8 ¡ OESOPHAGUS – 10 letters –T10 ¡ AORTIC HIATUS- 12 letters –T12 ¡ ------- ¡ “C3,4,5 keep the diaphragm alive” - Phrenic nerves supply diaphragm - Left phrenic supplies left hemidiaphragm and vice versa COSTOPHRENICANGLE Blunting is when the Where the ribs (costo-) meets costophrenic angle is greater the diaphragm (-phrenic) than 30 degrees. Can be caused by: Normal costophrenic angle measures approximately 30 - Pleural effusion degrees. - Lung Hyperexpansion Normally only a small amount - PleuralAbscess located within posterior and lateral of the lung comes into contact pleural space. with the angle. - HaemothoraxSBASANATRIAL SEPTAL DEFECT OFTEN OCCURSATTHE SITE OFAN EMBRYOLOGICAL INTERATRIAL SEPTAL SHUNT PRESENT INTHE FOETAL HEART.WHICH OFTHE FOLLOWING EMBRYOLOGICAL STRUCTURES OR FEATURES IS INVOLVED INTHIS DEFECT? A DuctusArteriosus B DuctusVenosus C Foramen Ovale D Fossa Ovalis E LigamentumVenosumANATRIAL SEPTAL DEFECT OFTEN OCCURSATTHE SITE OFAN EMBRYOLOGICAL INTERATRIAL SEPTAL SHUNT PRESENT INTHE FOETAL HEART.WHICH OFTHE FOLLOWING EMBRYOLOGICAL STRUCTURES OR FEATURES IS INVOLVED INTHIS DEFECT? A DuctusArteriosus B DuctusVenosus C Foramen Ovale D Fossa Ovalis E LigamentumVenosumA 96-YEAR-OLD MAN PRESENTSWITHATWO-WEEK HISTORY OF LEFT SHOULDER PAINACCOMPANIED WITH HOARSENESS OF VOICE. HAVINGTAKENA FULL HISTORYAND EXAMINATION OFTHE PATIENT,THE REGISTRAR ORDERSA CXR,WHICH IS SHOWN BELOW.WHICH OFTHE FOLLOWING IS INDICATED BYTHIS CXR? A Normal CXR B Left-Sided Pleural Effusion C Community-Acquired Pneumonia D PancoastTumour E Right PneumothoraxA 96-YEAR-OLD MAN PRESENTSWITHATWO-WEEK HISTORY OF LEFT SHOULDER PAINACCOMPANIED WITH HOARSENESS OF VOICE. HAVINGTAKENA FULL HISTORYAND EXAMINATION OFTHE PATIENT,THE REGISTRAR ORDERSA CXR,WHICH IS SHOWN BELOW.WHICH OFTHE FOLLOWING IS INDICATED BYTHIS CXR? A Normal CXR B Left-Sided Pleural Effusion C Community-Acquired Pneumonia D PancoastTumour E Right PneumothoraxA 30YEAR OLD MAN HAS PRESENTEDTOTHE EMERGENCY DEPARTMENTAFTER SEEING HIS GPWITHAN INTERMITTENT, HIGH-GRADE FEVER OFTWOWEEKS DURATION.ON EXAMINATION,THE PATIENT HAS POOR ORAL HYGIENEANDAN AUDIBLE END-SYSTOLIC MURMUR ONAUSCULTATION. ATRANSOESOPHAGEAL ECHOCARDIOGRAM IS PERFORMEDAND SHOWSTHE FOLLOWING.WHAT DOESTHE IMAGE SHOW? . A MitralValveVegetation B AorticValveVegetation C TricuspidValveVegetation D Aortic Regurgitation Patent Foramen Ovale EA 30YEAR OLD MAN HAS PRESENTEDTOTHE EMERGENCY DEPARTMENTAFTER SEEING HIS GPWITHAN INTERMITTENT, HIGH-GRADE FEVER OFTWOWEEKS DURATION.ON EXAMINATION,THE PATIENT HAS POOR ORAL HYGIENEANDAN AUDIBLE END-SYSTOLIC MURMUR ONAUSCULTATION. ATRANSOESOPHAGEAL ECHOCARDIOGRAM IS PERFORMED AND SHOWSTHE FOLLOWING.WHAT DOESTHE IMAGE SHOW? . A MitralValveVegetation B AorticValveVegetation C TricuspidValveVegetation D Aortic Regurgitation Patent Foramen Ovale EINDI ISA KNOWNASTHMATICWHO HAS PRESENTEDWITHA SUDDEN DETERIORATION IN HISASTHMA.HE IS STRUGGLINGTOVERBALISE DUETOANACUTE-ONSET SHORTNESS OF BREATHAND SHARP PLEURITIC CHEST PAIN. ON EXAMINATIONTHERE IS UNEQUAL CHEST EXPANSION BUTTHE PATIENT’STRACHEA REMAINS CENTRAL.THIS PATIENT’S CXR IS SHOWN BELOW.WHAT ISTHE DIAGNOSIS? A Right-SidedTension Pneumothorax B CardiacTamponade C Left-Sided Simple Pneumothorax D Pericardial Effusion E Right-Sided Simple PneumothoraxINDI ISA KNOWNASTHMATICWHO HAS PRESENTEDWITHA SUDDEN DETERIORATION IN HISASTHMA.HE IS STRUGGLINGTOVERBALISE DUETOANACUTE-ONSET SHORTNESS OF BREATHAND SHARP PLEURITIC CHEST PAIN. ON EXAMINATIONTHERE IS UNEQUAL CHEST EXPANSION BUTTHE PATIENT’STRACHEA REMAINS CENTRAL.THIS PATIENT’S CXR IS SHOWN BELOW.WHAT ISTHE DIAGNOSIS? A Right-SidedTension Pneumothorax B CardiacTamponade C Left-Sided Simple Pneumothorax D Pericardial Effusion E Right-Sided Simple PneumothoraxTENSION PNEUMOTHORAX CXRA 32-YEAR-OLD MAN IS BROUGHTTOTHE EMERGENCY DEPARTMENT COUGHINGANDWHEEZINGAFTER AN EPISODE OFALCOHOL INTOXICATION.ON EXAMINATION,HE HAS REDUCED BREATH SOUNDS ONTHE ONE SIDE.IMAGING STUDIES SHOW HE HASASPIRATEDA FOREIGN BODY,WHICH IS OCCLUDINGAN AIRWAY STRUCTURE.WHICH ISTHE MOST LIKELY LOCATION FORTHIS FOREIGN BODYTO BE STUCK IN? A Lower Lobe of Left Lung B Primary Bronchus of Left Lung C Primary Bronchus of Right Lung D Tertiary Bronchus of Left Lung E Tertiary Bronchus of Right LungA 32-YEAR-OLD MAN IS BROUGHTTOTHE EMERGENCY DEPARTMENT COUGHINGANDWHEEZINGAFTER AN EPISODE OFALCOHOL INTOXICATION.ON EXAMINATION,HE HAS REDUCED BREATH SOUNDS ONTHE ONE SIDE.IMAGING STUDIES SHOW HE HASASPIRATEDA FOREIGN BODY,WHICH IS OCCLUDINGAN AIRWAY STRUCTURE.WHICH ISTHE MOST LIKELY LOCATION FORTHIS FOREIGN BODYTO BE STUCK IN? A Lower Lobe of Left Lung B Primary Bronchus of Left Lung C Primary Bronchus of Right Lung D Tertiary Bronchus of Left Lung E Tertiary Bronchus of Right LungA 74-YEAR-OLDWOMAN PRESENTSWITH INTENSE FATIGUE,SHORTNESS OF BREATHANDANKLE OEDEMA. THE DOCTOR ON-CALLAUSCULTATESTHE PATIENT’S HEARTVALVES.THEY DETECTAN EJECTION SYSTOLIC MURMUR HEARD LOUDEST OVERTHEAORTICVALVE,SUGGESTINGAORTIC STENOSIS.WHERE DIDTHE DOCTOR PLACETHEIR STETHOSCOPETO HEARTHIS MURMUR? A Right 2 Intercostal Space nd B Left 2 Intercostal Space C Left 4/5 Intercostal Space D Apex Beat Sub-Xiphoid EA 74-YEAR-OLDWOMAN PRESENTSWITH INTENSE FATIGUE,SHORTNESS OF BREATHANDANKLE OEDEMA. THE DOCTOR ON-CALLAUSCULTATESTHE PATIENT’S HEARTVALVES.THEY DETECTAN EJECTION SYSTOLIC MURMUR HEARD LOUDEST OVERTHEAORTICVALVE,SUGGESTINGAORTIC STENOSIS.WHERE DIDTHE DOCTOR PLACETHEIR STETHOSCOPETO HEARTHIS MURMUR? A Right 2 Intercostal Space nd B Left 2 Intercostal Space C Left 4/5 Intercostal Space D Apex Beat Sub-Xiphoid E LEARNING OUTCOME: DESCRIBETHEARTERIAL SUPPY OFTHE HEART LO PRESENTED BY DOM JARVISTHE GREATVESSELS –AORTAAND DERIVATIVESCORONARYARTERIES Right CoronaryArtery à Marginal Branch Small CardiacVein à Sinoatrial Branch à Posterior Interventricular BranMiddle CardiacVein Left CoronaryArtery à LeftAnterior Descending Great CardiacVein à CircumflexCORONARYARTERIESECGTERRITORIES ECG leads represent different ‘territories’ of the myocardium depending on the placement position of the electrodes.GREATVESSELS -VEINS SuperiorVena Cava: ¡ Formed by merging of brachiocephalic veins rd ¡ Drains into superior part of right atrium at the 3 rib InferiorVena Cava: ¡ Formed in pelvis by common iliac veins ¡ Collects blood from hepatic,lumbar,gonadal,renal & phrenic veins ¡ Drains into inferior right atriumSBASA PATIENT HAS PRESENTEDTOTHE EMERGENCY DEPARTMENT COMPLAINING OF NEW-ONSET CHEST PAINAND SHORTNESS OF BREATH.AN ECG IS PERFORMEDWHICH SHOWS ST ELEVATION INTHEANTEROSEPTAL LEADS. ANGIOGRAPHY SHOWSTHE OCCLUSION OFA CORONARYVESSEL.INWHICHARTERY ISTHE OCCLUSION FOUND? A Right MarginalArtery B Right Main Coronary C LeftAnterior Descending D Diagonal Branches E Left CircumflexA PATIENT HAS PRESENTEDTOTHE EMERGENCY DEPARTMENT COMPLAINING OF NEW-ONSET CHEST PAINAND SHORTNESS OF BREATH.AN ECG IS PERFORMEDWHICH SHOWS ST ELEVATION INTHEANTEROSEPTAL LEADS. ANGIOGRAPHY SHOWSTHE OCCLUSION OFA CORONARYVESSEL.INWHICHARTERY ISTHE OCCLUSION FOUND? A Right MarginalArtery B Right Main Coronary C LeftAnterior Descending D Diagonal Branches E Left CircumflexMAX IS PLAYINGAN INTENSE GAME OF RUGBYAND HIS HEART RATE HAS INCREASEDTO MEETTHE OXYGEN DEMAND OF HIS MUSCLES. THE HEART RECEIVES ITS OWN OXYGENTO PUMPATTHIS INCREASED RATETHROUGH ITS CORONARY CIRCULATION. WHEN IS LEFT CORONARYARTERY BLOOD FLOW HIGHEST? A Early Diastole B Isovolumetric Phase of Contraction C Isovolumetric Phase of Relaxation D Late Diastole E Mid-SystoleMAX IS PLAYINGAN INTENSE GAME OF RUGBYAND HIS HEART RATE HAS INCREASEDTO MEETTHE OXYGEN DEMAND OF HIS MUSCLES. THE HEART RECEIVES ITS OWN OXYGENTO PUMPATTHIS INCREASED RATETHROUGH ITS CORONARY CIRCULATION. WHEN IS LEFT CORONARYARTERY BLOOD FLOW HIGHEST? A Early Diastole B Isovolumetric Phase of Contraction C Isovolumetric Phase of Relaxation D Late Diastole E Mid-SystoleEMILY IS REVISINGTHEANATOMY OFTHEAORTA.SHE REMEMBERSTHATTHEAORTA CAN BE DIVIDED INTO 3 PARTSANDTHAT EACH PART HAS DIFFERENTVESSELS BRANCHING FROM IT. WHAT ISTHETHIRD BRANCH OFTHEARCH OFTHEAORTA? A CoronaryArteries B Left Brachiocephalic C Left Common Carotid Left Subclavian D E Right BrachiocephalicEMILY IS REVISINGTHEANATOMY OFTHEAORTA.SHE REMEMBERSTHATTHEAORTA CAN BE DIVIDED INTO 3 PARTSANDTHAT EACH PART HAS DIFFERENTVESSELS BRANCHING FROM IT. WHAT ISTHETHIRD BRANCH OFTHEARCH OFTHEAORTA? A CoronaryArteries B Left Brachiocephalic C Left Common Carotid Left Subclavian D E Right BrachiocephalicJULIA ISAN F1WORKING ONTHE CARDIACWARDS.ONE OFTHE PATIENTS ONTHEWARD HAS RECENTLY EXPERIENCEDA MYOCARDIAL INFARCTIONWHICH RESULTED INATHIRD DEGREE HEART BLOCK.THIS WAS BECAUSETHE BLOOD SUPPLYTOTHEATRIOVENTRICULAR NODEWAS COMPROMISED.WHICH CORONARYVESSEL IS RESPONSIBLE FOR SUPPLYINGTHEAVNWITH BLOOD? A Left CircumflexArtery B LeftAnterior DescendingArtery C Right CoronaryArtery D Posterior InterventricularArtery E Coronary SinusJULIA ISAN F1WORKING ONTHE CARDIACWARDS.ONE OFTHE PATIENTS ONTHEWARD HAS RECENTLY EXPERIENCEDA MYOCARDIAL INFARCTIONWHICH RESULTED INATHIRD DEGREE HEART BLOCK.THIS WAS BECAUSETHE BLOOD SUPPLYTOTHEATRIOVENTRICULAR NODEWAS COMPROMISED.WHICH CORONARYVESSEL IS RESPONSIBLE FOR SUPPLYINGTHEAVNWITH BLOOD? A Left CircumflexArtery B LeftAnterior DescendingArtery C Right CoronaryArtery D Posterior InterventricularArtery E Coronary SinusNAOMI,A 63YEAR OLD FEMALE,HAS HADA SILENT MIAND IS NOW PRESENTINGWITH SYMPTOMS OF HEART FAILURE.HER HEART IS NOT PUMPING SUFFICIENTLYAND SOTHERE ISA BACK FLOW OF BLOOD FROMTHE HEART.THIS CAN BEASSESSED ON CLINICAL EXAMINATION OFTHE CARDIOVASCULAR SYSTEM BYVISUALISINGTHE PRESSURE IN ONE OFTHE GREATVEINS INTHE NECK.WHICH OFTHE FOLLOWING VEINS DOWE USE? A Right External JugularVein B Left Internal JugularVein C Right Internal JugularVein D Right BrachiocephalicVein E SuperiorVena CavaNAOMI,A 63YEAR OLD FEMALE,HAS HADA SILENT MIAND IS NOW PRESENTINGWITH SYMPTOMS OF HEART FAILURE.HER HEART IS NOT PUMPING SUFFICIENTLYAND SOTHERE ISA BACK FLOW OF BLOOD FROMTHE HEART.THIS CAN BEASSESSED ON CLINICAL EXAMINATION OFTHE CARDIOVASCULAR SYSTEM BYVISUALISINGTHE PRESSURE IN ONE OFTHE GREATVEINS INTHE NECK.WHICH OFTHE FOLLOWING VEINS DOWE USE? A Right External JugularVein B Left Internal JugularVein C Right Internal JugularVein D Right BrachiocephalicVein E SuperiorVena CavaTHE POSTERIOR INTERVENTRICULARARTERY SUPPLIESTHE POSTERIORTHIRD OFTHE INTERVENTRICULAR SEPTUMANDTHE INFERIORASPECT OFTHE MYOCARDIUM.WHICH CARDIACVEIN RUNSALONGSIDETHE POSTERIOR INTERVENTRICULARARTERY? A Small CardiacVein B Middle CardiacVein C Great CardiacVein D Coronary Sinus E AzygosVeinTHE POSTERIOR INTERVENTRICULARARTERY SUPPLIESTHE POSTERIORTHIRD OFTHE INTERVENTRICULAR SEPTUMANDTHE INFERIORASPECT OFTHE MYOCARDIUM.WHICH CARDIACVEIN RUNSALONGSIDETHE POSTERIOR INTERVENTRICULARARTERY? A Small CardiacVein B Middle CardiacVein C Great CardiacVein D Coronary Sinus E AzygosVein CORONAR Y HEART DISEASE LO PRESENTED BY SANYATRIKHA TRIKHAS@CARDIFF.AC.UK A 56-YEAR-OLD MALE PRESENTS TO THE HOSPITAL WITH CRUSHING CHEST PAIN THAT RADIATES TO HIS LEFT ARM. A CORONARY ANGIOGRAM IS DONE SHOWING 90% OBSTRUCTED LUMEN OF AN ARTERY THAT SUPPLIES THE POSTERIOR INTRAVENTRICULAR SEPTUM. WHICH ARTERY IS THIS? A Left anterior descending B Left marginal artery C Circumflex artery D Right coronary artery E Right marginal artery A 56-YEAR-OLD MALE PRESENTS TO THE HOSPITAL WITH CRUSHING CHEST PAIN THAT RADIATES TO HIS LEFT ARM. A CORONARY ANGIOGRAM IS DONE SHOWING 90% OBSTRUCTED LUMEN OF AN ARTERY THAT SUPPLIES THE POSTERIOR INTRAVENTRICULAR SEPTUM. WHICH ARTERY IS THIS? A Left anterior descending B Left marginal artery C Circumflex artery D Right coronary artery E Right marginal artery CARDIOVASCULARARTERIES https://teachmeanatomy.info/thorax/organs/heart/heart-vasculature/ECGATHEROSCELOROSIS Modifiable Risk Factor Non - Modifiable Hypertension Age Hyperlipidaemia Gender Smoking Ethnicity Alcohol Family history Diabetes Mellitus High BMI Exercise Food/ Diet A SOUTH ASIAN 40-YEAR-OLD MAN WITH A BMI OF 34KG/M2 HAS HYPERCHOLESTEROLAEMIA. HIS GP ASKS HIM TO LOSE WEIGHT AND MAKE SOME LIFESTYLE MODIFICATIONS. HE ALSO PRESCRIBES HIM A STATIN AS HE HAS A HIGH RISK OF MI IN FUTURE. HOW DOES A STATIN REDUCE HIS RISK? A It reduces his heart rate by interfering the Na+/K+ channels B It will decrease cardiac output and reduce blood pressure C Breaks down the plaque formed in the artery D Vasodilates the vascular smooth muscles to there are less chances of his arteries being fully occluded E Stabilizes the fibrous plaque and reduces the risk of rupture and full vessel occlusion A SOUTH ASIAN 40-YEAR-OLD MAN WITH A BMI OF 34KG/M2 HAS HYPERCHOLESTEROLAEMIA. HIS GP ASKS HIM TO LOSE WEIGHT AND MAKE SOME LIFESTYLE MODIFICATIONS. HE ALSO PRESCRIBES HIM A STATIN AS HE HAS A HIGH RISK OF MI IN FUTURE. HOW DOES A STATIN REDUCE HIS RISK? A It reduces his heart rate by interfering the Na+/K+ channels B It will decrease cardiac output and reduce blood pressure C Breaks down the plaque formed in the artery D Vasodilates the vascular smooth muscles to there are less chances of his arteries being fully occluded E Stabilizes the fibrous plaque and reduces the risk of rupture and full vessel occlusionCoronaryArtery Disease JANICE IS A 72-YEAR-OLD FEMALE WHO PRESENTS WITH CHEST PAIN THAT STARTED IN THE LAST 3 DAYS. TODAY HOWEVER, SHE DESCRIBES THE PAIN TO GETTING BE WORSE DESPITE TAKING GTN SPRAY. A ECG WAS CONDUCTED SHOWING T WAVE INVERSIONS AND ST DEPRESSION, BUT HER TROPONIN LEVEL WAS NORMAL. WHAT COULD BE HER DIAGNOSIS? A Stable angina B Unstable angina C NSTEMI D STEMI E Atrial Fibrillation JANICE IS A 72-YEAR-OLD FEMALE WHO PRESENTS WITH CHEST PAIN THAT STARTED IN THE LAST 3 DAYS. TODAY HOWEVER, SHE DESCRIBES THE PAIN TO GETTING BE WORSE DESPITE TAKING GTN SPRAY. A ECG WAS CONDUCTED SHOWING T WAVE INVERSIONS AND ST DEPRESSION, BUT HER TROPONIN LEVEL WAS NORMAL. WHAT COULD BE HER DIAGNOSIS? A Stable angina B Unstable angina C NSTEMI D STEMI E Atrial Fibrillation CORONARY HEART DISEASE CP at rest StableAngina Acute coronary syndrome CP on exertion Ischemia Artery may be occluded less than 70% Unstable NSTEMI STEMI Angina ≥ 90% apprx100 % ≥ 90% Infarction – sub Infarction – Ischaemia transmural endotheliumACUTE CORONARY SYNDROMESTABLEANGINA Clinical Presentation ¡ Crushing,central chest pain on exertion and relieved on rest ¡ Dyspnoea ¡ Sweating Investigation – Stress Test ECG and coronary angiogram Stress Test ECG – ST depression and T wave inversion.MANAGEMENT 1. Nitrates, e.g. GTN – release NO, symptom control 2. Beta-blockers, e.g. Bisoprolol – negative inotropy and chronotropy, prophylaxis 3. Ca2+ channel blocker, e.g. Diltiazem – negative inotropy and chronotropy, vasodilation, prophylaxis 4. Nicorandil – vasodilation 5. Ivabradine – rate limiter A 52-YEAR-OLD FEMALE WITH HISTORY OF HYPERTENSION PRESENTS WITH 6 MONTHS HISTORY CHEST PAIN ELEVATED ON PLAYING TENNIS. SHE TAKES ATORVASTATIN AND RAMIPRIL. HER GP PRESCRIBES HER GTN AND BISOPROLOL. WHAT IS THE MECHANISM OF ACTION OF GTN SPRAYS? A Conversion of myosin phosphate to myosin which causes vascular smooth muscle contraction. B Vasodilation by increasing the influx of Ca2+ in the vascular smooth muscle. C Inhibition of NO with dilates the muscles D Vasoconstriction of smooth muscles by reducing Ca2+ in the cells. E By binding to the beta 1 adrenoceptors A 52-YEAR-OLD FEMALE WITH HISTORY OF HYPERTENSION PRESENTS WITH 6 MONTHS HISTORY CHEST PAIN ELEVATED ON PLAYING TENNIS. SHE TAKES ATORVASTATIN AND RAMIPRIL. HER GP PRESCRIBES HER GTN AND BISOPROLOL. WHAT IS THE MECHANISM OF ACTION OF GTN SPRAYS? A Conversion of myosin phosphate to myosin which causes vascular smooth muscle contraction. B Vasodilation by increasing the influx of Ca2+ in the vascular smooth muscle. C Inhibition of NO with dilates the muscles D Vasoconstriction of smooth muscles by reducing Ca2+ in the cells. E By binding to the beta 1 adrenoceptorshttps://youtu.be/MyXuvis4hN4 - Mechanism of action of GTN A PATIENT PRESENTS TO THE HOSPITAL WITH ACUTE CENTRAL CHEST PAIN THAT HE DESCRIBES 10/10. THEY FELL SICK AND ARE HYPOXIC AND SWEATY. AN ECG DONE IS IMMEDIATELY. LOOKING AT THE ECG BELOW, WHAT CONDITION DOES THE PATIENT HAVE? A Stable angina B Aortic dissection C Non-ST elevation myocardial infarction D UnstableAngina E ST elevated myocardial infarction A PATIENT PRESENTS TO THE HOSPITAL WITH ACUTE CENTRAL CHEST PAIN THAT HE DESCRIBES 10/10. THEY FELL SICK AND ARE HYPOXIC AND SWEATY. AN ECG DONE IS IMMEDIATELY. LOOKING AT THE ECG BELOW, WHAT CONDITION DOES THE PATIENT HAVE? A Stable angina B Aortic dissection C Non-ST elevation myocardial infarction D UnstableAngina E ST elevated myocardial infarctionACS ¡Clinical Presentation ¡Chest Pain during rest.It may radiate to the jaw,neck or the left arm. ¡Dyspnoea ¡Sweating ¡Nausea and vomiting ¡Dizzy ¡Investigations – BloodTest,Troponin,ECG,EchoMANAGEMENT Symptom management – MONA • Morphine • Oxygen • Nitrates (GTN) - sublingual • Aspirin (dual antiplatelet in STEMI) Surgery - PCI – Within 120 mins (only for STEMI) NSTEMI – more of an elective PCI understanding their risks Secondary Management – Reduce the risk of getting it again ACEi Dual platelet therapy Beta blockers/ CCB Statin MR JONES IS A 42-YEAR-OLD WHO HAS A PAST MEDICAL HISTORY OF RHEUMATIC FEVER, ASTHMA, AND ECZEMA. HE HAS RECENTLY BEEN DIAGNOSED WITH INCREASED HEART RATE AND UNSTABLE ANGINA. WHICH OF THE FOLLOWING MEDICATIONS CAN HE BE GIVEN TO HELP HIM MANAGE BOTH HIS SYMPTOMS? A GTN spray B Losartan C Bisoprolol D Diltiazem E Ramipril MR JONES IS A 42-YEAR-OLD WHO HAS A PAST MEDICAL HISTORY OF RHEUMATIC FEVER, ASTHMA, AND ECZEMA. HE HAS RECENTLY BEEN DIAGNOSED WITH INCREASED HEART RATE AND UNSTABLE ANGINA. WHICH OF THE FOLLOWING MEDICATIONS CAN HE BE GIVEN TO HELP HIM MANAGE BOTH HIS SYMPTOMS? A GTN spray B Losartan C Bisoprolol D Diltiazem E Ramipril A 64-YEAR-OLD FEMALES ATTENDS THE ED WITH AN MI THAT STARTED 50 MINS BEFORE. HER ECG CHANGES SHOW AN ELEVATED ST ELEVATION IN LEADS V1 TO V4. SHE IS THEN TREATED FOR HER STEMI WITH DUAL ANTIPLATELET THERAPY OF ASPIRIN AND TICAGRELOR. WHAT IS THE MECHANISM OF ACTION OF TICAGRELOR? A Phosphodiesterase inhibitor B reversible COX inhibitor C irreversible COX inhibitor D P2Y12-ADP receptor antagonist E GPIIb-IIIa inhibitor A 64-YEAR-OLD FEMALES ATTENDS THE ED WITH AN MI THAT STARTED 50 MINS BEFORE. HER ECG CHANGES SHOW AN ELEVATED ST ELEVATION IN LEADS V1 TO V4. SHE IS THEN TREATED FOR HER STEMI WITH DUAL ANTIPLATELET THERAPY OF ASPIRIN AND TICAGRELOR. WHAT IS THE MECHANISM OF ACTION OF TICAGRELOR? A Phosphodiesterase inhibitor B reversible COX inhibitor C irreversible COX inhibitor D P2Y12-ADP receptor antagonist E GPIIb-IIIa inhibitor A LECTURE WAS HAPPENING ON ACS. THE LECTURER SPOKE ABOUT HOW DIFFERENT TYPES OF CARDIAC MARKERS ARE ELEVATED DURING A MYOCARDIAL INFARCTION. WHICH OF THE FOLLOWING IS THE FIRST CARDIAC MARKER TO BE ELEVATED IN A PATIENT SUFFERING FROM MI? A Creatinine Kinase B Troponin I C Troponin T D Troponin C E Myoglobin A LECTURE WAS HAPPENING ON ACS. THE LECTURER SPOKE ABOUT HOW DIFFERENT TYPES OF CARDIAC MARKERS ARE ELEVATED DURING A MYOCARDIAL INFARCTION. WHICH OF THE FOLLOWING IS THE FIRST CARDIAC MARKER TO BE ELEVATED IN A PATIENT SUFFERING FROM MI? A Creatinine Kinase B Troponin I C Troponin T D Troponin C E Myoglobin st • Myoglobin – 1 to rise • CK – less cardio specific, useful to look for reinfarction (CK-MB) • Troponin T + I – cardio specific – indicates myocardial damage/injury – undetectable in normal health WILL - A 32-YEAR MALE - HAD A ROAD ACCIDENT ON TUESDAY NIGHT AND IS ADMITTED AT UHW. HE HAS FRACTURED HIS LEG AND NEEDS TO UNDERGO A SURGERY FOR ITS FIXATION. BEFORE ADMINISTERING ANAESTHETICS, HIS ECG AND BLOOD TEST WERE TAKEN. ECG SHOWED TACHYCARDIA BUT NORMAL RHYTHM. HIS BLOOD SHOWED A VERY HIGH CK LEVELS. WHAT SHOULD BE THE NEXT PLAN OF MANAGEMENT FOR HIM AFTER HIS SURGERY? A Concentrate of his post-operative care as his heart is fine B Prescribe his bisoprolol for his heart condition C Speak to a cardiologist and ask for their opinion D Prescribe statins as prophylaxis for a possible MI in future Prescribe anti-coagulants as prophylaxis as there is a risk of stroke in the future E WILL - A 32-YEAR MALE - HAD A ROAD ACCIDENT ON TUESDAY NIGHT AND IS ADMITTED AT UHW. HE HAS FRACTURED HIS LEG AND NEEDS TO UNDERGO A SURGERY FOR ITS FIXATION. BEFORE ADMINISTERING ANAESTHETICS, HIS ECG AND BLOOD TEST WERE TAKEN. ECG SHOWED TACHYCARDIA BUT NORMAL RHYTHM. HIS BLOOD SHOWED A VERY HIGH CK LEVELS. WHAT SHOULD BE THE NEXT PLAN OF MANAGEMENT FOR HIM AFTER HIS SURGERY? A Concentrate of his post-operative care as his heart is fine B Prescribe his bisoprolol for his heart condition C Speak to a cardiologist and ask for their opinion D Prescribe statins as prophylaxis for a possible MI in future Prescribe anti-coagulants as prophylaxis as there is a risk of stroke in the future ETHANKYOU LCHANGESASSOCIATEDWITH NORMALANDACCELERATEDAGINGLLULAR LO PRESENTED BY HO HIN LAM SBA QUESTION:PATIENT PRESENTINGATTHE GPATWINTERTIME COMPLAINING OF PAINAND SWELLING INTHEIR FINGERS BILATERALLY,THIS HAPPENEDAFTERA RUN INTHE PARK.ONTHE EXAMINATIONYOU FOUND POOR NAIL GROWTHAND PALLOR INTHE FINGERS,TOESANDTHE EARLOBES,THEREARE NO SIGNS OF SYSTEMIC INFLAMMATONAND PATIENT HAS NO OTHER MEDICAL HISTORY. WHICH OFTHE FOLLOWING DIAGNOSIS ISTHE MOST LIKELY A RAYNAUD’S DISEASE B COMPLEX REGIONAL PAIN SYNDROME C LUPUS D RHEUMATOIDARTHRITIS BUERGER’S DISEASE E SBA QUESTION:PATIENT PRESENTINGATTHE GPATWINTERTIME COMPLAINING OF PAINAND SWELLING INTHEIR FINGERS BILATERALLY,THIS HAPPENEDAFTERA RUN INTHE PARK.ONTHE EXAMINATIONYOU FOUND POOR NAIL GROWTHAND PALLOR INTHE FINGERS,TOESANDTHE EARLOBES,THEREARE NO SIGNS OF SYSTEMIC INFLAMMATONAND PATIENT HAS NO OTHER MEDICAL HISTORY. WHICH OFTHE FOLLOWING DIAGNOSIS ISTHE MOST LIKELY A RAYNAUD’S DISEASE B COMPLEX REGIONAL PAIN SYNDROME C LUPUS D RHEUMATOIDARTHRITIS BUERGER’S DISEASE ERA YNAUD’S ¡ IDIOPATHICVASOSPASM – REVERSIBLEVASO CONSTRICTION CHARACTERISED BY EXPOSURETO COLD ¡ TYPICAL PRESENTATION – COLD-INDUCED DIGITAL PALLOR,CYANOSISAND RUBOR OR EMOTIVE STIMULI ( SOMETIMES NOSEAND EARLOBESTOO),THROBING PAINAND SWELLINGACCOMPANIES RECOVERY PHASE ¡ DEFINITIVETREATMENT – NIFEDIPINE SBA QUESTION:ATYPE II DIABETIC PATIENT SUFFERS FROM HYPERTENSIONAND IS BEING TREATEDWITH RAMAPRIL,BISOPRILOL,VALSARTAN,METFORMIN,DAPAGLIFLOZIN,PRESENTS WITH SIGNS OF RAYNAUD’SWHICH OFTHE FOLLOWING ISTHE LIKELY CUASE A BISOPRILOL B VALSARTAN C RAMAPRIL D METFORMIN E DAPAGLIFLOZIN SBA QUESTION:ATYPE II DIABETIC PATIENT SUFFERS FROM HYPERTENSIONAND IS BEING TREATEDWITH RAMAPRIL,BISOPRILOL,VALSARTAN,METFORMIN,DAPAGLIFLOZIN,PRESENTS WITH SIGNS OF RAYNAUD’SWHICH OFTHE FOLLOWING ISTHE LIKELY CUASE A BISOPRILOL B VALSARTAN C RAMAPRIL D METFORMIN E DAPAGLIFLOZINBETA BLOCKER ON ENDOTHELIAL CELLS ¡ Bisoprolol is a selective beta 1 – adrenergic receptor blocker with a low affinity for beta 2 – adrenergic receptors ¡ Beta 1 adrenergic receptors are mainly found in the cardiac myocytes and have a role in ionotropy and chromotropy ¡ Beta 2 adrenergic receptors can be found in bronchial smooth muscle,endothelial smooth muscles and fat cells, blockage can cause exacerbation ofAsthma,COPD exacerbation and in the case of peripheral smooth muscles can cause vasospasm leading to presentation of the Raynaud’s phenomenon. SBA QUESTION:WHICH OFTHE FOLLOWING ISAVASOCONSTRICTOR RELEASED BY THE ENDOTHELIAL CELLS A PGI-1 B Endothelin-1 C CO2 D NO E NORADRENALINE SBA QUESTION:WHICH OFTHE FOLLOWING ISAVASOCONSTRICTOR RELEASED BY THE ENDOTHELIAL CELLS A PGI-1 B Endothelin-1 C CO2 D NO E NORADRENALINEENDOTHELIAL REGULATION ( ENDOTHELIAL CELLS ) VASODILATION VASOCONSTRICTION NITRIC OXIDE PROSTACYCLIN ( PGL – 2) ENDOTHELIUM-DERIVED HYPERPOLARIZING ENDOTHELIN – 1 FACTOR VASODILATION VASOCONSTRICTION ACETYLCHOLINE ACE II CO2 O2 HISTAMINE NORADRENALINE / NOREPINEPHRINE BRADYKININ ADENOSINETRIPHOSPHATE SBA QUESTION: WHICH OFTHE FOLLOWING IS NOTAN EFFECT OFAGING ON ENDOTHELIAL CELLS A DECREASED PRODUCTION OF NITRIC OXIDE B INCREASED OXIDATIVE STRESS C INCREASED INFLAMMATION D ABNORMAL FOLDING OFTHE FIBRILLIN-1 PROTEIN E DECREASEDVASCULAR REGENERATIVE CAPCITY SBA QUESTION: WHICH OFTHE FOLLOWING IS NOTAN EFFECT OFAGING ON ENDOTHELIAL CELLS A DECREASED PRODUCTION OF NITRIC OXIDE B INCREASED OXIDATIVE STRESS C INCREASED INFLAMMATION D ABNORMAL FOLDING OFTHE FIBRILLIN-1 PROTEIN E DECREASEDVASCULAR REGENERATIVE CAPCITYMARFAN’S SYNDROME ¡ Pathophysiology: autosomal dominant mutation in the gene coding for fibrillin-1 which is responsible for regulatory function of microfibrils in the extracellular matrix,affecting mainly the alpha 2 chains of type 1 collagen ¡ Clinical features: ¡ Slender limbs and scoliosis,change in the shape of chest and palate ¡ Increased risk for aortic aneurysm and dissection ¡ Increased risk to myopia,cataracts and glaucoma ¡ Thin,translucent skins that bruises easily ¡ Pulmonary fibrosis ¡ Management: ¡ Monitoring for aneurysm and dissections and valvular disease ¡ Surgical,physiotherapy input for skeletal features ¡ Pain management ¡ Respiratory input for pulmonary fibrosis SBA QUESTION: WHICH OFTHE FOLLOWINGANTI-CLOTTINGAGENTS IS PRODUCED BYTHE ENDOTHELIAL CELLS A ANTITHROMBIN III B LOW MOLECULARWEIGHT HEPARIN C APIXIBAN D TISSUE FACTOR PATHWAY INHIBITOR E CLOPIDOGREL SBA QUESTION: WHICH OFTHE FOLLOWINGANTI-CLOTTINGAGENTS IS PRODUCED BYTHE ENDOTHELIAL CELLS A ANTITHROMBIN III B LOW MOLECULARWEIGHT HEPARIN C APIXIBAN D TISSUE FACTOR PATHWAY INHIBITOR E CLOPIDOGRELANTI-CLOTTING FUNCTION OF ENDOTHELIAL CELLS ¡ Produced by endothelial cells ¡ Tissue factor pathway inhibitor – prevent tissue factor (Xa)binding ¡ Prostacyclin – cytokine which has anti-inflammatory and vasodilation effects ¡ Nitric oxide – relaxes blood vessels and increases blood flow ¡ Produced by the liver ¡ Antithrombin III – neutralize thrombin ¡ Produced by mast cells ¡ Heparin – accelerates the action of antithrombin III,therefore dependent on antithrombin III LO 6:EXPLAIN LIPIDTRANSPORTAND METABOLISM IN RELATIONTO CARDIOVASCULAR HEALTHAND DISEASE LO PRESENTED BY HO HIN LAM SBA QUESTION: WHICH OFTHE HORMONES BELOW STIMULATES LIPOLYSIS A INSULIN B GASTRIN C PEPTIDEYY D SOMATOSTATIN E GLUCAGON SBA QUESTION: WHICH OFTHE HORMONES BELOW STIMULATES LIPOLYSIS A INSULIN B B-TYPE NATRIURETIC PEPTIDE C PEPTIDEYY D SOMATOSTATIN E GLUCAGON SBA QUESTION: WHICH OFTHE FOLLOWING PROTEIN ISAFFECTED IN FAMILIAL HYPERCHOLESTEROLEMIA A LDL-R B Apo-B100 C Abo-E D PeptideYY E Glucagon SBA QUESTION: WHICH OFTHE FOLLOWING PROTEIN ISAFFECTED IN FAMILIAL HYPERCHOLESTEROLEMIA A LDL-R B Apo-B100 C Abo-E D PeptideYY E GlucagonFAMILIAL HYPERCHOLESTEROLEMIA ¡ Genetics: ¡ Autosomal FH:most common type of FH,autosomal dominant where a single copy of the LDLR gene is defective ¡ Homozygous FH:more severe,where both copies of the LDLR gene are defective,the patient has extremely high levels of LDL cholesterol ¡ Clinical features: ¡ High cholesterol levels and LDL in blood ¡ Xanthomas ¡ Arcus cornealis ¡ Early onset cardiovascular disease ¡ Management: ¡ Lifestyle changes ¡ High-intensity statin ¡ Ezetimibe monotherapy ¡ Refer to endocrine specialist for homozygous FH SBA QUESTION: WHICH OFTHE FOLLOWING IS RESPONSIBLE FOR BRINGING EXCESS CHOLESTEROL BACKTOTHE LIVER FROM EXTRA-HEPATICTISSUE A Chylomicrons B VLDL C IDL D LDL E HDL SBA QUESTION: WHICH OFTHE FOLLOWING IS RESPONSIBLE FOR BRINGING EXCESS CHOLESTEROL BACKTOTHE LIVER FROM EXTRA-HEPATICTISSUE A Chylomicrons B VLDL C IDL D LDL E HDLLIPOPROTEINS FUNCTIONS CHYLOMICR VLDL IDL LDL HDL ONS CONTENTS DietaryTAG EndogenousTAG Endogenous Endogenous Endogenous cholesterol cholesterol cholesterol esters esters esters FUNCTION Transport Processed into Processed into Reabsorbed into Transport of DietaryTAG IDL,fatty acid LDL,fatty acids the liver for cholesterol to from intestine to deposited in deposited in further break extrahepatic liver adipose tissue adipose tissue down tissues for use SBA QUESTION:WHICH OFTHE FOLLOWING ISTHE MOA OFATORVASTATIN A BLOCK HMG-COA REDUCTASE B BINDINGTO BILEACIDTO REDUCE FATTYACIDAVAILABILTY C PCSK9 – INHIBITORS D INCREASETHE PRODUCTION OFADIPONECTIN E ACTIVATE PPARS FOR INCREASED UPTAKEAND OXIDATION SBA QUESTION:WHICH OFTHE FOLLOWING ISTHE MOA OFATORVASTATIN A BLOCK HMG-COA REDUCTASE B BINDINGTO BILEACIDTO REDUCE FATTYACIDAVAILABILTY C PCSK9 – INHIBITORS D INCREASETHE PRODUCTION OFADIPONECTIN E ACTIVATE PPARS FOR INCREASED UPTAKEAND OXIDATION SBA QUESTION:WHICH OFTHE FOLLOWING ISA CONTRA-INDICATION FOR ATORVASTATIN A CHRONIC KIDNEY FAILURE B HAIRT FAILURE C MYOCARDIAL INFARCT D PULMONARY FIBROSIS E 12YEARS OLD ORYOUNGER SBA QUESTION:WHICH OFTHE FOLLOWING ISA CONTRA-INDICATION FOR ATORVASTATIN A CHRONIC KIDNEY FAILURE B HAIRT FAILURE C MYOCARDIAL INFARCT D PULMONARY FIBROSIS E 12YEARS OLD ORYOUNGERANTI-CLOTTING FUNCTION OF ENDOTHELIAL CELLS ¡ Produced by endothelial cells ¡ Tissue factor pathway inhibitor – prevent tissue factor (Xa)binding ¡ Prostacyclin – cytokine which has anti-inflammatory and vasodilation effects ¡ Nitric oxide – relaxes blood vessels and increases blood flow ¡ Produced by the liver ¡ Antithrombin III – neutralize thrombin ¡ Produced by mast cells ¡ Heparin – accelerates the action of antithrombin III,therefore dependent on antithrombin III LO 2 & 5 LO PRESENTED BYYEW ERNAU LO 2:Explain the physiology of cardiovascular LO function including cardiac muscle,the cardiac cycle and cardiac outputYou are a medical student and you are asked to analyse a histological sample. What is this sample showing? A Skeletal muscle B Cardiac muscle C Smooth muscle Dense irregular connective tissue D E Dense regular connective tissueYou are a medical student and you are asked to analyse a histological sample. What is this sample showing? A Skeletal muscle B Cardiac muscle C Smooth muscle Dense irregular connective tissue D E Dense regular connective tissueYou are asked about the cardiac action potentials,and you recall that there are 5 phases of this process.In which phase do L-type long Ca2+ channels open? A Phase 0 B Phase 1 C Phase 2 Phase 3 D E Phase 4You are asked about the cardiac action potentials,and you recall that there are 5 phases of this process.In which phase do L-type long Ca2+ channels open? A Phase 0 B Phase 1 C Phase 2 Phase 3 D E Phase 4You are a medical student on your emergency block,and you are auscultating a patient’s heart valves.Upon completing the examination,the FY1 asks you about what sound represents what.What is the‘lub’ sound indicative of? A S1,AV valve closure B S2,AV valve closure C S1,Aortic & pulmonary valve closure S2,Aortic & pulmonary valve closure D E S3,rapid filling of the ventricles causing the chordae tendinae to snap openYou are a medical student on your emergency block,and you are auscultating a patient’s heart valves.Upon completing the examination,the FY1 asks you about what sound represents what.What is the‘lub’ sound indicative of? A S1,AV valve closure B S2,AV valve closure C S1,Aortic & pulmonary valve closure S2,Aortic & pulmonary valve closure D E S3,rapid filling of the ventricles causing the chordae tendinae to snap openYou are revising the cardiac cycle and the pressure changes within each chamber.Ventricular systole cannot occur forever,and you know that when the heart relaxes,there is an event that occurs when the aortic and pulmonary valves shut.What is this called? A AV valves close B AV valves open C Aortic valves open Aortic pressure has a sudden drop D E Dicrotic notch/incisuraYou are revising the cardiac cycle and the pressure changes within each chamber.Ventricular systole cannot occur forever,and you know that when the heart relaxes,there is an event that occurs when the aortic and pulmonary valves shut.What is this called? A AV valves close B AV valves open C Aortic valves open Aortic pressure has a sudden drop D E Dicrotic notch/incisuraA patient is having a review of their heart function,and the doctor mentions that their ejection volume is around 50%.You decide to revise your knowledge of cardiac physiology and remember that cardiac output is governed by various factors.What is the correct equation for cardiac output? A Cardiac Output = Stroke volume/Heart rate B Cardiac Output = Heart rate/Stroke volume C Cardiac output = Heart rate x Stroke volume Cardiac output = Mean arterial pressure/Systemic vascular resistance D E Cardiac output = Systemic vascular resistance/Mean arterial pressureA patient is having a review of their heart function,and the doctor mentions that their ejection volume is around 50%.You decide to revise your knowledge of cardiac physiology and remember that cardiac output is governed by various factors.What is the correct equation for cardiac output? A Cardiac Output = Stroke volume/Heart rate B Cardiac Output = Heart rate/Stroke volume C Cardiac output = Heart rate x Stroke volume Cardiac output = Mean arterial pressure/Systemic vascular resistance D E Cardiac output = Systemic vascular resistance/Mean arterial pressureCARDIAC MUSCLES HISTOLOGY ¡ Long ¡ Striated (a little) ¡ Branched ¡ Intercalated discs ¡ Adherens junctions ¡ Desmosomes ¡ Gap junctionsCARDIAC MUSCLES HISTOLOGY ¡ Long ¡ Striated (a little) ¡ Branched ¡ Intercalated discs ¡ Adherens junctions ¡ Desmosomes ¡ Gap junctionsEXCITATION-CONTRACTION COUPLING OF CARDIAC MYOCYTESACTION POTENTIALS OF CARDIAC MYOCYTESACTION POTENTIALS OF SINO-ATRIAL MYOCYTES CARDIAC CYCLE (SIMPLIFIED!!) ????????????????? ????????????????? ????????????????? ????????????????? ????????????????? ?????????????????CARDIAC CYCLE (SIMPLIFIED!!)CARDIAC CYCLE (SIMPLIFIED!!)CARDIAC CYCLE (SIMPLIFIED!!)CARDIAC CYCLE (SIMPLIFIED!!) CARDIAC OUTPUT Cardiac Output (CO) = Heart rate (HR) x StrokeVolume (SV) End DiastolicVolume (EDV) – End systolic volume (ESV) Cardiac output Heart rate Stroke volume Autonomic innervation Heart size Hormones Fitness level Fitness level Gender Age Contractility Contraction duration Preload (EDV) Afterload (resistance) LO 5:Apply the principles of cardiovascular LOphysiology to the regulation of blood pressureShort term blood pressure is maintained by a feedback control mechanism.What are the two receptors involved in this system,and what do they detect? A Baroreceptors (high pressure) and volume receptors (low pressure) B Mechanoreceptors (low pressure) and baroreceptors (high pressure) C Nociceptors (high pressure) and baroreceptors (low pressure) Baroreceptors (low pressure) and volume receptors (high pressure) D E Mechanoreceptors (low pressure) and nociceptors (high pressure)Short term blood pressure is maintained by a feedback control mechanism.What are the two receptors involved in this system,and what do they detect? A Baroreceptors (high pressure) and volume receptors (low pressure) B Mechanoreceptors (low pressure) and baroreceptors (high pressure) C Nociceptors (high pressure) and baroreceptors (low pressure) Baroreceptors (low pressure) and volume receptors (high pressure) D E Mechanoreceptors (low pressure) and nociceptors (high pressure)A 19 year old Medical Student has collapsed on the wards suddenly after standing up.They regain consciousness almost immediately and recalled‘seeing stars’ and‘darkness’.They are previously fit and well,with no significant past medical history.They recall that the night before they had been drinking with friends,for which she had been moderately intoxicated.What is the most likely cause? A Epidural haemorrhage B Subarachnoid haemorrhage C Subdural haemorrhage Vasovagal syncope D E Orthostatic hypotensionA 19 year old Medical Student has collapsed on the wards suddenly after standing up.They regain consciousness almost immediately and recalled‘seeing stars’ and‘darkness’.They are previously fit and well,with no significant past medical history.They recall that the night before they had been drinking with friends,for which she had been moderately intoxicated.What is the most likely cause? A Epidural haemorrhage B Subarachnoid haemorrhage C Subdural haemorrhage Vasovagal syncope D E Orthostatic hypotensionA 50 year old patient presents to the GP for a routine check up.They have their blood pressure recorded which shows 145/95 mmHg.They have a past medical history of hypertension,for which they usually take ACE inhibitors and amlodipine.The patient admits they have avoided the medication due to personal belief. What stage of hypertension are they in? A No hypertension B Stage 1 C Stage 2 Stage 3 D E SevereA 50 year old patient presents to the GP for a routine check up.They have their blood pressure recorded which shows 145/95 mmHg.They have a past medical history of hypertension,for which they usually take ACE inhibitors and amlodipine.The patient admits they have avoided the medication due to personal belief. What stage of hypertension are they in? A No hypertension B Stage 1 C Stage 2 Stage 3 D E SevereWhat is the long term regulator of blood pressure? A Heart rate B Baroreceptor reflex C Reticuloendothelial system RAAS D E Cardiac outputWhat is the long term regulator of blood pressure? A Heart rate B Baroreceptor reflex C Reticuloendothelial system RAAS D E Cardiac outputYou are studying the effect of the Renin-Angiotensin-Aldosterone System (RAAS) and you want to recall the synthesis of the effector molecules.What enzyme is responsible for converting angiotensin I to angiotensin II,and where does this enzyme come from? A Angiotensin Converting Enzyme (ACE) - lungs B Renin - lungs C Angiotensin Converting Enzyme (ACE) - liver Renin - liver D E HMG-CoA ReductaseYou are studying the effect of the Renin-Angiotensin-Aldosterone System (RAAS) and you want to recall the synthesis of the effector molecules.What enzyme is responsible for converting angiotensin I to angiotensin II,and where does this enzyme come from? A Angiotensin Converting Enzyme (ACE) - lungs B Renin - lungs C Angiotensin Converting Enzyme (ACE) - liver Renin - liver D E HMG-CoA ReductaseBLOOD PRESSURE FUNDAMENTALS ¡ Systolic pressure:The pressure exerted by the ventricles ¡ Diastolic pressure:The pressure against the aorta from the systemic arterial pressure (pressure required to open the aortic valve)WHAT ISA HEALTHY/UNHEALTHY BLOOD PRESSURE Systolic Diastolic Average blood pressure 90-120 mmHg 60-80mmHg Pre-Hypertension (Stage 1 120-139 mmHg 80-89 mmHg hypertension) Stage 2 Hypertension 140+ mmHg 90+ mmHg Hypertensive crisis 180 + mmHg 120+ mmHg PHYSIOLOGICAL REGULATORS OF BLOOD PRESSURE Short term Long term Baroreceptor reflex RAAS Chemoreceptor reflex Behavioural state (sleep,stress) Nociceptor reflex Fight or flight reflex ExerciseNEUROLOGICAL CONTROL OF BLOOD PRESSURE Baroreceptor reflex § The feedback control system consisting of: § Sensors § Central control system § Effectors § This is a short-term regulatory mechanism Sensors Baroreceptors Volume receptors Central control Hypothalamus Medulla Oblongata Effectors ANS to heart ANS to vesselsGRAVITYAND BLOOD PRESSURE ¡ Blood pressure is generally lower in the superior end of the body compared to the inferior end due to gravity favouring blood flowing inferiorly ¡ Lying down generally increases the blood pressure towards the superior end of the body to make it roughly equal ORTHOSTATIC (POSTURAL) HYPOTENSION ¡ Caused by standing from a lying position ¡ Sudden drop in blood pressure with the activation of the baroreceptor reflex ¡ HR,contractility and vasoconstriction increase ¡ Potential lightheadedness and loss of consciousness ¡ Diagnosis with the tilt-test VASOVAGAL SYNCOPE ¡ Temporary reduction/loss of blood supply to the brain ¡ Triggered by: ¡ Environmental triggers ¡ Emotional triggers ¡ Activation of the parasympathetic nervous system which leads to: ¡ Bradycardia ¡ Vasodilation ¡ Reduction of blood pressure results in cerebral hypoperfusionENDOCRINE CONTROL OF BLOOD PRESSURE