Cardiovascular Flashcards

Question

Symptoms of myocardial infarction

Answer 1

Cardiac chest pain that: - Is unremitting - usually severe but may be mild or absent - occurs at rest - associated with sweating, breathlessness, nausea and/or vomiting - one third occur in bed at night

Answer 2

- get to hospital ASAP - direct to primary PCI centre for transfer if paramedics detect ST elevation - take 300mg aspirin immediately - pain relief if needed

Answer 3

- make diagnosis -ECG - bed rest - oxygen therapy *if hypoxic* - pain relief - opiates or nitrates - dual anti platelet tx - aspirin +/- platelet P2Y12 inhibitor - beta blocker - other anti anginal therapy

Answer 4

Most cases caused by atherosclerotic plaques

Answer 5

- A protein complex made of 3 subunits Tropnin T, I + C - regulates actin:myosin contraction

Answer 6

Cardiac muscle injury - troponin T and I are highly sensitive indicators of cardiac muscle injury

Answer 7

- FALSE - May not represent permanent muscle damage

Answer 8

False troponin is non-selective **troponin is also positive in** - gram negative sepsis - pulmonary embolism - myocarditis - heart failure - arrhythmias - chronic renal failure - aortic dissection - cytotoxic drugs

Answer 9

Factors influencing psychological responses to the social environment and pathophysiological changes

Answer 10

1. Clinical risk factors (hypertension, lipids, diabetes) 2. Lifestyle/ behavioural risk factors (smoking, diet, physical inactivity) 3. Environmental risk factors (air pollution, chemicals) 4. Demographic risk factors (age, sex, ethnicity, genetic) 5. Psychosocial risk factors (behaviour pattern, depression/anxiety, work, social support)

Answer 11

- “Type A” behaviour - competitive, hostile and impatient

Answer 12

- clinical interview - Speech, Answer content - Psychomotor, Non-verbal - questionnaires - assessment usually done in psychological settings not day to day medical practice

Answer 13

* ADP is released by damaged endothelium --> platelet adhesion and secretion of more ADP

Answer 14

1. shape change 2. fibrinogen release which promotes blood clotting by forming bridges between platelets via GPIIb/IIIa - an integrin 3. thromboxane release which amplifies platelet activation + recruits more platelets. 4. dense granule formation -> ADP release -> amplification of platelet activation via P2Y1 and **P2Y12** receptors 5. thrombin generation which converst fibrinogen --> fibrin to form a more stable fibrin basaed clot. 6. alpha granule formation -> release of coagulation factos and inflammatory mediators.

Answer 15

1. unstable angina 2. STEMI 3. NSTEMI

Answer 16

An imbalance between the heart’s oxygen demand and supply, usually caused by an increased demand coupled with a limitation of supply

Answer 17

1. Age 2. Cigarette smoking 3. Diabetes mellitus 4. Family history 5. Male 6. Hyperlipidemia 7. Hypertension 8. Obesity 9. Kidney disease 10 physical inactivity 11. Stress

Answer 18

**factors affecting O2 supply** - anaemia - hypoxemia **factors affecting O2 demand** - hypertension - tachycardia - valvular heart disease - hyperthyroidism - hypertrophic cardiomyopathy **environmental factors** - exercise - cold weather - heavy meals - blood is diverted to the stomach - emotional stress

Answer 19

When diameter stenosis reaches 70%

Answer 20

Angina pain that has been steadily getting worse over prior weeks and months, due to coronary heart disease Serious and requires hospitalisation

Answer 21

Angina pain at rest, due to coronary hear disease Serious and requires hospitalisation

Answer 22

Coronary spasm that narrows the coronary arteries ➡️ symptoms of angina RARE

Answer 23

- The micro vessels are at fault , meaning they can’t relax to reduce the resistance and increase blood flow ➡️ angina - The main coronary arteries apparently normal - mostly affects females - Cause unknown

Answer 24

- The prognosis is not bad as those that are diagnosed with the condition go on to live with it for a while - Prevalence = the number of people with a condition - Incidence = the number of people that develop a condition

Answer 25

Personal details (demographics, identifiers) Presenting complaint History of PC + risk factors Past medical history Drug history, allergies Family history -1st degree relative <60years old Social history Systematic enquiry

Answer 26

- Chest pain / tightness/ discomfort / heaviness **on exertion** - Breathlessness - No fluid retention (unlike heart failure) - Palpitation (not usually) - Syncope or pre-syncope (very rare)

Answer 27

**OPQRST** Onset Position (site) Quality (nature / character) Relationship (with exertion, posture, meals, breathing and with other symptoms) Radiation Relieving or aggravating factors Severity Timing

Answer 28

- MI - pericarditis/ myocarditis - pulmonary embolism / pleurisy - chest infection - Gastro-oesophageal (reflux, spasm, ulceration) - Musculo-skeletal - Psychological - Aorta dissection - severe tearing pain **the description of the pain is helpful**

Answer 29

- Lifestyle - smoking - Weight - Exercise - diet - Advice for emergency - Medication - Revascularisation

Answer 30

- CT Coronary Angiography - exercise testing - myoview scan - stress echo - perfusion MRI = GOLD STANDARD. - coronary angiography

Answer 31

- CT Coronary Angiography - good at ruling out and spotting severe disease. - Shows the anatomy of the heart nor the function. - much less invasive than traditional angiogram - Long waiting times

Answer 32

- Pt walks on treadmill while hooked up to ECG continuously and the intensity is gradually increased. - Dependent on pts ability to walk on treadmill - diagnostic tool for IHD - useless in disabled, elderly, obese, arthritic etc

Answer 33

- small dose of radiolabel circulates through the heart and imaged using a gamma camera to determine which parts of the heart have low perfusion when stressed and if perfusion returns on rest. - Uses pharmacological stressor to Increase HR and CO - a diagnostic tool for IHD

Answer 34

- diagnostic tool for IHD - Pharmacological stressor administered and a highly skilled operative looks for a regional wall abnormality. - Not used often

Answer 35

- perfusion MRI = GOLD STANDARD.

Answer 36

- A catheter is inserted and guided to heart and contrast administered - X-ray taken to look at the coronary arteries - also treatment planning tool as a stent can be administered immediately if appropriate

Answer 37

Reduce the cholesterol by 30%

Answer 38

- aspirin - Beta-blocker or Calcium channel blocker [2nd line] - statin - nitrates - GTN and long acting

Answer 39

- negatively inotropic [rate] and chronotropic [contractility] ➡️ reduced cardiac output and reduced oxygen demand

Answer 40

- bradycardia - nightmares - depending on w=if water soluble or not - cold peripheries - erectile dysfunction

Answer 41

- mainly act on venous return by causing expansion of venous capacitance vessels, causing the veins to relax ➡️ reduced preload on the heart. - dilates the coronary arteries - dilates the arterioles

Answer 42

A headache caused by vasodilation - should stop within 3 days of use

Answer 43

- negatively inotropic ➡️ less left ventricular contraction - negatively chronotropic ➡️ lower heart rate - together this reduces the work the heart does and therefore the oxygen demand - lowers BP ➡️ reduced after load

Answer 44

- flushing - postural hypotension - swollen ankles

Answer 45

Gastric ulceration

Answer 46

They inhibit the enzyme HMG CoA reductase This prevents the production of cholesterol

Answer 47

**pros** - Less invasive - Convenient - Repeatable - Acceptable **cons** - Risk stent thrombosis - Risk restenosis - Can’t deal with complex disease - Dual antiplatelet therapy

Answer 48

**Pros** - Prognosis - Deals with complex disease **Cons** - Invasive - Risk of stroke, bleeding - Can’t do if frail, comorbid - One time treatment - Length of stay - Time for recovery

Answer 49

Coronary artery bypass graft The internal mammary artery is diverted from the chest back to the LAD beyond the blockage A graft from the leg [saphenous vein] is placed to another blockage

Answer 50

- STEMI - NSTEMI - stable angina

Answer 51

- NSTEMI - complex stable angina **never use for STEMI**

Answer 52

* brachocephalic trunk → right common carotid and right subclavian * left common carotid artery * left subclavian artery

Answer 53

a double layered sac covering the heart. * **inner layer** = serous pericardium: has simple squamous epithelium * visceral serous pericardium [epicardium] lines the outer surface of the heart * parietal serous pericardium lines the fibrous pericardium and secretes fluid. * **outer layer =** fibrous pericardium * tough connective tissue that anchors the heart to the mediastinum. * outside → in = FPSV * Fibrous, parietal serous, SPACE, visceral serous

Answer 54

sternal angle point at which the trachea bifurcates end of the aortic arch and begining of the thoracic aorta.

Answer 55

midclavicular line of the 5 intercostal space

Answer 56

the 2nd intercostal space at the right sternal margin

Answer 57

2nd intercostal space of the left sternal margin

Answer 58

the ascending aorta

Answer 59

on the anterior surface of the heart in the atrioventricular sulcus.

Answer 60

the right marginal artery posterior interventricular artery - present in 90% of people.

Answer 61

the ascending aorta

Answer 62

* left anterior descending * the left marginal artery / obtuse marginal artery * Circumflex artery * diagonals

Answer 63

* 90% of people have PIV supplied by the right coronary artery * 30% of people have the PIV supplied by the circumflex artery * 20% of people have **TWO** PIVs supplied by each

Answer 64

the atrioventricular node recieves blood supply from..

Answer 65

as the PIV supplies the AVN, disease could limit O2 supply → electrical blockage in the heart.

Answer 66

the Posterior interventricular artery supplies …

Answer 67

1. An excitation signal (an action potential) is created by the **sinoatrial (SA) node**. 2. The wave of excitation spreads across the **atria,** causing them to contract. 3. Upon reaching the **atrioventricular (AV) node**, the signal is delayed. 4. It is then conducted into the **bundle of His**, down the interventricular septum. 5. The bundle of His and the **Purkinje fibres** spread the wave impulses along the ventricles, causing them to contract

Answer 68

the sinoatrial node is a collection of pacemaker cells, located in the upper wall of the right atrium, at the junction where the superior vena cava enters.

Answer 69

located within the right atrioventricular septum, near the opening of the coronary sinus.

Answer 70

* right coronary artery = right atrium and ventricle * LAD = right and left ventricles and interventricular septum * obtuse / left marginal artery = left ventricle * circumflex = left atrium and ventricle * Right marginal = right ventricle and apex

Answer 71

120 days destroyed as they have no nucleus for self maintainance

Answer 72

phase 1 = platelet plug formation phase 2 = coagulation - stabilising the plug

Answer 73

3: 1. intrinsic: triggered by surface contact with collagen 2. extrinsic: triggered by endothelial damage 3. common

Answer 74

1. endothelial injury 2. exposure 3. adhesion 4. activation 5. aggregation

Answer 75

it's not activated by any other cell, it is in an automatic, constant cycle

Answer 76

* Increases heart rate (positively **chronotropic**) * Increases force of contraction (positively **inotropic**) * Increases cardiac output

Answer 77

* Decreases heart rate (negatively chronotropic) * Decreases force of contraction (negatively inotropic) * Decreases cardiac output

Answer 78

Adrenaline and noradrenaline + type 1 beta adrenoreceptors * Increases adenylyl cyclase → increased cAMP

Answer 79

ACh and M2 receptors – inhibit adenyl cyclase → reduced cAMP

Answer 80

the time in which the cell cannot depolarise again

Answer 81

* **P wave** * atria fills with blood → SA node firiing → atrial contraction * atrial systole occurs partway through the P wave * P-R = atrial systole / ventricle diastole * P-Q segment = time it takes for signal to pass from SAN → AVN * **QRS complex** * represents firing of AVN and depolarisation of the ventricles * R-S = isovolumetric contraction * AV valves are shut and semilunar valves are shut BUT the ventricle has started contracting * **ST segment** * represents the plateau in myocardial action pd = Ca²⁺influx → contraction * Thus ST segment = ventricular contraction - systole * **T wave** * ventricular repolarisation and diastole * end of T wave represents isovolumetric relaxation

Answer 82

* a protein that holds tropomyosin in place on actin and is involved in myocyte contraction * it has 3 subunits 1. TNI - inhibitory to prevent in actin and myosin interaction 2. TnT tropomyosin binding 3. TnC calcium binding

Answer 83

1. Mitral valve shutting 2. aortic valve shutting

Answer 84

the degree of ventricular stretch at the end of diastole - a **volume** venous blood pressure and rate of venous return

Answer 85

the **pressure** which the ventricles must overcome to eject blood i.e. systemic pressure and pulmonary pressure

Answer 86

- platelets - anti-platelet therapy is used

Answer 87

Right atrium Right ventricle Inferior aspect of left ventricle Posterior septal area

Answer 88

Left atrium Posterior aspect of left ventricle

Answer 89

Anterior aspect of left ventricle Anterior aspect of septum

Answer 90

Nausea and vomiting Sweating and clamminess Feeling of impending doom Shortness of breath Palpitations Pain radiating to jaw or arms

Answer 91

1. ECG carried out to determine if there is ST elevation or new left bundle branch block 2. Blood test for troponin levels to determine if there was an MI

Answer 92

Unstable angina Or another cause of chest pain such as MSK chest pain

Answer 93

ST segment depression in a region Deep T Wave Inversion Pathological Q Waves (suggesting a deep infarct – a late sign)

Answer 94

Chronic renal failure Sepsis Myocarditis Aortic dissection Pulmonary embolism

Answer 95

- Primary PCI (if available within 2 hours of presentation) - Thrombolysis (if PCI not available within 2 hours) - Using fibrinolytic drug to dissolve the clot such as alteplase, streptokinase or tenectplase

Answer 96

BATMAN B – Beta-blockers unless contraindicated A – Aspirin 300mg stat dose T – Ticagrelor 180mg stat dose (clopidogrel 300mg is an alternative if higher bleeding risk) M – Morphine titrated to control pain A – Anticoagulant: Fondaparinux (unless high bleeding risk ➡️ heparin) N – Nitrates (e.g. GTN) to relieve coronary artery spasm Give oxygen only if their oxygen saturations are dropping (i.e. <95%).

Answer 97

- A scoring system that gives a 6 months risk of **death** or **repeated MI** after an NSTEMI - It’s used to assess the need for PCI in NSTEMI - <5% Low Risk - 5-10% Medium Risk - >10% High Risk - medium -high risk considered for early PCI for underlying coronary artery disease

Answer 98

DREAD D – Death R – Rupture of the heart septum or papillary muscles E – “Edema” (Heart Failure) A – Arrhythmia and Aneurysm D – Dressler’s Syndrome

Answer 99

- post-myocardial infarction syndrome. - It usually occurs around 2-3 weeks after an MI. - It is caused by a localised immune response and ➡️ pericarditis

Answer 100

- pleuritic chest pain - low grade fever - pericardial rub on auscultation

Answer 101

- ECG ➡️ global ST elevation and T wave inversion - Echocardiogram ➡️ pericardial effusion - Raised inflammatory markers - CRP and ESR

Answer 102

DASLAB - D - Dual antiplatelet therapy - aspirin + clopidogrel or ticagrelor up to 12 months - A - Ace inhibitor - S - Statin - Astorvastatin 80mg - L - Lifestyle changes - A - Aldosterone antagonist for pts with clinical heart failure - eplerenone - B - Beta blocker titrated to max tolerated dose

Answer 103

**2 continuous layers** - Visceral single cell layer adherent to epicardium - Fibrous parietal layer 2mm thick - ~50 ml of serous fluid in between for lubrication

Answer 104

- the great vessels - all of the heart EXCEPT the left atrium

Answer 105

To restrain the filling volume of the heart

Answer 106

- The pericardium is similar to rubber in that it is initially stretchy but becomes stiff at higher tensions - this means the sac can only take on a small amount of fluid before it stiffens. Thus, it has a small reserve volume. - pericardial effusions occur when fluid enters the sac and the reserve volume is exceeded ➡️ the pericardial sac stiffens and prevents the heart from filling as normal.

Answer 107

A small increase or decrease in pericardial space fluid ➡️ dramatic effects on filling of the heart

Answer 108

- Slow accumulation of fluid within the pericardium allows the parietal pericardium to adapt and stretch. - the increase in compliance of the parietal layer reduces the effect on filling of the chambers - this allows for large effusions to accumulate - slowly accumulation effusions rarely cause tamponade

Answer 109

Acute pericarditis is an inflammatory pericardial syndrome with or without effusion

Answer 110

At least 2/4 of: 1. Chest pain 2. Friction rub 3. ECG changes 4. Pericardial effusion

Answer 111

**infectious** - **viral** - enteroviruses, herpes virus, adenovirus - ** bacterial** - mycobacterium tuberculosis **Non-infectious** - **autoimmune** - common, e.g. Sjögren syndrome, rheumatoid arthritis, scleroderma, - **Neoplastic** - secondary metastatic tumours - **metabolic** - uraemia and myxoedema - **traumatic** - direct or indirect injury - **iatrogenic** - amyloidosis, aortic dissection, CHF

Answer 112

* chest pain that is: * Severe * Sharp and pleuritic (without constricting crushing character of ischaemic pain) * Rapid onset * Left anterior chest or epigastrium * Radiates to arm more specifically trapezius ridge (co-innervation phrenic nerve) * Relieved by sitting forward exacerbated by lying down * dyspnoea * cough * hiccups * systemic disturbance * Skin rash, joint pain, eye Sx, weight loss (Cause) * Viral prodrome, Antecedent fever * past medical history of cancer, rheumatological conditions, MI or cardiac procedures.

Answer 113

- pericardial rub: sounds like crunching snow or scratching on the left sternal edge - sinus tachycardia - fever - signs of effusion - pulsus paradoxus - Beck's triad - elevated JVP - Hypotension - quiet heart sounds

Answer 114

* a pathogonomic sign. * sounds like crunching snow or scratching in the left sternal edge

Answer 115

- 3 symptoms and signs that are indicative of pericardial tamponade - low blood pressure - High jugular vein pressure - muffled/ quiet heart sounds

Answer 116

- an exaggerated fall in a patient's blood pressure during inspiration by greater than 10 mmHg caused by moderate or large effusions - paradox = the reduced cardiac output -> reduced volume of the peripheral pulse

Answer 117

- Clinical examination * Pericardial rub – pathognomonic, crunching snow * Sinus tachycardia * Fever * Signs of effusion (pulsus paradoxus, Kussmauls sign) * ECG * Bloods * Chest X-ray - effusion may cause cardiomegaly * Echocardiogram

Answer 118

* Saddle shaped ST elevation * Concave ST segment * diffuse ST elevation on ALL leads

Answer 119

- sedentary activity until resolution of symptoms and ECG and CRP - NSAID or aspirin at high dose - 2 weeks - colchicine - 3 months

Answer 120

viral pericarditis self-limiting conditions

Answer 121

FALSE this causes a bad sickness and high mortality

Answer 122

Hypertrophic cardiomyopathy (HCM) caused by sarcomeric protein gene mutations

Answer 123

unexplained primary cardiac hypertrophy

Answer 124

HCM may cause: * angina * dyspnoea * palpitations * dizzy spells or syncope.

Answer 125

Dilated cardiomyopathy (DCM) – often caused by cytoskeletal gene mutations

Answer 126

An Inherited arrhythmia caused by ion channel protein gene mutations. usually relates to potassium, sodium or calcium channels.

Answer 127

1. long QT 2. short QT 3. Brugada 4. CPVT - Catecholaminergic polymorphic ventricular tachycardia

Answer 128

- Channelopathies have a structurally normal heart - Channelopathies may present with recurrent syncope

Answer 129

- usually caused by an inherited condition - If so this is most likely a cardiomyopathy or ion channelopathy

Answer 130

an inherited abnormality of cholesterol metabolism

Answer 131

FH leads to serious premature coronary and other vascular disease

Answer 132

ICCs are usually dominantly inherited – offspring have 50% risk of inheritance

Answer 133

1. Viral pericarditis – most common cause in developed world 1. Purulent bacterial pericarditis and effusion – rare and high mortality rate 1. Tuberculous effusion TB pericarditis 1. Dressler’s syndrome

Answer 134

- it is an important preventable cause of premature morbidity and mortality as it is a major risk factor for numerous conditions

Answer 135

Stroke – ischaemic and haemorrhagic Myocardial infarction Heart failure Chronic renal disease Cognitive decline – dementia Premature death

Answer 136

Clinic BP 140/90 mmHg or higher

Answer 137

- Pts with high BP in clinic are fitted with ambulatory BP monitoring to confirm a diagnosis

Answer 138

1. Cardiac output 2. **Peripheral resistance** - KEY ISSUE IN HYPERTENSION 3. Local vascular vasoconstrictor and vasodilator mediators 4. Interplay between: a. Renin-Angiotensin-Aldosterone system b. Sympathetic nervous system (noradrenaline)

Answer 139

- hypertension - heart failure - diabetic nephropathy

Answer 140

1. Related to reduced angiotensin II formation a. Hypotension b. Acute renal failure c. Hyperkalaemia d. Teratogenic effects in pregnancy – stop before conception if possible. 2. Related to increased kinin production a. Cough b. Rash c. Anaphylactoid reactions

Answer 141

Angiotensin II Receptor Blockers

Answer 142

Hypertension Diabetic nephropathy Heart failure (when ACE-I contraindicated)

Answer 143

Symptomatic hypotension (especially volume deplete patients) Hyperkalaemia Potential for renal dysfunction Rash Angio-oedema

Answer 144

FALSE It’s contraindicated

Answer 145

Hypertension Ischaemic heart disease (IHD) – angina Arrhythmia (tachycardia)

Answer 146

- Dihydropyridines - amlodipine etc - Non-dihydropyridines - Phenylalkylamines: verapamil - Benzothiazepines: diltiazem

Answer 147

Preferentially affect vascular smooth muscle Peripheral arterial vasodilators

Answer 148

- verapamil - mainly affects the heart - negatively chronotropic and inotropic

Answer 149

- Diltiazem - effects on the heart and blood vessels - Negatively chronotropic - arterial vasodilation ➡️ reduced BP [increases smooth muscle relaxation

Answer 150

1. Due to peripheral vasodilatation (mainly dihydropyridines) Flushing Headache Oedema - usually benign and can be ignored Palpitations 2. Due to negatively chronotropic effects (mainly verapamil/diltiazem) Bradycardia Atrioventricular block 3. Due to negatively inotropic effects (mainly verapamil) Worsening of cardiac failure 4. Verapamil causes constipation

Answer 151

Ischaemic heart disease (IHD) – angina Heart failure Arrhythmia Hypertension

Answer 152

FALSE Selectivity is relative not absolute B2 receptors are found in the heart so no such thing as cardioselectivity. NEVER give any BB to asmatics regardless of se;ectivity claim

Answer 153

Fatigue Headache Sleep disturbance/nightmares Bradycardia Hypotension Cold peripheries Erectile dysfunction

Answer 154

- asthma - severely worsened NEVER give to these pts - peripheral vascular disease - Claudication or Raynauds - heart failure IF given a standard dose - must start on a low dose and slowly uptitrate.

Answer 155

- hypertension - heart failure

Answer 156

1. Thiazide like diuretics 2. Loop diuretics 3. Potassium sparing diuretics 4. Aldosterone antagonists

Answer 157

- bendroflumethiazide - indapamide - metolazone - chorthalidone - hydrochlorothiazide

Answer 158

- furosemide - bumetanide

Answer 159

- amiloride - triamterine - spironolactone - eplerenone

Answer 160

TRUE - they are mainly used in conjunction with thiazide or loop diuretics in pts with hypOkalaemia instead of K+ supplements

Answer 161

Spironolactone and eplerenone They intrinsically act on the RAAS system. Thus they are disease modifying and prevent K+ loss, making them K+ sparing diuretics too

Answer 162

- hypovolaemia and hypotension [ mainly loop diuretics] - hypokalaemia - hyponatraemia - hypomagnesaemia - hypocalcaemia - hyperuricaemia ➡️ gout - Impaired glucose tolerance [mainly loop diuretics] - erectile dysfunction [mainly thiazides]

Answer 163

- Moxonidine - methyldopa

Answer 164

1. Chronic heart failure - caused by: - Left Ventricular Systolic Dysfunction LVSD - Diastolic failure - heart failure with preserved ejection fraction HFPEF. 2. Acute heart failure - caused by MI

Answer 165

Heart failure is a complex clinical syndrome of symptoms and signs that suggest the efficiency of the heart as a pump is impaired. It is caused by structural or functional abnormalities of the heart. **Most common cause is coronary artery disease**

Answer 166

**Best** - Vasodilator therapy - neurohumoral blockade of the RAAS-SNS systems - *reduces peripheral resistance AND cardiac output* **Worst** - Left ventricle stimulant - **heart failure treatment aims to address the *response* to the impaired heart function rather than the heart function itself**

Answer 167

1. Symptomatic treatment for relief of oedema - usually loop diuretics 2. Disease influencing treatment via neurohumoral blockade - inhibition of RAAS-SNS systems 1. 1st line = ACE inhibitors and beta blocker therapy [Low dose and slow up-titration] 2. Give ARB if ACEi intolerant 3. give hydralazine/ nitrate combo if intolerant to ACEi + ARB 2. Add aldosterone antagonist [MRA] if no response 3. consider addition of digoxin, ivabradine or sacubitril/valsartan depending on preserved ejection fraction if poor response

Answer 168

YES - it produces natriuretic peptides in response to stretch - Atrial natriuretic peptide (ANP) - from the atria - B-(Brain) natriuretic peptide (BNP) – from the ventricles - stretching can be caused by raised atrial or ventricular pressures OR volume over load

Answer 169

Increase renal excretion of sodium (natriuresis) and water (diuresis) Relax vascular smooth muscle (except efferent arterioles of renal glomeruli) Increased vascular permeability Inhibit the release or actions of: Aldosterone, angiotensin II, endothelin, anti-diuretic hormone (ADH) **Counter-regulatory system to the renin-angiotensin system**

Answer 170

- The enzyme that breaks down the cardiac natriuretic peptides - Neutral Endopeptidase = NEP = neprilysin

Answer 171

Atrial natriuretic peptide (ANP) - atria B-(Brain) natriuretic peptide (BNP) – ventricles

Answer 172

- A neprilysin inhibitor - it increases the levels of natriuretic peptides ➡️ the inhibition of release or action of RAAS: - Aldosterone, angiotensin II, endothelin, anti-diuretic hormone (ADH) - Heart failure with <35% ejection fraction preserved

Answer 173

True Preserves ejection fraction and is cardioprotective

Answer 174

- arterial and venous vasodilators - reduce preload and after load - lower BP

Answer 175

- Ischaemic heart disease - angina - heart failure

Answer 176

- headache - GTN syncope - with the spray Dizziness

Answer 177

1. All pts receive - antiplatelet therapy - aspirin or clopidogrel - statins to lower cholesterol - GTN spray for acute attacks 2. 1st line treatment = - **Beta Blockers or CCBs** - if intolerant ➡️ **switch** - if not controlled ➡️ **combine** 3. If pt still uncontrolled or intolerant consider mono therapy or combinations with: - Long acting nitrate - Ivabradine (inhibits If current) - Nicorandil (K channel activator) - Ranolazine (inhibits late inward sodium current)

Answer 178

1. Pain relief: GTN spray, Opiates – diamorphine 2. Dual antiplatelet therapy: Aspirin plus ticagrelor or prasugrel or clopidogrel 3. Antithrombin therapy: Fondaparinux 4. Consider Glycoprotein IIb IIIa inhibitor *high risk cases*: tirofiban, eptifibatide, abciximab 5. Background angina therapy: beta blocker, long acting nitrate, calcium channel blocker 6. Lipid lowering therapy: Statins 7. Therapy for LVSD/heart failure as required: ACE-I, beta blocker, aldosterone antagonist

Answer 179

Antiarrhythmic drugs

Answer 180

A cardiac glycoside Antiarrhythmic drug

Answer 181

Inhibit Na/K pump [ leads to increased Ca++ in the heart ➡️ increased vagal tone ]

Answer 182

Bradycardia (increased vagal tone) Slowing of atrioventricular conduction (increased vagal tone) Increased force of contraction (by increased intracellular Ca)

Answer 183

- N+V - confusion - Diarrhoea - dizziness

Answer 184

- Used in atrial fibrillation (AF) to reduce ventricular rate response - Used in severe heart failure as positively inotropic - has a narrow therapeutic index so frequent monitoring required

Answer 185

Treatment of arrhythmias e.g. QT prolongation and Polymorphic ventricular tachycardia

Answer 186

Interstitial pneumonitis Abnormal liver function Hyperthyroidism / Hypothyroidism Sun sensitivity Slate grey skin discolouration Corneal microdeposits Optic neuropathy Many DDIs

Answer 187

- diabetic pts - elderly pts

Answer 188

* Essential (Primary origin) – 95% cases * Secondary causes * Renal e.g. CKD * Endocrine e.g. Conn’s syndrome, acromegaly, * Cushing’s syndrome * Coarctation of the aorta * Pre-eclampsia occurring during third trimester of pregnancy * Drugs – oestrogen-containing oral contraceptives, NSAIDs, vasopressin

Answer 189

Rapid rise in BP leading to vascular damage

Answer 190

Headache Visual disturbance

Answer 191

* Severe hypertension * Systolic > 200 mmHg * Diastolic > 130 mmHg * Bilateral renal haemorrhage = exudates = papilloedema

Answer 192

Hypertensive emergencies e.g: - acute kidney injury, - HF - encephalopathy

Answer 193

Sodium nitroprusside

Answer 194

- Angina due to coronary artery spasm, which can occur even in normal coronary arteries. - The pain usually occurs during rest and resolves rapidly with short-acting nitrates (eg GTN spray). - ECG during pain shows ST segment elevation.

Answer 195

TRUE during an episode of pain ST elevation is seen on the ECG

Answer 196

- avoid triggers + quit smoking - correct low magnesium - PRN GTN spray - CCBs - long acting nitrates - AVOID non-selective BB, aspirin and triptans

Answer 197

1. BP 1. Age 1. Smoking status 1. Cholesterol 1. Rheumatoid Arthritis 1. Diabetes Mellitus 1. Anti-hypertensives 1. BMI 1. Ethnicity

Answer 198

QRISK2 score predicts risk of CVD in next 10 years, considers:

Answer 199

coronary arterial disease which causes myocardial dysfunction.

Answer 200

* Breathlessness * Tiredness * Cold peripheries * Leg swelling * Increased weight

Answer 201

* Tachycardia * Laterally Displaced apex beat * Raised JVP * Added heart sounds and murmurs * Hepatomegaly, especially if pulsatile and tender * Peripheral and sacral oedema n Ascites

Answer 202

- loss of P-waves which show atrial depolarisation, due to contraction triggered by ectopic sites as well as SA node. - irregular rhythm on ECG due to irregular stimulation of the AV node from ectopic sites.

Answer 203

- AF causes loss of P-wave whereas ventricular ectopics doesn't. - both still cause palpitations + an irregular pulse

Answer 204

PR segment depression and widespread ST elevation with reciprocal changes in aVR (occurs during the first couple of weeks) Associated T wave flattening can also be seen from weeks 1 to 3. Sinus tachycardia is also seen in some cases due to the chest pain.

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Cardiovascular Flashcards

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