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78 Cards in this Set
- Front
- Back
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Normal pressure of RA
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0-5mmHg
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Normal systolic pressure of RV
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15-30mmHg
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Normal pressure of LA
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5-12mmHg
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Normal systolic pressure of LV
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90-140
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SA node is commonly supplied by which main coronary artery?
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RCA (60%)
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AV node is supplied by which main coronary artery
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RCA (90%)
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Cardiac Output =
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Heart Rate x Stroke Volume
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Stroke Volume is dependant on (3)
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Preload
Contractility Afterload |
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Starling law states that
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Preload is proportional to contraction force
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alpha adrenoreceptor - a peripheral vasoconstrictor or dilator?
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peripheral vasoconstrictor
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What is Pulsus Paradoxus
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A dramatic fall in BP on inspiration.
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Causes of pulsus paradoxus?
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Cardiac Tamponade
Severe airway obstruction |
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What's the name for angina caused by lying down?
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Decubitas angina
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In acute MI why do patients vomit and become bradycardic?
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Vagal stimulation
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AMI is almost always caused by thrombus formation - what two pathologies underly this?
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75% Plaque fissuring (deep cleft)
25% Endothelium ulceration |
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You notice ST elevation and Q waves in leads V1-4. What is the anatomical distribution of infarct and which vessel is the likely culpret?
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Anteroseptal MI
Left Anterior Descending (with its septal perforators) |
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You notice ST elevation and Q waves in leads V4-6, aVL and I. What is the anatomical distribution of infarct and which vessel is the likely culpret?
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Massive Anterolateral MI
Left Coronary Artery |
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You notice ST elevation and Q waves in leads II, III and aVF. What is the anatomical distribution of infarct and which vessel is the likely culpret?
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Inferior MI
RCA / LCX |
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You notice no ST elevation. But in leads V1-4 you notice ST depression and tall R waves. What is the diagnosis?
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Posterior inferior MI
(looking at reciprocal changes in anterior leads...) RCA occlusion |
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Talk me through the ECG changes through time of a full thickness MI.
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1) Normal
2) Acute ST elevation (mins) 3) Loss of R wave, Increased Q wave, resolution of ST elevation, terminal T wave inversion (hours) 4) Deepening Q waves, Full T wave inversion (days) 5) Q waves persist, T wave inversion less pronounced (weeks) |
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What is required for a definitive diagnosis of an MI?
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1) a typical rise of troponin or CK-MB, with one of...
a) ischaemic sx b) ST depression/elevation c) q waves |
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Name four plasma markers in the order they are raised following an MI
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1) CK (peak @ 12hrs)
2) Troponin I or T (peak @ 36hrs) 3) AST 4) LDH |
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What are the two specific side effects of giving streptokinase compared to tPA
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anaphylaxis (it is antigenic)
hypotension 10 per 1000 less survival improvement than tPA 1 per 1000 non-fatal strokes than tPA |
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You're in A&E and the nurse reckons you should thrombolyse a patient with 2 leads of ST elevation. What are the 6 ABSOLUTE contraindications to thrombolysis.
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1 Previous haemorrhagic stroke
2 Previous ischaemic stroke in prev year 3 Previous allergic reaction to fibrinolytic 4 Active internal bleed 5 Recent head trauma/surgery 6 Suspected aortic dissection |
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What is the triad of Dressler's Syndrome?
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Fever
Pericarditis Pleurisy autoimmune cause a few weeks after MI. lasts a few days. treat with high dose aspirin/NSAIDs. |
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What class of drug is Valsartan
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Angiotensin blocker with his buddy Candesartan
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Talk me through the pathology of atherosclerotic plaque formation
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1) Fatty streaks form at sites of high shear stress (bifurcation)
2) Activated overlying endothelium express adhesion molecules recruiting monocytes 3) Monocytes migrate to intima, ingest lipid, become foam cells 4) Monocytes release cytokines and growth factor which recruit smooth m cells from the media into the intima where they become morph to repair phenotype and form the fibrous capsule around the lipid core |
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Name four groups of drugs used in the treatment of angina
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Nitrates
B blockers Ca antagonists K channel activators |
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Which Ca antagonists should be used with B blockers and which should not
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Nifidipine, Nicardipine YES
Verapamil, Diltiazem NO |
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What types of prosthetic valves do you know (3)
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Ball and cage
Tilting single disk Tilting bi-leaflet |
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Compare and contrast the value of a biological valve replacement
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Bio is
less durable (good for elderly) no need for anti-coagulation but frequently end up in AF anyway good for mitral valve |
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5 signs of cardiac tamponade
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muffled hrt sounds
low bp high jvp pulsus paradoxus Kussmaul's sign (jvp rise with inspiration) |
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Ever heard of Cheyne-Stoke Respirations, what are they?
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Cyclical pattern of respiration. depressed, apnoea, depressed, hyperventilation etc.
associated with cerebral damage / barbituates, opiates |
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With a system, what are the causes of pulmonary oedema? (4headings)
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>Cap Permeability (pneumonia, ARDS, toxins (Cl, H2, Septicaemia))
>Cap Pressure (LHF, Fluid overload) <Oncotic pressure (<albumin - hepatic/renal) Lymph Obstruction - tumour/parasite |
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Define heart failure
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an imprecise term describing inadequate cardiac output
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6 catagory heading causes of heart failure
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<contractility (post-mi, dilated cardiomyopathy)
outflow obstruction (hypertension, aortic stenosis) inflow obstruction (mitral stenosis) arrhythmia (AF, heart block) vent overload (aortic regurg, VSD) diastolic dysfunction (tamponade, restricted cardiomyopathy) |
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What murmur if slow in onset can result in pulmonary hypertension due to reflex vasoconstriction with no pulmonary oedema
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slow onset mitral stenosis
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What is amrinone and how does it work in heart failure
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Amrinone is a friendly phosphodiesterase inhibitor which is a positive ionotrope.
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What is dobutamine used for in heart failure
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dobutamine, a b agonist, is used as a positive ionotrope.
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So you think your patients got Heart Failure, what investigations would you do?
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Bedside - ECG, BM
Blood - BNP, Cardiac enzymes, FBC, TFT, U&E Radio - CXR, Echocardiogram |
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and what 4 things would you be looking for on the CXR in heart failure?
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Abnormal distension of upper pulmonary veins
Inc vascularity Kerley B lines in lower zones Pleural effusions Memory aid = ABCDE Alveolar oedema (bat wings) kerley B lines (interstitial oedema) Cardiomegaly Dilated upper lobe vessels Effusions (pleural) |
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Talk me through the NICE medication guidelines for CCF
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Diuretic
ACEi B Block Digoxin (1st line in AF) Spironolactone |
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What would a quiet S1 make you suspect
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Quiet closure of mitral valve = regurgitation?
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Fixed wide splitting of S2
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ASD - leads to extra filling of RV and late pulmonary valve closing
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Variable S2 splitting
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if narrow - physiological on inspiration
if wide - RBBB/LBBB |
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What is S3 and its causes
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early diastole (after S2)
from rapid filling against vent wall pregnancy, young, HF, mitral regurg |
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S4 is caused by
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late diastolic filling in severe left ventricular hypertrophy
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causes of mitral stenosis
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rheumatic carditis
congenital |
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what is a plumb coloured malar flash called?
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Malar fascies
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In massive aortic regurg - the mitral valve can become so stenotic that it causes a murmur called
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Austin-Flint murmur
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Surgical management of aortic stenosis
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Valvuplasty
Comissurotomy Replacement |
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Top 5 commonest CHD's
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VSD (30%)
ASD (10%) PDA (10%) PS (7%) Coarctation (7%) |
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If i told you this patient has an ASD - what two pathological classifications are there for it, and what is the significance?
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Ostium Secundum (common, due to failure of foramen ovale closure)
Ostium Primum (true defect in septum which is associated with a cleft mitral valve) |
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Incidence of VSD
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VSD is the commonest CHD (30% of them)
Incidence = 1 in 500 |
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What is tetralogy of Fallot (4)
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Pulmonary stenosis
VSD Overiding of aorta over VSD RVH |
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What's it called when you get pulmonary hypertension and R to L shunt with this?
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Eisennmenger's Syndrome
associated with cyanosis, clubbing and polycythaemia |
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2 principal catagories of risk factors for endocarditis
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Bacteraemia
Abnormal Cardiac endothelium |
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Commonest 5 features of Endocarditis
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90% Varying murmur
65% Haematuria 50% Petechial, transient, rash 35% Splenomegaly 10% Digital clubbing/splinter haemorrhage, cerebral emboli |
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What's the main difference with subacute endocarditis rather than acute?
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Subacute more insidious,
tends to be more virilent organism Can obstruct Can embolise - kidney, brain, peripheral vessels |
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Describe the leads used in a "12-lead ECG"
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10 leads in reality
6 chest leads (V1-6) 3 limb leads + neutral (3 bipolar, 3 unipolar traces) |
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On a standard ECG one small square horizontally equals what period of time?
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40ms
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What is 2nd degree Heart block?
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When one or more (but not all) impuleses are not conducted through the AV node
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How is 2nd degree classified
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Motitz type 1 (wenckebach) = progressively increasing PR interval until skipped
Mobitz Type II = most beats conducted normally, occasional missing ventricular contraction. |
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What are the naturally depolarising rates of SA node, AV node and Ventricular myocardium
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SA = 70/min
AV = 50/min Ventricular = 30/min |
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Describe the commonest features of Atrial Flutter
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Atrial rate 300/min
Ventricular rate 150/min Sawtooth Atrial picture (beware p waves hidden in t wave) |
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What is Wolff-Parkinson-White syndrome and ecg findings...
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When an accessory bundle conducts between the atria and ventricles without the usual nodal delay.
Pre-excitation with a short PR interval and slurred upstroke of QRS |
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If there is ST elevation is it angina or infarction?
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Commonly infarction
Unless Prinzemetal angina with vasospasm. |
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Contrast the features of Atrial Arrest with Atrial Block
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Atrial Arrest the SA node stops completely and restarts out of synch with previous rhythmn.
Atrial block is depolarising normally, one or two of them don't get atrially conducted. When restarts - it does so in synch with previous rythmn |
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What are the risk factors for DVT?
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Virchow's Triad
1)Hypercoaguability (malignancy, oestrogen, protein c) 2)Stasis (surgery, immobility, dehydration) 3)Endothelial damage (previous dvt, smoking, >40) |
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CF's of DVT
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Swollen, tender, warm leg
Tachycardia Mild fever Pitting oedema Distended veins |
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So you suspect your patient has a DVT what investigations would you order (2)?
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Doppler U/S of leg
Venogram - the definitive test but only if doppler inconclusive |
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How would you manage a patient with a proven DVT?
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LMW Heparin
Warfarin 6/12 to lifelong |
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Given that 1% of patients in hospital die of a fatal PE how would you protect them from getting one. (2)
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Mechanical - elevation, stocking, pneumatic sequential compression device early ambulation
Medical - 5000 U SC heparin (Antithrombin III) or Warfarin |
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What CF's would you look for in a patient with suspected PE? (5+)
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>JVP
mild fever tachycardia, S2 splitting, pleural effusions, hypotension confusion |
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What is the most common finding on CXR with a patient with PE
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NORMAL
if lucky - pleural effusion, raised hemidiaphram, decreased vascularity, horizontal shadows |
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What ECG changes might you find with a PE
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Normal/Sinus Tachycardia
20% - RBBB, S1Q3T3 appearance |
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ABG findings on a PE?
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<PaO2
normal or <PaCO2 metabolic acidosis (lactic?) |
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How would you investigate a patient with suspected PE? (3)
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D-dimer - strong negative specificity only
V/Q scanning - only helpful if no underlying lung/heart pathology Pulmonary Angiography CT pulmonary Angiography (GOLD) |
