Cardiology Flashcards

(100 cards)

1
Q

What is heart failure?

A

A syndrome where cardiac output is not sufficient to meet the body’s requirements

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2
Q

What is systolic failure? What causes it (top 3)

A

Inability of the ventricle to contract normally, reduced CO, ejection fraction typically <40%

Causes: IHD, MI, cardiomyopathy (hypertension)

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3
Q

What is diastolic failure? What causes it (5)

A

Inability of the ventricle to relax and fill normally, increased filling pressure. Typical ejection fraction >50%.
Causes include ventricular hypertrophy, constrictive pericarditis, tamponade, restrictive cardiomyopathy, obesity

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4
Q

What are the symptoms of left ventricular failure?

A

Dyspnoea, poor exercise tolerance, fatigue, orthopnea, PND, nocturnal cough (+/- pink frothy sputum), wheeze, nocturia, cold peripheries, weigh loss.

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5
Q

What are the symptoms of right heart failure ?

A

Peripheral oedema, ascites, nausea, anorexia, facial engorgement, epistaxis

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6
Q

NY classification of heart failure

A

I: no undue breath,Essenes
II: Breathlessness during ADLs, not limiting
III: breathlessness during ADLs, limiting
IV: breathlessness at rest

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7
Q

Chest x-ray findings in heart failure (5)

A

Alveolar Oedema (bat wing appearance)
kerley B lines (interstitial oedema, also known as septal lines)
Cardiomegally (>50% cardiothoracic ratio)
Dilated prominent upper lobe vessels (diversion due to oedema)
Effusions (blunted costophrenic angle and cardiac border)

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8
Q

How should you investigate suspected heart failure?

A

BNP and ECG. If either abnormal echocardiogram. If abnormal ever to cardiology.

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9
Q

Management of heart failure (not specific drugs, 5 things)

A

1) treat cause e.g. valvular heart disease, arrhythmia.
2)treat exacerbating factors e.g. anaemia,infection
3 )lifestyle modification e.g smoking cessation, alcohol reduction, reduced salt diet, healthy eating, weight loss.
4)avoid exacerbating factors e.g. NSAIDS and negative inotropes e,g, verapamil
5) annual flu vaccine and one off pneumococcal vaccine

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10
Q

Pharmacological management of heart failure. (3 core things + 2 to add on)

A

Reduce workload of heart.

1) diuretics - furosemide or bumetanide
2) ACEi or ARB
3) beta blocker e.g. bisoprolol. Start low and go slow.
4) spironolactone if renal function allows and potassium >3.4 or arrhythmia or digoxin therapy. Use if other diuretics not achieving adequate symptom control or if LVSD in post MI patients
5) digoxin considered in all who have LVSD who are still symptomatic with above management.

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11
Q

Palliative care considerations for heart failure patients (5)

A

1) treat and prevent comorbid conditions e.g. flu vaccine
2) good nutrition, allow alcohol
3) involve GP - discuss prognosis
4) treat symptoms - consider opiates for pain and dyspnoea
5) be realistic about prognosis

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12
Q

Hypertension management (not drugs)

A

If >135/85 in clinic, monitor, lifestyle advice
If >140/90 in clinic, home recordings
If at home >135/85 then stage 1 hypertension.
No comorbid disease or over 80- monitor
Comorbid disease and under 80- drug treatment
If in clinic >150/95 drug treatment

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13
Q

Pharmacological management of hypertension

A

A=ACEi
C= CA2+ blocker
D= thiazide diuretic

if <55yrs or diabetic = A
if >=55yrs or Afro-Caribbean =C
Then A and C
Then A and C and D

Then consider adding spironolactone or increasing D, if not tolerated add an alpha or beta blocker
If doesn’t tolerate ACEi use ARB

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14
Q

What is the cardiac output of an average male at rest

A

5L/min

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15
Q

Leads I and aVL on an ECG refer to which territory and which artery is likely to supply this area?

A

Septal or lateral - circumflex artery

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16
Q

Leads II, III and aVF on an ECG refer to which territory and which artery is likely to supply this area?

A

Inferior - RCA or Circumflex

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17
Q

Leads V1 to V4 on an ECG refer to which territory and which artery is likely to supply this area?

A

Anteroseptal - LAD

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18
Q

Leads V1 to V6 (+/- aVL) on an ECG refer to which territory and which artery is likely to supply this area?

A

Anteriorlateral - LAD

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19
Q

What ECG change would make you suspicious of a posterior myocardial infarction? What should you do to confirm your suspicions?

A

ST depression in V1 to V3, there may also be reciprocal change in aVR

Repeat ECG with leads V7, V8 and V9 which are placed on the back, below the left scapula. You would expect to see moderate ST elevation in these leads.

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20
Q

Where does the ductus arteriosus run, what is it’s purpose and what does it become after birth?

A

Between the pulmonary artery and the aorta. Allows most of the semi-oxygenated blood to bypass the foetuses lungs which are fluid filled and therefore at high pressure.

It becomes the ligamentum arteriosus

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21
Q

What is the foremen ovale, and what does it become?

A

The foremen ovale is a hole in the interatrial septum providing a shunt for oxygenated blood between the right and left atrium, allowing it to bypass the non-functioning lungs.

After birth the foramen closes forming the fossa ovalis

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22
Q

What is the ductus venousus purpose and what does it become?

A

The ductus venous provides a shunt from the umbilical vein to the IVC, preventing the liver from using most of the the oxygenated blood from the placenta.
Becomes the ligamentum venosum, which separates the caudate lobe of the liver

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23
Q

Give two examples of acyanotic congenital heart defects

A

Atrial septal defect

Ventricular septal defect

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24
Q

Give two examples of cyanotic congenital heart defects

A

Tetralogy of fallot

Transposition of the great arteries

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25
What defects are present in tetralogy of fallot? | Which direction is the shunt?
Ventricular septal defect Overriding aorta Pulmonary stenosis Right ventricular hypertrophy Produces right to left shunt, therefore some degree of cyanosis. Severity depends on level of pulmonary stenosis (and therefore amount of blood shunted)
26
What autonomic receptors are found in the heart?
Beta 1 adrenoreceptors - increase rate and contractility | M2 muscarinic ACh receptor - decrease rate
27
What is starling’s law?
The stroke volume of the heart increases if there is an increased volume of blood in the heart (i.e. a greater preload will result in greater contractility)
28
How do you calculate cardiac output?
CO= stroke volume * heart rate
29
What is preload?
The end diastolic pressure -the volume at which the ventricles are stretched the most.
30
What is afterload?
The tension within the left ventricle during systole -depends on arterial or pulmonary pressures
31
Describe Stable angina
- transient ischaemia which is relived when O2 demand decreases - brief episodes of chest pain on breathlessness brought on by exertion or emotion and relieved by rest - resting ECG normal, ST depression on stress test, troponin normal
32
Describe unstable angina
- ischaemia even at rest - ST depression at rest - no raised troponin as no necrosis
33
Describe an NSTEMI
ST depression or T wave changes pm ECG Raised troponins Some infarction but not full thickness
34
Describe STEMI
ST segment elevation on ECG with reciprocal changes Troponins raised Full thickeners infarction
35
When is troponin I most raised? How long will it remain raised? When would you look at creatinine kinase?
Troponin I reaches its peak level 24hours post infarction It remains raised for approximately 1 week CK may be used if there is a second episode of chest pain within 2 days of a confirmed MI
36
NYHA scale of dyspnoea in heart failure... go!
I - no symptoms or limitation II - mild symptoms and slight limitation during ordinary activity III - marked limitation on activity due to symptoms e.g. walking short distances. Only comfortable at rest. IV - severe limitation, symptoms at rest, bed bound.
37
Causes of heart failure
``` Ischaemic heart disease Valvular disease Hypertension Arrhythmia Hypertrophic cardiomyopathy ```
38
What general advice would you give to someone with heart failure?
Regular, low level exercise, such as brisk walking Have a low salt diet STOP SMOKING Education about the disease and it’s progression Vaccination
39
Define cardiogenic shock
The inability of the heart to eject enough blood e.g. following myocardial infarction
40
What is a third heart sound and what can cause it?
Due to a stiff or dilated ventricle suddenly reaching its elastic potential which decelerates the incoming blood. “Lub...dub de” Normal in under 30s and children Causes include HF, MI, cardiomyopathy, hypertension
41
What is a fourth hear sound and what does it mean?
Low pitched sound of atrial contraction into a non-compliant or hypertrophied ventricle. “Le lub...dub” Always abnormal Heart failure, MI, cardiomyopathy, hypertension
42
What is the grading system for murmurs?
1- very faint 2- soft 3- heard easily 4- loud, with palpable thrill 5- very loud, with thrill. Heard with stethoscope partly off the chest 6- very loud, with thrill. Heard with stethoscope completely off the chest
43
What ECG changes in left ventricular hypertrophy?
S waves in V1 + r waves in V5/V6 = greater than 3.5 big squares
44
ECG changes 1st degree heart block
Constant but prolonged PR interval
45
Second degree heart block mowbitz 1 ECG changes
Progressively lengthening PR interval until a QRS is dropped
46
What are the ECG changes in mowbitz II 2nd Degree heart block
Occasional Failure of the AV node to conduct atrial depolarisations to the ventricle. May occur in a fixed pattern I.e. 2:1 or 3:1
47
What ECG changes in third degree heart block?
No relationship between the p waves and the qrs
48
What ecg changes are suggestive of right ventricular hypertrophy?
Right axis deviation Narrow QRS Dominant R waves in V1 ( 7mm or taller) Dominant S waves in V6 (7mm or deeper)
49
ECG changes in LBBB
Wide QRS W in V1, M in V6 (WiLLiaM)
50
What ECG changes in RBBB?
Wide QRS M in lead V1, W in lead V6 (MaRRoW)
51
Heart failure changes on CXR (abcde)
``` Air space shadowing Kerley B lines Cardiomegaly Diversion of blood to upper lobes Effusions - pleural ```
52
Class I antiarrythmics | Action
Sodium Channel Blockers (N -1 line) Ia - quinidine - ventricular dysrhythmias, atrial fibrillation Ib - lidocaine - VT & VF Ic - flecainide - paroxysmal AF, recurrent tachycardias incl. WPW
53
Class II antiarhytmics | Action, example
``` Beta Blockers (two lines for B) Bisoprolol, atenolol, propanol ```
54
Class III antiarhythmics | Action, example, use
K+ channel Blockers (3 lines to draw a K) | Amiodarone - end SVT in acute incl. WPW
55
Class IV antiarrythmics | Action, example
Calcium channel blocker, verapamil or diltiazem These are both examples of non-dihydropyridines which act centrally on the heart
56
Adenosine What is it? What is it used for.
Antiarrythmic - unclassified Rapid reversion to sinus rhythm of SVT including WPW Don’t use in broad complex irregular tachycardias as could be preexcited AF because could cause VT
57
Beta blockers Examples Action Indications
Bisoprolol, atenolol, propranolol. Negatively inotrophic (contractility) and chronotophic (rate) Indicated for ischaemic heart disease, dysrhythmias such as AF and is a third line option for hypertension.
58
Beta Blockers Side effects Contraindications
Vagal- GI disturbance, bradycardia, fatigue, cold peripheries, sexual dysfunction, exacerbation of Raynaud’s or intermittent claudication, bronchospasm. Contraindications - brittle asthma, marked bradycardia, heart block, peripheral vascular disease
59
Calcium channel Blockers | Two types - examples and uses
Non-dyhydropyridines - verapamil and diltiazem - act on myocardium - used in SVTs but should be cautioned in Heart failure (especially in combination with beta blockers) can be used for hypertension Dihydropyridines - act on arteries more than myocardium. E.g. amlodipine, felodipine,nifedipine 1st line for hypertension in over 55s and afrocarribeans of any age. Prevent angina.
60
Side effects of calcium channel blocker
Non-dihydropyridines - CONSTIPATION, nausea, flushing, headache, dizziness, fatigue Dihydropyridines - abdo pain, nausea, palpitations, flushing, oedema, headache, dizziness, fatigue
61
Contraindications for calcium channel blockers
Non-dihydropyridines - Heart failure, 2nd or 3rd Degree heart block, cardiogenic shock Dihydropyridines - unstable angina, significant atherosclerosis
62
Nitrates Examples Indications
Isosorbide mononitrate - oral GTN spray Stable angina (prevention and treatment) unstable angina, acute heart failure, chronic heart failure.
63
ECG Changes in posterior MI and which artery is most likely effected
Tall R waves in V1 and V2 | usually left circumflex, can be right coronary
64
CHADSVASc
``` Risk of thromboembolic disease in AF patients - used to inform anticoagulation decisions Congestive HF Hypertension Age >75 =2, 65-74=1 Diabetes Previous stroke or TIA =2 Vascular disease = IHD or PVD Sex= female ```
65
What is a third heart sound? | What causes it? (5)
'lub dub DE' blood rushing into ventricle during early diastole or a stiff or dilated ventricle suddenly reaches its limit and the incoming blood decelerates. ``` Causes: Normal in under 30s Heart failure myocardial infarction cardiomyopathy hypertension ```
66
What is a fourth heart sound? | What causes it? (4)
"LE lub dub" atrial contraction into a non-compliant or hypertrophied ventricle. low pitched ``` Causes: ALWAYS ABNORMAL Heart failure MI cardiomyopathy ( + hypertrophic) hypertension ```
67
``` Mitral Stenosis How best heard? What does it sound like? Causes (2) Effects ```
LUB De Derrr Loud S1, Opening snap 'De' followed by rumbling mid-diastolic murmur. Best heard with bell over apex with patient lying on left side. Causes - calcification in old age or rheumatic fever. Effects - raised LA pressure, pulmonary hypertension, eventually RHF.
68
ECG and CXR Changes in Mitral Stenosis
AF, Pifid P waves, RHF - right axis deviation and tall R waves in leads V1 and V2.
69
``` Mitral Regurgitation How best heard? What does it sound like? Causes (5) Effects ```
pan systolic murmur at the apex which radiates to the axilla 'burrrrr' Prolapsed mitral valve, rheumatic mitral regurgitation, papillary muscle rupture, cardiomyopathy, connective tissue disorder. left atrial and left ventricular enlargement - LHF
70
ECG and CXR Changes in Mitral regurgitation
bifid P wave, Left axis deviation due to LVH | CXR - cardiomegally
71
``` Aortic Stenosis How best heard? What does it sound like? Causes (3) Effects ```
Ejection systolic, radiates to the carotid Lub-whoshhh Dub Bicuspid aortic valve (under 65), age related calcification, rheumatic fever. Left heart failure
72
ECG and CXR Changes in aortic stenosis
Left ventricular strain - ST segment depression and T wave inversion in left ventricular leads - chest leads prominent, dilated aorta on CXR
73
``` Aortic Regurgitation How best heard? What does it sound like? Causes (5) Effects ```
High pitched, early diastolic murmur - best heard at left sternal edge, 4th intercostal space, with the patient leaning forwards. Lub Taaarrr rheumatic fever, bicuspid valve, infective endocarditis, Marfan's, tertiary syphilis LV dilation
74
Aortic regurge - changes on ECG
ECG - left ventricular hypertrophy
75
Left axis deviation on ECG
If lead I is positive and lead II is negative - i.e. they are Leaving each other (aVF also negative)
76
Right axis deviation on ECG
Lead I is negative and lead AVf is positive (I and II are Reaching for each other)
77
ECG changes in bundle branch block
QRS is broad up in V1, becoming progressively more negative = RBBB down in V1, becoming progressively more positive - LBBB
78
ECG changes in PE
``` TACHYCARDIA S1, Q3, T3 Large S waves in I Q wave inversion in III T wave inversion in III RAD ```
79
Pathophysiology of atherosclerosis formation
Superficial endothelial injury causes: -increased permeability causes lipoprotein accumulation - cytokine release causing macrophage recruitment macrophages phagocytose lipoproteins producing foam cells creating fatty plaque inflammation causes smooth muscle cell migration and proliferation and collagen production, creating a fibrous cap
80
pathophysiology of plaque thrombosis
the fibrous cap is ruptured or eroded platelets adhere and aggregate platelets release serotonin and thromboxane A2 causing localised thrombosis (which may embolise distally) and vasoconstriction reduced coronary blood flow causes myocardial ischaemia and later necrosis, causing an increase in serum troponins.
81
STEMI Management
MONA and PCI or thrombolysis
82
NSTEMI/Unstable angina management
``` Morphine nitrates, ACEi, Beta blocker, calcium channel blocker, statin aspirin, clopidogrel LMWH Consider PCI ```
83
Causes of acute LHF (5)
``` MI hypertension aortic stenosis or aortic incompetence mitral incompetence increased demand on heart i.e. shock - sepsis, hypovolaemia ```
84
Acute HF Mx (9)
``` ABCDE Sit upright 100% O2 via non-rebreathe IV access and ECG monitoring Morphine and antiemetic If systolic BP >100 GTN infusion Furosemide - caution if hypotensive CPAP - think ceiling of care address cause ```
85
Mx of Tachyarrhythmia with adverse features and what are adverse features
Shock, snycope, MI, HF | A to E, periarrest call, prepare to DC cardiovery
86
Mx narrow tachyarrhythmia
Regular - SVT so vagal manouvere, adenosine 6mg IV | Irregular - Probable AF - beta blocker if in HF consider digoxin or amiodarone
87
Mx broad tachyarrhythmia
Regular - VT so amiodarone 300mg over 20-60 mins if known SVT with BBB then beta blocker Irregular - ? AF with BBB beta blocker ?Preexcided AF - ?amiodarone
88
infective organism endocarditis
strep viridans most common | staph aureus in IVDU, central lines
89
presentation of infective endocarditis
systemic infection - malaise, pyrexia, myalgia, weight loss, fatigue Cardiac- heart murmur, heart failure, conduction abnormalities Embolic disease immune vasculitis - Roth spots, Osler's nodes, Janeway lesions, clubbing, splinter haemorrhages, glomerulonephritis.
90
Mx of infective endocarditis
involve micro and cardiology | empirical ABx gentamycin and penicillin IV
91
presentation of pericarditis
chest pain - sharp, worse on inspiration, central, radiating to left shoulder, eased by sitting forward +/- dyspnoea and fever
92
ECG changes in pericarditis
1) saddle shaped ST elevation in most leads 2) days later - ST normalises, T wave flattening 3) T wave then inverts 4) Weeks to months later - ECG normalised.
93
Ix Pericarditis
Bloods - FBC, U&E, LFT, CRP, CK, Trop I Virology screen, blood culture Rheumatology panal Tuberculin and sputum for acid fast bacilli Imaging - ECHO for effusion, CT/MRI
94
Causes of pericarditis (7)
``` Viral - cocksakie idiopathic tuberculosis bacterial secondary to MI, neoplasm renal failure rheumatological - RA, sarcoid, SLE ```
95
Mx of pericarditis
treat cause supportive care high dose NSAIDs unless MI
96
What is rheumatic fever
immunological reaction to a strep infection - usually URTI
97
Diagnostic criteria for rheumatic fever
``` Confirmed Strep infection - swab or increasing antibodies 2 major or 1 major + 2 minor Major: erythema marginatum sydenham's chorea polyarthritis carditis and valvulitis subcutaneous nodules Minor: raised CRP/ESR pyrexia arthralgia if no arthritis prolonged PR interval ```
98
Ix rheumatic fever
``` blood culture antistreptolysin titre throat swab ECG Echocardiogram CXR ```
99
Mx Rheumatic fever
admit and bed rest oral aspirin IM penicillin 1.2mg followed by 10 day course long term Abx may be required to prevent cardiac damage
100
BP targets in diabetes
No end-organ damage - 140/80 | End organ damage - 130/80