Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Medicine Specialities > Cardiology > Flashcards

Cardiology Flashcards

1
Q

define atherosclerosis

A

atheromas - fatty deposits in artery walls and sclerosis - hardening of walls
affects medium and large arteries
causes a chronic inflammation and activates immune system causing deposits of lipids in the walla dn fibrous plaques

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is the results of the plaque formation in artery walls?

A

stiffening of artery walls - cause hypertension, staining heart
stenosis, reducing blood flow - angina
plaque rupture - thrombus causing ischaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are the non modifiable risk factors for atherosclerosis?

A

old age
family history
male

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what are the modifiable risk factors for atherosclerosis?

A

Smoking
Alcohol consumption
Poor diet (high sugar and trans-fat and reduced fruit and vegetables and omega 3 consumption)
Low exercise
Obesity
Poor sleep
Stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what co morbidities are associated with atherosclerosis?

A

Diabetes
Hypertension
Chronic kidney disease
Inflammatory conditions, such as rheumatoid arthritis
Atypical antipsychotic medications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what can result from atherosclerosis?

A

Angina
Myocardial Infarction
Transient Ischaemic Attacks
Stroke
Peripheral Vascular Disease
Mesenteric Ischaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what is involved in the primary prevention of CVD?

A

diet exercise, weight loss, stop smoking, alcohol, treat co morbidity
perform a QRISK 3 score - percentage risk that a patient will have a stroke or myocardial infarction in the next 10 years. > 10% risk of having a stroke or heart attack over the next 10 years then you should offer a statin (current NICE guidelines are for atorvastatin 20mg at night).

All patients with chronic kidney disease or type 1 diabetes for more than 10 years should be offered atorvastatin 20mg.

check lipids at 3months and increase dose if required to aim for 40% in non HDL cholestrol

check LFT’s within 3 months and 12 months - mild rise in ALT, AST (normal if less than 3 times the upper limit)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is involved in the secondary prevention of CVD?

A

A – Aspirin (plus a second antiplatelet such as clopidogrel for 12 months)
A – Atorvastatin 80mg
A – Atenolol (or other beta-blocker – commonly bisoprolol) titrated to maximum tolerated dose
A – ACE inhibitor (commonly ramipril) titrated to maximum tolerated dose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are the side effects of statins?

A

myopathy
type 2 DM
haemorrhagic stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is the cause of angina?

A

narrowing of coronary arteries..ishcaemia to myocardium
high demands of exercise so is stable if relieved by rest or GTN
unstable if randomly comes on while at rest and is considered an acute coronary syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

which investigations are required to investigate angina?

A

CT coronary angiography - inject contrast and taking CT of coronary arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

which other investigations are required to have a basline for angina

A

Physical Examination (heart sounds, signs of heart failure, BMI)
ECG
FBC (check for anaemia)
U&Es (prior to ACEi and other meds)
LFTs (prior to statins)
Lipid profile
Thyroid function tests (check for hypo / hyper thyroid)
HbA1C and fasting glucose (for diabetes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

how is angina managed?

A

R – Refer to cardiology (urgently if unstable)
A – Advise them about the diagnosis, management and when to call an ambulance
M – Medical treatment
P – Procedural or surgical interventions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

how is angina medically treated?

A

GTN - vasodilation, repeat after 5 mins then call ambulance if still pain
long term - bisoprolol, amlodipine
secondary prevention - Aspirin (i.e. 75mg once daily)
Atorvastatin 80mg once daily
ACE inhibitor
Already on a beta-blocker for symptomatic relief.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what surgical intervention is required to treat angina?

A

percutaneous coronary intervention with coronary angioplasty (dilate BV with balloon and inserting stent)
catheter into brachial or femoral artery up to coronary arteries under x ray guidance and inject contrast so areas of stenosis were highligted
or
coronary artery bypass graft (CABG) - opening chest along sternum (midline sternotomy scar) taking a graft vein from great saphenous and sew to affected coronary artery to bypass stenosis (slower recovery, hgiher rate of complications)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

how can you examine a patient to work out previous surgeries?

A

When examining a patient that you think may have coronary artery disease, check for a midline sternotomy scar (previous CABG), scars around the brachial and femoral arteries (previous PCI) and along the inner calves (saphenous vein harvesting scar) to see what procedures they may have had done and to impress your examiner

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

define acute coronary syndrome

A

usually the result of a thrombus from an atherosclerotic plaque blocking a coronary artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is the main medications to be used for acute coronary syndromes?

A

thrombus forms usually from platelets -
anti platelet medications - aspirin, clopidogrel and ticagrelor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what does the RCA supply?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what does the circumflex artery supply?

A

Left atrium
Posterior aspect of left ventricle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what does the LAD supply?

A

Anterior aspect of left ventricle
Anterior aspect of septum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what are the three types of acute coronary syndrome/

A

Unstable Angina
ST Elevation Myocardial Infarction (STEMI)
Non-ST Elevation Myocardial Infarction (NSTEMI)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

how is an ACS diagnosed?

A

ECG - ST elevation or new left bundle branch blOCK = STEMI.

If there is no ST elevation then perform troponin blood tests:

If there are raised troponin levels and other ECG changes (ST depression or T wave inversion or pathological Q waves) the diagnosis is NSTEMI
If troponin levels are normal and the ECG does not show pathological changes the diagnosis is either unstable angina or another cause such as musculoskeletal chest pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what are the sx of ACS?

A

Nausea and vomiting
Sweating and clamminess
Feeling of impending doom
Shortness of breath
Palpitations
Pain radiating to jaw or arms
>20 mins, settled with rest
diabetic patients do not experience typical sx - silent MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

which other investigations are required for stable angina?

A

Physical Examination (heart sounds, signs of heart failure, BMI)
ECG
FBC (check for anaemia)
U&Es (prior to ACEi and other meds)
LFTs (prior to statins)
Lipid profile
Thyroid function tests (check for hypo / hyper thyroid)
HbA1C and fasting glucose (for diabetes)
Chest xray to investigate for other causes of chest pain and pulmonary oedema
Echocardiogram after the event to assess the functional damage
CT coronary angiogram to assess for coronary artery disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what is the acute stemi treatment protocol?

A

Primary PCI (if available within 2 hours of presentation)
Thrombolysis (if PCI not available within 2 hours) -
injecting a fibrinolytic medication (they break down fibrin) that rapidly dissolves clots. There is a significant risk of bleeding which can make it dangerous. Some examples of thrombolytic agents are streptokinase, alteplase and tenecteplase.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what is the acute nstemi treatment?

A

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)

N – Nitrates (e.g. GTN) to relieve coronary artery spasm

Give oxygen only if their oxygen saturations are dropping (i.e. <95%).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

how is the severity of NSTEMi scored?

A

GRACE score - 6 month risk of death or repeat MI after having NSTEMI
<5% Low Risk
5-10% Medium Risk
>10% High Risk
If they are medium or high risk they are considered for early PCI (within 4 days of admission) to treat underlying coronary artery disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what are the complications of MI?

A

D – Death

R – Rupture of the heart septum or papillary muscles

E – “Edema” (Heart Failure)

A – Arrhythmia and Aneurysm

D – Dressler’s Syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

define dressler’s syndrome

A

post myocardial infarction syndrome
2-3 weeks after
by localised immune response
causes pericarditis
pleuritic chest pain, low grade fever, pericardial rub on auscultation, can cause pericardial effusion
ECG - global ST elevation and T wave inversion
echo - pericardial effusion
raised CRP, ESR
managed with NSAIDS and steroids
pericardiocentesis to remove fluids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what is the secondary prevention medical managed of ACS?

A

Aspirin 75mg once daily
Another antiplatelet: e.g. clopidogrel or ticagrelor for up to 12 months
Atorvastatin 80mg once daily
ACE inhibitors (e.g. ramipril titrated as tolerated to 10mg once daily)
Atenolol (or other beta blocker titrated as high as tolerated)
Aldosterone antagonist for those with clinical heart failure (i.e. eplerenone titrated to 50mg once daily)
Dual antiplatelet duration will vary following PCI procedures depending on the type of stent that was inserted.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what are the 4 types of MI?

A

Type 1: Traditional MI due to an acute coronary event
Type 2: Ischaemia secondary to increased demand or reduced supply of oxygen (e.g. secondary to severe anaemia, tachycardia or hypotension)
Type 3: Sudden cardiac death or cardiac arrest suggestive of an ischaemic event
Type 4: MI associated with PCI / coronary stunting / CABG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

define acute left ventricular failure

A

when left ventricle unableto adequately move blood through left side of heart and out so backlog increases pressure in ledt atrium, pulmonary veins and lungs. they leak fluid and unable to reabsorb it so causes pulmonary oedema, intefering with gas exchange

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what are the triggers of acute left ventricular heart failure?

A

Iatrogenic (e.g. aggressive IV fluids in frail elderly patient with impaired left ventricular function)
Sepsis
Myocardial Infarction
Arrhythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

how does acute left ventricular failure present?

A

rapid onset breathless
exacerbated by lying flat and improves sitting up
causes type 1 resp failure
SOB
cough - frothy white/pink sputum
look unwell
Chest pain in ACS
Fever in sepsis
Palpitations in arrhythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what are the examination findings of acute left ventricular failure?

A

Increase respiratory rate
Reduced oxygen saturations
Tachycardia
3rd Heart Sound
Bilateral basal crackles (sounding “wet”) on auscultation
Hypotension in severe cases (cardiogenic shock)
Raised Jugular Venous Pressure (JVP) (a backlog on the right side of the heart leading to an engorged jugular vein in the neck)
Peripheral oedema (ankles, legs, sacrum)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

which investigations are required for acute left ventricular failure?

A

ECG
ABG
chest X ray
bloods - routine for infection, kidney function, BNP, troponin
echo - ejection fraction should be >50% if normal
chest x ray - cardiomegaly, Upper lobe venous diversion. Usually when standing erect the lower lobe veins contain more blood and the upper lobe veins remain relatively small. In LVF there is such a back-pressure that the upper lobe veins also fill with blood and become engorged (referred to as upper lobe diversion). This is visible as increased prominence and diameter of the upper lobe vessels on a chest xray. or Bilateral pleural effusions
Fluid in interlobar fissures
Fluid in the septal lines (Kerley lines)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

treat or investigate first acute left ventricular failure

A

treat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what is BNP?

A

hormone released from the hearts ventricles when myocardium is stretched beyond normal range
high = heart overloaded with blood
BNP - relaxes smooth muscle in blood vessels, reduces systemic resistance, acts on kidneys as a diuretic, reducing circulating volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what is the problemw ith BNP?

A

Testing for BNP is sensitive but not specific. This means that when negative it is useful in ruling out heart failure, but when positive result can have other causes. Other causes of a raised BNP include:

Tachycardia
Sepsis
Pulmonary embolism
Renal impairment
COPD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

how is acute left ventricular failure managed?

A

Pour away (stop) their IV fluids
Sit up
Oxygen
Diuretics
ay also use IV opiates, NIV CPAP, inotropes -for oedema or cardiogenic shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

define chronic HF

A

chronic version of acute HF
due to either impaired LV contraction -systolic HF, or LV relaxation - diastolic HF…chronci back pressure of blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

what are the key features of chronic HF?

A

Breathlessness worsened by exertion
Cough. They may produce frothy white/pink sputum.
Orthopnoea (the sensation of shortness of breathing when lying flat, relieves by sitting or standing). Ask them how many pillows they use at night.
Paroxysmal Nocturnal Dyspnoea (see below)
Peripheral oedema (swollen ankles)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

what is PND caused by?

A

fluid settling across a large SA of their lungs as they lie flat, when stand up, sinks to lung bases and upper lungs clear
also during sleep the resp centre in the brain becomes less responsive so their resprate does not increase in response to oxygen sats like it would do so hypoxic
also less adrenalin during sleep, so myocardium more relaxed worsening CO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

how is chronic HF diagnosed?

A

clinical diagnosis
BNP blood test (specifically “N-terminal pro-B-type natriuretic peptide” – NT‑proBNP)
Echocardiogram
ECG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

what are the causes of chronic HF?

A

Ischaemic Heart Disease
Valvular Heart Disease (commonly aortic stenosis)
Hypertension
Arrhythmias (commonly atrial fibrillation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

how is chronic HF managed?

A

Refer to specialist (NT-proBNP > 2,000 ng/litre warrants urgent referral)
Careful discussion and explanation of the condition
Medical management (see below)
Surgical treatment in severe aortic stenosis or mitral regurgitation
Heart failure specialist nurse input for advice and support
Additional management:

Yearly flu and pneumococcal vaccine
Stop smoking
Optimise treatment of co-morbidities
Exercise at tolerated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

what is the first line medical tx for chronic HF?

A

ACE inhibitor (e.g. ramipril titrated as tolerated up to 10mg once daily) or ARB (avoid ACEi in valvular heart disease)
Beta Blocker (e.g. bisoprolol titrated as tolerated up to 10mg once daily)
Aldosterone antagonist when symptoms not controlled with A and B (spironolactone or eplerenone) (when reduced EF and sx not controlled by ACEi and BB)
Loop diuretics improves symptoms (e.g. furosemide 40mg once daily)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

what should be monitored during HF treatment due to the side effects of the drugs used?

A

UandE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

define cor pulmonale

A

right side HF caused by respiratory disease
increased pressure and resistance in pulmonary arteries cuasing pulmonary hypertension so unable to pump out of ventricle..back pressure in RA, vena cava, and venous system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

what are the respiratory causes of cor pulmonae?

A

COPD is the most common cause
Pulmonary Embolism
Interstitial Lung Disease
Cystic Fibrosis
Primary Pulmonary Hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

what are the sx of cor pulmonale?

A

asx
SOB
peripheral oedema
breathlesness of exertion
syncope

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

what are the examination findings of cor pulmonale?

A

Hypoxia
Cyanosis
Raised JVP (due to a back-log of blood in the jugular veins)
Peripheral oedema
Third heart sound
Murmurs (e.g. pan-systolic in tricuspid regurgitation)
Hepatomegaly due to back pressure in the hepatic vein (pulsatile in tricuspid regurgitation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

how is cor pulmonale managed?

A

treat sx and underlying cause
long term o2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

what is quanitively diagnosed as hypertension?

A

140/90 in clinic or 135/85 with ambulatory or home readings

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

what are the causes of hypertension?

A

essential/primary - no cause (95% of the time)
secondary -
R – Renal disease. This is the most common cause of secondary hypertension. If the blood pressure is very high or does not respond to treatment consider renal artery stenosis.
O – Obesity
P – Pregnancy induced hypertension / pre-eclampsia
E – Endocrine. Most endocrine conditions can cause hypertension but primarily consider hyperaldosteronism (“Conns syndrome”) as this may represent 2.5% of new hypertension. A simple test for this is a renin:aldosterone ratio blood test.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

what are the complications of hypertension?

A

Ischaemic heart disease
Cerebrovascular accident (i.e. stroke or haemorrhage)
Hypertensive retinopathy
Hypertensive nephropathy
Heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

how is hypertension diagnosed?

A

measure every 5 yrs to screen
more often if borderline for diagnosis
every year if have type 2 DM
clinic blood pressure between 140/90 mmHg and 180/120 mmHg should have 24 hour ambulatory blood pressure or home readings to confirm the diagnosis
measuring blood pressure in both arms, and if the difference is more than 15 mmHg using the reading from the arm with the higher pressure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

what is white coat syndrome?

A

Having your blood pressure taken by a doctor or nurse often results in a higher reading. This is commonly called “white coat syndrome”. The white coat effect is defined as more than a 20/10 mmHg difference in blood pressure between clinic and ambulatory or home readings.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

what are the stages of hypertension?

A

Stage

Clinic Reading

Ambulatory / Home Readings

Stage 1 Hypertension

> 140/90

> 135/85

Stage 2 Hypertension

> 160/100

> 150/95

Stage 3 Hypertension

> 180/120

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

how should complications of hypertension be investigated?

A

Urine albumin:creatinine ratio for proteinuria and dipstick for microscopic haematuria to assess for kidney damage
Bloods for HbA1c, renal function and lipids
Fundus examination for hypertensive retinopathy
ECG for cardiac abnormalities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

which medication can be used to control BP?

A

A – ACE inhibitor (e.g. ramipril 1.25mg up to 10mg once daily)
B – Beta blocker (e.g. bisoprolol 5mg up to 20mg once daily)
C – Calcium channel blocker (e.g. amlodipine 5mg up to 10mg once daily)
D – Thiazide-like diuretic (e.g. indapamide 2.5mg once daily)
ARB – Angiotensin II receptor blocker (e.g. candesartan 8mg to up 32mg once daily)
Angiotensin receptor blockers are used in place of an ACE inhibitor if the person does not tolerate ACE inhibitors (commonly due to a dry cough) or the patient is black of African or African-Caribbean descent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

how is hypertension managed?

A

diagnose
investigate causes and organ damge
advice on lifestyle - diet, smoking, alcohol, caffeine, salt, exercise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

when is medical management implemented?

A

All patients with stage 2 hypertension
All patients under 80 years old with stage 1 hypertension that also have a Q-risk score of 10% or more, diabetes, renal disease, cardiovascular disease or end organ damage.
There are slightly different guidelines for younger patients and those aged over 55 or black:

Step 1: Aged less than 55 and non-black use A. Aged over 55 or black of African or African-Caribbean descent use C.
Step 2: A + C. Alternatively A + D or C + D. If black then use an ARB instead of A.
Step 3: A + C + D
Step 4: A + C + D + additional (see below)
For step 4, if the serum potassium is less than or equal to 4.5 mmol/l consider a potassium sparing diuretic such as spironolactone. If the serum potassium is more than 4.5 mmol/l consider an alpha blocker (e.g. doxazosin) or a beta blocker (e.g. atenolol).

Seek specialist advice if the blood pressure remains uncontrolled despite treatment at step 4.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

what must be monitored due to the medical management of hypertension>

A

U and E for hyperkalaemia - ACEi and spirinolactone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

what are the treatment targets of hypertension?

A

Age

Systolic Target

Diastolic Target

< 80 years

< 140

< 90

> 80 years

< 150

< 90

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

what is S1 caused by?

A

the closing of AV valves - tricuspid and mitral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

what is S2 caused by?

A

closing of semilunar valves - pulmonary and aortic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

what is S3 caused by?

A

heard 0.1 seconds after s2
rapid ventricular filling causing the chordae tendineae to pull their full length
normal if young (15-40 yrs) - as ventricles easily allow rapid filling
older patients - heart failure as ventricles and chordae are stiff and weak so reach limit mcuh faster than normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

what is S4 caused by?

A

heard directly before S1
abnormal and rare
indicates stiff or hypertrophic ventricle caused by tubulent flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

which end of the stethoscope is better for which pitch of sound?

A

bell - low pitched
diaphragm - high pitched

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

where do you hear for each valve?

A

Pulmonary: 2nd I.C.S left sternal border
Aortic: 2nd I.C.S right sternal border
Tricuspid: 5th I.C.S left sternal border
Mitral: 5th I.C.S mid clavicular line (apex area)
“Erb’s point”. This is in the third intercostal space on the left sternal border and is the best area for listening to heart sounds (S1 and S2).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

when manouvering a pt to the left side, which murmur is emphasised?

A

mitral stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

when manouvering a pt leaning forward, sat up and holding exhalation, which murmur is emphasised?

A

aortic regurg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

how do you assess a murmur?

A

S – Site: where is the murmur loudest?
C – Character: soft / blowing / crescendo (getting louder) / decrescendo (getting quieter) / crescendo-decrescendo (louder then quieter)
R – Radiation: can you hear the murmur over the carotids (AS) or left axilla (MR)?
I – Intensity: what grade is the murmur?
P – Pitch: is it high pitched or low and grumbling? Pitch indicates velocity.
T – Timing: is it systolic or diastolic?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

how do you grade murmurs?

A

Difficult to hear
Quiet
Easy to hear
Easy to hear with a palpable thrill
Can hear with stethoscope barely touching chest
Can hear with stethoscope off the chest
- usually grade 2 or 3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

how do you describe a murmur?

A

“This patient has a harsh / soft / blowing, Grade …, systolic / diastolic murmur, heard loudest in the aortic / mitral / tricuspid / pulmonary area, that does not / radiates to the carotids / left axilla. It is high / low pitched and has a crescendo / decrescendo / crescendo-decrescendo shape. This is suggestive of a diagnosis of mitral stenosis / aortic stenosis”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

mitral stenosis causes…

A

left atrial hypertrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

aortic stenosis causes…

A

left ventricular hypertrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

mitral regurg causes…

A

left atrial dilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

aortic regurg causes…

A

left ventricular dilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

define dilation

A

leaky valve allows blood flow back in causing stretching of the muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

define stenosis

A

pushing against a stenotic valve, muscle tries harder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

what is mitral stenosis caused by?

A

Rheumatic Heart Disease
Infective Endocarditis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

what noise is made by mitral stenosis?

A

mid diastolic low pitched rumbling due to low velocity of blood flow
loud S1 due to thick valves - will be able to palpate it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

which sx are associated with mitral stenosis?

A

malar flush - back pressure of blood into pulmonary system so increased CO2 and vasodilation
afib - left atrium struggles to pish through stenotic valve causing electrical disruption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

what does mitral regurg cause?

A

congestive cardiac failure because the leaking valve causes a reduced ejection fraction and a backlog of blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

what murmur is heard in mitral regurg?

A

pan-systolic, high pitched “whistling” murmur due to high velocity blood flow through the leaky valve. The murmur radiates to left axilla. You may hear a third heart sound.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

what are the causes of mitral regurg?

A

Idiopathic weakening of the valve with age
Ischaemic heart disease
Infective Endocarditis
Rheumatic Heart Disease
Connective tissue disorders such as Ehlers Danlos syndrome or Marfan syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

what murmur is heard in aortic stenosis?

A

ejection-systolic, high pitched murmur (high velocity of systole). This has a crescendo-decrescendo character due to the speed of blood flow across the value during the different periods of systole. Flow during systole is slowest at the very start and end and fastest in the middle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

what other signs might be heard on examination of aortic stenosis?

A

murmur radiates to cartoid as turbulence comes to neck
slow rising pulse and narrow pulse pressure
exertional syncope

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

what are the causes of aortic stenosis?

A

Idiopathic age related calcification
Rheumatic Heart Disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

what murmur is heard in aortic regurg?

A

early diastolic, soft murmur
t can also cause an “Austin-Flint” murmur. This is heard at the apex and is an early diastolic “rumbling” murmur. This is caused by blood flowing back through the aortic valve and over the mitral valve causing it to vibrate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

what pulse is felt in aortic regurg?

A

corrigan’s pulse - collapsing pulse and is a rapidly appearing and disappearing pulse at carotid as the blood is pumped out by the ventricles and then immediately flows back through the aortic valve back into the ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

what are the two main types of valves?

A

bioprosthetic - can come from a pig, life of 10 yrs
mechanical - life of 20 yrs but require warfarin and INR of 2.5-3.5

96
Q

what are the three types of mechanical valves?

A

starr-edwards
tiliting disc valve
st jude valve

97
Q

what are the complications from a mechanical heart valve?

A

thrombus
infective endocarditis
haemolysis causing anaemia

98
Q

what sound is caused from a mechanical valve?

A

click

99
Q

what less invasive procedure can be used for treatment for severe aortic stenosis?

A

transcatheter aortic valve implantation
catheter into femoral artery, feeding under x ray guidance to aortic valve
inflate balloon and implant a bioprosthetic valve
Long term outcomes for TAVI are still not clear as it is a relatively new procedure. Therefore in younger, fitter patients open surgery is still the first line option.

Patient that have a TAVI do not typically require warfarin as the valve is bioprosthetic.

100
Q

what are the 3 bacterial causes of endocarditis?

A

Staphylococcus
Streptococcus
Enterococcus

101
Q

define afib

A

where the contraction of the atria is uncoordinated, rapid and irregularly. This due to disorganised electrical activity that overrides the normal, organised activity from the sinoatrial node

102
Q

what will be see on ECG of afib?

A

absent p waves
Narrow QRS Complex Tachycardia
Irregularly irregular ventricular rhythm

103
Q

what does afib result in?

A

Irregularly irregular ventricular contractions
Tachycardia
Heart failure due to poor filling of the ventricles during diastole
Risk of stroke

104
Q

what are the sx of afib?

A

Palpitations
Shortness of breath
Syncope (dizziness or fainting)
Symptoms of associated conditions (e.g. stroke, sepsis or thyrotoxicosis)

105
Q

what are the two differentials for an irregularly irregular pulse?

A

afib
ventricular ectopics - disappear when HR gets over certain threshold

106
Q

what is valvular versuses non valvular af?

A

Valvular AF is defined as patients with AF who also have moderate or severe mitral stenosis or a mechanical heart valve. The assumption is that the valvular pathology itself has lead to the atrial fibrillation

107
Q

what are the most common causes of af?

A

Sepsis
Mitral Valve Pathology (stenosis or regurgitation)
Ischemic Heart Disease
Thyrotoxicosis
Hypertension

108
Q

how is afib treated?

A

Rate control-
Beta blocker is first line (e.g. atenolol 50-100mg once daily)
Calcium-channel blocker (e.g. diltiazem) (not preferable in heart failure)
Digoxin (only in sedentary people, needs monitoring and risk of toxicity)
rhythm control-
cardioversion or long term control

109
Q

NICE guidelines (2014) suggest all patients with AF should have rate control as first line unless:

A

There is reversible cause for their AF
Their AF is of new onset (within the last 48 hours)
Their AF is causing heart failure
They remain symptomatic despite being effectively rate controlled

110
Q

Rhythm control can be offered to patients where:

A

There is a reversible cause for their AF
Their AF is of new onset (<48 hours)
Their AF is causing heart failure
They remain symptomatic despite being effectively rate controlled

111
Q

what are the two types of cardioversion?

A

Immediate cardioversion if the AF has been present for less than 48 hours or they are severely haemodynamically unstable.
Delayed cardioversion if the AF has been present for more than 48 hours and they are stable (should be anticaoged min of 3 weeks before)

112
Q

what are the two options for cardioversion?

A

pharmacological - flecanide, amiodarone
electrical - sedation or a general anaesthetic and using a defib
long term - beta blocker, dronedrone, amidarone

113
Q

define paroxymsal afib?

A

when af comes and goes in episodes
not more than 48 hrs
anti coagulated based on CHADSVASc score. They may be appropriate for a “pill in the pocket” approach. This is where they take a pill to terminate their atrial fibrillation only when they feel the symptoms of AF starting - only if no stricutal heart disease, usually flecanide used

114
Q

what is the risk of clotting in afib?

A

WITHOUT anticoagulation, patients with AF have around a 5% risk of stroke each year (depending on CHADSVASc score).
WITH anticoagulation, patients with AF have around a 1-2% risk of stroke each year (depending on CHADSVASc score). Anticoagulation reduces the risk of stroke by about 2/3.

115
Q

what is the risk of a pt having a bleed while on anticoag?

A

HAS-BLED score - 3%

116
Q

how does warfarin work?

A

vitamin K antagonist. Vitamin K is essential for the functioning of several clotting factors and warfarin blocks vitamin K. It prolongs the prothrombin time, which is the time it takes for blood to clot.

117
Q

how is warfarin monitored?

A

INR -
1 is normal
if 2 - twice as long to form a clot
target for afib - 2-3

118
Q

what are the interactions of warfarin?

A

Warfarin is affected by the cytochrome P450 system in the liver. This system is involved in the metabolism of warfarin. The INR will be affected by other drugs that influence the activity of the P450 system. This includes many antibiotics.

INR is also affected by many foods such those that contain vitamin K such as leafy green vegetables and those that affect P450 such as cranberry juice and alcohol

119
Q

how are DOAC’s reversed?

A

Andexanet alfa (apixaban and rivaroxaban)
Idarucizumab (a monoclonal antibody against dabigatran)

120
Q

what are the advanages of DOAC’s compared to warfarin?

A

No monitoring is required
No major interaction problems
Equal or slightly better than warfarin at preventing strokes in AF
Equal or slightly less risk of bleeding than warfarin

121
Q

how is a pt with afib assessed if they require anticoagulation?

A

higher score - higher risk, if one risk - consider, if more than 1 - offer anticoag
CHA2DS2-VASc
C – Congestive heart failure
H – Hypertension
A2 – Age >75 (Scores 2)
D – Diabetes
S2 – Stroke or TIA previously (Scores 2)
V – Vascular disease
A – Age 65-74
S – Sex (female)

122
Q

how is the risk of bleeding assessed of a pt on anticoag?

A

ORBIT
Low haemoglobin or haematocrit
Age (75 or above)
Previous bleeding (gastrointestinal or intracranial)
Renal function (GFR less than 60)
Antiplatelet medications
or HAS-BLED

123
Q

what are the 4 cardiac arrest rhythms?

A

Shockable rhythms:
Ventricular tachycardia
Ventricular fibrillation

Non-shockable rhythms:
Pulseless electrical activity (all electrical activity except VF/VT, including sinus rhythm without a pulse)
Asystole (no significant electrical activity)

124
Q

how is tachycardia treated?

A

Unstable patient:
Consider up to 3 synchronised shocks
Consider an amiodarone infusion

In a stable patient:
Narrow complex (QRS < 0.12s)
Atrial fibrillation – rate control with a beta blocker or diltiazem (calcium channel blocker)
Atrial flutter – control rate with a beta blocker
Supraventricular tachycardias – treat with vagal manoeuvres and adenosine

Broad complex (QRS > 0.12s)
Ventricular tachycardia or unclear – amiodarone infusion
If known SVT with bundle branch block treat as normal SVT
If irregular may be AF variation – seek expert help

125
Q

define atrial flutter

A

aused by a “re-entrant rhythm” in either atrium. This is where the electrical signal re-circulates in a self-perpetuating loop due to an extra electrical pathway. The signal goes round and round the atrium without interruption. This stimulates atrial contraction at 300 bpm. The signal makes its way into the ventricles every second lap due to the long refractory period to the AV node, causing 150 bpm ventricular contraction

126
Q

what are the ECG changes for atrial flutter?

A

“sawtooth appearance” on ECG with P wave after P wave.

127
Q

which conditions are associated with atrial futter?

A

Hypertension
Ischaemic heart disease
Cardiomyopathy
Thyrotoxicosis

128
Q

how is atrial flutter treated?

A

Rate/rhythm control with beta blockers or cardioversion
Treat the reversible underlying condition (e.g. hypertension or thyrotoxicosis)
Radiofrequency ablation of the re-entrant rhythm
Anticoagulation based on CHA2DS2VASc score

129
Q

define supraventricular tachycardia

A

caused by the electrical signal re-entering the atria from the ventricles. Once the signal is back in the atria it travels back through the AV node and causes another ventricular contraction. This causes a self-perpetuating electrical loop without an end point

130
Q

what are the ECG changes seen in supraventricular tachycardia?

A

fast narrow complex tachycardia (QRS < 0.12). It looks like a QRS complex followed immediately by a T wave, QRS complex, T wave and so on.

131
Q

what are the 3 main tupes of SVT?

A

“Atrioventricular nodal re-entrant tachycardia” is when the re-entry point is back through the AV node.
“Atrioventricular re-entrant tachycardia” is when the re-entry point is an accessory pathway (Wolff-Parkinson-White syndrome).
“Atrial tachycardia” is where the electrical signal originates in the atria somewhere other than the sinoatrial node. This is not caused by a signal re-entering from the ventricles but instead from abnormally generated electrical activity in the atria. This ectopic electrical activity causes an atrial rate of >100bpm.

132
Q

how are stable pts acutely managed with SVT?

A

continuous ECG
Valsalva manoeuvre. Ask the patient to blow hard against resistance, for example into a plastic syringe.
Carotid sinus massage. Massage the carotid on one side gently with two fingers.
Adenosine (see below)
An alternative to adenosine is verapamil (calcium channel blocker)
Direct current cardioversion may be required if the above treatment fails

133
Q

how does adenosine work?

A

works by slowing cardiac conduction primarily though the AV node. It interrupts the AV node / accessory pathway during SVT and “resets” it back to sinus rhythm. It needs to be given as a rapid bolus to ensure it reaches the heart with enough impact to interrupt the pathway. It will often cause a brief period of asystole or bradycardia

134
Q

what are the consideration of administering adenosine?

A

Avoid if patient has asthma / COPD / heart failure / heart block / severe hypotension
Warn patient about the scary feeling of dying / impending doom when injected
Give as a fast IV bolus into a large proximal cannula (e.g. grey cannula in the antecubital fossa)
Initially 6mg, then 12mg and further 12mg if no improvement between doses

135
Q

what is the long term management of pts with paraxysmal SVT?

A

Medication (beta blockers, calcium channel blockers or amiodarone)
Radiofrequency ablation

136
Q

define wolff-parkinson white syndromq

A

an extra electrical pathway connecting the atria and ventricles. Normally there is only one pathway connecting the atria and ventricles called the atrio-ventricular node. The extra pathway that is present in Wolff-Parkinson White Syndrome is often called the Bundle of Kent.

137
Q

what is the definitive treatment of WPW syndrome?

A

radiofrequency ablation of accessory pathway

138
Q

what are the ECG changes of WPW?

A

Short PR interval (< 0.12 seconds)
Wide QRS complex (> 0.12 seconds)
“Delta wave” which is a slurred upstroke on the QRS complex

139
Q

how does radiofrequency ablation work?

A

insert catheter into femoral veins into venous system under x ray, when in heart placed against different areas to test electrical signals
The operator may try to induce the arrhythmia to make the abnormal pathways easier to find. Once identified, radiofrequency ablation (heat) is applied to burn the abnormal area of electrical activit - leaving scar tissue which can not conduct

140
Q

define torsades de pointes

A

type of polymorphic (multiple shape) ventricular tachycardia. It translates from French as “twisting of the tips”

141
Q

what are the ecg changes of torsades de pointes?

A

normal ventricular tachycardia on an ECG however there is an appearance that the QRS complex is twisting around the baseline. The height of the QRS complexes progressively get smaller, then larger then smaller and so on. It occurs in patients with a prolonged QT interval.

142
Q

what occurs as a result of torsades de pointes?

A

When a patient develops Torsades de pointes it will either terminate spontaneously and revert back to sinus rhythm or progress in to ventricular tachycardia. Usually they are self limiting but if they progress to VT it can lead to a cardiac arrest.

143
Q

what are the causes of prolonged QT?

A

Long QT Syndrome (inherited)
Medications (antipsychotics, citalopram, flecainide, sotalol, amiodarone, macrolide antibiotics)
Electrolyte Disturbance (hypokalaemia, hypomagnesaemia, hypocalcaemia)

144
Q

what is the acute management of torsades de pointes?

A

Correct the cause (electrolyte disturbances or medications)
Magnesium infusion (even if they have a normal serum magnesium)
Defibrillation if VT occurs

145
Q

what are the long term management of prolonged QT syndrome?

A

Avoid medications that prolong the QT interval
Correct electrolyte disturbances
Beta blockers (not sotalol)
Pacemaker or implantable defibrillator

146
Q

what are ventricular ectopics?

A

premature ventricular beats caused by random electrical discharges from outside the atria. Patients often present complaining of random, brief palpitations (“an abnormal beat”). They are relatively common at all ages and in healthy patients however they are more common in patients with pre-existing heart conditions (e.g. ischaemic heart disease or heart failure).

They can be diagnosed by ECG and appear as individual random, abnormal, broad QRS complexes on a background of a normal ECG.

147
Q

define bigeminy

A

the ventricular ectopics are occurring so frequently that they happen after every sinus beat. The ECG looks like a normal sinus beat followed immediately by an ectopic, then a normal beat, then ectopic and so on.

148
Q

firhow are ventricular ectopics managed?

A

Check bloods for anaemia, electrolyte disturbance and thyroid abnormalities
Reassurance and no treatment in otherwise healthy people
Seek expert advice in patients with background heart conditions or other concerning features or findings (e.g. chest pain, syncope, murmur, family history of sudden death)

149
Q

define first degree HB

A

PR >0.2

150
Q

define second degree HB

A

type 1 - increased PR until absent QRS
type2 -miss QRS but PR normal, risk of asystole
2:1 - 2 P waves for each QRS complex. Every second p wave is not a strong enough atrial impulse to stimulate a QRS complex. It can be caused by Mobitz Type 1 or Mobitz Type 2 and it is difficult to tell which.

151
Q

define third degree HB

A

NO relationship between P and QRS
sig risk of asystole

152
Q

how is bradycardia/AVN block treated?

A

Stable:
Observe

Unstable or risk of asystole (i.e. Mobitz Type 2, complete heart block or previous asystole):
First line: Atropine 500mcg IV

No improvement:
Atropine 500mcg IV repeated (up to 6 doses for a total to 3mg)
Other inotropes (such as noradrenalin)
Transcutaneous cardiac pacing (using a defibrillator)

In patients with high risk of asystole (i.e. Mobitz Type 2, complete heart block or previous asystole):
Temporary transvenous cardiac pacing using an electrode on the end of a wire that is inserted into a vein and fed through the venous system to the right atrium or ventricle to stimulate them directly
Pacemaker

153
Q

what are pacemakers?

A

deliver controlled electrical impulses to specific areas of the heart to restore the normal electrical activity and improve the heart function. They consist of a pulse generator (the little pacemaker box) and pacing leads that carry electrical impulses to the relevant part of the heart. The box is implanted under the skin (most commonly in the left anterior chest wall or axilla) and the wires are implanted into the relevant chambers of the heart

154
Q

what are the indications for a pacemaker?

A

Symptomatic bradycardias
Mobitz Type 2 AV block
Third degree heart block
Severe heart failure (biventricular pacemakers)
Hypertrophic obstructive cardiomyopathy (ICDs)

155
Q

what are the types of pacemaker?

A

single chamber - RA or RV
dual chamber - RA and RV
triple chamber/CRT - RA, RV, LV

156
Q

what are implantable cardioverter defibrillators?

A

continually monitor the heart and apply a defibrillator shock to cardiovert the patient back in to sinus rhythm if they identify a shockable arrhythmia.

157
Q

what are the ECG changes seen with a pacemaker?

A

A sharp vertical line in all leads before either the P or QRS but not the other indicates a single-chamber pacemaker
A line before both the P and QRS indicates a dual-chamber pacemaker

158
Q

how does coarctation appear on chest x ray?

A

white lines on ribs

159
Q

how does htn appear on chest x ray?

A

cardiomegaly

160
Q

what are the clinical fx of aortic dissection?

A

In aortic dissection, a pulse deficit may be seen:
weak or absent carotid, brachial, or femoral pulse
variation in arm BP

161
Q

what is the most common ECG finding of PE?

A

most common ECG finding in patients with pulmonary embolism is sinus tachycardia

162
Q

what is a side effects of acei?

A

After starting an ACE inhibitor, significant renal impairment may occur if the patient has undiagnosed bilateral renal artery stenosis

163
Q

Define decompensated HF

A

When heart failure becomes severe enough to cause symptoms requiring immediate medical treatment, it is called decompensated heart failure

164
Q

How is infective endocarditis managed?

A

Prosthetic - vanc, gent, rifampicin

165
Q

Atrial flutter v fibrillation

A

Flutter - saw tooth appearance of baseline, give flecainide
Fibrillation - more wavy baseline

166
Q

how are palpitations with no seeming cause managed?

A

Palpitations should first be investigated with a Holter monitor after initial bloods/ECG

167
Q

what is bumetanide and what is a prominent side effect?

A

Bumetanide is a loop diuretic that is known to cause hypokalaemia

168
Q

what is the medical tx of heart failure?

A

1st line - beta blocker and acei
2nd - add spirinolactone
3rd - add ivabradine or digoxin

169
Q

how does pericarditis present on ECG?

A

There is widespread ST elevation without reciprocal changes and marked PR depression

170
Q

when is an echo used?

A

echocardiogram is the investigation of choice for the diagnosis of heart failure and measurement of left ventricular ejection fractio

171
Q

how is bradycardia treated

A

atropineh

172
Q

how are supraventricular tachycardias treated?

A

IV adenosine is used to manage cases of supraventricular tachycardia. The pulse of these patients is fast and regular

173
Q

which valves are most commonly affected in endocarditis?

A

The most commonly affected valve overall is the mitral valve, and the most commonly affected valve in patients who inject drugs intravenously is the tricuspid valve.

174
Q

how is first degree heart block managed?

A

not serious - normal in atheletes

175
Q

what is the mechanism of action of bendroflumethiazide and side effects?

A

Thiazide diuretics work by inhibiting sodium reabsorption at the beginning of the distal convoluted tubule (DCT) by blocking the thiazide-sensitive Na+-Cl− symporter. - hypokalaemia, hyponatraemia

176
Q

what are the ecg changes assoicated with hypercalcaemia?

A

shortening of the QT interval

177
Q

pci versus other options

A

. In a stable but symptomatic adult patient with aortic stenosis, valve replacement would be the most appropriate treatment.

178
Q

What is the difference between AF and supraventricular tachycardia?

A

AF is a kind of type of supraventricular tachycardia
But af is irregularly irregular, wheras SVT is regular
SVT is very different on ecg on how it looks and also has p wave inversion in II, III avF
Both can be treated with flecanide

179
Q

Define tachy Brady syndrome and how it is treated

A

A period of fast heart rates is often followed by very slow heart rates. When there are periods of both slow and fast heart rates (rhythms) the condition often will be called tachy-brady syndrome
With pacemaker

180
Q

Left bundle branch b’ock

A

V1 - negative Q (looks like M)
V6 - very prominent W in Q wave

181
Q

What is a cause of chest pain which is non cardiac?

A

Anaemia

182
Q

What should you ask about in the history of chest pain?

A

Shortness of breath
Cough
Palpitations

183
Q

Ivabradine

A

Ivabradine is a class of anti-anginal drug which works by reducing the heart rate. It acts on the If (‘funny’) ion current which is highly expressed in the sinoatrial node, reducing cardiac pacemaker activity.

Adverse effects
visual effects, particular luminous phenomena, are common
headache
bradycardia, heart block

There is no evidence currently of superiority over existing treatments of stable angina.

184
Q

Nicorandil

A

Nicorandil is a vasodilatory drug used to treat angina. It is a potassium-channel activator with vasodilation is through activation of guanylyl cyclase which results in increase cGMP.

Adverse effects
headache
flushing
skin, mucosal and eye ulceration
gastrointestinal ulcers including anal ulceration

185
Q

What is the protocol for management following fibrinolysis of STEMI?

A

If fibrinolysis is given for an ACS, an ECG should be repeated after 60-90 minutes - then urgent PPCI if not resolved

186
Q

How is orthostatic hypotension diagnosed?

A

Orthostatic hypotension can be diagnosed when there is a drop in SBP of at least 20 mmHg and/or a drop in DBP of at least 10 mmHg after 3 minutes of standing

187
Q

Aortic dissection diagnosis

A

Transoesophageal echocardiography (TOE) may be a useful investigation in clinically unstable patients with a suspected aortic dissection

188
Q

Rivoroxiban v thrombolysis PE

A

Rivaroxaban would be offered for haemodynamically stable PE, as DOACs are now increasingly used in PE. However she is hypotensive and tachycardic so this would not be suitable in her case.

189
Q

PE treatment

A

if 2-level PE Wells score is ≤ 4 and D-dimer is negative then stop anticoagulation and consider alternative diagnosis

190
Q

how is axis deviation interpreted?

A

leads 1 and 111 - if reaching for each other - R side devation, if leaving each other - left sided

191
Q

define long QT syndrome and some causes

A

Long QT syndrome (LQTS) is an inherited condition associated with delayed repolarization of the ventricles. It is important to recognise as it may lead to ventricular tachycardia/torsade de pointes and can therefore cause collapse/sudden death
- drugs - amiodarone, haloperidol
- acute MI
- electrolyte imbalances - hypocalcaemia

192
Q

how is complete heart block managed?

A

Complete heart block is a risk factor for asystole and therefore needs prompt treatment. The most appropriate treatment for this patient is transvenous pacing w

193
Q

when is a TOE used?

A

Transoesophageal echocardiography (TOE) may be a useful investigation in clinically unstable patients with a suspected aortic dissection

194
Q

v tach management

A

IV amiodarone is the first-line treatment for regular broad complex tachycardias without adverse features

195
Q

long qt syndrome durgs

A

Antipsychotic medications have a higher probability of causing a prolonged QT interval

196
Q

diabetes and >55

A

ace i

197
Q

posterior MI on ecg

A

ST depression and tall R waves in the anterior leads

198
Q

infective endocarditis orgnaisms

A

staph aureus
unless - Staphylococcus epidermidis if < 2 months post valve surgery

199
Q

LBBB

A

New LBBB is always pathological and never normal
Important for meLess important
This patient is experiencing an ST-elevation myocardial infarction evidenced by the new left bundle branch block on the ECG.

200
Q

HF with reduced ejection fraction

A

vabradine should be considered in heart failure if the patient has sinus rhythm > 75/min and a LVEF < 35% and have not responded to to ACE-inhibitor, beta-blocker and aldosterone antagonist therapy

201
Q

nstemi management - require ppci

A

NSTEMI management is determined by a risk assessment score such as GRACE - >3%

202
Q

broad complex v narrow complex tachycardia tx

A

broad complex - This patient presents with a regular broad complex tachycardia with a palpable pulse and the adverse feature of shock (systolic blood pressure <90mmHg), therefore a synchronised DC cardioversion is indicated. If this patient had no adverse features an intravenous amiodarone infusion would be indicated.

narrow complex - Intravenous adenosine and vagal manoeuvres (e.g carotid massage, Valsalva manoeuvre) are indicated for the termination of a regular narrow complex tachycardias.

203
Q

takayasu arteritis

A

Takayasu’s arteritis is a vasculitic disorder generally affecting young Asian women. It affects the aorta and its branches and causes both systemic features and those specific to which vessels coming off of the aorta are affected.

It is associated with renal artery stenosis and so this is the correct answer.

204
Q

cardiac tamponade ecg changes

A

Electrical alternans is a relatively specific but non-sensitive ECG sign of cardiac tamponade. Electrical alternans is characterised by beat to beat variation in QRS amplitude and morphology. This variability is due to the heart ‘swinging’ in the pericardial fluid.

205
Q

hypertrophic obstruction cardiomyopathy features

A

auto dominant

Features
often asymptomatic
exertional dyspnoea
angina
syncope
typically following exercise
due to subaortic hypertrophy of the ventricular septum, resulting in functional aortic stenosis
sudden death (most commonly due to ventricular arrhythmias), arrhythmias, heart failure
jerky pulse, large ‘a’ waves, double apex beat

206
Q

rate control

A

Beta-blockers and calcium channel blockers are first line for rate control in patients with atrial fibrillation. Diltiazem would be the most appropriate drug for rate control in this case because the patient has a background of asthma and beta-blockers are contraindicated.

207
Q

pulmonary stenosis v aortic stneosis

A

louder on inspiration v expiration

208
Q

beta blockers contraindications

A

Beta-blockers combined with verapamil can potentially cause profound bradycardia and asystole.

209
Q

AV block cause

A

AV block can occur following an inferior MI

210
Q

NSTEMI management based off risk

A

NSTEMI management: patients with a GRACE score > 3% should have coronary angiography within 72 hours of admission

211
Q

pharmacological optionsfor orthostatic hypotension

A

Fludrocortisone increases renal sodium reabsorption and increases the plasma volume. This helps to counteract the physiological orthostatic vasovagal reflex.

212
Q

intracranial haemorrhage on warfarin

A

Intracranial haemorrhage on warfarin → give IV vitamin K 5mg + prothrombin complex concentrate

213
Q

ventricular tachycardia tx

A

no shock - IV loading dose of amiodarone
shock - 1 synchronised DC shock

214
Q

tricsupid regug

A

lower left sternal edge
louder on inspiration
pansysttolic

215
Q

proxiaml aortic dissection

A

An inferior myocardial infarction and AR murmur should raise suspicions of an ascending aorta dissection rather than an inferior myocardial infarction alon

216
Q

louder on expiration

A

mitral aortic

217
Q

louder on imspiration

A

pulmonary tricuspid

218
Q

WPW

A

short PR intervals

219
Q

provoked PE tx

A

Rivaroxaban for 3 months is correct as the first-line option for treating a provoked PE is a DOAC (such as rivaroxaban) for 3 months.

220
Q

stable angina not helped by beta blocker

A

add amlodipine or nifedipine

221
Q

aortic dissection neuro

A

horners syndrome cna also cocur

222
Q

Gout + htn

A

For a patient with hypertension who is already taking an ACE inhibitor, a history of gout would favour a calcium channel blocker over a thiazide as the next step

223
Q

Hypertrophic obstructive cardiomyopathy

A

HOCM may present with ejection systolic murmur, louder on performing Valsalva and quieter on squatting

224
Q

If diabetic first line anti hypertensive

A

Ramipril

225
Q

When should u thrombliysis in PE

A

If shock - hypotension

226
Q

Pathological q waves can look like

A

St elevation

227
Q

Only give oxygen in non stable angina if

A

<92%

228
Q

Electrical cardio version in AFib

A

If 48 hrs
Or haemodynamically unstable

229
Q

Cxr aortic dissection

A

Widened mediastinum

230
Q

Aortic dissection investigations

A

CT TAP

231
Q

Step 4 anti hypertensive

A

If k lower than 4.5 - spironooavtone
If higher - arb or beta blocker

After 4 drugs and not controlled - specialist review

232
Q

Stable angina treatment

A

all patients should receive aspirin and a statin in the absence of any contraindication
sublingual glyceryl trinitrate to abort angina attacks
NICE recommend using either a beta-blocker or a calcium channel blocker first-line based on ‘comorbidities, contraindications and the person’s preference’

233
Q

Contraindication to ace inhibitor

A

Moderate ro severe aortic stenosis

234
Q

Acute pericarditis ecg

A

Widespread ST elevation

235
Q

Pulmonary stenosis can result in

A

Right sided heart failure

Medicine Specialities (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions