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Cardiovascular System > General cardio/ vascular - COPIED > Flashcards

General cardio/ vascular - COPIED Flashcards

1
Q

In addition to severe chest pain, what else do you get with MI?

A

autonomic symptoms; pale and clammy patient, marked sweating. thready pulse, significant hypotension. Bradycardia or tachycardia.

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2
Q

Why do you have to be careful adminstering verapamil for angina if the patient also has heart failure?

A

Because it suppress cardiac contractility.

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3
Q

When do you use the Qrisk2 calculator?

A

If you do not already have a diagnosis of coronary heart disease (including angina or heart attack) or stroke/transient ischaemic attack.

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4
Q

PE and acute pulmonary oedema, what could be a differentiating factors re: sob?

A

acute pulmonary oedema; prefers upright

PE; more comfortable lying flat and may faint if sitting upright.

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5
Q

How long does it take for myocardial necrosis after coronary artery occlusion?

A

15-30 mins

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6
Q

If pain doesn’t subside after 3 sprays (5 min interval) of GTN then….

A

assume myocardial infarction.

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7
Q

Do all patients with AF experience palpitations?

A

NO, especially the elderly.

Need to take case history to find cause.

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8
Q

What is the common mechanism of acute coronary syndrome?

A
  • rupture or erosion of the fibrous cap of a coronary artery plaque.
  • platelet aggregation and adhesion
  • localised thrombosis, vasoconstriction and distal thrombus embolization
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9
Q

Apart from exercise, what else can bring on stable angina?

A

emotional stress

heavy meals

If pain is very transient I.e. few seconds, then unlikely to be angina.

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10
Q

How do B Blockers reduce myocardial oxygen demand?

A

<< Heart Rate

<< heart contractility

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11
Q

ECG and STEMI….

A

persistent ST-elevation

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12
Q

What is the most common symptom of peripheral vascular disease?

A

intermittent claudication; calf pain on walking (comes and goes).

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13
Q

What can damage the endothelial integrity? (5)

A
  • mechanical shear stresses (eg. hypertension)
  • biochemical abnormalities (eg. > LDL, diabetes)
  • immunological factors (eg. free radicals from smoking)
  • inflammation from infection
  • genetic alteration
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14
Q

What are the complications of pericardial effusion?

A

Pericardial effusions can compress adjacent lung parenchyma causing dyspnea.

Ventricular filling is compromised (termed cardiac tamponade) and cardiogenic shock can occur (sob, weakness, syncope, cough, etc).

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15
Q

MI and the elderly/ diabetes mellitus. What do I need to remember?

A

30% of patients have NO pain

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16
Q

Definition of heart failure

A

“when the heart is not pumping enough blood around the body to meet its needs”

IMP> It’s not a diagnosis, it just refers to the reduced function of the heart.

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17
Q

What are some causes of cor pulmonale?

A

ARDS, COPD, primary pulmonary hypertension, PE, ILD, sarcoidosis, etc.

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18
Q

Examination; clinical features of pericardial effusion…

A

heart sounds soft and distant

apex beat commonly obsured

frictional rub (only at early stages, quieter as fluid accumulates)

Raised JVP

Friedreich’s sign

Kussmaul’s sign

Pulsus paradoxus

< CO

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19
Q

Angina pain (that isn’t stable), if MI hasn’t been diagnosed, what is it termed?

A

Acute coronary syndrome

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20
Q

What physiologically factors could bring on angina?

A

Anything that increases myocardial oxygen demand:

  • >> cardiac contraction
  • >> Heart Rate
  • >> Blood pressure (cold weather can cause peripheral vasoconstriction)
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21
Q

Predisposing factors for aortic dissection?

A

Marfan’s syndrome

severe hypertension

trauma

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22
Q

What often gets confused with angina?

A

oesphageal pain

Rem: oesphageal pain can often wake the patient up at night, not rapidly relieved by rest but often relieved by nitrates. Maybe retrosternal or epigastric in origin. variable duration

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23
Q

What is cor pulmonale?

A

enlargement and failure of the right ventricle of the heart as a response to increased vascular resistance or pulmonary hypertension in the lungs

Maybe parasternal heave (due to RV hypertrophy)

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24
Q

What are the four classes of shock?

A
  • Distributive
  • Cardiogenic
  • Hypovolemic
  • Obstructive
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25
Q

What is Takotsubo or ‘bloken heart’ syndrome?

A

Extreme stress - LV enlargement and weakened.

Usually temporary, improves with time.

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26
Q

What can cause orthopnoea?

A
  • Fluid accumulating in the lungs due to congestive heart failure
  • Asthma (maybe trigggered by oesophageal reflex)
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27
Q

Physiologically, what are the two categories that can cause coronary heary disease?

A
  1. Mechanical obstructions
  • atheroma
  • thrombosis
  • spasm
  • coronary arteritis (eg. in SLE)
  1. decrease in flow of oxygenated blood to myocardium
  • Anaemia
  • hypotension (causing decrease coronary perfusion pressure)
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28
Q

What are the traditional risk factors for CAD?

A

Age

Gender (men > women, although similar postmenopausally)

Family history, Smoking

Diet, Weight (worse with fat around the abdomen - visceral fat)

Hypertension

Hyperlipidaemia

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29
Q

What’s the difference between nitrates and CCBs with reducing cardiac work?

A

Nitrates: act primarily on venous tissue, thus affect preload.

CCBs act mostly on arteriolar muscle to reduce afterload.

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30
Q

What common things can bring on palpitations?

A

>> caffeine

Nicotine from smoking

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31
Q

Severe carotid artery disease causes a bruit on auscultation, but is this always the case?

A

NO because stenosis may cause very reduced blood flow and the flow is too slow to cause a bruit.

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32
Q

What is included in acute coronary syndromes?

A
  • ST-elevation myocardial infarction (STEMI)
  • Non-ST-elevation myocardial infarction (NSTEMI)
  • Unstable angina (UA)
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33
Q

What is Kussmaul’s sign?

A

Rise in JVP/ increased neck vein distension during inspiration.

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34
Q

Do you get chest pain with cardiac tamponade?

A

No. Unless surrounding pain sensitive structures are affected, eg. parietal pleura.

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35
Q

ACS and ECG?….

A

ST Depression

T wave inversion

(+ anginal chest pain)

ST-elevation - STEMI

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36
Q

Severe tearing chest pain radiating through to the back

A

aortic dissection

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37
Q

What happens physiologically when the LV is obstructed?

A

>> LV pressure and compensatory LV hypertrophy.

This leads to relative ischaemia of the LV myocardium, consequently angina, arrthymias and LV failure.

Symptoms with be worse with exercise because narrowing prevents the increase in cardiac output causing a fall in blood pressure and thus an increase in coronary ischaemia.

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38
Q

If infective endocarditis is suspected, what is important to ask about?

A

recent dental work, IV drug use, skin infections (causes of bacteraemia)

(damage to peripheral vessels, eg. an infected false aneurysm of common femoral artery can be a source for infective endocarditis)

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39
Q

What is ‘walk though’ angina?

A

peripheral vasodilation during exercise decreases myocardial workload; angina eases

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40
Q

What could be a patient’s description of AF?

A

Heart jumping about or racing

Associated breathlessness

(may be unnoticed)

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41
Q

Palpitations/ syncope ; are these important?

A

YES.

Urgent investigation. Could have malignant but treatable arrhythmia (usually bradyarrhymias)

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42
Q

Why can angina occur at night/ lying flat?

A
  • increase in venous return
  • possibly anti-angina drugs wearing off

(indicates severe CHD)

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43
Q

Myocardial oxygen demand is determined by the amount of energy to support the heart. What three factors influence cardiac work?

A
  1. Heart Rate
  2. Cardiac contractility
  3. Myocardial wall tension (pressure exerted on the myocardial wall)
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44
Q

paroxysmal noctural dyspnoea could be asthma or heart failure, so what could be differentiating symptom?

A

asthma; wheeze

heart failure; also have frothy, bloodstained sputum

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45
Q

Coronary atherosclerosis isn’t the only cause of myocardial ischemia. Name two others

A

hypertrophic cardiomyopathy

aortic stenosis

(a loud systolic murmur may point to these findings)

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46
Q

Definition of crescendo angina

A

>> frequency with << reason

but not at rest

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47
Q

Why are Beta blockers used to treat angina?

A

Tachycardia decreases the time when the heart is in diastole;

tachycardia decreases myocardial perfusion.

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48
Q

What’s the difference between UA and NSTEMI?

A

NSTEMI;

occluding thrombus - myocardial necrosis - rise in serum troponins

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49
Q

Pharmaceutical management of angina

A
  • Aspirin
  • GTN spray (symptomatic relief)
  • ACE inhibitor
  • statins
  • (surgical - percutaneous coronary intervention)
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50
Q

What’s the commonest cause of heart failure?

A

coronary artery disease

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51
Q

What pharmaceutical intervention for low-risk CHD patients? (3)

A

aspirin/ clopidogrel (reduce platelet aggregation)

beta-blockers

nitrates

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52
Q

What factors can cause an obstruction to LV flow? (3)

A

aortic stenosis

LV hypertropic (narrowing of lumen)

supravalvular narrowing

congenital subvalvular aortic stenosis (formation of a ridge/ diaphragm)

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53
Q

What are the symptoms of stable angina?

A
  • Crushing sensation in chest or neighbouring areas
  • associated with effort
  • relieved by rest of nitroglyerin
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54
Q

Can you get arrhymias due to hypotension?

A

Yes

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55
Q

Can PE cause syncope?

A

YES

and frequently overlooked reason!!

PE can obstruct outflow from the right ventricle.

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56
Q

Definition of dissection

A

tear in the intima of aortic wall allows blood under high BP to penetrate the medial layer, causing cleaving.

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57
Q

What is coronary artherosclerosis?

A

an inflammatory process characterized by accumulation of lipid, macrophages and smooth muscle cells in the intima endothelium of large/ medium coronary arteries.

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58
Q

non-cardiogenic causes of oedema

A

nephrotic syndrome

Liver disease

Immobility

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59
Q

Signs and symptoms of pericarditis

A

sharp central chest pain exacerbated by movement, respiration and lying down. Typically relieved by sitting forwards.

Classic sign- pericardial friction rub. Stethoscope; lower left sternal edge, end of expiration, patient leaning forwards.

Fever if due to infection. Possible pericardial effusion. Effusion can compress adjacent lung parenchyma causing dyspnea.

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60
Q

Important case history questions to ask re CVD

A

What degree of activity causes chest pain or breathlessness?

eg. walking up stairs?

Can they continue with their normal activities/ hobbies?

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61
Q

What are the four main cardiovascular causes of syncope?

A
  • postural hypotension
  • neurocardiogenic syncope (eg. standing for long time in warm place)
  • arrhymias (esp. AF)
  • mechanical obstruction to cardiac output - hypertrophy or aortic stenosis, PE
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62
Q

What drugs can cause hypovolemia?

A

diuretics

chronic use of Beta-Blockers (slows heart and << contractility). Bradycardia often produces hypotension.

chronic use of Alpha-Blockers

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63
Q

If px is syncopic, can you hold them upright?

A

NO

Because continued cerebral hypoperfusion can cause an anoxic seizure.

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64
Q

What can you get transient murmurs of mitral regurgitation with unstable angina/ MI?

A

Ischaemia may have affected the papillary muscle.

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65
Q

If the JVP is not elevated but the patient has oedema, what does this mean?

A

origin is NOT cardiogenic

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66
Q

What’s the most common cause of myocardial ischaemia?

A

Obstructive coronary artery disease in the form of coronary atherosclerosis.

NB> one in every six coronary attacks present with sudden death as first, last, and only symptom.

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67
Q

What’s the difference between angina and MI pain?

A

Pain is similar, but MI pain is more severe and lasts longer.

MI pain lasts 20 mins or more and is not relieved by nitrates.

If sweating, nausa and vomiting present then >> chance of MI>

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68
Q

List of common causes of heart failure

(reduced capacity for the heart to pump)

A

Coronary heart disease

cardiomyopathy

valvular disease

heart rhythm disturbances

High systemic or pulmonary BP

Congenital causes

myocarditis (viral)

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69
Q

General managment of cardiomyopathy

A

Can’t be cured.

Beta blockers to control HR

Anti-coagulants

diruretics

ICD (implantable cardioverter defibrillators)

Heart transplant

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70
Q

sharp central chest pain that is worse with movement or respiration but relieved with sitting forwards

A

pericarditis pain

71
Q

What’s the most common cause of hypotension?

A

hypovolemia

Often induced by excessive use of diuretics

72
Q

Management of stable angina (generally)

A
  • Treat the underlying cause (eg. anaemia)
  • management of coexisting problems (diabetes, hypertension)
  • Evaluation of risk factors
73
Q

What’s the most common cause of rigt heart failure?

A

Left heart failure!!

It’s not pulmonary parenchymal or vascular disease

74
Q

What could cause Pulseless Electrical Activity (PEA); i.e. normal ECG, no CO?

A
  • tension pneumothorax
  • hypovolaemia
  • tamponade
  • thrombosis
75
Q

Definition of syncope

A

Loss of consciousness due to cerebral hypoperfusion

Presyncope ; feeling of impending loss of consciousness

76
Q

Indications for defibrillation

A

Ventricular arrhythmias (VT/ VF) with no pulse.

77
Q

What is the most common symptom of peripheral vascular disease?

A

Calf leg pain on walking (intermittent claudication)

NB> B-blockers, anti-hypertensives can impair peripheral circulation and aggravate intermittent claudication.

78
Q

What kind of heart failure can develop with chronic lung disease?

A

Right sided heart failure

79
Q

Which drugs (including recreational) can precipitate or exacerbate angina?

A

Starting thyroxine

cocaine & amphetamines - can cause MI, arrhythmias

Also NSAIDS

80
Q

Which is the pulse of choice during cardiac arrest?

A

Carotid pulse

81
Q

Pulse qualities - causes for

(a) regularly irregular

(b) irregularly irregular

A

(a) regular ectopic beats or 2nd AV block

(b) AF!!!!

82
Q

Fluid challenge and central venous cannula/ measurement of CVP; what’s that about?

A

If CVP doesn’t rise or rises transiently and then falls, then px is ‘underfilled’.

83
Q

symptoms of cardiogenic shock

A
  • chest pain, palpitations, history of IHD, AF
  • Cold sweaty peripherae; weak pulse, JVP raised, tachycardia
  • pulmonary oedema
84
Q

What % of px presenting to hospital with strokes, fulfill criteria for thrombolytic tx, and what is the drug?

A

2%

Actilyse; recombinant tissue plasminogen activator alteplase

85
Q

What is the risk of thrombolytic tx of ischaemic stroke?

And the incidence?

A

significant risk of primary intracerebral haemorrhage

1 in 30

86
Q

In the case of ischaemic stroke, what is the window for treatment?

A

3 hours from onset of symptoms.

(this includes getting a CT scan!)

87
Q

Thrombolysis; remember that…

A

lots of exclusion criteria!!!

Including:

  • seizures
  • px on warfarin
  • previous stroke within three month
  • BP >110 diastolic, > 185 systolic
  • hypoglycaemic/ hyperglycaemic
88
Q

Risk factors for CVD?

A

hypertension

hyperlipidaemia

diabetes mellitus

obesity

family history

smoking

89
Q

What are Charcot-Bouchard aneurysms?

A

Aneurysms in the small penetrating blood vessels of the brain.

They are associated with hypertension.

The common artery involved is the lenticulostriate branch of the middle cerebral artery.

90
Q

How effective is prophylaxic treatment of AF with warfarin in preventing strokes?

A

yearly risk of cerebral embolism reduced from 3% to 1%.

91
Q

Aspirin, stroke, no CT scan results. What’s the story?

A

No evidence that starting aspirin before CT findings are known adversely affects prognosis.

92
Q

When is a CT scan URGENT following a stroke?

A
  • if 3 hour window to start thrombolytics
  • evidence of head injury
  • severe headache at the time of onset of weakness
  • GCS score deteriorating
  • prior anticoagulation treatment
93
Q

Are px with carotid artery stenosis at risk of embolic stroke?

+ exclusions?

A

Yes, especially if stenosis 70-99% (very high risk). Also: is px well enough to receive tx?

Carotid stenosis diagnosis; doppler

Exclusions?

haemorrhagic strokes - TACI or POCI

94
Q

Stroke tx whilst awaiting CT scan results

A

Px NBM

Nasogastric tube, IV fluids

Oxygen mask, monitor cardiac rhythm (digoxin if needed)

Possibly catheter to monitor output

Aspirin 75mg

Statins (low dose) even if lipid levels normal

TED (thromboembolic disease) stockings

95
Q

Why don’t you treat HT immediately following a stroke?

A
  1. cerebral autoregulation of blood flow is disturbed and therefore risk of hypoperfusion.
  2. Watershed infarction; there can be an extension of the stroke due to reduced blood supply around area of infarction.

NB. continue with regular BP meds if taken previously.

96
Q

High BP two weeks after stroke. Which meds?

A

ACE inhibitors (perindopril - take at bedtime because can become dizzy)

thiazide diuretics

97
Q

What is Ortner’s syndrome?

A

A rare form of recurrent laryngeal palsy from CV disease.

A dilated left atrium due to mitral stenosis can cause voice hoarseness as the recurrent nerve is compressed.

98
Q

Which is the most common valvular heart disease?

A

Mitral regurgitation

  • abnormal leaking of blood from the LV to the LA during systole.
100
Q

What are some of the causes of mitral regurgitation?

A

Acute mitral regurgitation; commonly endocarditis (S. Aureus).

Also; papillary muscle rupture/ dysfunction, mitral valve prolapse

101
Q

What’s the pathology of mitral value regurgitation?

A

As LV volume increases over time with >> regurgitation, the LV contractile function deteriorates resulting in a decline in CO.

102
Q

Why is aortic stenosis often asymptomatic?

A

a hypertrophied LV can generate the elevated intraventricular pressures required for a normal stroke volume.

103
Q

Some causes of aortic stenosis include;

A

Calcification

Congenital

Endocarditis

Rheumatic fever

104
Q

What are the symptoms of aortic stenosis?

A

Symptoms only develop when stenosis is moderately severe (reduced to 1/4 of original size)

  • angina (CHD isn’t only cause of angina!)
  • dyspnoea
  • exercise induced syncope (and pre-syncope)

Poor prognosis when patient develops these symptoms. NB> At auscultation elderly px, murmour more at apex (misinterpreted as mitral regurgitation)

105
Q

What are the risk factors for calcific aortic valvular disease (CAVD)?

A
  • mainly occurs in the ELDERLY
  • more common in males
  • elevated LDL (low density lipoprotein)
  • hypertension
  • diabetes
  • smoking
106
Q

What’s the most important diagnostic aid for valvular disorders?

A

Echocardiography

107
Q

Two diagnostic tests for heart failure - NICE guidelines

A
  • trans-thoracic echocardiography
  • measure serum natriuretic peptides
108
Q

Why use transthoracic testing for px with heart failure? (3)

A
  • to exclude important valve disease
  • to assess the systolic (and diastolic) function of the the left ventricle
  • to detect intracardiac shunts
109
Q

What routine tests would be done for heart failure?

A
  • CXR
  • Kidney tests (U & E, eGFR)
  • thyroid tests
  • LFT
  • fasting lipids, glucose
  • FBC
  • urinalysis
  • spirometry
110
Q

Baseline drugs for heart failure

A
  • titrate ACE inhibitor and monitor Kidney function with increments.
  • Beta blockers. titrate and assess HR, BP
  • diuretics; titrate
111
Q

If comorbid hypertension/ angina then can add….

A

amlopidine CCB

(NOT verapamil or diltiazem)

112
Q

Why are ACEIs used for heart failure?

A

Because they lower both venous and arterial pressure.

<< venous pressure lowers oedema

Dilating of arteries reduces cardiac afterload, thus increasing cardiac output.

IMP: ACEIs also slow or reverse CARDIAC REMODELING.

113
Q

What is the skin like with LVF?

A

grey, clammy, cold skin

(assess peripheral perfusion)

114
Q

ECG - normal, then what?

What findings?

A

strongly consider an alternative diagnosis

ST elevation/ depression

115
Q

Acute LVF Management - What would you include in D - disability?

A

access consious level

blood sugar levels

116
Q

What breathlessness signs are associated with LVF?

A

orthopnea

paroxysmal nocturnal dyspnea

dyspnoea on exertion.

117
Q

What sounds would you hear with LVF?

A

LUB-DUB-uh

“galloping horses”

  • too much fluid
118
Q

Acute LVF Management: What investigations?

A

ABG

ECG

BP, etc.

CXR

chest examination. Need to rule out other causes of breathlessness

119
Q

Acute LVF Management: What would you find on ascultation?

A

bilateral crackles; widespread.

‘Fine’ crackles

3rd heart sound or gallop

120
Q

Initial treatment of LVF

A
  • Sit up patient
  • Give oxygen
  • If COPD do ABG early
  • Treat arrthymias (esp. tachycardia/ bradycardia)
  • Ensure STEMI has been excluded (Call reg if STEMI)
  • If BP >100mmHg give 0.5mg GTN S/L
121
Q

Acute LVF Management: What drugs for/to :

Speed up

Slow down

Irregular HR

A

Atropine - to speed up

Adenosine - to slow down (can be given very quickly)

Amiodarone - irregular HR (potassium channel blocker)

Used to suppress AF and flutter

122
Q

What features would you find on a CXR with pulmonary oedema?

A

bilateral interstitial or alveolar shadowing

upper lobe blood diversion

pleural effusions

cardiomegaly

Kerley B lines

123
Q

Acute LVF Management : What routine blood test would you do?

A

FBC

U + E

LFT

CRP

Troponin I

(anaemia + differential WBC)

124
Q

Acute LVF management; what other causes do you need to rule out?

A
  • pneumonia (consolidation, course crackles)
  • infective exacerbation of COPD
  • pneumothorax
  • pulmonary embolus

CASE HISTORY VERY IMPORTANT

Rem. Well’s criteria

125
Q

Mild LVF management

A

Start on furosemide 40mg.

If already on furosemide then give normal dose twice per day

126
Q

Moderate LVF management (acute)

A
  • Larger dose of furosemide and given via IV (50mg) - can be increased with renal impairment px
  • BP > 140 start GTN (25mg with 25 saline @ 0.5mg-10mg/hr)

Titrate; keep BP above 100mmHg

  • hypoxic? CPAP. careful of resp failure II
  • Morphine presided by Metoclopramide
127
Q

Acute LVF Management: What is morpine used for?

+ dose

A

Reduces sympathetic activity

reduces anxiety and work of breathing

“Titrate to good and bad symptoms”

Dose IV 1-4mg IV over 5-10 mins (preceeded by 10mg of metoclopramide)

128
Q

What is metoclopramide used for?

A

Given with morphine (increases GI motility)

129
Q

Acute LVF Management: What is the danger of morphine?

A

Resp failure II; caution with COPD, renal failure, or the elderly.

Give very slowly and reduce slowly.

* don’t give morphine orally because cannot regulate *

130
Q

Severe LVF management

A
  • Furosemide 50mg IV (increase if patient has renal impairment)
  • CPAP
  • Treat arrhythmias
  • lots of discussion with senior staff
  • dobutamine as inotrope in cardiogenic shock - consultant
131
Q

LVF Bundle

A
  1. ABCDE, then oxygen
  2. perform ECG, bloods, CXR, and ABG
  3. treat arrhythmias >150 or <40
  4. Call cardiologist reg BP <100, or STEMI
  5. GTN 0.5mg if BP>100
  6. Furosemide
132
Q

What pulse values might signify arrhythmias?

A

bradycardic <40

tachy cardic >140

or irregular

133
Q

What is the skin like with LVF?

A

grey, clammy, cold skin

(assess peripheral perfusion)

134
Q

ECG - normal, then what?

What findings?

A

strongly consider an alternative diagnosis

ST elevation/ depression

135
Q

What would you include in D - disability?

A

access consious level

blood sugar levels

136
Q

How would you assess conscious level?

A

AVPU

Alert,

Voice,

Pain,

Unresponsive

137
Q

What breathlessness signs are associated with LVF?

A

orthopnea

paroxysmal nocturnal dyspnea

dyspnoea on exertion.

138
Q

What sounds would you hear with LVF?

A

LUB-DUB-uh

“galloping horses”

  • too much fluid
139
Q

What investigations?

A

ABG

ECG

BP, etc.

CXR

chest examination. Need to rule out other causes of breathlessness

140
Q

What would you find on ascultation?

A

bilateral crackles; widespread.

‘Fine’ crackles

3rd heart sound or gallop

141
Q

Manageble O2 Sats for

COPD

Normal patients

A

88-92%

94-98%

142
Q

Initial treatment of LVF

A
  • Sit up patient
  • Give oxygen
  • If COPD do ABG early
  • Treat arrthymias (esp. tachycardia/ bradycardia)
  • Ensure STEMI has been excluded (Call reg if STEMI)
  • If BP >100mmHg give 0.5mg GTN S/L
143
Q

What drugs for/to :

Speed up

Slow down

Irregular HR

A

Atropine - to speed up

Adenosine - to slow down (can be given very quickly)

Amiodarone - irregular HR (potassium channel blocker)

Used to suppress AF and flutter

144
Q

What features would you find on a CXR with pulmonary oedema?

A

bilateral interstitial or alveolar shadowing

upper lobe blood diversion

pleural effusions

cardiomegaly

Kerley B lines

145
Q

What routine blood test would you do?

A

FBC

U + E

LFT

CRP

Troponin I

(anaemia + differential WBC)

146
Q

Acute LVF management; what other causes do you need to rule out?

A
  • pneumonia (consolidation, course crackles)
  • infective exacerbation of COPD
  • pneumothorax
  • pulmonary embolus

CASE HISTORY VERY IMPORTANT

Rem. Well’s criteria

147
Q

Mild LVF management

A

Start on furosemide 40mg.

If already on furosemide then give normal dose twice per day

148
Q

Moderate LVF management (acute)

A
  • Larger dose of furosemide and given via IV (50mg) - can be increased with renal impairment px
  • BP > 140 start GTN (25mg with 25 saline @ 0.5mg-10mg/hr)

Titrate; keep BP above 100mmHg

  • hypoxic? CPAP. careful of resp failure II
  • Morphine presided by Metoclopramide
149
Q

What is morpine used for?

+ dose

A

Reduces sympathetic activity

reduces anxiety and work of breathing

“Titrate to good and bad symptoms”

Dose IV 1-4mg IV over 5-10 mins (preceeded by 10mg of metoclopramide)

150
Q

Acute LVF Management: What is the danger of morphine?

A

Resp failure II; caution with COPD, renal failure, or the elderly.

Give very slowly and reduce slowly.

* don’t give morphine orally because cannot regulate *

151
Q

Severe LVF management

A
  • Furosemide 50mg IV (increase if patient has renal impairment)
  • CPAP
  • Treat arrhythmias
  • lots of discussion with senior staff
  • dobutamine as inotrope in cardiogenic shock - consultant
152
Q

LVF Bundle

A
  1. ABCDE, then oxygen
  2. perform ECG, bloods, CXR, and ABG
  3. treat arrhythmias >150 or <40
  4. Call cardiologist reg BP <100, or STEMI
  5. GTN 0.5mg if BP>100
  6. Furosemide
153
Q

What are the 4 types of arrhythmia?

A
  • premature (extra beats)
  • supraventricular arrhythmias
  • ventricular arrhythmias
  • bradyarrhythmias
154
Q

Premature beats don’t really need treatment unless..

A
  • autonomic signs; pale, sweaty with heatbeats change pace.
  • chest pain
  • dyspnoea
  • syncopic sensations
155
Q

Management of AF

A

cardioversion if < 48 hour onset

Rate and rhythm control

CCB - verapamil or a Beta Blocker

Rate control; amiodarone

anticoagulants to prevent thromboembolism/ stroke

surgical catheter ablation

156
Q

What can cause PVC (premature ventricular contractions)?

NB. ECG; these look like broadened QRS complexes with greater amplitude.

A
  • Hypokalaemia makes spontaneously polarization more likely.
  • Hypomagnesaemia also makes poloriziation more likely.
  • Existing damage to myocardium can provoke PVCs (scarring due to previous MIs, or surgery)
  • Inflammation cause cause increases in cytokine levels are increase irritability of myocytes.
157
Q

Name the four types of supraventricular arrhythmias

A
  • AF
  • Atrial flutter
  • PSVT (paroxysmal supraventricular tachycardia)
  • WPW (wolff-Parkinson-White) syndrome
158
Q

What’s the two major risks of AF?

A
  • embolic stroke
  • heart failure
159
Q

What underlying CARDIAC conditions predispose to AF. What are these?

A
  • HTN
  • CAD
  • RHD
  • Also inflammation plays a role.
160
Q

What underlying NON-CARDIAC conditions predispose to AF?

A
  • hyperthyroidism
  • >> alcohol
  • increase risk with age
161
Q

There are two possible routes for blood coagulation management with AF patients; What are they?

A
  • Oral anticoagulation (prefererable)
  • Or aspirin + clopidogrel
162
Q

AF management

A

Life-threatening instability, new-onset (less than 48 hours) – CARDIOVERSION

Stable, but new-onset (less than 48 hours) – rate or rhythm control.

Rate control if >> 48 hours, or uncertain.

If criteria for cardioversion is not met, and patient is likely to need long-term rate control then consider cardioversion AFTER three weeks of anti-coagulation therapy.

Usually rate control is first-line strategy.

163
Q

Rate control;

Rate control is First Line tx

A

Rate control; a beta-blocker other than sotalol

Or a rate-limiting CCB

Or digoxin monotherapy for sedentary px.

If rate not controlled then can combine medications: eg.

Beta blocker, diltiazem, digoxin.

Amiodarone is not indicated for long-term rate control.

164
Q

Rhythm control

NB> Used AFTER rate control if monotherapy ineffective.

A

Cardioversion

Can consider amiodarone for 12 months after electrical cardioversion to maintain sinus rhythm.

Torsades de pointes is an example of….. ventricular fibrillation

What can cause Torsades of pointes?

  • Imbalances in Potassium, Calcium, or magnesium.
  • People with long QT syndrome are at increased risk.
165
Q

PACs?

PVCs?

A

Premature Atrial Contractions

Premature Ventricular Contractions

166
Q

Rapid recognition of atrial flutter….

A

narrow QRS complexes at 150 bpm

Turn ECG upside down and look at leads II, III + aVF

167
Q

What cardiac conditions can cause PACs?

A

infection

genetic defects

narrow/ blocked vessels

valve disease

168
Q

What does hypokalaemia do to myocardiocytes?

A

Makes them more likely to depolarise spontaneously.

  • Also hypomagnesaemia

(Also hypercalcaemia although clinically less significant)

169
Q

Name some causes of PVCs

A
  • hypokalemia
  • hypercalcaemia (less so)
  • hypomagnesaemia
  • Existing myocardial scarring
  • Inflammation of the myocardium (eg. myocarditis)
170
Q

What causes AF?

A

Damage to the heart’s conducting system, often from other cardiac conditions

  • high BP
  • CAD
  • rheumatic heart disease

+ commonly inflammation

171
Q

What are the non-cardiogenic causes of AF?

A
  • Hyperthyroidism
  • >> alcohol
  • aging
  • idiopathic
172
Q

AF management

A

Rate control

Rhythm contol

Anticoagulation control

173
Q

CHA2DS2-VASc - breakdown

A

C - Congestive heart failure

H - Hypertension

A - Age >75

D - Diabetes

S - prior stroke/ TIA/ thromboembolism

V - ascular disease

A - 64-75

S - sex (gender)

174
Q

What group of people (ECG) is at risk of Torsades de Pointes - type of ventricular fibrillation.

A

People who have long QT syndrome are at
increased risk for torsades

(also - imbalanced amounts of
potassium, calcium, or magnesium in the
bloodstream can cause this condition)

175
Q

What is Sotalol?

A

Drug used for serious abnormal heart rhythms.

Can cause prolongation of the QT interval along with a small risk of life-threatening polymorphic ventricular tachycardia known as torsade de pointes.

Non-selective beta-adrenergic receptor blocker that also exhibits class III antiarrhythmic properties.

Cardiovascular System (1 decks)

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