Brainscape's Knowledge GenomeTM

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


See full index

Final > Cardio > Flashcards

Cardio Flashcards

1
Q

How to do ECG rate?

A

300/number of squares in R-R interval
OR
Number of QRS X6 (10 sec strip)

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

Normal ECG axis and how to calculate

A

-30 - +90
Look at leads I and aVF If these are both positive then axis is between -30 and +90

Also Leads I and II leaving returning rule for L and R deviation

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

What is P-wave & what increases & makes absent

A

This is atrial depolarisation

Inc = Cor pulmonale, PE
Absent = AF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is PR interval
Prolonged = ?
Shortened = ?

A

Time from atrial to ventricular depolarisation (120-200ms)

Prolonged = AV block, digoxin, hypokalaemia, rheumatic fever, sarcoidosis (RF and Sarc give AV node fibrosis)

Shortened = Accessory pathway e.g. WPW (assoc with Delta wave - upstroke on QRS due to retrograde impulse activity).

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

QRS breadth

Narrow =
Broad =

A

Normally 80-120ms

Narrow = normal HIS/Purkinje

Broad = ventricular ectopic, accessory pathway (non His-Purkinj)

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

What is R-wave progression?

A

This is normal phenomenon where QRS become more positive

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

What can cause tall T-waves

A

Hyperacute STEMI

Hyperkalaemia

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

What can cause inverted T-waves

A 
Ischaemia
Digoxin toxicity
SAH
PE
Brugada syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What can cause prolonged QT (interval over 500ms)?

Why is this important?

A

Citalopram
Antipsychotics
Macrolides (erythromycin)
Genetic

Risk of arrhythmias (longer relative refractory period means ectopics can cause arrhythmias)

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

First 4 steps in ECG interp

A

Patient name
Rate
Rhythm
Axis

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

Leads for Circumflex occlusion?

A

Leads I, V5, V6

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

Leads for Right coronary occlusion?

A

Leads II, III, aVF

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

Leads for LAD occlusion?

A

V1-V4

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

What are some causes of an irregular tachycardia

A

VF
Torsades (give Mg Sulphate)
AF+WPW (can be seen in association)

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

What can cause Left axis deviation

A

LBBB
WPW with right sided accessory pathway
hyperkalaemia
ASD

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

Causes of right axis deviation

A

RV hypertrophy

lung disease: cor pulmonale, PE

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

ST elevation causes

What causes prolonged ST elevation

A

MI
Pericarditis
LV aneurysm (cause of persistent STEMI)
Prinzmetals angina

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

ST depression causes

A

Can be seen secondary to abnormal QRS (LVH, RBBB/LBBB)
Ischaemia (e.g. inferior infarct)
digoxin
hypokalaemia

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

LBBB (WiLLiaM) causes

A

ALWAYS pathological
Ishcaemia: Ischaemic heart disease, MI (Sgarbossa criteria helps diagnose)
Aortic stenosis
Cardiomyopathy

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

RBBB (MaRRoW) causes

A

Can be normal variant seen with age

RVH e.g due to corpulmonale/PE

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

Hypokalaemia ECG

A 
U waves
small/absent T-waves
Prolonged PR
Long QT
ST depression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Hyperkalaemia ECG

A

Widened QRS
ST depression
Tall Tented T-waves
p-wave depression

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

Hypothermia ECG

A

Brady - 1st degree heart block
Long QT
Arrhythmia

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

Degrees of Heart Block

A

1st - PR over 0.2 (benign)

2nd type 1 Wenkebeck

  • Inc PR until dropped beat
  • AV nodal failure

2nd type 2
- PR constant until dropped beat (bundle branch conduction failure - can progress to complete block)

3rd

  • Complete.
  • P not assoc with QRS
  • Broad complex QRS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Which 2nd degree heart block is higher risk?

A

Type II - due to bundle branch failure

More commonly progress to complete failure

Pacing might be required

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

What is Bradycardia?

Physiological and pathological causes.

A

Under 60bpm
Phys = young (increased Nodal tone), fit

Pathological = acute MI, drugs (BB, digoxin, amiodarone), hypothyroid, hypothermia, inc ICP

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

Bradycardia symptoms & Tx

A 
Syncope
Fatigue
Dizzyness
Ischeamic chest pain
Palpitations

Tx: only if less than 40 bpm

  • IV atropine: anti-cholinergic. reduces vagal tone
  • Temp pacing wire
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Sick sinus pathophys, ECG changes and Tx.

A

Cause = fibrosis of AV node (idopathic, ischemis, digoxin, toxicity, sarcoid/amyloid)

ECG = sinus block/arrest with escape rhythms. Bursts of atrial tacky interspersed with Brady

Brady: dual chamber pacing
Tachy: Digoxin or Verapamil (CCB)

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

Investigating Bradycardia

A

ECG, U&E, Glucose, Ca, Mg, TFT, drugs, FBC

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

Tx in Bradycardia

A 
Treat any underlying (remove negative chronotrope, tx electrolyte disturbances)
IV atropine (if poor response e.g. heart block do transcutaneous pacing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Tachycardia Presentation

A 
Palpitations
Fatigue
Dizzyness
Chest discomfort
Syncope
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Tx of tachycardia (Acute pres)

Tx if unstable (high HR, low BO)

Tx if irregular tachy

Tx if regular tachy

A 
O2 and IV access
If HR over 200, BP under 90, MI or HF then GA + IV amiodorone (class III - K+ channel block)

If irregular tachycardia (usually AF) control with IV BB or Diltiazem. If onset less than 48 hours amiodarone cardioversion

If regular IV adenosine

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

Tachy Precipitating factors

A

MI/Ischamia
Thyrotoxicosis
Electrolyte disturbances
Drug/Caffeine/Alcohol

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

SVT - What is it, possible site or origin and what is the main concern

A

HR over 100bpm
Narrow complexes
Can be from Atria (AF and flutter)
Can be from AV node (nodal re-entry tachycardia)

Increased HR means decreased coronary filling time (angina type symptoms, chest pain, faintness, SOB)

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

Causes and Tx of sinus tachycardia (100-200bpm, regular with P-waves)

A

Physiological - pain, anxiety, exertion

Pathological - fever, anaemia, hypovolaemia, thyrotoxicosis, phaeo

Pharmacological - sympathomimetics, adrenaline, alcohol, caffeine, salbutamol

Tx: treat underlying (e.g. hypovolaemia), vagal manoeuvres (carotid massage, valsalva).
If ongoing sinus SVT give BB or non-dihydropyridine CCB (diltiazem, verapamil-

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

AV node re-entry pathophysiology.

A
  • Two pathways in AV node one fast with slow refractory and one slow with fast refractory
  • usually slow pathway is blocked as common pathway is in refractory when impulse arrives
  • if an impulse goes down the slow pathway when not in refractory then impulse can travel up fast pathway giving a re-entry circuit
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

AV node re-entry ECG

A

Narrow QRS
Rate 130-250
retrograde conduction = inverted P=waves in II, III and aVF

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

AV node re-entry Tx

A

Vagal manoeuvres 1st line
Adenosine 2nd line (transient AV block fees like death)

Long term: Beta block or digoxin, diltiazem, verapamil, flecanide (class 1c Na channel blocker – increases QRS time)

Cure: Radiofrequency ablation

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

AVRT ?

A

WPW

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

WPW pathophys

A

Bundle of Kent usually light sided. formed due to developmental failure.

Accessory pathway allows re-entry circuit formation (critical timing needed when pathways not in refractory)

Broad complex (anterograde)

Narrow (Orthodromic 90% - retrograde up accessory path used to get impulse back to atria)

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

WPW Tx

  • Acute
  • Prophylaxis
  • Cure
A

Vagal manoeuvres ± adenosine

Prophylaxis Flecainide (1c- inc refractory period) or sotalol (3)

Cure: RFA

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

What is AF

A

Chaotic firing of ectopics in atria.

Leads to irregularly irregular ventricular rhythm on ECG

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

AF complications

A

Stagnation of blood in atria can cause thrombus and inc risk stroke.

Reduced cardiac output may lead to HF

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

Types of AF

A

Paroxysmal: spontaneous termination in less than 7 days (usually 48hr)

Recurrent: 2+ episodes

Persistent: lasts over 7 days (may become permanent)

Permanent: long-standing (over 1 year) not terminated by cardioversion

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

AF

Symptoms & Signs

ECG

Other Presentations

A

Symptoms: Palpitations, Dyspnoea, Chest pain

Signs: Irregularly irregular heart beat

ECG: No P-waves, Oscillating baseline

Other: Syncope, TIA, stroke

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

AF Investigations

A

24 hour ECG
TFT, FBC (anaemia can cause), U&E (Potassium), LFT/Coag
Imaging - trans thoracic echo

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

AF management: Three areas to address

A

Rate
Rhythm
Anticoagulation

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

Rate control in AF

A

Beta blocker or CCB (Diltiazem) 1st line

Combination therapy 2nd line (NOT Verapamil - risk heart block) adding the above two OR adding in Digoxin

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

Rhythm control in AF

  • What should be considered
  • Who should get this
  • What is used
A
  • Thromboembolism
  • Only those with short term symptoms (less than 48 hours) or anticoagulant for over 3W
  • DC cardioversion or Amiodarone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Risk Control score in AF

A 
Chronic heart failure (1)
HTN over 140/90 (1)
Age of 75 (2)
DM (1)
Prior Stroke/TIA (2)
Vasc disease (PVD, MI)(1)
Age over 65 (1)
Sex: Female (1)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

When to offer anticoagulant in AF

A

CHA2DS2VASc
Consider Warfarin or NOAC in males with 1 and anyone over 2 points
INR 2-3 (n.b prostetic heart valves/post MI = 2.5-3.5)
If poor warfarin control switch to NOAC

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

Bleeding Risk score

A 
Hypertension
Abnormal Liver/Renal
Stroke
Bleeding
Labile INRs
Elderly (over 65 years)
Drugs or alcohol (1 point each)

in those with score one 3 use Warfarin with care

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

What is atrial flutter, causes and ECG

A

This is due to re-entry circuits in the atria

Causes: HTN, CAD, hyperthyroid, Obesity, alcohol

ECG: sawtooth appearance

Tx: anticoagulation then DC cardioversion / Amiodarone / sotalol / flecainide
Recurrent = RFA

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

What causes broad complex tachycardia?

A

Ventricular origin.

Either ventricular conduction (BBB) problem OR not using AV node.

Note any SVT with poor conduction can present as broad complex too

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

Causes of:

Regular VT
Irregular VT

A

Reg - monomorphic VT (all QRS look the same) most commonly due to MI

Irregular - Torsades de Points (Plyomorphic VT), VF

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

Pathophysiology of Monomorphic VT

A

Re-entry circuits in zones of fibrosis/ischaemia

e.g. iscahmia/damaged myocardium post MI

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

Pathophysiology of Torsades

A

Commonly due to electrolyte disturbance.

Treated by giving Magnesium sulphate

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

ECG in VT - P waves and capture beats

A

Broad complex (ventricular)

  • VT: regular
  • VF: irregular

P wave dissociation: AV node continues independently of ventricle

Capture beats are when some P-waves translate into normal QRS complexes intermittently

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

Broad complex Tachy symptoms

A

Dizziness, palpitations, syncope, chest pain, HF

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

Broad complex Tachy Tx

A

ABC, O2 and venous access

in unstable DC cardioversion (3 shocks) may be needed

Amiodarona IV

In Plyomorphic VT give magnesium 2g for non-Torsades, IV Mg sulphate for TdP

VT is usually due to damage so BB/CCB and consider Implantable cardioversion defibrillator

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

Torsades de Points

Causes
Morphology
Tx

A

Hypokalaemia, hypomagnesia,
Class III antiarrhythmics (amiodarone/sotalol)
Antibacterials (erythromycin, trimethoprim)

Varied axis and amplitude of QRS

Tx: Magnesium sulphate IV

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

VF

  • Causes
  • Morphology
  • Acute/Long term Tx
A

Cause of cardiac arrest and sudden death.
Random contracting of ventricular fibres giving failed ventricular function.

  • Antiarrhythmic drugs, AF, hypoxia, ischaemia, heart disease
  • Chaotic (varying amplitudes, no identifiable P, QRS, T
    -Acute: Defibrillation
    Long term: BB, implantable cardioverter defibrillates
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What are shockable rhythms?

A

VF and Pulseless VT

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

Non-shockable rhythms?

A

Asystole and PEA (Pulseless electrical activity)

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

Brugada

What is?
ECG?
Tx?

A
  • Geneticalli inherited condition affecting sodium channels. Family history of sudden death less than 45 yrs
  • Risk of sudden death
  • Coved ST segment elevation followed by negative T
  • ICD (implantable defibrillator)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

PE ECG

A

S1Q3T3

Deep S in I, Deep Q in III Deep T in III

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

Class 1
Class 2
Class 3
Class 4

A 
1 = Na channel blocker
2 = CCB
3 =  Potassium channel blocker
4 = Beta blocker
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Amiodarone

  • Use
  • Mech
  • Adverse
A

For irregular tachycardia (AF, SVT)

Block/Na/K/Ca, antagonist alpha and beta adrenergic
Reduces automaticity/conduction in atria

Hypotension, Pneumonitis (upper lobe fibrosis), AV block, grey skin, hypothyroidism

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

Adenosine

  • Use
  • Mech
  • Adverse
A
  • Used in certain SVT that don’t respond to Vagal maneouvers
  • Causes trainsient block in the AV node by causing hyperpolarization through inc potassium flux
  • Short term: Feeling of impending doom
  • Long term: Chest pain, Bronchospasm (caution in asthmatics), can cause increased conduction down accessory pathways - caution here
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Digoxin (cardiac glycoside)

  • Use
  • Mech
  • SE
A

Reduces ventricular rate after CCB and BB
3rd line in HF

Negative chronotropic(reduced AV node conduction), positive inotropic (Ca accumulation intracellular)

Toxicity - arrhythmias, low therapeutic index

  • GI upset
  • nausea
  • Hypokalaemia (competes with K+ and Na/K pump
  • visual disturbance (yellow)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Types of CCB

A

Dihydropyridine (More smooth muscle relax)
- Amlodipine
Non-dihydropyridine (more cardiac depression - SA and AV node block)
- Verapamil, Diltizem

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

Mechanism of CCB

A

Decrease Calcium entry to vascular and cardiac cells

  • induce relaxation and vasodilation in arterial smooth muscle
  • suppress cardiac conduction esp at the AV node
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

CCB effect in HF/IHD

A

Reduced rate and after load, decreases oxygen demand preventing angina

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

Amlodipine SE

A

ankle swelling, flushing

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

Verapamil facts

A

ONLY CCB which can be given IV in SVT

DONT give with BB (both negatively chronotropic and inotropic so = Heart block

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

Beta blockers use

A

IHD - reduces angina

Congestive HF - improves prognosis

AF - reduces rate and maintain rhythm

SVT - restore sinus rhythm

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

Receptors and action of BB

A

B1 (heart) - reduces force and rate of conduction in heart (prolonged AV refractory period).
= reduced cardiac work and oxygen demand. increased myocardial perfusion

B2 (vasc smooth muscle) - lower peripheral vasc resistance and also lowers BP through reducing renin secretion.

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

SE of BB

A

Fatigue, cold extremities, headache, impotence

Asthma - causes bronchospasm so contraindicated (choose B1 specific e.g. atenolol not non-specific e.g. Bisoprolol)

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

Where to listen for mitral area?

A

Mid clavicular

5th intercostal space

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

Where to listen for Tricuspid?

A

inferior right sternal

4th intercostal space

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

Where to listen for Pulmonary valve?

A

Left 2nd intercostal

Next to sternum

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

Where to listen for Aortic valve?

A

Right 2nd intercostal next to sternum

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

S1 and S2?

A

S1 = closure of mitral and tricuspid

S2 = closure of aortic and pulmonary

there may be delayed P2 (pulm part of S2) in inspiration. Third heart sound in diastole (aka after s2 is pathological)

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

Mitral regurgitation

A

Pansystolic blowing murmur at apex radiating to axilla

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

Mitral stenosis

A

Loud opening snap in S1 and mid-diastolic murmur

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

Aortic stenosis

A

Radiates to carotids
Soft S2
crescendo decrescendo murmur between S1 and S2

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

Aortic Regurg

A

Diastolic murmur
Collapsing pulse
not well transmitted to carotids

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

PDA murmur

A

Late systolic best heard across back

Continusous machinery murmur

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

VSD murmur

A

Harsh systolic murmur best a left sternal edge

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

Starlings Law

A

Preload or degree fo stretch is critical factor for stroke volume.

Thus increased end-diastolic volume increases stretch and also contractility giving a lower end systolic volume (after load)

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

Aortic stenosis

  • Triad
  • other features
  • Cause
  • Investigations
A
  • Chest pain, HF (LV hypertrophy due to obstruction), syncope (insufficient blood)
  • slow rising pulse, narrow pulse pressure (higher pressure needed to eject), transmitted to carotids
  • calcification of aortic ring
  • ECG (LV strain), Transthoracic echo, CXR (Calcifications)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Aortic valve anatomy

A

Tricuspid valve

Coronary sinus sits behind

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

Aortic stenosis Tx and complications of Tx

A

1st line is valve replacement

2nd line saloon valvuloplasty

SE of infection (need Abx prophylaxis) and risk emboli (esp metal valves) needing anticoagulant aiming for 2.5-3.5 INR

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

Aortic regurgitation

  • Causes
  • Associated diseases
  • Presentation
A
  • Bicuspid aorta, thematic fever (autoimmune), infective endocarditis, collagen disease, age (degenerative)
  • SLE, Marfans, Ehlers-Danlos, Turner’s, Ank spond
  • Shortness of breath, orthostatic/nocturnal dyspnoea
  • Wide pulse pressure and collapsing water hammer pulse
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Aortic regurgitation

  • Investigations
  • Tx
  • screening
A
  • ECG (may have LVH), CXR (HF due to fluid overload), Transthoracic echo
  • acute surgery (valve replace) is symptomatic, give ace inhibitor if chronic

screen those with assoc diseases e.g. marfans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Mitral stenosis

- complications

A
  • Inc LA and pulmonary artery pressure.
  • May progress to cause RV failure and subsequent raised JVP, liver congestion, ascites and peripheral oedema
  • Thromboembolic risk due to blood stasis in atria
97
Q

Mitral stenosis

  • Causes
  • Pres
  • Signs
A
  • congenital, rheumatic fever, degenerative calcification in elderly
  • progressive breathlessness, palpitations due to AF, systemic emboli effects, hoarseness (LA hypertrophy)
  • Malar flush (CO2 retention), raised JVP, Laterally displaced apex, RV heave, signs of RHF (hepatomegaly, ascites etc)
98
Q

Mitral Stenosis

  • Investigation
  • Tx
  • Prevention
A
  • ECG (P- mitrale = bifid), CXR - LA enlargement & interstitial oedema (Kerly B lines) & prominent pulmonary vessels
  • diuretics and nitrates fo SOB, BB or CCB for exercise tolerance, valve balloon if symptomatic
  • Prophylaxis for rheumatic fever and infective endocarditis is penicillin
99
Q

Mitral regurgitation

  • Causes
  • Presentation
  • Complications
  • Investigations
  • Tx
A
  • advancing age, rheumatic fever (less commonly), MI, IHD, post surgical, ehlers-Danlos, SLE
  • Acute forms lead to rapid pulmonary oedema (e.g. papillary muscle rupture).
  • Chronic forms give HF, Breathlessness, can cause pulmonary HTN
  • ECG P-mitrale, CXR left heart hypertrophy, Echo
  • Surgery (valve repair), ACEi, nitrates, diuretics
100
Q

Rheumatic fever

A
  • Antigen mimicry to strep pyoges (Group A beta haemolytic)
  • affects joint skin heart and nervous system 2-4 weeks post infection (sore throat)
  • IV Benzylpenicillin for strep, NSAIDs suppress inflammation
  • long term MR due to papillary muscle fibrosis and shortening
101
Q

Why is Rhematic fever less common

A

Group A - Strep Pyogenes infection is less common

102
Q

infective endocarditis

  • Pathogenesis
  • presentation
  • complications
  • RF
A
  • strep viridian’s (dental procedures), Staph aureus (invasive procedures IVDUs). Poor blood supply to valves (hard for WBC and drugs to reach), fibrin-platelet/organisms vegetation formed –> destroys valve leaflets
  • Fever + New Murmur = endocarditis until proven otherwise
  • valvular insufficiency, systemic emboli (can have embolic or infective effect (block or make abscess), immune complexes (cutaneous, kidney, arthritis)
  • structural heart defect, IVDU, previous IE
103
Q

Infective endocarditis features

A

Fever + new murmur (usually MR, tricusp with Staph aureus)

Roth’s spots - eyes, retinal haemorrhage with pale centre

Osler’s nodes - painful red blisters @ terminal phalanges and toes

Janeway lesions - painless red maculae on thenar eminence

Nail haemorrhage - splinter - red and linear

Embolic phenomena e.g. stroke
Subacute: clubbing

104
Q

Infective endocarditis Tx

A

Amoxicillin + Gentomycin IV

Surgery may be needed if damaged heart valves

105
Q

What is cardiomyopathy

A

Functional/Structural abnormality of heart muscle WITHOUT Coronary/valvular/congenital disease HTN

106
Q

Classification of cardiomyopathy

A

Dilated - most common. imparted contraction, most common need for transplant

Hypertrophic - (HOCM) L/R ventricular hypertrophy. usually familial due to data-myosin dysfunction

Restrictive - rare. reduced diastolic filling

107
Q

Causes of cardiomyopathy

A

Dilated - Ischaemic, Alcohol, Thiamine deficiency (Beri Beri), SLE

Hypertrophic = familial

Restrictive - amyloidosis, sarcoidosis, radiation, haemochromatosis

108
Q

Presentation, Investigation and Tx of dilated cardiomyopathy

A
  • congestive HF, Right sided HF, cardiomegaly, AF or VT, thromboembolism by stasis
  • CXR ABCDE (Alveolar oedema, Batwing, kersey B, interstitial Cardiomegaly, Dilated upper lobe vessels, pleural Effusion
    Bloods - BNP (b-type natriuretic peptide)
  • Loop diuretics / thiazide, ACEi (Digoxin if doesn’t respond)
    Nitrates, Warfarin, pacing

Most common cause for heart transplant

109
Q

Most common cause of sudden cardiac death in young people

A

Hypertrophic cardiomyopathy.

Genetic inheritance
gene coding for Beta myosin

Mitral regurgitation may be present giving atrial enlargement

110
Q

Management of Restrictive cardiomyopathy

A

Amiodarone if ventricular arrhythmia, anticoagulant, BB and CCB if AF

Transplant sometimes indicated

111
Q

What is Myocarditis and how does it occur?

A

acute/chronic inflammation of myocardium (fatigue, chest pain, fever)

might be due to viral (Coxsakie), immune mediated (SLE, Sarcoid, scleroderma), Alcohol, Heavy metals, Electric shock

112
Q

Heart failure features

A 
Dyspnoea
Cough - worse at night (pink frothy sputum)
Orthopnoea/nocturnal dyspnoea
Wheeze
Weight loss
Bibasal crackles 
Peripheral oedema/ascites
113
Q

HF acute management

A 
O2
diuretics (furosemide)
Opiates (for SOB)
Vasodilators
Inotropes
CPAP
114
Q

HF - Drug management

A

1st - ACei and BB
2nd - Aldosterone agonist or hydralazine in combo with nitrates
Diuretics for fluid overload
Annual influenza vaccine and pneumococcal vaccine

3rd line is digoxin

115
Q

HF classification

A

NYHA
I = no sympt

II = mild symptoms, slight limitation

III = moderate symptoms, unable to carry our physical activity without discomfort

IV = severe, symptoms of HF at rest

116
Q

HF investigations

A

BNP (released my myocardium stretched)
ECG for aetiology at Tx

Gallop murmur due to S3

117
Q

Causes of HF

A

Mostly IHD and HTN, 10% valvular (AS causing LVH)

Myocardial disease - ischaemia, cardiomyopathy, HTN, drugs (bb, cbb, doxorubicin), alcohol and cocaine, infiltrative (haemochromatosis, sarcoidosis)

high output: anaemia, pregame’s, hyperthyroidism, pagers disease of bone

118
Q

Atherosclerosis

4 stages

A

1) Fatty streak formation - this is due to endothelial dysfunction causing lipid and monocyte infiltration.monocytes engulf fat to become foam cells = fatty streak
2) Intimal hyperplasia - platelet derived growth factor, TGF-B from macrophages and SMC causes hyperplasia
3) Fibrous cap formation - SMC produce collagen
4) Plaque formation or Rupture - may have a fatty necrotic core. Plaque might continue growing to narrow lumen or become unstable and rupture

119
Q

What can be found within intimal plaques in Atherosclerosis?

A

Lipid
Macrophages
Smooth Muscle cells

120
Q

Two type of Cholesterol

A

HLD - Carries fat away from arteries to Liver for synthesis of bile salts and steroids

LDL - Carry fat towards arteries causing plaque formation

121
Q

What carries fat from intestine to muscle

A

Chylomicrons

122
Q

Statins:

  • Mechanism
  • When NICE recommend
  • SE
  • Which statin
  • Monitoring
A
  • HMG-CoA reductase inhibitor
  • QRISK2 over 10%, Hx of CVD, familial hypercholesterolaemia, over 65
  • Myalgia, stiffness, weakness, cramping
  • Atorvastatin 20mg (primary prev), 80mg for secondary prev
  • LFTs
123
Q

HTN complications

A

Stroke, IHD, MI, CKD

124
Q

HTN modifiable RF

A

Smoking, weight, alcohol, stress, exercise, salt

125
Q

HTN non-modifiable RF

A

AGe, Fam Hx, Ethnicity, Gender

126
Q

HTN stages and when to Tx

A

Stage 1: over 140/90 (135/85 ABPM/HBPM)
Stage 2: over 160/100 (150/95ABPM/HBPM)
Stage 3: over 180/110

Intervene at stage 2

127
Q

Symptoms of HTN and screening

A

Often no symptoms (unless 200 systolic then headaches etc)

Screen adults every 5 years up to 80

128
Q

Causes

A

Primary - Essential HTN (95%) env, gene etc

Secondary - Renal disease (inc renin due to dec perfusion), Endocrine (Cushing, Conns, Thyroid, Phaeo), Pre-eclampsia and preg, Drugs (steroids, COCP, decongestant)

129
Q

What is malignant HTN

A

High BP or fast inc in BP

Causes end-organ damage

130
Q

End organ damage in HTN

A 
Brain - Seizure, Vomit, Stroke
Dissection
Pulmonary oedema (HF)
Nephropathy
Retinopathy (grade 1 = tortuous retinal arteries, grade 4 = papilloedema)
131
Q

Investigations for secondary HTN

A

Lipids and FBC

VMA - breakdown prod of adrenaline

Urinary free cortisol

Renin/aldosterone levels

Plasma Ca

MRI renal arteries

132
Q

Treatment of HTN

A

LIFESTYLE!
diet, weight, salt, all, exercise, smoking

Target of under 140/90

A or C (amlodipine - ankle swelling)

  • A for under 55
  • C for afrocarib or over 55

A + C

A + C + D (indapamide )

if still then if K+ low add Spironolactone if high then inc ‘D’

133
Q

IHD Causes

A

Mechanical obstruction of CA (atherosclerosis, thrombosis, spasm-prinzmetals, arteritis)

Decrease blood O2 (anaemia, decreased CO - HF, poor oxygenation in lung)

inc heart demand = more O2 and reduced coronary filling time (HTN, valvular disease, hyperthyroid, fever, exercise)

134
Q

IHD symptom

A

Angina (stable is when exercise induced, unstable is at rest)

135
Q

IHD RF

A

modifiable:
- smoking, poor diet, weight, low exercise, alcohol, stress, HTN, depression, diabetes, hyperlipidaemia

non-modifiable:
- age, male, genetics, FH

136
Q

What is stable angina?

A

Narrow lumen from atherosclerosis decrease blood flow = chest pain on exertion

constricting discomfort front of neck/shoulder/jaw/arms

Brought on by exercise, received by rest/GTN

137
Q

What is Prinzmetals angina?

A

Angina due to coronary spasm

138
Q

Referral of new angina

A

All cases to acute chest pain clinic for confirmation of Dx and severity assess

within 2 week

139
Q

How does unstable angina occur

A

Either progressive luminal narrowing or Plaque rupture.

140
Q

Angina Dx

A 
MI - if pain over 5 mins
Pericarditis - worse on inspiration or lying flat
MSK - worse on moving
PE - pleuritic
GORD
141
Q

Investigation of angina

A 
ECG - S/T or T flattening or inversion
FBC (anaemia), Blood glucose diabetes)
LFT (baseline befor statin)
U&E (renal function)
TFT

Coronary angiography will confirm (this is invasive)

142
Q

Stable angina management:

A

Modify CV RF + educate patient

GTN (if doesn’t relieve then 2nd dose after 5 min and third dose after 5 min then wait 5 min then call 999)

1s line: BB (atenolol - dec HR and BP, brady, cold hands, fatigue) or CCB (diltiazem (ankle swelling flushing)

2nd line dihydroperidine CCB + BB

To reduce RF: Aspirin or Clopidogrel, Statin if indicated

143
Q

Angina not controlled by medications

A

PCI

CABG

144
Q

ACS ECG

ST elevation =
No ST elevation =

A

STEMI

NSTEMI (if cardiac markers raised)

Unstable angina if they are not raised

145
Q

ACS investigation

A

ECG - ST elevation (acute infarct) ST depression/T-inverstion (unstable angina or NSTEMI)

Cardiac enzymes: (best 3-6 hours post infarct, max at 12-24hours troponin T, troponin I, Creatine kinase
–> minimal inc may suggest future risk

Bloods (FBC - anaemia, glucose - if high poor prognosis, renal/tyroid function)

Imaging:
CXR - complications like pulmonary oedema, PE, pneumothorax, TAA

146
Q

ACS presentation

A

New onset angina, prolonged anginas pain at rest (over 20 min)

Other: sweating, vomit, fatigue, SOB, palpitations

147
Q

Initial management of ACS

A

MONA

morphine, O2, Nitrates, Aspirin

Monitor with ECG

148
Q

Risk assessments in ACS

A

TIMI - bleeding risk in MI thrombolysis

GRACE - assess Tx of NSTEMI

149
Q

GRACE

A

used in ACS to predict 6 month mortality

Low risk = Clopidogrel 12 months

Medium risk = angiography within 4 days

High risk = PCI or CABG for revascularisation

150
Q

Dressler’s syndrome

A

late pericarditis. Inflammatory reaction to necrotic tissue occurring 2-8 weeks after ACS

151
Q

Discharge management for ACS

A

Cant drive for 4 weeks (1 week if angioplasty)

ACEi, dual platelet (aspirin+clopidogrel), BB, Statin, monitor BP and renal function regularly.

IF HF offer Spironolactone

LIFESTYLE - smoking, weight

152
Q

ACS complications

A

Acute MI
Pericarditis
Dresslers syndrome

153
Q

MI complications

A 
Death
Dresslers
PEricarditis
Rupture of free wall
Aneurysm (persistent ST elevation)
Tamponade (Becks)
HF
Shock (cariogenic)
VT
154
Q

Cardiac arrest management

A

call 999
A+B
C once airway secured (30:2 uninterrupted)
D - automatic defibrillates
2 mins CPR between defibrillates attempts
after 3rd shock adrenaline + Amiodarone
2min CPR.. Adrenaline etcetcetc

155
Q

Pericarditis

  • Anatomy
  • Pathogen
  • Causes
A

Pericardium is outer fibrous layer and inner serous membrane with 5ml fluid. Fixes heart to pericardium and prevent dilation.

inflammation results in exudate/adhesions/effusions (haemorrhage or serous)

viral (Coxsackie, EBV, staph)
Rheum (RA, SLE, Sarcoid)
MI (dresslers)
Other (drugs e.g. hydralazine, fungal)

156
Q

Acute pericarditis

- Presentation, Signs/sympt

A

Chest pain (dull, sharp, burning),

Substernal/precordial radiates to neck or leg trapezius

Aggravated - Cough, lying flat
Relieved - siting up

tachypnoea, tachycardia, fever

If tamponade may have becks

60-85% have pericardial friction rub

157
Q

Acute Pericarditis Investigations

A

ECG - Concave ST elevation (saddle shape)

Bloods - FBC (WCC), ESR/CRP (raised), U+E (uraemia can cause), Cardiac enzymes (point to MI as cause of pericarditis)

Echo - if suspecting fluid or tamponade (over 20mm free fluid)

158
Q

Pericarditis Tx

A

If RA or Ventricular collapse on echo - Pericardiocentesis

Stable Patients:

  • Rest, Treat cause, NSAIDs (naproxen)
  • If uraemia consider dialysis
159
Q

When to admit for Pericarditis

A 
Fever
evidence of tamponade
Large effusion (echo free space over 20mm)
On Warfarin
Trauma
Fail to respond to NSAIDs
160
Q

Complications of Pericarditis

A

Falling BP and shock - suspect tamponade

161
Q

What is Cardiac Tamponade.

Why Important?

A

Blood/Fluid/Pus/Gas in pericardial space.

Large volume = reduced ventricular filling leading to haemodynamic compromise
medical emergency

162
Q

Causes of Tamponade

A

Pericarditis, malignancy, Dressler’s (post MI), infective (HIV, TB), connective tissue disease (SLE, RA, dermatomyositis, systemic sclerosis), Trauma.

163
Q

Presentation of Tamponade

A

Anxiety, Fatigue, Oedema (peripheral, pulmonary), SOB, tachycardia, tachypnoea

164
Q

Becks Triad: when and what

A

Seen in ACUTE Tamponade

1) Muffled Heart sounds
2) Raised JVP
3) Hypotension

165
Q

Tamponade ECG

A

Low voltage QRS

166
Q

Tamponade CXR

A

Water bottle shaped heart

167
Q

Gold standard Investigation in Tamponade

A

Transthoracic Echo

168
Q

Tamponade Tx

A 
O2
Volume Expansion
Increase venous return (legs up)
Inotrope (dobutamine)
Pericardiocentesis
169
Q

What is peripheral artery disease?

A

Narrowing of peripheral vasculature

Most often due to atherosclerosis

170
Q

Peripheral artery disease classification

A

1) Asymptomatic
2) Intermittent Claudication
3) Ischaemic rest pain
4) Critical limb ischaemia (P’s - Pulseless, perishing cold, Painful, Pale, Parasthesia, Paralysed)

171
Q

Intermittent Claudication:

A

Cramping pain in calf/thigh/buttock on walking.

symptoms worse uphill/stairs
relieved by rest

172
Q

Intermittent Claudication - determinants of severity

A

Claudication distance

Rest time

173
Q

Ischaemic rest pain

A

Unremitting pain in limb.

Wakes from sleep, relieved on dangling foot/cold floor

174
Q

Peripheral artery disease other signs

A

Skin changes (atrophic)

Hairless

175
Q

Peripheral artery disease DDx

A

Sciatica
Spinal stenosis
DVT
Nerve entrapment

176
Q

Peripheral artery disease investigations

A 
FBC (anaemia aggravates)
ESR (giant cell arteritis)
Thrombophilia screen (DVT)
ECG (look for coronary disease)
Doppler US to calc ABPI
- Normal = 1
- 0.9 mild, 0.8 mod, below 0.5 ischaemic rest pain.
177
Q

Acute limb ischaemia

  • 6 P’s
  • Cause
  • Investigation
  • Tx
  • Complications
A
  • Pulseless, Paralysed, Parasthesia, Pale, Perishing cold, Pain
  • Thrombus or Embolism giving sudden occlusion
  • Urgent doppler and urgent angiography
  • Revascularisation in 4-6 hours with immediate heparinisation (embolectomy for embolus, thrombolysis/angioplasty/bypass if thrombotic
  • Infection, poor healing, gangrene
178
Q

General management of Peripheral Limb Ischaemia.

A

RF: smoking, weight, statins, ACEi (beware renal artery stenosis), Manage DM/HTN

Antiplatelet - Clopidogrel

179
Q

Management of intermittent claudication

A

Vasodilator therapy - Naftidrofuryl oxalate

Supervised exercise

ABPI (doppler USS) ± CT angio

Revascularisation if tried lifestyle improve (angioplasty + stenting

180
Q

Management of Critical ischaemia

A

Pain: para+opioid
doppler USS ± contrast angio

Revascularisation with angioplasty and stenting

Some cases may need amputation

181
Q

Aortic Dissection what is it?

A

Intimal tearing gives disruption of media

Intramural bleeding separates layers leading to a false lumen creation

182
Q

Aortic Dissection Types

A 
Type A (70%) aortic arch + ascending aorta
Type B (30%) descending aorta
183
Q

Aortic Dissection RF

A

Cardiovascular disease
Aortic disease
Cocaine/amphetamines
Bicuspid aortic valve

184
Q

Aortic Dissection Presentation

  • Acute
  • possible systemic effect
A
  • Sudden tearing/sharp pain. Radiates to back, Pulse loss

- Spinal arteries (paraplegia), Distal aorta (limb ischaemia), Carotids (Neurological deficit), Coronary (angina)

185
Q

Aortic Dissection expansion phase

A
  • Cardiac tamponade

- Pleural Haemothorax

186
Q

Important Dx in Aortic Dissection

A

Differentiate from MI as thrombolysis will be fatal in Aortic Dissection

187
Q

Aortic Dissection investigations

A

CXR - widened mediastinum (if -ve can’t exclude dissection)

TTUS - site and extent of dissection

MRI - good for diagnosis and looking for other vessel involvement

ECG - needed to differentiate if MI suspected

188
Q

Aortic Dissection Tx

A

IV access, analgesia (morphine) and O2 initially

ICU

Aggressive HTN management aim for BP 100-120 systolic

  • IV BB (labetalol) to reduce contraction
  • IV nitropruside (emergency Vasodilation)

Surgical repair

  • Type A gets graft
  • Type B TEVAR
189
Q

TAA

  • True aneurysm
  • Location
  • Pathogenesis
  • RF
A
  • Involves all three layers
  • Ascending aorta (51%), arch, descending
  • Inflammation, proteolysis and reduced SMC survival
  • CTD (marfans etc), genetic, Infective (HIV, syphilis), Aortitis (GCA, RA, Takyasu’s arteritis, Trauma (weight lifting), Cocaine/amphetamines, bicuspid aortic valve, HTN, smoking, age
190
Q

What level is Aortic Hiatus in diaphragm?

A

T12

191
Q

TAA presentation

A

Pain - chest, neck, upper back, epigastrium. dissection sudden tearing
Compression symptoms - hoarseness, SVC obstruction, stridor

if rupture: acute pain, collapse/shock, haematemesis/haemoptysis, haemothorax/tamponade

192
Q

TAA investigations

A

Acute: FBC, clotting, U&E, LFT, CT contrast, ECG, MR angio

Non-acute: above plus USS, TTE

193
Q

TAA Tx

A

Surgery: TEVAR
smoking cessation, Tx CV RF
6 monthly MRI/CT
Inform DVLA if above certain size

194
Q

TAA surgery complications

A

paraplegia (spinal ischaemia)
Stroke
AKI

195
Q

AAA

  • Location
  • Causes
A
  • Mainly below level of renal arteries
  • Atherosclerotic disease, FH, smoking, male, inc age, cardiovasc disease/RF, Arteritis (Takyasu, Behcets), CTD ( marinas etc), infective (TB, HIV)
196
Q

AAA

  • Presentation
  • Examination findings
A
  • Often incident finding, pain in back/loin (DDX for loin to groin), pulsatile abode swelling, rupture = shock
  • Bimanual palpation, Abdominal bruit, retroperitoneal haemorrhage - Grey Turner sign (flank bruising)
197
Q

AAA investigations

A 
FBC, clotting, U&E (renal), LFTs, Crossmatch, 
USS --> initial assess
ECG
CXR
CT --> more anatomical detail

MRI angio

198
Q

AAA Management

A

USS monitoring

  • 3-4.5cm = yearly
  • 4.5-5.5cm = 3mnthly

Over 5.5 consider surgery

Inform DVLA over 6cm

surgery - over 5.5cm or rapid expansion over 1cm/year or if symptomatic

  • Open repair
  • EVAR
199
Q

AAA rupture

  • Pres
  • Investigation
  • Management
  • Prognosis
A
  • Thoracic chest pain, Haemoptysis ± tamponade, pale, sweaty, weak pulse, hypotension. Triad
    1) flank/back pain
    2) hypotension
    3) pulsatile abdo mass
  • FBC, crosshatch, baseline U&E, CXR, ECG
  • Large bore IV access, Immediate theatre - Prosthetic graft repair and stem bleeding
  • 1 in 3 reach hospital alive
200
Q

Types of shock

A

Cardiogenic - heart can’t supply enough blood (dec CO)

Septic - dec systemic vasc resistance

Anaphylactic - Type I hypersensitivity, mast cell histamine and vasoactive mediators dec systemic vasc resistance

Neurogenic - spinal cord injury, epidural/spinal anaesthesia causes dec vasc resist

201
Q

Triad seen in shock?

A

Triad

1) Coagulopathy
2) hypothermia
3) Metabolic acidosis

202
Q

Shock and Organ systems

A

Kidney - acute tubular necrosis
Lung - ARDS
Heart - MI
Brain - Confusion, Coma

203
Q

Sepsis def

Septic shock def

A
  • Life threatening organ dysfunction from dysreg response to host infection (dec SOFA 2 points or more)
  • Circulatory and metabolic dysfunction as a result of sepsis
204
Q

Hypovolaemic shock

  • Aim of resus
  • Presentation
  • Investigations
A
  • correct hypo perfusion of vital organs e.g. kidneys
  • Pale, sweaty, tachycardia/pnoea, cold periphery, inc cap refill time, hypotension
  • FBC (Hb), U&E (kidney), Group and Crossmatch, ABG+Lactate, urine output
205
Q

Hypovolaemic shock

staging

A 
Like Tennis:
Class I 15% loss
Class II 30%
Class III 40%
Class IV over 40%
206
Q

Compensation mechanisms to hypovolaemia

A

Baroreceptor feedback (via CN IX sensation) causes vagal inc in contractility, tachycardia, vasoconstriction

Release of Vasopressin, Aldosterone, Renin (Kidney compensation)

207
Q

what is occurring in hypovolaemia which is:

  • Uncompensated
  • Irreversible
A
  • Myocardial depression and failure of vasomotor reflex, inc capillary permeability, lactic acidosis
  • End organ failure
208
Q 
Features of:
Class I
Class II
Class III
Class IV

When to transfuse

A

Class I: Physiological compensation

Class II: postural hypotension, dec urine

Class III: Tachycardia over 120 bpm, urine under 20ml/hr, confused

Class IV: marked hypotension, tachycardia

209
Q

Tx Hypovolaemic shock

A
  • Raise legs (venous return)
  • ABCDE
  • Fluid resus: Saline or - Hartmann’s 500ml over 15 min
  • If haemorhhagic give O -ve blood
  • Pain relief (pain inc metabolic rate and inc ischaemia) IV opiates
  • Surgery may need fro stem blood loss
210
Q

Cariogenic shock

  • Cause
  • Presentation
  • Management
A
  • MI mostly, can also be Tamponade/constrictive pericarditis/PE/tension pneumothorax
  • Dyspnoea, sweat, confusion, palpitations, pale, mottled, slow cap refill, hypotension
  • A+B = intubation and ventilation, C = venous access (may need central due to peripheral shut down, IV morphine, cardiac inotropes
211
Q

Anaphylactic shock

  • Definition
  • Presentation
A
  • Type 1 hypersensitivity due to mast cell histamine/other vasomediator release. sudden onset, life threatening airway + circulatory problems
  • breathless/wheeze, profound vasodilation (warm periphery, low BP, tachycardia), angio-oedema/hives, oedema of face/pharynx/larynx
212
Q

Anaphylactic shock Tx

A

A (call help if signs of obstruction), B (treat rest distress - O2), C (assess with colour, pulse, BP), D (responsive?)

Give:

  • high flow O2
  • raise legs (venous return)
  • IM adrenaline (most important) 0.5mg adult
  • Expert intubation
  • IV fluid challenge: 500ml CRYSTALLOID in 5-10 min
  • IV chlorphenamine + hydrocortisone
  • Bronchodilators: IV salbutamol (or nets), ipratropium inhaled, Aminophylline (IV)
213
Q

Sepsis Presentation

A 
Bounding pulse
temperature
Rigors
Rapid cap refill
Vasodilation
warm peripheries
214
Q

Sepsis BUFALO

A
  • Blood cultures
  • Urine output - monitor hourly
  • Fluid resus
  • Abx - Tazocin, Gent (according to local guidelines)
  • Lactate (ABG/VBG)
  • Oxygen to correct hypoxia
215
Q

Sepsis complications

A

DIC
Renal failure
Cardiorespiratory failure

216
Q

ECG Hyperkalaemia

A

Peaking of T waves (occurs first)
Loss of P waves
Broad QRS complexes
Ventricullar fibrillation

217
Q

Hypercalcaemia features

A

Bones, Stones, Groans and Psychic moans.

ShortenedQT interval on ECG

218
Q

DVLA and driving with cardio disease

A 
Angioplasty - 1 week
CABG - 4 week
ACS - 4 week
Pacemaker - 1 week
AA over 6cm - tell DVLA
219
Q

When is BNP released?

Effects on BNP

What can cause a rise in BNP?

A

Hormone prod. mainly in LV in response to strain

Vasodilator, diuretic and natriuretic (suppresses both RAAS and sympathetic tone)

ischaemia, valvular disease, an LV dysfunction

220
Q

What is Buerger’s Disease

A

Small and medium vessel vasculitis assoc with smoking

Causes IgA nephropathy but also Intermittent Claudication, Ischaemic ulcers, Raynauds

221
Q

TOF

A
  • Over-riding aorta
  • VSD
  • LVH
  • Pulmonary stenosis
222
Q

Types of ASD

A 
Ostium Secundum (most common)
Ostium primum
223
Q

Ostium Secundum Aetiology

A

70% due to failed closure of Foramen Ovale

224
Q

Clopidogrel

  • Action
  • When used
  • Names of similar drugs
A
  • Blocks ADP receptor (P2Y12) inhibiting platelet activation
  • 1st line in ischaemic stroke and peripheral artery disease
  • Ticagrelor, Prasugrel
225
Q

Antiplatelet use

  • NSTEMI
  • STEMI
  • TIA
  • Ischaemic stroke
  • Periphreal artery disease
A
  • Aspirin (lifelong), clopidogrel/ticagrelor (12mnth)
  • Aspirin (lifelong), clop 1 month
  • Clopi (lifelong)
  • Clopi (lifelong)
  • Clopi (lifelong)
226
Q

ACEi SE

A

Cough in 15% due to inc bradykinin levels

Small risk angio-oedema

Hyperkalaemia

227
Q

Cautions and contraindications ACEi

A

Pregnancy and BF

Renovascular disease risk renal impairment if bilateral renal artery stenosis

228
Q 
Action of antiarrhythmics 
Class 1 -
Class 2 -
Class 3 -
Class 4 -
A

Class 1 - sodium channel blockers
Class 2 - B-block (Propanolol)
Class 3 - K+channel block (Amiodarone, Sotalol)
Class 4 - Ca channel block (verapamil, diltiazem)

229
Q

Class 1 antiarrhythmics examples

A

1a (moderate): Quinidine
1b (weak): Lidocaine, phenytoin
1c (strong): Flecainide

230
Q

Action potential changes of Antiarrhythmics

A

Class 1: Change slope of phase 0
Class 2: decrease HR and conduction velocity
Class 3: inc AP duration and absolute refractory period, prolong repolarization
Class 4: slow rise of action potential. prolonged depolarisation at AV node

231
Q

When does ductus arterioles close

  • What drug keeps open & what one closes early
A

2-3 days

PG

NSAID

232
Q

Reduced femoral pulse / Radio femoral delay.. what is diagnosis

A

Coarctation (constriction) of the aorta

233
Q

What is 1st management of Pulseless electrical activity

A

Chest compression then

Give 1mg IV adrenaline

234
Q

In VF/VT when is adrenaline given

A

After chest compression started

235
Q

In Asystole what should be done

A

2 mins chest compressions and see if changes

236
Q

CCB used in HTN

A

Dihydroperidones: Amlodipine

237
Q

When is electrical rather than pharmacological cardioversion used in AF?

What should be done prior?

A

Any AF lasting for over 48 hour s= DC cardioversion

Must receive oral anticoagulant for 3 weeks prior if AF symptoms last over 48hr

238
Q

Definition of Pulseless electrical activity

A

Sinus tachy on eCG

No pulse felt

Final (26 decks)

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