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MBBS3 > CARDIO > Flashcards

CARDIO Flashcards

1
Q

Non ST Elevation MI ACS

What are the ECG Changes?

A
  • ST depression
  • T wave inversion
  • non specific/may be normal
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2
Q

Which cardiac enzyme is most sensitive and specific markers for myocardial necrosis?

A

Troponin (T and I)
Go up within 3-12 hours from onset of chest pain
Peak at 24-48 hours
Return to baseline 5-14 days
If normal 6 hours after peak of chest pain + normal ECG = MI risk is 0.3%

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3
Q

There are 3 isoenzymes for creatinine kinase.
Where is CKMM?
where is CKBB?
Where is CKMB?

A

CKMM- skeletal muscles- peaks after trauma/seizure ++ exercise

CKBB- brain

CKMB- HEART- increase 3-12 hours after onset of chest pain, peak 24hrs and return to baseline 48-72 hrs
Levels peak earlier if reperfusion occurs

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4
Q

What does myoglobin do in MI?

A

Rise within 1-4 hrs from onset of chest pain

Highly sensitive but not specific

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5
Q

What proportion of deaths occur within 2 hours of the onset of symptoms in acute MI?

A

50%

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6
Q

What are the 2 key questions if someone has chest pain? Clinical tests

A

1) is there ST elevation
2) is there a troponin rise?

If symptoms settle without these happening, no myocardial damage has occurred and good prognosis

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7
Q

What proportion acute MI die before discharge?

A

7%

Worst prognosis if old, LV failure, ST changes

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8
Q

Management of MI up to doing an ECG

A

1) 300mg aspirin , clopidogrel 300mg, heparin
2) GTN sublingually
3) 5-10mg morphine i.v
4) 10mg metaclopramide I.v NOT I.M- high risk of bleeding)
5) if sats >90% O2.
6) -/+b blocker- metoprolol

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9
Q

Do an ECG and find it’s an ST elevation MI- immediate management is done- what next?

A

1) primary angioplasty or thromblysis
Is PCI available within 120mins?
Yes- PCI. (Must use injectable anticoagulant- bivalirudin preferred. If not use enoxaparin -/+ GP II b/IIIa blocker.
No- fibrinolysis then transfer to PCI center. Either rescue PCI if fibrinolysis is unsuccessful or angiography.
Don’t do fibrinolysis if chest pain >24hrs
2) b blocker- atenolol- iv 5mg
3) ACE inhibitor - lisinopril 2.5 mg in all normotensive pts within 24 hrs of acute MI- especially if evidence of heart failure.
4)consider clopidogrel 300mg loading followed by 75mg per day for 30 days

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10
Q

Do ECG and non ST elevation MI is confirmed. Basic management complete- what next?

A

1) b blocker- atenolol 5mg iv
2) iv nitrates
3) antithrombotic- fondaparinux- if low bleeding risk and no angioplasty planned for 24 hrs. OR if angioplasty is planned in 24 hrs, LMWH- enoxaparin- s/c for 2-8 days.
4) then assess risk - GRACE SCORE
If high risk:
1) GP IIb/IIIa antagonist eg tirofiban or bivalirudin (thrombin inhibitor)
2) angiography within 96hrs

If low risk:

1) give clopidogrel in addition to aspirin. Consider life long. if risk is >1.5-3% per year
2) oral b blocker- metoprolol 50mg/12h if HTN, High HR Or LV function 100mmHg

repeat troponin- if negative discharge

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11
Q

GRACE SCORE for determining if someone is high or low risk for MI after an non ST elevation MI and whether they should have angioplasty within 96hrs or not- what is high and low risk?

A

High risk:

  • persistent/recurring ischemia
  • ST depression /dynamic ST changes
  • diabetes
  • raised troponin
  • GRACE SCORE >140 need PCI within 24 hrs
  • if low risk GRACE SCORE need PCI within 72 hrs.
  • LVEF
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12
Q

When after MI do you give warfarin?

A
  • large anterior MI
  • give for 3 months
  • helps against systemic embolism from LV mural thrombus
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13
Q

After MI, what medications should people be put on?

A

1) aspirin 75mg- reduces vascular events and vascular death by 29% lifelong.
AND ADP Receptor blocker (clopidogrel/ticagrelor/prasugrel) for 12 months
2) B blocker- bisoprolol 2.5mg or enough to bring HR to

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14
Q

Complication of MI

Treatment of bradycardia or heart block ?

A

Atropine 0.6-1.2mg iv
If sinus bradycardia

If unresponsive or poorly tolerated consider temporary pacing

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15
Q

40% of people who develop 1st degree heart block post MI go on to develop higher degrees of heart block. 1st degree heart block is most commonly seen in what type of infarction?
What meds should you stop?

A
  • inferior Infarcts

- if develop higher degrees of heart block need to stop B Blockers and CCB

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16
Q

Complication of MI

Mobitiz type 1 treatment

A

Does not need pacing unless poorly tolerated

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17
Q

Complications of MI

Treatment of Mobitz type 2

A

Should be paced as carries a high risk of developing suddenly complete AV block

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18
Q

Complications of MI

Complete heart block

What is the exception to this treatment?

A

Insert pacemaker and usually resolves in a few days

Exception- if inf infarction and narrow qrs complex with reasonably stable pulse at about 40-50bpm

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19
Q

3 things that pre dispose to arrhythmias

A

Low K+
Hypoxia
Acidosis

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20
Q

Complication of MI
Treatment of AF or atrial flutter
A)!if compromised
B) otherwise

A

A) DC cardio version

B) Control rate with digoxin -+ b blocker.
Can try amiodarone or sotalol with intermittent AF or atrial flutter

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21
Q

Complication of MI

Define non sustained VT

A

> =3 consecutive premature ventricular beats. HR 100bpm and lasting >30secs

If this happens

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22
Q

Complications of MI

Define sustained VT

How do you treat it?

A

> =3 premature ventricular beats, HR >100bpm, for >30 secs

If stable- amiodarone
If unstable- Give DC shock

Recurrent VT may need pacing

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23
Q

Complication of MI

When does ventricular fibrillation most commonly occur?

A

80% occurs within 12 hours

If occurs later indicates pump failure or cardiogenic shock.

Need to give DC shock for both

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24
Q

What ejection fraction do you consider giving someone an implantable cardiac defib?

A
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25
Q

How do you measure R sided heart pressures?

A

Swan ganz catheter- guides fluid replacement

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26
Q

How does a RVF/ infarction present?

A

Low CO, raised JVP

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27
Q

How does pericarditis present?
What are the ECG changes?
What is the treatment?

A

Central chest pain relived by moving forward.
ECG- saddle shaped ST elevation
Treatment- NSAIDS and check ECHO for effusion

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28
Q

How does cardiac tamponade present?

Treatment

A
  • low CO
  • pulsus paradoxus
  • raised JVP
  • muffled HS

Treatment- pericardial aspiration for tempory relief then surgery

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29
Q

Complication of MI

How does mitral regurge present?

A

Pulmonary oedema
LVF

Consider valve replacement

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30
Q

Complication of MI.

How does VSD present?

A

Pan systolic murmur
Raised JVP
HF

diagnose on echo
50% mortality in 1st week
Treatment- surgery

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31
Q

Complication of MI

When do late malignant ventricular arrhythmias occur?

A

1-3weeks post MI
Avoid hypokalaemia
24hour ECG monitoring

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32
Q

Complication of MI

Dressler’s syndrome- what is it?
When does it occur?
How do you treat it?

A

Recurrent pericarditis, pleural effusions, fever, anaemia, ESR raised.

Occurs 1-3 weeks post MI

treatment- NSAIDS or steroids if severe.

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33
Q

complications of MI

How do LV aneurysms present?

What does the ECG show?

A
  • occurs late- 4-6 w post MI
  • presents with LVF, angina, recurrent VT or systemic embolism

-ECG shows persistent ST elevation

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34
Q

Give 5 indications for a CABG

A

1)left main stem disease
2) multi vessel disease
3)multiple severe stenoses
These it improves survival

4) refractory angina
5) pts unsuitable for angioplasty or angioplasty has failed
These it relieves symptoms

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35
Q

If pt has single vessel CAD and normal LV function, what is the best treatment option?

A

PCI

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36
Q

If pt has triple vessel disease and abnormal LV function what is the best treatment?

A

CABG

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37
Q

Positives and negatives of CABG

A

Positives-

  • procedural mortality rates same as PCI
  • provides more complete long term relief of angina in patients and less repeated revasularisation procedures

Negatives-
Longer recovery time and Los
Increased risk of stroke

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38
Q

What is the life span of a vein graft?

A

50% close in 10 years

Low dose aspirin can help prevent this.

Internal mammary artery lasts longer but may cause chest wall numbess

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39
Q

After CABG

What if still have angina?

A
  • poor graft run off
  • atheroma
  • graft occlusion

Restart anti anginal drugs and consider angioplasty

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40
Q

After CABG

Getting back to normal

A

Drive after 1 month

Mood, sex and intellectual problems are common- rehab helps.

Back to work 3 months

Aspirin 75mg/day lifelong

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41
Q

When preforming PCI must use injectable anticoagulant.

What is preferred?

A

bivalirudin preferred. If not use enoxaparin -/+ GP II b/IIIa blocker.

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42
Q

Whet ECG changes would you get with RV infarct?

A

ST elevation in inferior leads ( II, III, aVF)

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43
Q

ECG Changes in LAD problem

A

Anterior leads

C1-4

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44
Q

ECG changes if problem with circumflex

A

I, aVL, c5,c6

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45
Q

What is the ECG criteria for thromblysis?

A

-ST elevation >1mm in 2 or more limb leads
Or
- >2mm in 2 or more chest leads.
Or
-New LBBB
Or
-Posterior changes- deep ST depression and tall r waves in leads V1-V3.

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46
Q

What are the major contraindications for thrombolysis?

A

1) previous intracranial haemorrhage
2) aortic disscection
3) known incompressible puncture -

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47
Q

What are the relative contraindications for thrombolysis?

A

1) TIA180/110mmHg)
6) active peptic ulcer
7) infective endocarditis

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48
Q

What drug is used for thrombolysis?

A

Tissue plasminogen activators
Alteplase/ reteplase/ tenecteplase.

Should follow alteplase with unfractionated heparin infusion

All associated with fewer deaths than streptokinase

Though slight increase in stroke risk

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49
Q

What should you not use with verapamil??

A

B blocker- risk asysole

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50
Q

What O2 sats do you give low flow O2 to in MI?

A

90%

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51
Q

Who is high risk of death from NON ST elevation MI?

A
  • > 70
  • previous MI
  • hx of unstable angina
  • ST Depression or wide spread t wave inversion.
  • raised troponin
  • poor LV function
  • diabeties
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52
Q

What is the pathophysiology of MSTEMI?

A

Acute thrombosis induced by ruptured or eroded atherosclerotic plaque
With or without
Concomitant vasoconstriction causing a sudden reduction in coronary blood flow

THROMBUS IS PLATELET RICH
PARTIALLY OR INTERMITTENTLY OCCLUSIVE AND MAY FRAGMENT AND EMBOLISE

(Primary aggregation pathway dominates following plaque ruptured)

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53
Q

What is the pathophysiology of a STEMI?

A

Acute thrombosis induced by ruptured or eroded atherosclerotic plaque
With or without
Concomitant vasoconstriction causing a sudden reduction in coronary blood flow

THROMBUS IS FIBRIN RICH
COMPLETELY OCCLUSIVE

(secondary aggregation pathway dominates following plaque ruptured)

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54
Q

What is a vunerable plaque??

A

Large lipid core
Lots of inflammatory cells
Thin fibrous cap

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55
Q

What does the 300mg loading dose of aspirin do?

A

1) reduce CV Mortality
2) reduce reoccusion
3) reduce non fatal MI
4) in 40% reduction from unstable angina to MI

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56
Q

How do thienopyrides work?

Examples

A

Clopidogrel and prasugrel

Inhibit ADP mediated stimulation of the P2Y12 receptor resulting in inhibition of platelet activation and aggregation.

Reduces major cardiac events, thrombosis and restenosis rate.

ACS & DES: 12 months

34% of people are non responders.

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57
Q

Clopidogrel

How many days do you need to withdraw before surgery?

A

5 days

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58
Q

Clopidogrel

How long does it take to work

A

2-4 h

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59
Q

Clopidogrel

How long is it’s duration of effect?

A

3-10 days

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60
Q

Prasugrel
What is it?
How long is it onset of effect?

A

Irreversible
Thienopyride
30 mins

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61
Q

Prasugrel
What is it?
How long is the duration of it’s effect?

A

Thienopyride

5-10 days

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62
Q

Prasugrel
What is it?
How long do you withdraw it before surgery?

A

Thienopyride

7 days

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63
Q

What is ticagrelor?

A

Triazolopyrimide
Anti platelet a bit like clopidogrel
Active drug takes 30 mins to work. And last 3-4 days
Withhold 5 days before surgery

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64
Q

Post PCI when can you drive?

A

1 week

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65
Q

What do nitrates do to help the heart?

A

1) decrease O2 demand
- Lower dose venous vasodilation
- high dose arterial vasodilation

2) improve coronary blood flow
- vasodilate coronary arteries
- help collateral flow
- reverse coronary artery spasm

66
Q

ECG changes on acute MI

A
  • Hyper acute t waves
    -ST elevation or new LBBB
    These occur within hours if transmural infarction
    -T wave inversion and development of pathological q waves
    This happens after hours - days
67
Q

What valve problem can cause an arrhythmia?

A

Mitral valve

Also pericarditis, myocarditis, cardiomyopathy, CAD, MI, LV aneurysm.

68
Q

What meds can cause arrhythmias?

A 
Digoxin
B2 agonists 
L dopa
Tricyclics 
Doxorubicin (cytotoxic)

Pneumonia
Caffeine
Alcohol
Smoking

69
Q

What is sick sinus syndrome?

A
  • sinus node dysfunction
  • causes bradycardia+- arrest
  • sino atrial block or SVT alternating with bradycardia/a systole. (Tachy Brady syndrome)
  • associated with ischemia or valvular lesions.
  • can use permanent pacing
70
Q

Define sinus tachycardia

A

Normal p wave followed by normal qrs >100bpm

Qrs

71
Q

Define SVT

A

P wave is absent or inverted after qrs

> 100bpm
Qrs

72
Q

Define atrial fibrillation

A

P wave is absent and irregular qrs

73
Q

Define atrial flutter

A

Rate usually >300bpm
Giving flutter/saw tooth waves

Ventricular rate usually 150bpm (2:1 block)

74
Q

Define Atrial tachycardia

A

Abnormally shaped p waves- outnumber qrs morphologies

75
Q

Define multi focal atrial tachycardia

A

3 or more p waves per qrs

76
Q

What is junctional tachycardia?

A

Rate 150-250 bpm

P wave either buried in qrs complex or occurring after qrs complex

77
Q

How do you manage narrow complex tachycardias?

A

1) vasovagal manoovers
2) if insuccessful give adenosine (causes transient AV Block) show underlying atrial rhythm
Half life is short- 10-15 secs. If doesn’t work after 1-2 mins give more.

78
Q

When is adenosine for narrow complex tachycardias contraindicated?

A

Asthma
2/3rd degree heart block
Sino atrial node disease.
If taking dipyridamole (anti platelet)

Use smaller dose if transplanted heart,

79
Q

If adenosine fails cardioverting SVT, what do you try next?

A

Verapamil

NOT IF ON B BLOCKER

80
Q

What can atrial tachycardia be due to!

A

Digoxin toxicity

81
Q

When is multi focal atrial tachycardia more commonly seen?

A

-COPD- correct hypoxia and hypercapnia.

Can try verapamil or b blocker is rate remains >110bpm

At least 3 morphologically distinct p waves with irregular p-p intervals.

82
Q

What rhythm can be treated with radio frequency ablation?

A

Junctional tachycardias-

1) AV node re entry tachy
2) AV re entry tachy
3) his bundle tachy

Ablation good in AV re entry tachycardia.

83
Q

ECG findings for Wolfe parkinson white syndrome?

A

1) short pr interval
2) wide qrs (due to slurred upstroke/delta wave)
3) ST-T changes.

84
Q

Why do pts with WPW Syndrome present with SVT?

A 
- AV re entry tachycardia 
Or 
- pre excited AF 
OR 
-pre excited atrial flutter
85
Q

What is the most common rhythm disorder in someone with holiday heart syndrome?

A

SVT- AF

Stop drinking- resolves- advise against future binge drinking

86
Q

Define broad complex tachycardia

A

> 100bpm
Qrs >120ms.

NB if no clear qrs it is VF or asystole…

If in doubt treat as VT (most common cause incl torsade de pointe)

87
Q

What ECG criteria are in favour of VT?

A

1) marked left axis deviation
2) fusion beats or capture beats
3) AV dissociation- 25% or 2:1 or 3:1 AV block
4) brugada critera (can duck off)
5) positive qrs concordance in chest leads

88
Q

Treatment of stable VT

A

MONITOR and send investigations
High flow O2

  • amiodarone ivi

If this fails or arrest- DC Shock

After corrected- keep amiodarone as maintenance

Refractory cases- radiofrequency ventricular tachycardia ablation can be tried

89
Q

Treatment of ventricular fibrillation- pulse less

Or unstable VT

A

A synchronised DC shock

90
Q

Treatment of polymorphic stable VT

A 
(This is torsade de points) 
Give magnesium sulphate 
MONITOR 
If this fails/cardiac arrest 
DC Shock
91
Q

What is the most common post MI Arrhythmia?
What is the risk?
When do you intervene?

A

Ventricular extrasystoles (ectopics)
Risk- VF
Intervene if frequent (>10/min)

92
Q

Define AF

A

Chaotic irregular atrial rhythm at 300-600 bpm- AV node responding intermittently and you get an irregular ventricular rate

93
Q

With AF What does your CO drop by?

A

10-20% poor priming by the atria

94
Q

What proportion of elderly people have AF?

A

9%

95
Q

What are possible causes of AF?

A 
Low K+ 
Low Mg 
HF / ischemia 
MI 
HTN 
PE 
mitral valve disease 
Pneumonia 
Hyperthyroidism 
Caffeine
Alcohol 
Post operative 
Rare causes 
Cardiomyopathy 
Constructive pericarditis 
Sick sinus syndrome 
Lung cx 
Atrial myxoma
Endocarditis 
Haemochromatosis 
Sarcoidosis
96
Q

Who gets acute AF? (

A

Very ill

Haemodynamically unstable

97
Q

What is the treatment of acute AF?

A

O2
Find and treat cause
Cardioversion- iv sedation. 200j, 360j. 360j. Relapses are common

Therefore drug cardioversion is preferred. Amiodarone ivi or po for 1 week.
Can also use flecainide (strong negative inoptrope) NOT if WPW or IHD.

Can control ventricular rate: verapamil or bisoprolol

2nd line:
Digoxin or amiodarone

98
Q

What are the goals of treatment for chronic AF?

A

Rate control

Anticoagulation

99
Q

How do you rate control in AF?

A

1) b blocker or rate limiting CCB
2) if fails- add digoxin
3) if fails, consider amiodarone

100
Q

When do you need to rhythm control in AF?

What do you use?

A
  • symptomatic or CCF
  • younger
  • presenting for the 1st time with lone AF
  • AF from a corrected precipitant- eg low k or mg

First, do ECHO

Use to treat:
If no structural abnormality then flecainide
If structural abnormality use amiodarone

101
Q

What is the ‘pill in the pocket’ in people with paroxysmal AF?

A

Sotalol or flecainide PRN
ONLY GIVE IF
No past LV dysfunction
BP >100mmHg

102
Q

When do you anticoagulate with heparin in acute AF?

A

Use until full assessment of emboli risk is made

103
Q

When do you anticoagulate with warfarin in acute AF?

A 
Target INR 2-3 
If emboli risk is high 
-past ischemic stroke /TIA/emboli 
->\=75 years old 
-HTN
-diabeties 
-poor LV Function 
-evidence of valve disease 
- large left atrium size
104
Q

When do you not anticoagulate in acute AF?

A

If stable sinus rhythm has been restored and NO risk factors for emboli AND AF recurrence is unlikely

105
Q

What do you anticoagulate with in chronic AF?

A

Warfarin target INR 2-3

106
Q

What is CI to warfarin and have chronic AF?

A

Aspirin 300mg per day

107
Q

What is the risk of major bleed in person years for someone taking warfarin?

A
  • > 80 yo 13/100 person years

-

108
Q

What is dabigatran?

A

Direct thrombin inhibitor
Expensive but can be used as an alternative to warfarin
CI- severe liver/renal impairment.
Need to decrease dose if eGFR >50 avoid if >30

109
Q

What does the CHA2DS-VASc score measure?

A

Your risk of stroke if you have AF

110
Q

CHA2DS-VASc score what scores 1 point?

2points?

A 
1 point
HF 
Diabeties 
HTN 
Vascular disease 
Female 
>65 yo 
2 points 
>/=75 yo
Prior stroke
Prior TIA 
Piror thromboembolic event.
111
Q

CHA2DS-VASc score
What is your annual stroke risk of score is 2?
What score do you anticoagulate?

A

2.2%
>2 oral Anticoagulation
>1 if younger

112
Q

What does the CHADS2 score calculate?

A

Bleeding risk if being anti-coagulated

113
Q

Outline the CHADS2 score

A 
C chd
H  HTN (>140/90 or on meds treating it)
A age >75
D diabeties
S2 prior stroke or TIA or thromboembolism (2 points)

Rest are 1 pont each

114
Q

What is pacemaker syndrome?

A
  • happens in single chamber pacing
  • retrograde conduction to atria makes them contract during ventricular contraction
  • therefore get retrograde flow in pulmonary veins
  • results in decrease in CO, dyspnoea, palpitations, malaise, syncope
115
Q

Define systolic heart failure

A

EF

116
Q

Define diastolic heart failure

A

Ventricle can’t relax and fill properly- get increased filling pressures
EF is >50%
Causes- constrictive pericarditis, restrictive cardiomyopathy, tamponade, HTN

117
Q

Symptoms of L sides HF

A 
Dyspnoea
Poor exercise tolerance 
Fatigue 
Orthopnoea 
Paroxysmal nocturnal dyspnoea 
Noctural cough (-/+ pick frothy sputum) 
Wheeze 
Nocturia 
Cold peripheries 
Weight loss 
Muscle wasting
118
Q

Symptoms of R sides heart failure

A 
Peripheral oedema 
Ascities 
Nausea 
Anorexia 
Facial engirgement 
Pulsation in neck and face (tricuspid regurge) 
Epistaxis
119
Q

What criteria are used to diagnose congestive heart failure?

A

Framingham criteria
Need 2 major
Or
1 major and 1 minor

120
Q

What are the major and minor Framingham criteria for the diagnosis for CCF?

A

Major:

  • s3 gallop
  • distended neck veins
  • heptojugular relex
  • acute pulmonary oedema
  • weight loss (4.5kg in 5 days in response to treatment)
  • raised CVP
  • cardiomegaly
  • paraoxysmal Noctural dyspnoea
  • crepitation
Minor: 
Bilateral ankle oedema 
Tachycardia >120bpm
Dyspnoea on normal exertion 
Nocturnal cough 
Hepatomegaly 
Pleural effusion 
Decrease in vit capacity by 1/3rd from max recorded.?
121
Q

What is ezetimibe?

A

Inhibits the NPC1L1 transporter
Lowers cholesterol
Enhances actions of all statins

122
Q

What is sitosterol?

A

Stops cholesterol being released into the lumen.

Lowers cholesterol

123
Q

If someone has FH what is the main aims of treatment ?

A
  • screen family LDL-C mutation
  • put on statin irregardless of CVD risk
  • combo therapy may be needed to reduce LDL-C to
124
Q

What is the LBBB ECG criteria?

A

Qrs duration >/- 120ms
Broad, notched or slurred r waves in leads I, aVL, V5, V6
ST and T waves usually in opposite directions

125
Q

Other causes of ST Elevation that are not MI

A
  • acute pericarditis
  • massive PE (v1-v2 occasionally)
  • brugada (v1-v3 with RBBB morphology)
  • hyperkalaemia (v1-v2)
  • hypothermia
  • hypercalcaemia
126
Q

When do you use catheter ablation to treat AF?

A
  • drug treatment failed to control symptoms

- drug treatment is unsuitable

127
Q

What is pro arrhythmia?

A

People who have long QT Syndrome (congenital) can be triggered into Torsades de Pointes by many medications including quinidine.
Due to promotion of 1:1 conduction on AF- very treatment resistant once pro arrhythmia is established- so people with long QT Syn need to carry warning,

128
Q

What is HFREF?

A

Heart failure with reduced ejection fraction

Systolic failure
EF

129
Q

What are the compensatory mechanisms to improve cardiac function in HFREF

A
  • activation of SAS (sympathetic activation)
  • RAAS system
  • endothelin
  • AVP (vasopressin/antidiuretic hormone)
  • inflammatory cytokines
  • oxidative stress

Long term consequences:

  • hypertrophy
  • remodelling
  • apoptosis
130
Q

Equation for MAP (mean arterial pressure)

A

MAP=COxTPR

131
Q

What does ADH do in HFREF?

A

Made by hypothalamus and released by post pit. In response to central baro receptors but also helped by ATII and under control of a negative feedback loop.
Vasoconstriction, and water retention. increase MAP.
Long term ventricular remodelling

132
Q

What does ANP, c type natriuretic peptide and BNP do?

A

They counteract the vasoconstricting actions of other neuro hormones.
ANP, BNP: atria and ventricles- released during ventricular stress and stretch
CNP
In CNS
INHIBITS
renin, aldosterone, vasopressin

133
Q

What effect does TNFa, IL1, IL6 and IFa all have on the heart?

A

Negative inotropes- decrease contractility

High levels associated with worst clinical outcomes

134
Q

What is the most common cause of chronic heart failure ?

A

Ischemic cardiomyopathy post MI (24% of pts)

135
Q

What are the 4 conditions to diagnose HFpEF?

A
  • normal or mildly abnormal EF
  • evidence of abnormal LV relaxation, filling, diastolic distensibility, stiffness
  • symptoms of HF.
  • signs of HF
136
Q

What are the X ray findings for LVHF?

A 
Alveolar oedema (bat wings) 
Kerley B lines (interstitial oedema) 
Pleural effusion 
Cardiomegaly 
Prominent upper love vessels
137
Q

Outline the New York classification of HF

A

I: heart disease present, no undue dyspnoea from ordinary activity
II: comfortable at rest, dyspnoea on ordinary activity
III: less than ordinary activity levels causes dyspnoea which is limiting
IV: dyspnoea at rest all activity causes discomfort

138
Q

When do you use a B blocker and Ace inhibitor in HF?

A

If EF is

139
Q

What is important to remember when prescribing ace inhibitors?

A

1) cough is common
2) stop other nephrotoxic drugs - they mess up your kidneys
3) stop if K+ is >5.5mmol
4) stop other vasodilators if symptomatic hypotension

140
Q

What are contraindications for b blockers?

A

Asthma
NOT COPD
second or 3rd degree AV block in the absence of a permanent pacemaker

141
Q

Define stages of hypertension

A

Normotensive:
Stage 1:
Stage 2
Stage 3

142
Q

Define accelerated hypertension

A

Sudden increase in blood pressure over a baseline level that could if untreated pose a threat of damage to organs and tissues

  • severe HTN with associated grade 2-3 Keith-Wagner-baker retinopathy
  • aka hypertensive urgency
143
Q

Define benign intracranial hypertension.

A

Old term now called Idiopathic intracranial hypertension. Increased pressures in absence of tumour or other diseases

144
Q

Define pseudo hypertension

A

Seen in the elderly

Non compressibility artery syndrome due to calcified arteries leading to a falsely high reading

145
Q

What proportion of >60 have isolated systolic hypertension?

A

50%

Result of arteriosclerosis- stiffening of the arteries

146
Q

What is your increased risk of MI if have HTN?

CVA?

A

MI- double

CVA- triple

147
Q

What is the pathological hallmark of malignant/accelerated HTN?
What else might you get??

A

Fibroid necrosis

Retinal haemorrhages, exudates, papilloedems

148
Q

Mortality rate of untreated malignant HTN?

A

Untreated 90% die in 1 year

Treated 70% survive 5 years

149
Q

Who is malignant HTN more common in?

A

Younger afrocarribbean pts

150
Q

I idiopathic HTN There are multiple genetic polymorphisms implicated. Which ones in particular?

A

RAAS system- especially polymorphisms in the angiotensinogen locus and angiotensin receptor locus

151
Q

In idiopathic HTN what are the interacting environmental factors?

A 
Stress 
Obesity 
Smoking 
Physical inactivity
Heavy consumption of salt
152
Q

What are the end organ damage complications HTN can cause?

A
  • atherosclerosis
  • cardiac hyper trophy bad cardiac failure
  • aortic dissection
  • renal failure - nephroscerlosis (cortical surfaces have fine even granularity)
  • multi- infarct dementia- lacuna infarct (caudate and putamen supply)
153
Q

What can malignant HTN do to the lumen if the artery?

A

Hyper plastic arteriosclerosis (onion skinning) causes obliteration of the lumen.
Creates concentric laminations-
- smooth muscle cells with thickened re duplicated basement membranes
- accompanied by fibrinoid deposits and vessel wall necrosis (necrotizing arteriolitis) espec in the kidney

154
Q

Define malignant HTN

A

Severe HTN with associated grade 4 Keith Wagner baker retinopathy including papiloedema -/+ evidence of impending or progressive target/end organ dysfunction
-aka hypertensive emergency (crisis)
Mortality high - 90% 1 year if untreated

NB THIS AND ACCELERATED HTN DO NOT DEPENT ON ABSOLUTE LEVELS OF BP

155
Q

What type of end organ damage is associated with malignant HTN?

A 
Hypertensive encephalopathy 
Intracerebral haemorrhage 
Acute thrombotic stroke 
Ischemic heart disease (most common) - ACS and acute LVF with PO 
-aortic dissection
-eclampsia
156
Q

Withdrawal of which drug can cause malignant HTN?

A

Clonidine

157
Q

What drug do you not use with ivi GTN?

A

Tadalafil- huge vasodilatory effect and can cause fatal hypotension

158
Q

What don’t you use with labetalol?

A

Dilazem

159
Q

Side effect of iv hydralazine

A

Lupus like syndrome

160
Q

After MI when does lactate dehydrogenase rise and peak?

A

8-12 hrs

24-48

161
Q

What are the ECG changes for hypokalaemia ?

A

U waves
Small it absent t waves
Prolonged PR interval
Long QT

MBBS3 (6 decks)

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