CARDIO Flashcards
(161 cards)
1
Q
Non ST Elevation MI ACS
What are the ECG Changes?
A
- ST depression
- T wave inversion
- non specific/may be normal
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%
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
4
Q
What does myoglobin do in MI?
A
Rise within 1-4 hrs from onset of chest pain
Highly sensitive but not specific
5
Q
What proportion of deaths occur within 2 hours of the onset of symptoms in acute MI?
A
50%
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
7
Q
What proportion acute MI die before discharge?
A
7%
Worst prognosis if old, LV failure, ST changes
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
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
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
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
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
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
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
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
16
Q
Complication of MI
Mobitiz type 1 treatment
A
Does not need pacing unless poorly tolerated
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
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
19
Q
3 things that pre dispose to arrhythmias
A
Low K+
Hypoxia
Acidosis
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
21
Q
Complication of MI
Define non sustained VT
A
> =3 consecutive premature ventricular beats. HR 100bpm and lasting >30secs
If this happens
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
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
24
Q
What ejection fraction do you consider giving someone an implantable cardiac defib?
A
25
How do you measure R sided heart pressures?
Swan ganz catheter- guides fluid replacement
26
How does a RVF/ infarction present?
Low CO, raised JVP
27
How does pericarditis present?
What are the ECG changes?
What is the treatment?
Central chest pain relived by moving forward.
ECG- saddle shaped ST elevation
Treatment- NSAIDS and check ECHO for effusion
28
How does cardiac tamponade present?
Treatment
- low CO
- pulsus paradoxus
- raised JVP
- muffled HS
Treatment- pericardial aspiration for tempory relief then surgery
29
Complication of MI
How does mitral regurge present?
Pulmonary oedema
LVF
Consider valve replacement
30
Complication of MI.
| How does VSD present?
Pan systolic murmur
Raised JVP
HF
diagnose on echo
50% mortality in 1st week
Treatment- surgery
31
Complication of MI
| When do late malignant ventricular arrhythmias occur?
1-3weeks post MI
Avoid hypokalaemia
24hour ECG monitoring
32
Complication of MI
Dressler's syndrome- what is it?
When does it occur?
How do you treat it?
Recurrent pericarditis, pleural effusions, fever, anaemia, ESR raised.
Occurs 1-3 weeks post MI
treatment- NSAIDS or steroids if severe.
33
complications of MI
How do LV aneurysms present?
What does the ECG show?
- occurs late- 4-6 w post MI
- presents with LVF, angina, recurrent VT or systemic embolism
-ECG shows persistent ST elevation
34
Give 5 indications for a CABG
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
35
If pt has single vessel CAD and normal LV function, what is the best treatment option?
PCI
36
If pt has triple vessel disease and abnormal LV function what is the best treatment?
CABG
37
Positives and negatives of CABG
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
38
What is the life span of a vein graft?
50% close in 10 years
Low dose aspirin can help prevent this.
Internal mammary artery lasts longer but may cause chest wall numbess
39
After CABG
| What if still have angina?
- poor graft run off
- atheroma
- graft occlusion
Restart anti anginal drugs and consider angioplasty
40
After CABG
| Getting back to normal
Drive after 1 month
Mood, sex and intellectual problems are common- rehab helps.
Back to work 3 months
Aspirin 75mg/day lifelong
41
When preforming PCI must use injectable anticoagulant.
| What is preferred?
bivalirudin preferred. If not use enoxaparin -/+ GP II b/IIIa blocker.
42
Whet ECG changes would you get with RV infarct?
ST elevation in inferior leads ( II, III, aVF)
43
ECG Changes in LAD problem
Anterior leads
| C1-4
44
ECG changes if problem with circumflex
I, aVL, c5,c6
45
What is the ECG criteria for thromblysis?
-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.
46
What are the major contraindications for thrombolysis?
1) previous intracranial haemorrhage
2) aortic disscection
3) known incompressible puncture -
47
What are the relative contraindications for thrombolysis?
1) TIA180/110mmHg)
6) active peptic ulcer
7) infective endocarditis
48
What drug is used for thrombolysis?
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
49
What should you not use with verapamil??
B blocker- risk asysole
50
What O2 sats do you give low flow O2 to in MI?
90%
51
Who is high risk of death from NON ST elevation MI?
- >70
- previous MI
- hx of unstable angina
- ST Depression or wide spread t wave inversion.
- raised troponin
- poor LV function
- diabeties
52
What is the pathophysiology of MSTEMI?
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)
53
What is the pathophysiology of a STEMI?
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)
54
What is a vunerable plaque??
Large lipid core
Lots of inflammatory cells
Thin fibrous cap
55
What does the 300mg loading dose of aspirin do?
1) reduce CV Mortality
2) reduce reoccusion
3) reduce non fatal MI
4) in 40% reduction from unstable angina to MI
56
How do thienopyrides work?
| Examples
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.
57
Clopidogrel
| How many days do you need to withdraw before surgery?
5 days
58
Clopidogrel
| How long does it take to work
2-4 h
59
Clopidogrel
| How long is it's duration of effect?
3-10 days
60
Prasugrel
What is it?
How long is it onset of effect?
Irreversible
Thienopyride
30 mins
61
Prasugrel
What is it?
How long is the duration of it's effect?
Thienopyride
| 5-10 days
62
Prasugrel
What is it?
How long do you withdraw it before surgery?
Thienopyride
| 7 days
63
What is ticagrelor?
Triazolopyrimide
Anti platelet a bit like clopidogrel
Active drug takes 30 mins to work. And last 3-4 days
Withhold 5 days before surgery
64
Post PCI when can you drive?
1 week
65
What do nitrates do to help the heart?
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
ECG changes on acute MI
- 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
What valve problem can cause an arrhythmia?
Mitral valve
| Also pericarditis, myocarditis, cardiomyopathy, CAD, MI, LV aneurysm.
68
What meds can cause arrhythmias?
```
Digoxin
B2 agonists
L dopa
Tricyclics
Doxorubicin (cytotoxic)
```
Pneumonia
Caffeine
Alcohol
Smoking
69
What is sick sinus syndrome?
- 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
Define sinus tachycardia
Normal p wave followed by normal qrs >100bpm
| Qrs
71
Define SVT
P wave is absent or inverted after qrs
>100bpm
Qrs
72
Define atrial fibrillation
P wave is absent and irregular qrs
73
Define atrial flutter
Rate usually >300bpm
Giving flutter/saw tooth waves
Ventricular rate usually 150bpm (2:1 block)
74
Define Atrial tachycardia
Abnormally shaped p waves- outnumber qrs morphologies
75
Define multi focal atrial tachycardia
3 or more p waves per qrs
76
What is junctional tachycardia?
Rate 150-250 bpm
| P wave either buried in qrs complex or occurring after qrs complex
77
How do you manage narrow complex tachycardias?
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
When is adenosine for narrow complex tachycardias contraindicated?
Asthma
2/3rd degree heart block
Sino atrial node disease.
If taking dipyridamole (anti platelet)
Use smaller dose if transplanted heart,
79
If adenosine fails cardioverting SVT, what do you try next?
Verapamil
| NOT IF ON B BLOCKER
80
What can atrial tachycardia be due to!
Digoxin toxicity
81
When is multi focal atrial tachycardia more commonly seen?
-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
What rhythm can be treated with radio frequency ablation?
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
ECG findings for Wolfe parkinson white syndrome?
1) short pr interval
2) wide qrs (due to slurred upstroke/delta wave)
3) ST-T changes.
84
Why do pts with WPW Syndrome present with SVT?
```
- AV re entry tachycardia
Or
- pre excited AF
OR
-pre excited atrial flutter
```
85
What is the most common rhythm disorder in someone with holiday heart syndrome?
SVT- AF
| Stop drinking- resolves- advise against future binge drinking
86
Define broad complex tachycardia
>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
What ECG criteria are in favour of VT?
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
Treatment of stable VT
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
Treatment of ventricular fibrillation- pulse less
| Or unstable VT
A synchronised DC shock
90
Treatment of polymorphic stable VT
```
(This is torsade de points)
Give magnesium sulphate
MONITOR
If this fails/cardiac arrest
DC Shock
```
91
What is the most common post MI Arrhythmia?
What is the risk?
When do you intervene?
Ventricular extrasystoles (ectopics)
Risk- VF
Intervene if frequent (>10/min)
92
Define AF
Chaotic irregular atrial rhythm at 300-600 bpm- AV node responding intermittently and you get an irregular ventricular rate
93
With AF What does your CO drop by?
10-20% poor priming by the atria
94
What proportion of elderly people have AF?
9%
95
What are possible causes of AF?
```
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
Who gets acute AF? (
Very ill
| Haemodynamically unstable
97
What is the treatment of acute AF?
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
What are the goals of treatment for chronic AF?
Rate control
| Anticoagulation
99
How do you rate control in AF?
1) b blocker or rate limiting CCB
2) if fails- add digoxin
3) if fails, consider amiodarone
100
When do you need to rhythm control in AF?
| What do you use?
- 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
What is the 'pill in the pocket' in people with paroxysmal AF?
Sotalol or flecainide PRN
ONLY GIVE IF
No past LV dysfunction
BP >100mmHg
102
When do you anticoagulate with heparin in acute AF?
Use until full assessment of emboli risk is made
103
When do you anticoagulate with warfarin in acute AF?
```
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
When do you not anticoagulate in acute AF?
If stable sinus rhythm has been restored and NO risk factors for emboli AND AF recurrence is unlikely
105
What do you anticoagulate with in chronic AF?
Warfarin target INR 2-3
106
What is CI to warfarin and have chronic AF?
Aspirin 300mg per day
107
What is the risk of major bleed in person years for someone taking warfarin?
- >80 yo 13/100 person years
| -
108
What is dabigatran?
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
What does the CHA2DS-VASc score measure?
Your risk of stroke if you have AF
110
CHA2DS-VASc score what scores 1 point?
| 2points?
```
1 point
HF
Diabeties
HTN
Vascular disease
Female
>65 yo
```
```
2 points
>/=75 yo
Prior stroke
Prior TIA
Piror thromboembolic event.
```
111
CHA2DS-VASc score
What is your annual stroke risk of score is 2?
What score do you anticoagulate?
2.2%
>2 oral Anticoagulation
>1 if younger
112
What does the CHADS2 score calculate?
Bleeding risk if being anti-coagulated
113
Outline the CHADS2 score
```
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
What is pacemaker syndrome?
- 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
Define systolic heart failure
EF
116
Define diastolic heart failure
Ventricle can't relax and fill properly- get increased filling pressures
EF is >50%
Causes- constrictive pericarditis, restrictive cardiomyopathy, tamponade, HTN
117
Symptoms of L sides HF
```
Dyspnoea
Poor exercise tolerance
Fatigue
Orthopnoea
Paroxysmal nocturnal dyspnoea
Noctural cough (-/+ pick frothy sputum)
Wheeze
Nocturia
Cold peripheries
Weight loss
Muscle wasting
```
118
Symptoms of R sides heart failure
```
Peripheral oedema
Ascities
Nausea
Anorexia
Facial engirgement
Pulsation in neck and face (tricuspid regurge)
Epistaxis
```
119
What criteria are used to diagnose congestive heart failure?
Framingham criteria
Need 2 major
Or
1 major and 1 minor
120
What are the major and minor Framingham criteria for the diagnosis for CCF?
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
What is ezetimibe?
Inhibits the NPC1L1 transporter
Lowers cholesterol
Enhances actions of all statins
122
What is sitosterol?
Stops cholesterol being released into the lumen.
| Lowers cholesterol
123
If someone has FH what is the main aims of treatment ?
- screen family LDL-C mutation
- put on statin irregardless of CVD risk
- combo therapy may be needed to reduce LDL-C to
124
What is the LBBB ECG criteria?
Qrs duration >/- 120ms
Broad, notched or slurred r waves in leads I, aVL, V5, V6
ST and T waves usually in opposite directions
125
Other causes of ST Elevation that are not MI
- acute pericarditis
- massive PE (v1-v2 occasionally)
- brugada (v1-v3 with RBBB morphology)
- hyperkalaemia (v1-v2)
- hypothermia
- hypercalcaemia
126
When do you use catheter ablation to treat AF?
- drug treatment failed to control symptoms
| - drug treatment is unsuitable
127
What is pro arrhythmia?
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
What is HFREF?
Heart failure with reduced ejection fraction
Systolic failure
EF
129
What are the compensatory mechanisms to improve cardiac function in HFREF
- activation of SAS (sympathetic activation)
- RAAS system
- endothelin
- AVP (vasopressin/antidiuretic hormone)
- inflammatory cytokines
- oxidative stress
Long term consequences:
- hypertrophy
- remodelling
- apoptosis
130
Equation for MAP (mean arterial pressure)
MAP=COxTPR
131
What does ADH do in HFREF?
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
What does ANP, c type natriuretic peptide and BNP do?
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
What effect does TNFa, IL1, IL6 and IFa all have on the heart?
Negative inotropes- decrease contractility
| High levels associated with worst clinical outcomes
134
What is the most common cause of chronic heart failure ?
Ischemic cardiomyopathy post MI (24% of pts)
135
What are the 4 conditions to diagnose HFpEF?
- normal or mildly abnormal EF
- evidence of abnormal LV relaxation, filling, diastolic distensibility, stiffness
- symptoms of HF.
- signs of HF
136
What are the X ray findings for LVHF?
```
Alveolar oedema (bat wings)
Kerley B lines (interstitial oedema)
Pleural effusion
Cardiomegaly
Prominent upper love vessels
```
137
Outline the New York classification of HF
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
When do you use a B blocker and Ace inhibitor in HF?
If EF is
139
What is important to remember when prescribing ace inhibitors?
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
What are contraindications for b blockers?
Asthma
NOT COPD
second or 3rd degree AV block in the absence of a permanent pacemaker
141
Define stages of hypertension
Normotensive:
Stage 1:
Stage 2
Stage 3
142
Define accelerated hypertension
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
Define benign intracranial hypertension.
Old term now called Idiopathic intracranial hypertension. Increased pressures in absence of tumour or other diseases
144
Define pseudo hypertension
Seen in the elderly
| Non compressibility artery syndrome due to calcified arteries leading to a falsely high reading
145
What proportion of >60 have isolated systolic hypertension?
50%
| Result of arteriosclerosis- stiffening of the arteries
146
What is your increased risk of MI if have HTN?
| CVA?
MI- double
| CVA- triple
147
What is the pathological hallmark of malignant/accelerated HTN?
What else might you get??
Fibroid necrosis
Retinal haemorrhages, exudates, papilloedems
148
Mortality rate of untreated malignant HTN?
Untreated 90% die in 1 year
| Treated 70% survive 5 years
149
Who is malignant HTN more common in?
Younger afrocarribbean pts
150
I idiopathic HTN There are multiple genetic polymorphisms implicated. Which ones in particular?
RAAS system- especially polymorphisms in the angiotensinogen locus and angiotensin receptor locus
151
In idiopathic HTN what are the interacting environmental factors?
```
Stress
Obesity
Smoking
Physical inactivity
Heavy consumption of salt
```
152
What are the end organ damage complications HTN can cause?
- 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
What can malignant HTN do to the lumen if the artery?
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
Define malignant HTN
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
What type of end organ damage is associated with malignant HTN?
```
Hypertensive encephalopathy
Intracerebral haemorrhage
Acute thrombotic stroke
Ischemic heart disease (most common) - ACS and acute LVF with PO
-aortic dissection
-eclampsia
```
156
Withdrawal of which drug can cause malignant HTN?
Clonidine
157
What drug do you not use with ivi GTN?
Tadalafil- huge vasodilatory effect and can cause fatal hypotension
158
What don't you use with labetalol?
Dilazem
159
Side effect of iv hydralazine
Lupus like syndrome
160
After MI when does lactate dehydrogenase rise and peak?
8-12 hrs
| 24-48
161
What are the ECG changes for hypokalaemia ?
U waves
Small it absent t waves
Prolonged PR interval
Long QT
