Lec 14- Stroke and ischemic hearth disease Flashcards

1
Q

Definition of stroke and TIA

A
  • Insufficient blood to the brain due to a block (ischemic) or rupture of arteries (haemorrhagic)
  • TIA- transient ischemic attack (temporary interruption)
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2
Q

Those at risk from stroke

A
  • HTN
  • Diabetes
  • AF
  • High cholesterol
  • Smokers
  • High alcohol intake
  • Positive family history
  • Often associated with older people 65+, but 25% occur in younger people
  • Ethnicity also a risk factor: south Asian; African or Caribbean
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3
Q

Symptoms of stroke

A
  • Sudden numbness or weakness of the face, arm or leg, especially if it occurs on one side of the body
  • Sudden confusion, trouble speaking or understanding
  • Sudden trouble seeing in one or both eyes, double vision
  • Sudden trouble walking, dizziness, loss of balance or coordination
  • Sudden severe headache
  • F.A.S.T
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4
Q

Diagnosis and treatment of stroke (If ischemic)

A

-Diagnosis through brain imaging (CT scan) –> urgency dependant on presentation
IF ISCHEMIC:
-Alteplase therapy (if within 4.5 hours of stroke)
-Mechanical clot removal
-Decompressive hemicraniectomy (middle cerebral artery infarction)
-Immediately start anti-platelet therapy
AFTER: SALT assessment, stroke rehab and statin therapy

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5
Q

Treatment of stoke if Haemorrhagic

A

-Referal to neurology
-Surgery or conservative management depending on size of bleed and predisposing factors
AFTER: SALT assessment, stroke rehab and statin therapy

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6
Q

Monitoring following acute stroke

A
  • Swallowing reflex
  • O2 sat
  • BM’s
  • BP
  • GCS
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7
Q

Angina

A
  • The pain of angina is variously described as tightness and gripping sensation in the chest
  • Pain may also be described in arm, neck, jaw, ear
  • Symptom not a disease- usually due to underlying atherosclerosis
  • Often but not always associated with exertional breathlessness
  • Need to distinguish from non-cardiac causes of chest pain e.g. GI-reflux, psychological pain
  • Brought on by exertion and stress
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8
Q

Prevalence of angina

A
  • 1.5 million sufferers in UK
  • Considered to affect 9% of males 55-64 and 5% of females. Age 65-74 14% male and 8% female
  • 40-50% of angina patients have silent angina: estimated that 60-70% of all ischaemic episodes are silent
  • Diabetics are most likely to have silent angina
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9
Q

Cardiac O2 supply and demand

A
  • O2 supply: oxygenation of the blood + blood flow (microvasculature is autoregulated)
  • O2 demand: ventricular wall tension + HR+ contractility (increased by sympathetic B-stimulation
  • Double product = HR x SBP (demand)
  • NB- triple product = aortic pressure x HR x ejection time
  • NB- increase in ventricular wall tension and marked increases HR may reduce blood flow
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10
Q

Diastolic crunch

A
  • Most coronary flow occurs during diastole
  • Sub-endocardial regions receive least flow
  • Sub-endocardial perfusion pressure = diastolic BP (DBP) - ventricular end diastolic pressure (VEDP)
  • Pain is caused by high pressure during diastole
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11
Q

Classification of angina

A

ANGINA PECTORIS: (exertional angina)- angina of effort and or emotion
-Most common form
-the onset of pain is predictable (usually stress or exercise)
UNSTABLE ANGINA: ‘intermediate syndrome’ due to the breakup of unstable plaques causing embolism or thrombosis. may precede AMI
-Symptoms are more severe and last longer
-Symptoms may occur at rest; may also involve arterial spams
-Symptoms may be more frequent

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12
Q

Classification of angina (prinzmetals angina)

A

VARIANT ANGINA

  • Caused by spasm of epicardial coronary arteries due- to electrical instability associated with arterial tone (in 25% of cases AT is not present)
  • Varient angina can occur at rest or at night
  • High incidence among cocaine users
  • Arterial spasm is also likely if angina is variable threshold
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13
Q

Classification of angina (prinzmetals angina)

A

VARIANT ANGINA

  • Caused by spasm of epicardial coronary arteries due- to electrical instability associated with arterial tone (in 25% of cases AT is not present)
  • Variant angina can occur at rest or at night
  • High incidence among cocaine users
  • Arterial spasm is also likely if angina is variable threshold
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14
Q

Glyceryl Trinitrate (GTN)

A

Mode of action is due to liberation of NO, activation of guanyl cyclase and increased levels of c-GMP:

  • Enzymatic conversion to NO involving thiols
  • Ineffective if injected into coronary arteries
  • Effective if administered systematically
  • Sublingual administration
  • Treatment of angina attacks
  • S/E: headache, hypotension
  • Recurring pain after 2 administrations= hospital
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15
Q

Other nitrate based therapies

A

ORAL
-Isosorbide dinitrate active SL and orally
-Isosorbide and dinitrate are usually modified release preps
-Tolerance does occur and is clinically significant- incorporate nitrate free period
-Normal preps of ISMN use BD or TDS
-MR preps of ISMN OD and ISDN use BD or TDS
TOPICAL
-Patched used for once daily application, usually when oral route unavailable
IV
-Emergency reduction of BP or ischemic pain

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16
Q

BB (beta blocker) regular therapy

A

-Drugs of choice for regular symptom control
-Trials show no other agent better relief when given in monotherapy
MODE OF ACTION
+Decrease HR and contractility
+Decrease O2 demand
+Decrease SBP. Most effective during exercise
+May decrease mortality
-Care when prescribing in asthma/COPD
-Care with LV dysfunction- start low
-If patient has COPD or asthma, this will cause bronchoconstriction

17
Q

BB- disadvantage

A
  • Increased duration of diastole may increase VEDV (an effect that may be reversed by nitrates; BB also will prevent the reflex tachycardia of nitrates or the dihydropyridine calcium entry blocker)
  • May exacerbate arterial spasm
  • They shouldn’t be used in combination with cardio-depressant calcium entry blockers or if signs of LV dysfunction
  • Acute withdrawal can precipitate increased coronary events- avoid
18
Q

Calcium entry blockers

A

ARTERIOSELECTIVE e.g. nifedipine, nicardipine
-Dilate peripheral arteries and arterioles; decreased afterload
-also some dilation of coronary arteries (cf nitrates)
-Risk of reflex tachycardia- less than other vasodilation
CARDIOSELECTIVE e.g. verapamil
-Reduction in HR and contractility (c.f. BB)
-Little or no demonstrable effect on veins (preload)
-Affect the heart and arterioles e.g. diltiazem
-No tachycardia because of -ve chronotropic action
-Verapamil and diltiazem may be used with nitrates, but not usually with BB

19
Q

Use of CEBs

A

ANGINA PECTORIS
-Verapamil and Diltiazem; may be used as monotherapy reducing HR, contractility and afterload (should not normally be combined with BB-WHY?)
Nifedipine and nicardipine; less useful as monotherapy because of reflex tachycardia. (therefore ideal candidates for combination with BB). These agents (particularly nicardipine) may also have beneficial effects if coronary vasospasm is suspected
VARIANT ANGINA
-Drugs of choice for this condition

20
Q

Use of CEBs

A

ANGINA PECTORIS
-Verapamil and Diltiazem; may be used as monotherapy reducing HR, contractility and afterload (should not normally be combined with BB-WHY?)
Nifedipine and nicardipine; less useful as monotherapy because of reflex tachycardia. (therefore ideal candidates for combination with BB). These agents (particularly nicardipine) may also have beneficial effects if coronary vasospasm is suspected
VARIANT ANGINA
-Drugs of choice for this condition

21
Q

Nicorandil- 2nd line

A
  • K+ channel opener and NO donor
  • Dilates arteries and veins (NO)
  • Also dilates arterioles
  • Not suitable if LV dysfunction or hypotension
  • Trial evidence showed effective as add-on therapy
  • If patient doesn’t tolerate nitrates- will probably not tolerate nicorandil (due to mechanism of action)
  • USE: Not currently a first line agent
22
Q

Ivabradine- 2nd line

A
  • Blocks If (pacemaker) current in SA pacemaker cells- contributes to depolarization prior to Apd
  • Reduces HR and so cardiac work
  • Don’t use for angina if HR <60/min
  • Patients will actually feel better on this agent- not just reduction in attacks
  • Side effects: bradycardia; heart block; visual disturbance (phosphenes and blurred vision).range of hypersensitivity reactions possible
  • Use: not currently 1st line agent
23
Q

Ranolazine- 2nd line

A
  • Inhibits the late I(Na) in myocardial cells during systole which is enhanced in ischemia
  • Improves exercise tolerance, reduced angina attack frequency and use of GTN
  • Useful for patients where low BP contra-indicated titration of other agents
  • Side effects: dizziness; nausea; constipation
  • Uses: not currently 1st line agent
24
Q

Choice of drug regimen- monitor symptoms and exercise tolerance

A

-<2 attacks/week: GTN (sublingual)
->2 attacks/week: Add BB; low dose if LV dysfunction (start low rise slow)
OR CEB. (note verapamil and diltiazem CI if LV dysfunction
-If BB or CEB not effective alone then combine BB and DHP CEB (NOT verapamil or diltiazem)
-If BB or CEB contra-indicated one of the 2nd line agents can be used as monotherapy or add-on therapy
-Try to control on 2 agents- offer 3rd agent if not controlled on 2 agents or awaiting revascularisation or revascularisation not appropriate

25
Q

Combination therapy

A
  • Rationale different modes of action:
  • Nitrates reduced preload/increase collateral flow
  • BB reduce contractility and O2 demand
  • Ca2+ entry blockers reduce afterload
  • All 3 theoretical benefit (little evidence in practise)
  • 2ndary prevention: aspirin 75mg OD; ACEI if diabetic; Statin (atorvastatin 20mg OD); treatment of HTN
26
Q

Advice

A

ADVICE TO REDUCE CARDIOVASCULAR RISK
+Stop smoking
+reduce weight
+Controlled exercise programme
+Stress/excitement avoidance (watching football); take things easier in the morning
+Avoid sympathomimetics (pseudoephedrine)
-Attention to other risks factors (hypertension; hyperlipidaemia)
-Structured/supervised exercise programme
-Drugs should be used prophylactically

27
Q

Surgical intervention: CABG and PCI

A

-For all patient consider and particularly when symptoms are not satisfactorily controlled
-PCI: Percutaneous Coronary Intervention; feed cannula back from the femoral radial artery. Balloon angioplasty and stenting
Preferred over CABG as minimally invasive and less risk of complications
See video link on atherosclerosis
-CABG: Coronary Artery Bypass Graft- single, double, triple, quadruple.
+Would need angiogram to access
+Not all patients candidates for surgery (3-6 hrs; open chest; bypass machine)
+Large number of possible complications including kidney failure; AF; Blood clots

28
Q

Acute Coronary Syndrome

A
  • Encompass a range of conditions- unstable angina; MI with or without ST-segment elevation
  • Unstable angina and NSTEMI both involve atheromatous plaque rupture. Unstable angina doesn’t show evidence of myocardial cell necrosis
29
Q

Prognosis of AMI

A
  • Prognosis is related to severity of disease not symptoms
  • Mortality for angina pectoris is 4% (20% for unstable)
  • Angina is caused when myocardial O2 demands exceed myocardial O2 supply The resting heart extracts 2 to 3 times as much O2 as other tissues- very dependant on increasing flow to increase supply
  • Pain for >30 minutes, usually indicates AMI
  • Pain relieved by GTN is usually angina
  • Diagnosis: First Line is angiogram; 2nd line is non-invasive, stress echo, myocardial perfusion scan
30
Q

GTN-Actions

A

-Preferential ventilation: reduce preload and improves subendocardial perfusion (Reduced venous return reduces CO and BP)
-Also dilate epicardial coronary arteries (even if stenosed)
+No interference with metabolic autoregulation- no steal
+There is a favourable re-distribution of flow- dilation of collateral vessels
+This ability to dilate epicardial arteries is of use if spasm is suspected
-Low dose may reduce after load (arterial). High doses cause reflex tachycardia
+Increasing O2 demands
+A fall in diastolic BP may reduce subendocardial perfusion