Ischaemic Heart Disease (Clinical) Flashcards
What is prinzmetal’s angina
Spasm in the artery causing a functional obstruction.
Unlike classical angina, which is triggered by exertion or exercise, commonly occurs in individuals at rest or even asleep. It is caused by vasospasm, a narrowing of the coronary arteries due to contraction of the smooth muscle tissue in the vessel walls. This contrasts with classical angina which is due the permanent occlusion of these vessels by atherosclerosis (i.e. buildup of fatty plaque and hardening of the arteries).[2]
A 60-year-old woman was awakened early one morning with extreme chest discomfort
radiating to both her arms. She felt weak and light-headed and she fainted when she tried to
get up. On admission to hospital, her blood pressure heart rate and ECG were normal. She
was a cigarette smoker with no other risk factors. Continuous ECG monitoring was
performed. She experienced several further episodes of nocturnal chest pain, which were
accompanied by transient ST-segment elevation and, in one case, polymorphic ventricular
tachycardia also occurred. A coronary angiogram showed normal coronary arteries.
However, infusion of acetylcholine (50 μg) induced multifocal hyper-reactive
vasoconstriction (spasm) in some coronary segments, but mild vasodilation elsewhere. The
spasm was promptly resolved by intracoronary infusion of nitroglycerine. Variant angina due
to vasospasm was diagnosed and treatment with nifedipine was started.
Explain the nocturnal chest discomfort.
A night, the fluid gets reabsobed into the circulation, which gives the heart moreto deal with (distribution of blood when lying down)
- PNS active at rest/at night (-> Ach -> Vasopasm)
- Anginal pain and work of breathing increase (pulmonary congestion)
- Symptoms worse when lying since
- Increased venous return leads to increased RV and LV filling wrt standing)
- Greater LV filling - greater LV load and increased O2 demand
- Impaired IV function -> greater pulmonary congestion
A 60-year-old woman was awakened early one morning with extreme chest discomfort
radiating to both her arms. She felt weak and light-headed and she fainted when she tried to
get up. On admission to hospital, her blood pressure heart rate and ECG were normal. She
was a cigarette smoker with no other risk factors. Continuous ECG monitoring was
performed. She experienced several further episodes of nocturnal chest pain, which were
accompanied by transient ST-segment elevation and, in one case, polymorphic ventricular
tachycardia also occurred. A coronary angiogram showed normal coronary arteries.
However, infusion of acetylcholine (50 μg) induced multifocal hyper-reactive
vasoconstriction (spasm) in some coronary segments, but mild vasodilation elsewhere. The
spasm was promptly resolved by intracoronary infusion of nitroglycerine. Variant angina due
to vasospasm was diagnosed and treatment with nifedipine was started.
Why did the woman faint when she tried to get up?
When you’re getting up, there’s less blood, less preload (postural hypotension)
Postural hypotension
- Venous return reduced when standing (gravity, dsitends veins)
- Reduces ‘preload’
- Reduces CO
- Leads to reduced MAP
- Ledas to reduced cerebral perfusion (faint)
- Leads to reduced MAP
A 60-year-old woman was awakened early one morning with extreme chest discomfort
radiating to both her arms. She felt weak and light-headed and she fainted when she tried to
get up. On admission to hospital, her blood pressure heart rate and ECG were normal. She
was a cigarette smoker with no other risk factors. Continuous ECG monitoring was
performed. She experienced several further episodes of nocturnal chest pain, which were
accompanied by transient ST-segment elevation and, in one case, polymorphic ventricular
tachycardia also occurred. A coronary angiogram showed normal coronary arteries.
However, infusion of acetylcholine (50 μg) induced multifocal hyper-reactive
vasoconstriction (spasm) in some coronary segments, but mild vasodilation elsewhere. The
spasm was promptly resolved by intracoronary infusion of nitroglycerine. Variant angina due
to vasospasm was diagnosed and treatment with nifedipine was started.
_Give a possible reason why acetylcholine provoked vasospasm in some coronary
segments and explain why this was reversed by nitroglycerine_
Normal endothelium
- ACh binds to M3 receptors on endothelial cells which leads to the release of NO = relaxation of SM
Dysfunction/absent endothelium:
- ACh acts directly through M3 and M2 receptors of VSM activating Gq and Gi pathways leading to increased intracellular Ca2+ levels and increased interaction between myosin and actin (as a result of increased phosphorylation of myosin light cahins) and thus contraction.
Nitroglycerine increases NO levels- acts directly on VSM (mitochondrial aldehyde dehydrogenase responsible for the conversion)
A 60-year-old woman was awakened early one morning with extreme chest discomfort
radiating to both her arms. She felt weak and light-headed and she fainted when she tried to
get up. On admission to hospital, her blood pressure heart rate and ECG were normal. She
was a cigarette smoker with no other risk factors. Continuous ECG monitoring was
performed. She experienced several further episodes of nocturnal chest pain, which were
accompanied by transient ST-segment elevation and, in one case, polymorphic ventricular
tachycardia also occurred. A coronary angiogram showed normal coronary arteries.
However, infusion of acetylcholine (50 μg) induced multifocal hyper-reactive
vasoconstriction (spasm) in some coronary segments, but mild vasodilation elsewhere. The
spasm was promptly resolved by intracoronary infusion of nitroglycerine. Variant angina due
to vasospasm was diagnosed and treatment with nifedipine was started.
Explain the S-T segment elevation in her ECG during the angina attacks.
If you’ve got an area of damage, it may have a different electrical potential ***FINiSH((
Action potentail magnitude and duration reduced in schaemic region
Systloic or diastolic injury current
Refelcted in ST segmenet election in ECG leads “addressing” that region.
A 60-year-old woman was awakened early one morning with extreme chest discomfort
radiating to both her arms. She felt weak and light-headed and she fainted when she tried to
get up. On admission to hospital, her blood pressure heart rate and ECG were normal. She
was a cigarette smoker with no other risk factors. Continuous ECG monitoring was
performed. She experienced several further episodes of nocturnal chest pain, which were
accompanied by transient ST-segment elevation and, in one case, polymorphic ventricular
tachycardia also occurred. A coronary angiogram showed normal coronary arteries.
However, infusion of acetylcholine (50 μg) induced multifocal hyper-reactive
vasoconstriction (spasm) in some coronary segments, but mild vasodilation elsewhere. The
spasm was promptly resolved by intracoronary infusion of nitroglycerine. Variant angina due
to vasospasm was diagnosed and treatment with nifedipine was started.
_Explain what is meant by the term polymorphic ventricular tachycardia. Outline key
factors that may have contributed to ventricular tachycardia in this case. Why is the
tachycardia polymorphic?_
The arrhythmia is moving around. = polymorphic
- Often polymorphic arrhythmia is triggered by ischaemia*
- Often monomorphic is assicated with scarring*
Reentrant tachycardia requires
- trigger -DADs
- Unidirectional propagation
- A relatively short wavelength (refractory period * conduction velocity)
These are all probable in schaemia in where there is
- Reduced ATP and thus CA2+ ATPase activity -> Increased Ca2+i -> DADs
- Spatial inhomogenities in electrical properites
- Shortened AP duration as a result of hyperkaelaemia and activation of IK(ATP)
- Slow propataion due to partial depoalrsation (hyperkaelaemia), inactivation of Na2+ channels and gap junction uncoupling.
A 56 year old woman with no previous history of angina pectoris, experiences chest pain with
moderate exercise. She is found to be anaemic and has partial narrowing of her left anterior
descending coronary artery. The following data are also obtained at rest in clinical tests:
After treatment to correct haemoglobin levels, the patient no longer experiences angina
pectoris with exercise
Explain why someone with Anaemia will have elevated cardiac output and heart rate at rest - Mechanisms
Oxygen supply is reduced in aneamia
- V(dot) oxtgen = Q x Hb (SaO2-SvO2)
- Reduced Hb, therefore to maintain O2 supply, people increase cardiac output
This woman is anaemic therefore she needs to increase CO (SV and HR)
- Total peripheral resistance reduced
- Local control (vasodilator metabolites)
- Low viscosity (anaemia)
- Increased ANS activity (to maintain BP and flow)
- Increased HR and inotropic state
- Increased CO
- Increased HR and inotropic state
A 56 year old woman with no previous history of angina pectoris, experiences chest pain with
moderate exercise. She is found to be anaemic and has partial narrowing of her left anterior
descending coronary artery. The following data are also obtained at rest in clinical tests:
After treatment to correct haemoglobin levels, the patient no longer experiences angina
pectoris with exercise
Why is the patient’s pulse pressure high?
Pulse pressure = Systolic-Diastolic
Large pulse pressure as a result of the peripheral vasodilation (lowered total peripheral resistance)
- leading to rapid runoff, and lowered diastolic pressure
This patient has dilated peripheries- therefore she has hyperdynamic pulse.
A 56 year old woman with no previous history of angina pectoris, experiences chest pain with
moderate exercise. She is found to be anaemic and has partial narrowing of her left anterior
descending coronary artery. The following data are also obtained at rest in clinical tests:
After treatment to correct haemoglobin levels, the patient no longer experiences angina
pectoris with exercise
Explain the elevated resting coronary blood flow in this patient. Reasons
Increased myocardial demand requires icnreased coronary flow
Anaemia-> extra 2x coronary flow required for enough O2 delivery at rest
When HR increases and increases inotropic state, int his case because of reqirement for increased CO it leads to further increase in O2 requirement.
A 56 year old woman with no previous history of angina pectoris, experiences chest pain with
moderate exercise. She is found to be anaemic and has partial narrowing of her left anterior
descending coronary artery. The following data are also obtained at rest in clinical tests:
After treatment to correct haemoglobin levels, the patient no longer experiences angina
pectoris with exercise
Explain Angina pectoris is experienced with moderate exercise prior to treatment.
- Patient’s coronary reserve capcity substantially utilised at rest (anaemia)
- Exercise futther increases demands described above
- Coronary flow not sufficient to deliver enough O2 to myocardium
- Demand/supply mismatch first occurs in regions distal to narrowed LAD
- Angina symtpoms arise from LAD territory
A 56 year old woman with no previous history of angina pectoris, experiences chest pain with
moderate exercise. She is found to be anaemic and has partial narrowing of her left anterior
descending coronary artery. The following data are also obtained at rest in clinical tests:
After treatment to correct haemoglobin levels, the patient no longer experiences angina
pectoris with exercise
Explain why Exercise angina is relieved after treatment for anaemia.
- Restoration of Hb levels increase coronary reserve
- Even with narrowed vessel
- Is now enough coronary flow for angia-free moderate exercise.
A 56 year old woman with no previous history of angina pectoris, experiences chest pain with
moderate exercise. She is found to be anaemic and has partial narrowing of her left anterior
descending coronary artery. The following data are also obtained at rest in clinical tests:
After treatment to correct haemoglobin levels, the patient no longer experiences angina
pectoris with exercise
_What do these data indicate about the risk associated with coronary artery narrowing in
this patient._
- Underperfusion of myocardium when there are other compromising factors
- Has narrowed LAD
- Monitor for progression (?Development of exercise angina)
Note: can get angina with anaemia, without coronary narrowing.
A 58 year-old obese, hypertensive male air traffic controller has a history of dyspepsia, which
has been treated with antacids and proton pump inhibitors. Recently, he has experienced
chest pain on exertion that has been relieved by rest and antacids. These discomforts are a
heavy sensation centrally and anteriorly with radiation to the arms and jaw. On occasion,
there is some belching and acid wash feelings in the back of his throat, more often with a tight
squeezing sensation that may last for up to half an hour. There is a family history of
premature heart disease and this man’s smoking history and dyslipidaemia was noted in an
insurance medical examination.
What are the major symptomatic problems?
- Chest pain on exertion (nature, distribution)
- Dyspepsia
A 58 year-old obese, hypertensive male air traffic controller has a history of dyspepsia, which
has been treated with antacids and proton pump inhibitors. Recently, he has experienced
chest pain on exertion that has been relieved by rest and antacids. These discomforts are a
heavy sensation centrally and anteriorly with radiation to the arms and jaw. On occasion,
there is some belching and acid wash feelings in the back of his throat, more often with a tight
squeezing sensation that may last for up to half an hour. There is a family history of
premature heart disease and this man’s smoking history and dyslipidaemia was noted in an
insurance medical examination.
What are the key cardiac risk factors?
- Hypertension
- Smoking
- Dyslipidaemia
- Family history
- Male + Age
- ?Stress at work
His GP prescribes aspirin, metoprolol and a nitrate spray (to be taken for the discomforts).
This treatment markedly reduces the incidence of chest pain with exertion. The nitrate spray
typically relieves chest pain within seconds when it does occur and is also useful for the
longer ‘indigestion’ discomforts. However, the patient experiences a number of new
symptoms after starting the metoprolol. These include fatigue, reduced exercise tolerance and
sleep disturbance from nightmares.
- *Explain how the balance of myocardial oxygen supply and demand is altered with
exercise. **
Oxygen demand
- Inotropic state?
- Heart rate?
Oxtgen supply
- Narrowing BP- reduce Q?
