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2 - Diseases Of The Human System > CV Medicine - 2 > Flashcards

CV Medicine - 2 Flashcards

1
Q

blood vessel narrowing VS blood vessel occlusion

A

Blood vessel narrowing
* ischaemia developing in the tissues supplied by the affected blood vessel causing cramp felt as pain
* over many years specialised cardiac tissue will become fibrotic and muscle tissue will reduce

Blood vessel occlusion
* no oxygen delivery - tissue death
* more severe pain
* loss of function of tissue

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2
Q

Where in the vessels does atherosclerosis occur?

A

occurs at areas where there is turbulent bloodflow i.e. areas with increased stress

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3
Q

At what time does permanent damage occur if there is total occlusion?

A

reversible <20 min
permanent >20 min

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4
Q

What are the 3 main forms of acute ischaemic events affecting the heart?

A

atherosclerosis with blood clot
atherosclerosis
spasm

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5
Q

What are the characteristics of stable angina?

A

pain develops where there is increased demand in the setting of a stable atherosclerotic plaque.
vessel is unable to dilate enough to allow adequate blood flow to meet the myocardial demand
mostly due to exercise
lactic acidosis

normal troponin levels and ECG

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6
Q

What are the characteristics of unstable angina?

A

plaque ruptures and a thrombus forms around ruptured plaque causing partial occlusion of the vessel. angina pain occurs at rest or progresses rapidly over a short period of time
can happen at any time i.e. sitting
troponin levels are normal
ECG can show inverted T waves, ST depresssion or just normal
no cardiac tissue death but ischaemia

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7
Q

What are the characteristics of NSTEMI?

A

non-elevated st

during an nstemi, the plaque rupture and thrombus formation causes partial occlusion to the vessel that results in injury and infarct to the subendocardial myocardium (damage has happened to heart muscle)
troponion level is elevated
ECG can show inverted T waves, ST depression or normal

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8
Q

What are the characteristics of STEMI?

A

complete occlusion of the blood vessel lumen, resulting in entire wall (transmural0 injury and infarct to myocardium which is reflected by ECG changes and elevated troponins
ECG shows hyperacute T waves or ST elevation

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9
Q

What are the steps to diagnosing ACS?

A

History - (PMH may show patient has has central crushing chest pain)
ECG findings (STEMI, NSTEMI)
Biomarkers (troponin)

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10
Q

When testing troponin what is recommened?

A

tested on admission then 24 hours later because troponin levels can change

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11
Q

What do all angina pectoris symptoms share?

A
  • All describe ‘central crushing chest pain’
    – radiation to arm, back, jaw possible (embryological)
    coronary artery narrowing (mostly due to plaque)
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12
Q

What are the symptoms of classic angina?

A
  • No pain at rest
  • pain with certain level of exertion
    – worse with cold weather/emotion
  • pain relieved by rest
  • patient lives within limits of tolerance
  • gradual deterioration
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13
Q

What conditions can worsen angina?

A

– anaemia
– hyperthyroidism
– hypovolaemia

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14
Q

What are the tests for angina?

A
  • ECG -resting and exercise
    – shows area of myocardial ischaemia
  • Test and eliminate other disease
    – thyroid, anaemia, valve
  • Angiography
  • Echocardiography
  • Isotope studies (function assessment)
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15
Q

What is an exercise ECG?

A
  • Tests ischaemia of the heart in real time
  • Allows changes to be seen and stopped at the ’reversible’ stage
  • ST- segment depression increases as ischaemia increases – asymptomatic to the patient
  • ECG changes resolve when exercise stops
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16
Q

How are blood vessels visualised?

A

with an injection of dye

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17
Q

What are the two ways angina can be treated?

A

reduced oxygen demands of the heart
increase oxygen delivery to the tissues

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18
Q

How can oxygen demands be reduced?

A

– reduce afterload (blood pressure)
– reduce preload (venous filling pressure, starling’s law)
– Correct mechanical issues – failing heart valves, septal defects

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19
Q

How can oxygen delivery be increased?

A

– dilate blocked/narrowed vessels
* angioplasty
– bypass blocked/narrowed vessels
* Coronary Artery Bypass Grafting (CABG)

20
Q

What are the non-drug therapies?

A

Live within limitations - limited activity/mobility
Modify risk factors - smoking, exercise, cholesterol

21
Q

What are the drug therapies and what do they do?

A
  • Reduce MI risk – ASPIRIN
  • Hypertension
    – diuretics, Ca channel antagonists – ace inhibitors, b blockers
  • Reduce heart filling pressure / dilate coronary vessels – nitrates - short acting & long acting
22
Q

What are the disadvantages of CABG?

A

– benefit not always obtained
– major surgery
- mortality risk, requires opening the chest and stopping the heart
– limited benefit - 10 years
* less in smokers who continue to smoke

23
Q

What are the disadvantages of angioplasty and stenting?

A

– lower risk but lower benefit
– risk of vessel rupture during procedure

24
Q

Where are the veins taken from for a CABG?

A

from the leg

25
Q

What drugs are required after angioplasty?

A

dual antiplatelet therapy to reduce platelet aggregation on metal stent

26
Q

Where is the cannula inserted in a angioplasty?

A

femoral artery in the leg OR
radial/brachial artery in arm

27
Q

What is peripheral vascular disease?

A

narrowed or blocked arteries reduce blood flow to the limbs, typically the legs and feet. causes pain, cramping, numbness

28
Q

What can peripheral vascular disease cause?

A
  • Limitation of Function
  • Poor wound healing
  • May lead to tissue necrosis & gangrene
    – Chronic slow process
    – Amputation
29
Q

How does ischaemia turn into infarction?

A

Atheroma in vessels

Plaque surface/ platelets detach
* travel downstream and BLOCK
vessels
* no blood flow to that area - infarction

30
Q

Where can infarctions occur?

A
  • Heart
  • coronary artery atheroma
  • Limb
  • femoral & popliteal arteries
  • Brain
  • carotid arteries
31
Q

What can be done to treat infarction?

A

REDUCE tissue loss from necrosis - open blood flow
* thrombolysis - drugs
* Angioplasty - surgery
* bypass obstruction via CABG, Fem/pop bypass - surgery requires to be carried out within a short time of the blockade which is sometimes not practical

32
Q

What can be done to prevent further infarcts?

A

risk factor management
aspirin

33
Q

How does a stroke occur?

A

platelet clot and other clots embolise up the internal carotid artery and into the brain
this causes ischcemia and eventually infarction of brain tissue

34
Q

What if the embolise is solely platelets in a stroke?

A

cause loss of function and obstruction however the platelets are removed quickly from circulation and vessels will open up within 24 hours

35
Q

What are the symptoms and signs of MI?

A

pain, nausea, pale, sweaty
crushing chest pain
some MIs are silent

36
Q

What is the effect of MI?

A

death
functional limitation from reduced cardiac muscle action

37
Q

How can myocardial infarction be diagnosied?

A
  • History
  • ECG findings
  • Biomarkers -Troponin mainly
38
Q

What is the primary care treatment of MI?

A
  • aim to get patient to hospital alive!
  • Analgesia, Aspirin & reassurance
  • Basic life support if required
  • Cardiac arrest situation
39
Q

Does MI always cause cardiac arrest?

what is cardiac arrest

A

MI does not always cause Cardiac Arrest but this might happen due to an arrhythmia from altered electrical conduction in the heart tissues

complete and sudden stop of pumping - leads to death in minutes

40
Q

What treatment can be done in the hospital?

A
  • Up to 3 hours from onset of symptoms - Primary PCI
  • acute angioplasty & stenting (if available)
  • Up to 6 hours from onset of symptoms - thrombolysis if suitable and angioplastly not possible
  • Medical (drug) treatment to reduce tissue damage – improve penumbra (damaged tissue surrounding MI)
  • prevent recurrence/complications
  • Secondaryprevention
41
Q

How is an angioplasty and stent carried out?

A
  • Catheter inserted through artery
  • Femoral or radial
  • Moved to site of blockage under x- ray control
  • Balloon inflated to open blockage
  • Metal stent clicks rigid to hold vessel open and allow blood flow
42
Q

What is the best option of treatment for no access to angioplasty & stent (PCI)?

A

thrombolysis

43
Q

Why might thrombolysis be dangerous?

A
  • injury/surgery/IM injections – recent blood clots would be dissolved
  • severe hypertension, active PUD – would exacerbate active bleeding
  • diabetic eye disease, liver disease, pregnancy
44
Q

What are the complications of MI?

A
  • Death
  • Post MI Arrhythmias
  • Heart Failure
  • Ventricular hypofunction & mural thrombosis
45
Q

What are long term treatment plans?

A
  • Prevent next MI
  • risk modification & aspirin
  • b blocker
  • ACE inhibitor
  • treat complications
  • heart failure
  • arrhythmias
  • psychological distress

2 - Diseases Of The Human System (19 decks)

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