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Medical Studies 1 > Module 5a > Flashcards

Module 5a Flashcards

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USMLE® Step 1 flashcards
1
Q

What are the major roles of the cardiovascular system?

A
  • Gas, nutrient, and waste transportation
  • pH & fluid balance
  • Defence against toxins and pathogens
  • Body temperature regulation
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2
Q

What is the space between the lungs where the heart sits called?

A

Mediastinum

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3
Q

How much blood is delivered to the myocardium each minute?

A

200 – 250mls during rest

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4
Q

What artery carries 85% of the blood to the myocardium?

A

Left coronary artery

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5
Q

What are the two main branches of the left coronary artery?

A
  • Left anterior descending LAD

- Circumflex artery

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6
Q

What are the two main branches of the right coronary artery?

A
  • Right anterior descending RAD

- Marginal branch

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7
Q

The cardiac cells are automaticity cells, what does that mean?

A

They are specialised fibres that can beat autonomously

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8
Q

What rate at does the SA and NA nodes stimulate a contraction?

A

SA: 60-100bpm
NA: 40 – 60bpm
Bundle of His: 30 – 40bpm
Purkinje fibres: 20 – 40bpm

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9
Q

What are the 6 steps to the Cardiac Conduction Cycle?

A
  1. Atrial depolarisation initiated by the SA node, cause the P wave.
  2. With atrial depolarisation complete, the impulse is delayed at the AV node.
  3. Ventricular depolarisation begins at the apex, causing the QRS complex. Atrial repolarisation occurs.
  4. Ventricular depolarisation is complete.
  5. Ventricular repolarisation begins at the apex, causing the T wave.
  6. Ventricular repolarisation is complete.
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10
Q

Where is the cardiac control centre located and where does it receive its input from?

A

Located in the Medulla Oblongata. Input received from the baroreceptors in the aorta & internal carotid arteries.

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11
Q

What are the roles of Beta1, Beta 2 and Alpha receptors?

A

Remember B1 = heart as there is only 1 heart, B2 = Lungs as there is two lungs
Beta 1:
Chronotropic: Increased rate
Dromotropic: Increased conduction velocity
Inotropic: Increased Force of contraction

Beta 2:
Vasodilation of bronchioles of the lungs and blood vessels of smooth muscles

Alpha:
Vasoconstriction of bronchioles of the lungs and blood vessels of smooth muscles

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12
Q

An increased sympathetic tone (fight or flight) leads to …?

A
  • Positive chronotropic, dromotropic & inotropic effect (increase HR, velocity, and strength)
  • Vasoconstriction
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13
Q

An increase parasympathetic (vagal) tone leads to..?

A
  • Negative chronotropic, dromotropic & inotropic effect (decrease HR, velocity, and strength)
  • Vasodilation
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14
Q

What are some factors that determine peripheral resistance?

A
  • Viscosity of blood
  • Turbulence
  • Vasotone
  • Main changes in BP are via arterioles responding to humoral and neural stimuli
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15
Q

What is the leading cause of ischemic heart disease?

A

Coronary artery disease (CAD)

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16
Q

Define arteriosclerosis.

A

The general term for all arterial changes.

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17
Q

What occurs during atherosclerosis?

A

Progressive narrowing of the lumen within medium and large arteries as a result of endothelial injury. Mechanism of injury genetic factors (males) age (over 50) lifestyle (obesity) mechanical stresses (hypertension).

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18
Q

What is the process of atherosclerosis?

A
  1. Endothelial injury
  2. Inflammatory response – platelet adhesion and clotting
  3. Smooth muscle cells may move from the middle muscle layer into the lining of the artery forming atheroma
  4. Atheroma becomes fibrous and hardens over injury site
  5. Artery becomes occulated
  6. Reduced flow due to narrowed lumen
  7. Should the atheroma become damaged the process above will repeat upon the already establish atheroma and cause an obstruction resulting in a sudden heart attack.
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19
Q

How is collateral circulation developed?

A

Through aerobic exercise by creating an oxygen demand increasing vessel growth.

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20
Q

What are the two main effects of atherosclerosis on the blood vessels?

A
  1. Disrupts the innermost lining of the vessels – causes loss of elasticity and increased clots
  2. Reduces the diameter of the vessel – decreased blood supply and insufficient nutrients to tissues.
21
Q

What is the relationship between atherosclerosis and ACS?

A

Atherosclerotic plague the ability of the vessel to respond to messages to vasoconstrict and vasodilate and obstructs the lumen. Any interruption to blood flow within the coronary arteries will create ACS.

22
Q

What are the risk factors for atherosclerosis?

A
  • Age
  • Diet
  • Lack of exercise
  • Gender
  • Genetic predisposition
23
Q

What treatments are there for atherosclerosis?

A
  • Stents
  • Blood thinners
  • Bypass valve
  • Diet and exercise
  • Antihypertensive and anti-cholesterol medication
24
Q

Acute Myocardial Infarction (AMI) and Unstable Angina are both collectively referred to as …?

A

Acute Coronary Syndrome

25
Q

What is the underlying pathophysiology of ACS?

A

Ruptured or eroded atheromatous plaque resulting in arterial blockage.

26
Q

What are the treatment goals and how will you achieve that for ACS?

A
  1. Reduce the workload of the heart and increase oxygen delivery.
  2. Preserve the myocardium and reduce necrosis
  3. Minimise clot formation and platelet aggregation
  4. Initiate cardiac re-perfusion measures ASAP and preserve systemic tissue perfusion
  5. Prevent progression to life threatening events
  • Rest and reassurance (decreases HR and workload)
  • Oxygen administration (increases O2)
  • GTN (vasodilates) and pain relief (fentanyl 1mcg/kg max of 100mcg, repeat dose every 5 mins)
  • Aspirin (stops clot development) and fibrinolytics (blood thinner e.g. heparin)
27
Q

What is angina?

A

An imbalance between myocardial oxygen supply and demand due to a build up of lactic acid and CO2 in ischaemic myocardium tissues. These metabolites irritate nerve endings and stimulate pain.

28
Q

What are the 3 types of anginas and how do they present?

A

Stable Angina:

  • Occurs during physical or emotional distress
  • Resolves quickly (with rest & GTN)
  • Pain typically lasts 1 – 5 minutes

Unstable Angina:

  • Unpredictable pain – occurs during period of low exertion
  • Atypical onset to previous angina (patients’ pain will be different)
  • Slower response to rest and medication
  • Sense of impending doom

Prinzmetal Angina:
- Occurs unpredictably at night or rest due to coronary artery vasospasms

29
Q

What conditions can mimic the signs and symptoms of angina?

A
  • GORD
  • Pancreatitis
  • Pericarditis
  • Chest wall trauma
  • Respiratory infection
  • Aortic dissection
  • Pneumothorax
30
Q

What are the differences between stable and unstable angina? **

A

Stable vs Unstable
Onset: Whilst physically active or stressed / during rest or minimal exertion.
Duration: 1-5 mins / 10mins+
Presentation: Typical to previous / New or worsened symptoms.
Pain: Relieved by rest, oxygenation and nitrates / not always relieved by rest, oxygen, and nitrates.

31
Q

What is the typical presentation of a patient with angina?

A
  • Left-sided or central chest discomfort
  • Crushing, heavy or tight in nature
  • Levine’s sign (gripping chest with hand)
  • Radiation of pain to upper back, jaw, shoulder, and left arm

Can be accompanied by

  • SOB
  • Anxiety
  • Clammy skin
  • Nausea
  • Fatigue
  • Headache
  • Generalised weakness
32
Q

In ACS what determines the level of injury?

A

The extent and duration of occlusion.

33
Q

When does acute myocardial infarction (AMI) occur?

A

When blood flowing through a coronary artery is blocked, affecting the myocardium supplied by that artery. This can be caused by ischemia, cellular injury and necrosis.

34
Q

What determines the extent of an AMI?

A
  • Location & presences of prolateral circulation.
35
Q

What is the pathophysiology of an acute myocardial infarction?

A
  • Formation of atherosclerotic plague
  • Disruption to smooth arterial lining resulting in uneven surfaces
  • Creates turbulent blood flow which can result in the rupturing of the plague
  • Injured tissue is exposed t o circulating platelets
  • Results in the formation of a thrombus that osculates the artery (acute thrombotic occlusion)
  • As the thrombus enlargers it further reduces blood flow in the coronary vessel
36
Q

What is the leading cause of AMI?

A

Acute thrombotic occlusion

37
Q

Other than an acute thrombotic occlusion, what are other causes of heart attacks?

A
  • Coronary spasm
  • Coronary embolism (clot traveling from elsewhere)
  • Sever hypoxia
  • Haemorrhage into diseased atrial wall
  • Reduced blood flow after any form of shock
38
Q

Who is predisposed to suffer from silent MI?

A
  • Diabetics
  • Those with neuropathic disorders
  • Elderly
  • Previous heart transplant/chest surgery
  • Women
39
Q

In a MI where does the necrosis occur?

A

Distal to the occlusion

40
Q

The size of a myocardial infarct is determined by …?

A
  • The need of the tissue typically supplied by the now occluded vessel
  • The presence of collateral circulation
  • The time it takes to re-establish perfusion
41
Q

Where do most AMI’s occur and why?

A

Within the left ventricle or interventricular system because these areas are supplied by the two main coronary arteries.

42
Q

Where area of the heart can be impacted by an AMI in the left coronary artery? And how would they be referred to?

A

Impact to left atrium and ventricle, interventricular septum. Referred to as anterior, lateral or septal wall infarctions.

43
Q

Where can an AMI in the right coronary artery impact and how are they referred to?

A

Inferior-posterior wall of left ventricle referred to as Inferior wall infarction

44
Q

When does a STEMI occur?

A

When a thrombus has completely occluded coronary vessel for a prolonged period of time.

45
Q

How do we diagnose a STEMI?

A
  • Elevated ST segments in two or more contiguous ECG leads.

- Height of the ST increases 1mm+ in limbs and 2mm+ in chest above isoelectric line

46
Q

When does a NON-STEMI occur?

A

When micro-emboli from thrombus become lodged in distal coronary arteries (side streets are blocked instead of the freeway)

47
Q

What would you expect to see on the ECG of a patient suffering a NON-STEMI?

A

ST depression and T wave inversion

48
Q

What type of response can you expect for an anterior vs. interior MI?

A

Anterior: Sympathetic response
Inferior: Parasympathetic response

49
Q

What is “tombstone” presentation on an ECG?

A

Highly elevated ST segment = STEMI

Medical Studies 1 (11 decks)

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