Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

A Pathophysiology- BN607 > Lecture 4: Cardiac conditions lecture > Flashcards

Lecture 4: Cardiac conditions lecture Flashcards

1
Q

What is the thickest layer of the heart wall and what is it composed of?

A

Myocardium
Mainly composed of cardiac muscle cells (myocytes) which generate the pumping action of the heart.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Is the hearts conduction system controlled by intrinsic or extrinsic factors?

A

Both. Can work independently of extrinsic stimulation, but also responds to extrinsic stimulation from the autonomic nervous system.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Name the order of blood flow (10)

A

1) Vena cava (IVC & SVC)
2) Right atrium
3) Right ventricle
4) Pulmonary trunk
5) Pulmonary circulation
6) Pulmonary viens
7) Left atrium
8) Left ventricular
9) Aorta
10) Systematic circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What does the systematic circuit do?

A

Highly oxygenated blood is pumped into this circuit by the left ventricle via the aorta.

This circuit distributes this highly oxygenated blood to all the body’s tissue via the systematic arteries into the systemic capillaries where gas exchange occurs.

From the systemic capillaries the now poor oxygenated blood is transported via the systemic veins into the IVC and the SVA which empty this poor oxygenated blood into the right atrium.

Blood is propelled through this circuit under high pressure generated by the much thicker wall of the left ventricle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What does the pulmonary circuit do?

A

Poorly oxygenated blood is pumped into this circuit by the right ventricle via the pulmonary trunk.

This circuit takes the poorly oxygenated blood into the lungs via the left and right pulmonary arteries which subsequently branch within the lungs giving rise to the pulmonary capillaries where gas exchange occurs.

From these pulmonary capillaries, the now highly oxygenated blood is transported via the pulmonary veins into the left atrium.

Blood is propelled through this circuit under lower pressure compared to the systemic circuit because the right ventricle wall is thinner than the left ventricle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Why does the heart have its own vascular system?

A

The walls of the heart are too thick for most of the myocardium to obtain oxygen and nutrients from the blood flowing through the heart chambers, thus the heart wall also contains a vascular network that is part of thesystemic circulationknown as the coronary circulation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the “pacemaker” of the heart?

A

The sinoatrial (SA) node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the importance of the the sinoatrial (SA) node?

A

Generates action potentials at a rate of about 100 times per second (this is the intrinsic heart rate).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the steps/ order of the cardiac conduction system?

A

The sinoatrial (SA)

Signals are then sent across the atria (to stimulate atrial contraction)

The atrioventricular (AV) node

The AV node then regenerates action potentials (delaying the signal by about 0.1 second) and transmits them via the remaining parts of the conduction system.

The purkinje fibers stimulate individual myocytes throughout the ventricular walls, thus resulting in ventricular contraction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What mechanical actions do the electrical activity of the heart lead to?

A

Contraction and subsequent changes in pressures within the heart chambers that open and close the heart valves and allow blood to move.
Diastole and systole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe mid ventricular diastole

A

The atria and ventricles are both relaxed and blood entering the atria from the veins pushes open the AV valves and flows freely into the ventricles. The semilunar valves are closed.

There is NOelectrical activity happening in the conduction system at this time.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe late ventricular diastole/Atrial systole

A

Atria contract, forcing blood through the open AV valves into the relaxed ventricles. This finishes the filling of the ventricles during diastole. The volume of blood in the ventricles at the end of thisstage is referred to as theend diastolic volume (EDV).

The SA node has fired and electrical signals spread throughout the atria to cause atrial contraction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe early ventricular systole

A

Atria relax while the ventricles begin contracting. This increases pressure within the ventricles forcing the AV valves closed. The semilunar valves remain closed.

Electrical signals hadreached the AV node and rapidly spreadthroughout the rest of the conduction system to initiate ventricular contraction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe late ventricular systole

A

Atria remain relaxed and passively fill with blood while theventricles continue contraction. This continued ventricular contraction further increases the pressure within the ventricles, forcing the semilunar valves open and blood rapidly flows into the pulmonary trunk and aorta under high pressure. Some bloodwill remain in the ventricles and this volume of blood is known as theend systolic volume (ESV).

Electrical signals are still passing through the myocytes at this stage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe early ventricular diastole

A

The atria remain relaxed and the ventricles now relax(dropping intraventricular pressure). Blood in the pulmonary trunk and aorta fall back towards the ventricles, thus closing the semilunar valves.

Electrical activity in the conduction system & myocytes has ceased.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

In an ECG what does the P wave represent?

A

When the atria are filled with blood,
The SA node fires and electrical signals spread throughout the atria and cause them to depolarize.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

In an ECG what does the P-Q wave represent?

A

Signals the time traveled from the SA node and the AV node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

In an ECG what does the QRS complex wave represent?

A

Firing of the AV node. Represents ventricular depolarization.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

In an ECG what does the Q wave represent?

A

Depolarization of the interventricular septum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

In an ECG what does the R wave represent?

A

Depolarization of the main mass of the ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

In an ECG what does the S wave represent?

A

Last phase of ventricular depolarization at the base of the heart.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

When does atrial repolarization occur?

A

It occurs during the QRS complex wave but is obscured by the huge wave.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

In an ECG what does the S-T wave represent?

A

Represents the plateau in myocardial action potential.

This is when the ventricles contract and pump blood.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

In an ECG what does the T wave represent?

A

Ventricular repolarization immediately before ventricular diastole.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

During what phase of an ECG is ventricular contraction?

A

S-T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What is cardiac output (CO)

A

The amount of blood pumped out of a ventricle each minute

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the amount of blood pumped out of a ventricle each minute called?

A

Cardiac output (CO)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is the equation for cardiac output?

A

CO= SV x HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the baseline CO?

A

5 L/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is HR regulated through?

A

The autonomic nervous system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is stroke volume?

A

The definition of stroke volume is the volume of blood pumped out of the left ventricle of the heart during each systolic cardiac contraction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is SV regulated through?

A

While stroke volume is regulated by aspects of the autonomic nervous system, but also factors that affect body fluid dynamics (e.g. blood volume).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is coronary artery disease?

A

Coronary artery disease involves the narrowing, stiffeningand/or blockage of coronary arteries, mostly due to atherosclerosis.

34
Q

What is atherosclerosis?
“A- thuh - row - skluh - row - suhs”

A

Atherosclerosis thickening or hardening of the arteries. It is caused by a buildup of plaque in the inner lining of an artery. Plaque is made up of deposits of fatty substances, cholesterol, cellular waste products, calcium, and fibrin.

35
Q

What is myocytes?

A

The muscle cell, also known as the myocyte is the smallest subunit of all muscular tissues and organs throughout the body

36
Q

What is anaerobic respiration

A

Anaerobic respiration is the type of respiration through which cells can break down sugars to generate energy in the absence of oxygen.
Anaerobic respiration can build up lactic acid

37
Q

What are the risk factors of CAD

A
  • Family history
  • Increasing age > 45 males, postmenopausal females
  • Hypercholesterolemia
  • Smoking
  • Hypertension
  • Diabetes
  • Obesity
  • Physical inactivity
38
Q

What is Angina?

A

Angina is chest pain that occurs when the oxygen demand of the myocardium outweighs the available supply. It is usually transient and typically occurs with increased physical exertion or stress.

39
Q

What is the two classification of angina?

A
  • Stable: angina is predictable (e.g. occurs with exertion) and resolves with rest or use of nitroglycerine
  • Unstable: angina is unpredictable, may occur at rest and is of increasing severity, length and/or frequency
40
Q

What is unstable angina often associated with?

A

With atherosclerotic plaque rupture, or outer erosion, which results in transient episodes of thrombotic occlusion and vasoconstriction.

Unstable angina is a strong predictor of myocardial infarction.

Management of unstable angina generally requires some type of antithrombotic.

41
Q

What is angina often accompanied by?

A
  • pallor (an unhealthy pale appearance.)
  • diaphoresis (sweating, especially to an unusual degree as a symptom of disease or a side effect of a drug.)
  • dyspnoea (Difficult or laboured breathing.)
42
Q

What is a myocardial infarction (MI)?

A

Myocardial infarction (MI), or heart attack, occurs when there is an occlusion of blood flow within a coronary artery causing prolonged myocardial ischemia which leads to myocyte necrosis.

As cardiac muscle cells are unable to repair/replace themselves, there will be permanent loss of muscle tissue in this area.

Areas surrounding the site of necrosis also experience various levels ofischemia, further affecting systolic function.

43
Q

What are the signs and symptoms of MI?

A
  • Prolonged pain, tightness/pressure ordiscomfort in the chest (angina), shoulder, arm, neck, jaw and/or back. Onset is typically sudden and severe. Pain/discomfort does not subside or respond to rest and/or medications
  • Diaphoresis
  • Pallor
  • Nausea/vomiting
  • Feeling anxious
  • Shortness of breath or dyspnoea
  • Extreme fatigue (more common in females)

Additional signs that may be detected upon examination include:
- Abnormal heart sounds or murmurs
- Increased heart rate & blood pressure
- ECG changes (e.g. T wave inversion, ST elevation or depression)
- Elevated cardiac enzymes

44
Q

Whats the process of an MI?

A

Myocardial infarction occurs when there is sustained myocardial ischemia.

Prolonged myocardial ischemia leads to irreversible hypoxic damage.

Oxygen deprived cardiomyocytes convert to anaerobic respiration, resulting in a build up of lactic acid.

They will alsorelease inflammatory chemicals.

Eventually they willlose the ability to contract.

45
Q

How long after heart ischemia do cardiac muscles start to become necrotic?

A

20 minutes. Beginning in the area just below the endocardium and progressing towards the epicardium.

46
Q

Why does the detection of cardiac enzymes indicate MI?

A

As myocytes become necrotic, there is a breakdown of the sarcolemma which results in leakage of intracellular cardiac enzymes,
including creatine kinase myocardial band (CK-MB), myoglobin and troponin.

Thesecardiac enzymes/biomarkersbecome detectible in blood and are used in the diagnosis of MI.

47
Q

How can an MI be diagnosed

A
  • Non S-T elevation myocardial infarction (NSTEMI): there is no elevation of the S-T segment onECG (though other ECG changes are often present such as S-T depression or T wave inversion), but cardiac biomarkers are present. NSTEMI is generally associated withsubendocardial infarctiondue to only partial occlusion orsome level of re-perfusion occurring (e.g thrombus breaks up) prior to full necrosis.
  • S-T elevation myocardial infarction (STEMI): there is elevation of the S-T segment on the ECG. This is due to complete and sustained blockage in the coronary artery, resulting intransmural infarction.
48
Q

Can cardiac muscle cells regenerate new cells after some die from necrosis?

A

Cardiac muscle cells do not replicate, tissue repair results in necrotic cardiac muscle cells being replaced by fibrous scar tissue.

As scar tissue is non-contractile, it results in a portion of the myocardium that can no longer contract after MI.

49
Q

What are complications that can arise after an MI?

A
  • angina
  • re-infarction or infarct extension
  • arrhythmias
  • valvular incompetence
  • cardiogenic shock
  • left ventricular anuerysm
  • pericarditis
  • rupture of the ventricular wall
  • heart failure
  • sudden death
50
Q

What is initiated upon diagnosis of MI?

A

Reperfusion therapy.

Reperfusion therapy is a medical treatment to restore blood flow, either through or around, blocked arteries, typically after a heart attack.

Reperfusion therapy includes drugs and surgery.

The drugs are thrombolytics and fibrinolytics used in a process called thrombolysis.

MONA- Morphine, oxygen, nitroglycerin and asprin

51
Q

What is percutaneous coronary intervention (PCI)

A

A percutaneous coronary intervention (PCI) is a minimally invasive procedure to open blocked coronary (heart) arteries.

PCI involves the use ofangiographyto visualize the coronary arteries and identify any blockages and to then open up the blocked artery- typicallyviaangioplastywith stent.

52
Q

What additional interventions can you use for an MI?

A

Balloon angioplasty with stent

Medications- ACE inhibitors, beta blockers, anti-platelet therapy

CABG- Coronary artery bypass graft surgery

Management of underlying conditions- Hyperlipidemia, hypertension or diabetes.

53
Q

Whats an arrhythmia?

A

Alterations of cardiac conduction. If you experience an arrhythmia, the rhythm of your heartbeat is too fast or too slow.

No rhythm

54
Q

Whats a dysrhythmia?

A

If you experience dysrhythmia, the rate of your heartbeat is irregular, but it’s still within a normal range.

Bad rhythm

55
Q

What are some dysrhythmias?

A

Atrial fibrillation

Ventricular tachycardia
Ventricular fibrillation
Asystole

56
Q

Whats atrial fibrillation?

A

Chaotic signals in theatria cause them to quiver, leading to an irregular, and often rapid, heart rate.

Atrial fibrillation is the most common type of dysrhythmia, particularly in the older adult. Though atrial fibrillation itself is not life-threatening, it does carry a significant risk for thromboembolism (and therefore pulmonary embolism or stroke) because blood can pool in the atria, resulting in clot formation.

57
Q

What is three life threatening dysrhythmias?

A

Ventricular tachycardia
Ventricular fibrillation
Asystole

58
Q

What is ventricular tachycardia?

A

Abnormal and rapid discharge of electrical signals in the ventricles.

This manifests as a very high HR (~150-200 bpm) which decreases filling time (diastole) and therefore decreases CO and subsequently BP.

This may manifest withpalpitations, shortness of breath, chest pain, dizziness and loss of consciousness.

If lasting for more than a few seconds, this dysrhythmia becomes life threatening as CO will rapidly drop, eventually leading to cardiac arrest.Defibrillation can be used to re-establish more normal hearth rhythms.

59
Q

What are ways that you can treat ventricular tachycardia?

A

Defib
Amiodarone- Block K+ channels, slows repolarisation
Lignocaine- Blocks voltage gated sodium channels
Bretylium- Prolongs refractory period

60
Q

What is ventricular fibrillation?

A

Ventricles quiver instead of contracting. Without proper contractions, there is no CO from the ventricles, thus cardiac arrest ensues.

There will be a loss of consciousness andbreathing stops.

Defibrillation can be used to re-establish more normal hearth rhythms.

61
Q

How to treat ventricular fibrillation?

A

immediate defib and ACLS protocol

62
Q

What is asystole?

A

Cessation of electrical signals (also known as a ‘flatline’). Without electrical activity in the heart, there is no mechanical activity (so no pumping). This is the terminal rhythm of cardiac arrest.

This is not a shockable rhythm, thus defibrillation will not work.

Instead, high quality CPR must be instigated, usually with the use of adrenaline (epinephrine) tofirsttry and establish some electrical activity.

63
Q

How to treat asystole?

A

CPR
Artificial pacing
Adrenaline
Atropine

64
Q

What is heart failure?

A

Heart failure, sometimes known as congestive heart failure, occurs when there is inadequate perfusion of tissues due to cardiac dysfunction.

Perfusion is the passage of fluid through the circulatory system or lymphatic system to an organ or a tissue, usually referring to the delivery of blood to a capillary bed in tissue.

65
Q

What relieves stable angina?

A

Nitroglycerine

66
Q

What is myocardial stunning?

A

Temporary loss of contractility lasting hours to days after reperfusion

(Reperfusion is the restoration of blood flow to an organ or tissue after having been blocked)

67
Q

What is myocardial hibernation?

A

Prolonged loss of contractility post sustained ischemia and reperfusion

68
Q

Whats myocardial remodeling?

A

Permanent loss of contractility with cellular hypertrophy

69
Q

What kind of procedure is an angioplasty?

A

Opens blocked arteries with a balloon?

70
Q

What is a major consequence of left sided heart failure?

A

Pulmonary oedema. A condition caused by excess fluid in the lungs.

71
Q

What is systolic heart failure?

A

Decreased ability of a ventricle to pump blood. resulting in a reduced SV and fall in the ejection fraction.

72
Q

What is diastolic heart failure?

A

Decreased ability for ventricle to fill with blood, resulting in a reduced SV, but not necessarily a change in the ejection fraction (As there is less total blood available to pump in the first place)

73
Q

What are the two kind of MI?

A

Transmural and subendocardial

74
Q

What is a transmural MI?

A

Associated with atherosclerosis involving a major coronary artery.

Can be subclassed into anterior, posterior, inferior, lateral or septal.

Extend through the whole thickness of the heart muscle and are usually a result of complete occlusion of the areas blood supply

ST elevation and Q waves are seen on ECG

75
Q

Whats a subendocardial MI?

A

Involving an area of the subendocardial wall of the left ventricle, ventricular septum, or papillary muscles.

Subendocardial area is particularly susceptible to ischemia

ST depression is seen on ECG

76
Q

What cardiac enzymes in the blood suggest an MI?

A

Myoglobin
(Its main function is to supply oxygen to the cells in your muscles (myocytes).)

Total CK
Creatine kinase.
(CK’s job is to add a phosphate group, a group of natural chemicals, to creatine, a substance in your muscle cells that helps your muscles produce energy)

Troponin 1
Cardiac troponin I (cTnI) is a key regulatory protein in cardiac muscle contraction and relaxation. it binds to actin in thin myofilaments to hold the actin-tropomyosin complex in place. Troponin I prevents myosin from binding to actin in relaxed muscle.

CK-MB
Also known as creatine kinase-myocardial band. Further test after the creatine kinase test to distinguish if the elevated CK was due to skeletal muscle or cardiac muscle. CK-MB is normally undetectable or very low in the blood.

77
Q

Describe left sided heart failure

A

Most common. Occlusion of LAD/ circumflex arteries

Aortic valve stenosis

Mitral valve regurgitation

Chronic systemic hypertension- Increased afterload, heart generates more force to open aortic valve and eject blood into the circulation

Blood tends to back up into the pulmonary veins and arteries. Pulmonary congestion and increased pulmonary arterial & venous pressures

Due to the pressure fluid leaves the blood vessels & accumulates in the interstitial spaces of the lungs and alveoli

Lung compliance is reduced- they become more difficult to inflate.

Gas exchange is impaired and pulmonary edema may result

Dyspnea on exertion and fatigue

Cyanosis my reflect hypoxia

78
Q

Describe right sided heart failure

A

Can be occlusion of R coronary artery. Can follow L ventricular failure -> pulmonary hypertension, increased load on R ventricle

Tricuspid valve regurgitation

Characterised by venous hypertension
Peripheral oedema, fatigue, hepatic congestion and ascites, cyanosis

79
Q

Describe cor pulmonale

A

R side HF due to COPD. Hypoxia of part of lung -> vasoconstriction of corresponding blood vessles

Loss of pulmonary blood vessles means same amount of blood conducted via fewer -> increased pressure and R ventricular load

Result pulmonary hypertension, increased afterload, then heart failure

80
Q

Whats cardiac hypertrophy ?

A

Growth of heart muscles!

Can be genetic abnormality. Increased mass of individual cardiac cells in response to increased “afterload”. Increased myocardial muscle mass may not be accompanied by equivalent increase in myocardial vasculature.

Ischemia to some regions of the heart may occur -> fibrosis and reduced contractility

Hypertrophied cardiac muscle means that the cardiac chambers are smaller so stroke volume and cardiac output eventually decrease

Valves may be distorted by muscle overgrowth compounding the problems

81
Q

What are the treatment aims for HF?

A

Increase cardiac contractility.
Reduce fluid volume / edema
Reduce myocardial work load
Medications

A Pathophysiology- BN607 (28 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions