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Lex Patho Exam 2 > 1. The Heart > Flashcards

1. The Heart Flashcards

1
Q

Heart blood flow

A

R side.

  1. Sup/inf vena cava
  2. R atrium
  3. Tricuspid
  4. R ventricle
  5. Pulmonary valve
  6. Pulmonary artery

L side

  1. Pulmonary vein
  2. L atrium
  3. Bicuspid/mitral
  4. L ventricle
  5. Aortic valve
  6. Aorta
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2
Q

Pulmonary circulation

A

Transports deoxygenated blood From the right side of the heart to the lungs

Pulmonary circulation is supported by right atrium and right ventricle

RIGHT side

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3
Q

Systemic circulation

A

Carries oxygenated blood from the left side of the heart to all the tissues in the body

Removes waste from tissues and returns deoxygenated blood to the right side of the heart

Supported by left atrium and left ventricle (major player in cardiac output)

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4
Q

Electrical system of the heart

A

Electrical impulse is generated by the sinoatrial node (SA node) generates 60-100 times per minute

Travels from SA node to AV node then travels to ventricle bundle via bundle of His

Bundle of His divides the right and left pathways to stimulate the right and left ventricles

Fine branching of bundle of His into the purkinje network which stimulated the right and left ventricles

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5
Q

Excitation / contraction

A

Excitation: generation of action potential trigged by electrical impulse

Contraction: shortening of muscle cells triggered by excitation

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6
Q

Single cardiac cycle divided into:

A

Diastole: period of time when ventricles are relaxed at the end of diastole both atria contract (time heart fills)

Systole: period of time when the ventricles contract and eject blood into the aorta and pulmonary artery

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7
Q

Three layers of the heart

A

Epicardium: outer layer

Myocardium: middle layer (cardiac muscle)

Endocardium: internal layer (CT and squamous cells continuous with endothelium)

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8
Q

Pericardium

A

Three layers are enclosed in a double lined membrane sac

Parietals : touches body
Visceral: touches heart

Acts as physical barrier
Contains pain receptors and mechanoreceptors

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9
Q

End-diastolic volume (EDV)

A

The filled volume of ventricle prior to contraction

Prior to diastole (Relaxation)

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10
Q

End-systolic volume (ESV)

A

The residual volume of blood remaining the ventricle after contraction

Prior to systolic (contraction)

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11
Q

Stroke volume (SV)

A

The volume of the blood pumped out by the left ventricle in one contraction

SV = EDV - ESV

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12
Q

Preload

A

The ventricle volume at the end of diastole, approximated by LVEDV

Amount of volume of blood before contraction, blood entering ventricles

Wind that makes biking easier

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13
Q

After load

A

The ventricular wall tension during contraction, depends on the arterial blood pressure and vascular tone. Resistance ventricles must overcome two circulate blood

Increase after load (resistance) = increase cardiac workload = Decrease SV

Rocky road that biker has to push against

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14
Q

Cardiac output

A

The amount of blood the heart pumps in 1 minute

Depends on HR,
contractibility (EDV, sympathetic stimulation, myocardial oxygen supply)
preload (end-systolic volume ESV, venous return - increase water = increase venous return)
After load (aortic pressure, total peripheral resistance)

CO (ml/min)= SV (ml) x HR (bpm)

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15
Q

Ejection fraction (EF)

A

The percentage of blood that’s pumped out of a filled ventricle with each heartbeat

Usually only measured in left ventricle (LVEF)

EF= SV/EDV %

Less then 40% bad
50-70% is normal

Used to measure hearts squeezing ability and assess heart failure

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16
Q

Chronotropic effect

A

Increase or decrease in HR

positive chronotropic: major effect increase HR (sympathetic stim norepi and epi)(increase CO2)

Negative chronotropic: decrease HR (parasympathetic stim -acetylcholine)(decrease O2 hypoxia)(increase calcium)

DIrect relationship with HR

17
Q

Ionotropic effect

A

Force/strength of myocardial contraction

Positive ionotropic: strengthen force of heart
Negative ionotropic: weaken force of heart

direct relationship

18
Q

Normal left ventricular pressure-volume relationship in association with SV

A

Preload (EDV) DIRECT- Increase in venous BP forces more blood to flow into the heart - increase SV increase stretch increase venous BP!

Myocardial contractibility: DIRECT -Higher contractibility allows the heart to pump out more blood into the vasculature - increased SV

After load: an inverse relationship - Decrease in after load (wall tension) can increase SV

19
Q

Frank-Starling Law

A

Relationship between force and stretch (DIRECT)

SV rises in response to an increase in preload (EDV) - heart under influence of sympathetic nervous system (epi and norepi) = more force

Large volume of blood in ventricles - more stretch - more force from cardiac muscle

Increase stretch = increase force

20
Q

Nervous control

A

Higher centers: medulla oblongata

Sympathetic nervous system (SNS) - Controls SA node, release epi and norepi, increase HR and contractibility

Parasympathetic nervous system (PNS) - Mainly controls AV noded, releases acetylcholine, decreased HR, little effect on contractibility

21
Q

Hormonal control

A

ADH and aldosterone - affect BP (where salt goes water goes)

ADH decrease excretion of fluid increase BP

Epi and angiotensin II - affect BP , increase BP and vasoconstriction

22
Q

Cardio vascular disease occurs as a consequence of one more more mechanism

A

Pump failure - poor contractibility or relation of heart

Blood flow obstruction atherosclerotic plaque, aortic valve stenosis

Regurgitating flow - output form each contraction directed backwards - volume overload and decreased forward blood flow

Shunted flow - abnormal blood flow

Abnormal cardiac conduction - uncoordinated myocardial contractions

Rupture of the heart of major vessel

23
Q

Ischemic Heart Disease (IHD)

A

IHD frequently referred to as coronary heart disease - Mismatch between cardiac demand and supply of oxygenated blood

Etiology:

In more then 90% of cases IHD is due to atherosclerotic disease - reduced blood flow to coronary arteries

Myocardial ischemia in the absence of chest discomfort is “silent ischemia”

24
Q

Pathophysiology of myocardial ischemia

A

Mismatch between supply and demand

Demand determined by HR, systolic BP, myocardial tension, myocardial contractibility

Supply determined by oxygen carrying capacity of the blood, the degree of unloading from the hemoglobin to tissues

Coronary artery blood flow delivered to the myocardium which is determined by:

Perfusion pressure
Collateral blood flow
HR

25
Q

Conditions provoking or exacerbating ischemia

A

Sympathomimetic toxicity (cocaine use) - norepi and epi is usually increased, increase HR, BP

HT - increase supply decrease demand

Anxiety flight/flight increase blood flow

Tachycardia - increase HR reduction in tissue perfusion - inefficient pumping - increase O2 demand decrease supply

Hypoxemia - decrease in blood, not enough supply in tissues

Hyperviscocity Blood flow decrease RBC impair flow of blood

Aortic stenosis decrease blood flow and decrease O2

26
Q

Pathologic mechanisms do myocardial ischemia

A

Irreversible loss of myocardium (infarction)

Partially reversible loss of contractibility - still viable

Hibernating myocardium (chronic) - persistent ischemia can respond to therapy

Stunned myocardium (transient) - ischemia not prolonged - if repeatedly stunned heart will hibernate

27
Q

Acute coronary syndrome (ACS)

A

Types

Unstable angina: chest pain that does not respond to therapy

Stable angina: periodically happens

ST segment elevation - STEMI

Non-ST elevation - NSTEMI

Causes of MI

Type I - atherosclerosis plaque
Type II - mismatch

28
Q

Mechanism of Angina

A

Insufficient blood flow to heart muscle from narrowing coronary artery may cause angina.

29
Q

Myocardial Infarction (MI)

A

Clinical or pathologic event caused by myocardial ischemia with evidence of injury or necrosis

Pathogenesis: coronary artery occlusion (Type I)

Coronary artery atheromatous plaque undergoes erosion, ulceration, rupture and or intraplaque hemorrhage

Platelets become activated and aggregate

Activation coagulation cascade

The expansion of thrombus can completely occlude the coronary artery - necrosis= infarction

30
Q

Myocardial response to ischemia

A

Anatomic region supplied by the occluded coronary artery is referred to as an “area at risk”

Only severe ischemia (blood flow 10% or less than normal) lasting 20 to 30 minutes or longer leads to necrosis of cardiac myocytes

Significance:

Delay in onset of necrosis is window for rapid diagnosis MI

Disruption of integrity of Scromeres causes intracellular proteins to leak out of necrotic cells into the vasculature and lymphatics

Release of intracellular myocardial proteins into the circulation is the basis for blood tests

31
Q

Diagnosis of acute MI

A

Evidences

Acute myocardial injury (myocyte death)

Clinical evidence of ischemia

Preferred serologic test:

Cardiac troponin I (cTnl) and T (cTnT)
Skeletal muscle can be the source for elevations of cTnT detected in the blood
Cardiac troponin concentrations usually begin to rise 2 to 3 hours after onset of acute MI

32
Q

Outcomes of myocardial ischemia

A

Shift in metabolism (aerobic - anaerobic because of lack of O2)

Acidosis (LA decrease pH), decrease ATP due to anaerobic respiration

Loss of cellular pump
Loss of membrane integrity
generate ROS

Role of platelets: adhere and aggregation platelets secreted serotonin to activate aggregation of platelets

33
Q

Oxygen demand determined by

A

HR
Systemic BP
Myocardial wall tension
Myocardial contractibility

34
Q

Oxygen supply determined by

A

oxygen carrying capacity of blood

Degree of oxygen unloading from hemoglobin to tissues

Coronary artery blood flow delivered to myocardium determined by:
Perfusion pressure
Collateral blood flow
HR

35
Q

Area at risk

A

Necrosis begins in a small area beneath the endocardium and “area at risk” begins to expand

Area around necrotic region

36
Q

4 determinants of Cardiac output

A

1 HR (positive/negative chronotropic effects)

2 Preload- increase blood entering ventricle increase myocardial stretching increase preload, increase SV

  1. Afterload
  2. Contractility
    positive ionotropic - sympathetic stim, hypercalciemia (Ca 2+)
    negative ionotropic - parasympathetic, decrease Ca, increase potassium, myocardial hypoxia

Lex Patho Exam 2 (10 decks)

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