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5043 > L3 cardio > Flashcards

L3 cardio Flashcards

1
Q

Cardiovascular System function

A

– Primarily TRANSPORT for cellular respiration

– Mediated by perfusion of ~ 40 billion capillaries

– Supply cells with O2 and nutrients

– Removes waste (Inc. CO2)

– Heat regulation

– Endocrine hormonal transport

– Immune function supply

– Regulation of blood volume

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2
Q

what is cardiovascular system composed of :

A
  • heart
  • pumonary circulation (low pressure system ~ 25mmHg)

– systemic circulation (high pressure system ~ 120mmHg)

Supplies cells with nutrients + O2, matches demand

output of pulmonary go to the input of systemic

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3
Q

circulatory system

A

The heart pumps blood through two separate circulatory systems:

– systemic circulation (LH to body) – pulmonary system (RH to lungs)

Both systems are interconnected so a problem with blood flow in one affects the other.

Blood always moves in one direction (RH to pulmonary circulation to LH to systemic circulation and back to RH)

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4
Q

structure of heart

A
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5
Q

heart anatomy

A
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6
Q

heart wall layers, functions, pathology

A
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7
Q

myocardium: structure, function and pathology

A
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8
Q

Myocarditis

A

– RARE infection to the myocardium

– Inflammatory substances infiltrate the heart muscle causing thickening, or, heart gets dilated and floppy.

– This interferes with filling and pumping… Causes catastrophic drop in blood pressure

– Often occurs in young, previously healthy people

– Usually requires heart transplant

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9
Q

Myocardial hypertrophy

A

It will develop to some degree through aerobic training

As a disease process develops

– from long standing high blood pressure

– The thickened muscle wall makes it difficult for the heart chambers to fill and muscle contraction becomes less effective

– The conductions system runs through the muscle layers and gets ‘messed up’ causing rhythm problems

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10
Q

endocardium

A

– epithelial tissue that lines entire vasculature

– thin layer continuous with endothelium of arteries, veins, and capillaries

– prone to infection

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11
Q

Anatomy of the Heart Wall

A
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12
Q

valve of the heart

A

AV (atrioventricular) – prevent blood entering atria from ventricle during systole

– TRICUSPID: Right Atrium + Right Ventricle

– MITRAL: Left Atrium + Left Ventricle

SEMILUNAR – prevent blood entering ventricle from arterial (pulmonary + aorta) tree during diastole

– AORTIC: Left Ventricle + Aorta
– PULMONARY: Right Ventricle + Pulmonary Artery

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13
Q

valve of the heart structure

A
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14
Q

valve regurgitation

A

– Blood flows back and forth across valve

– Blood flow from the heart reduced

– Poor cardiac output

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15
Q

valve stenosis

A

– Blood trying to squeeze through narrow valve opening

– Blood flow from the heart reduced

– Poor cardiac output

– ?poor coronary artery filling

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16
Q

valve pathology

A
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17
Q

Coronary circulation

A

– The heart is a “hungry beast” – high oxygen requirements

– Myocardial O2 consumption > skeletal muscle – (65% extracted vs 25%)

– Left and right coronary arteries
– increase myocardial metabolic demand = increase coronary blood flow – Local response not ANS

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18
Q

Blood Vessels associated with the Heart

A

Vessels returning blood to the heart include:

– Superior and inferior

venae cavae

– Right and left pulmonary veins

Vessels conveying blood away from the heart:

– Pulmonary trunk, which splits into right and left pulmonary arteries

– Ascending aorta

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19
Q

vasclature layers

A

Tunica intima: endothelium, single layer of flattened cells

Tunica intermedia: smooth muscle and elastic tissue regulated by sympathetic nervous system: controls vessel constriction and dilation

Tunica adventitia: fibrous connective tissue and collagen

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20
Q

Cardiac Output

A

HRXSV=CO

– Cardiac output is the amount of blood pumped by each ventricle in one minute

– Cardiac output is the product of heart rate (HR) and stroke volume (SV)

– Heart rate is the number of heart beats per minute

– Stroke volume is the amount of blood pumped out by a ventricle with each beat

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21
Q

determinants of CO

A

– Preload – amount ventricles are stretched by contained blood

– Afterload – resistance against which the ventricles have to overcome to eject blood into the large arteries

– Contractility – cardiac cell contractile force e Calcium ions, actin & myosin binding

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22
Q

preload

A

– Volume of blood that fills the ventricles during diastole

– Influenced by total blood volume

– The greater the venous return, the more the myocardial fibres will stretch

– Frank Starling’s Law – “the greater the myocardial stretch, the greater the force of contraction”

– Preload increased in systolic heart failure – (because blood backs up in the pulmonary system)

– Preload decreased in hypovolaemia

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23
Q

afterload

A

Afterload

– Afterload - Resistance to ventricular ejection

– Load the ventricle must move during contraction

– Controlled by the sympathetic nervous system

– increase Resistance to flow in systemic circulation (SVR)

– Hypertension

– vasoconstriction

– Aortic & pulmonary valve stenosis

– Increased blood viscosity

– Disease

– eg Atherosclerosis

– Coarctation of aorta

– Reduced by hypotension & vasodilation

24
Q

Contractility

A

– Ability of myocardium to contract when no change in preload or afterload

– Contractility determines force of contraction which determines SV

– 2 factors influence force of contractility:

(i) changes in stretching of myocardium caused by changes in preload
(ii) alterations in SNS

– β adrenergic receptors are stimulated by noradrenaline – circulating adrenaline

– Altered by hypoxaemia

25
Q

CO flowchat

A
26
Q

HR

A

HR x stroke volume = cardiac output

– So… The faster the heart rate the better the cardiac output?… Up to a point

Too fast a heart rate:

– Less time for ventricular filling

– So less stretch on the ventricle wall… so less force of contraction

– Also less time for coronary artery filling during diastole

27
Q

BP

A

– Average blood pressure in aorta

– BP = CO x PR

– CO in the volume of blood per min

– PR is total resistance against which blood must be pumped

28
Q

factors affecting BP flowchat

A
29
Q

Hypertension

A

– Hypertension (high blood pressure) is defined as the consistent elevation in systemic arterial pressure.

– It is estimated that 3.7 million Australians aged over 25 years have high blood pressure or are on medication to treat high blood pressure.

– Diagnosis is based on serial blood pressure (BP) measurements at different times.

– A diagnosis of hypertension will be made when systolic blood pressure is consistently equal to or greater than 140 mmHg or diastolic pressure is 90 mmHg or greater.

– Genetic and lifestyle risk factors contribute to the development of hypertension.

30
Q

Chronic Heart Failure definition, causes

A

Defined as cardiac impairment with inability to fill or eject blood volume

Causes:

– ischaemic heart disease (over 50% of new cases)

– hypertension (about two-thirds of cases)

– idiopathic dilated cardiomyopathy (around 5–10% of cases)

–Left ventricular failure most common (congestive heart failure)

–Right sided heart failure may also occur (often due to lung pathology eg COPD)

31
Q

chronic heart failure

A

Prevalence:
– 2% of total population – 3-5% > 65 years old – 10%>75yearsold

– Hypertension and coronary heart disease most common cause.

– Left ventricular failure most common (congestive heart failure).

– Defined as cardiac impairment with inability to fill or eject blood volume.

– Mortality 5 years from diagnosis.

32
Q

systolic VS diastolic heart failure

A

– Systole is when the heart squeezes, diastole is when the heart relaxes and fills.

33
Q

New York Heart Association (NYHA) Classification of Heart Failure

A
34
Q

cardiac cycle

A

Cardiac Cycle

– Cardiac cycle refers to all events associated with blood flow through the heart

– Systole – contraction of heart muscle

– Diastole – relaxation of heart muscle

35
Q

Conduction System of the Heart

A
36
Q

bundle branches and purkinje system

A
37
Q

normal P QRS T complex

A

– Normal PR Interval
– 0.12 - 0.20 secs
– ( 3 – 5 small boxes)

– Normal QRS
– less than 0.12 sec
– Less than 3 small boxes

38
Q

normal sinus rhythm

A
39
Q

tauonomic crl of the heart

A
40
Q

what influence normal heart rates

A
41
Q

the sinus node and ageing

A

Sinus node activity is correlated with age

– lengthening of time sino-atrial node takes to recover

– lengthening of time sino-atrial node takes conduct.

– progressive lengthening of sinus cycle length

Progressive decrease of parasympathetic activity with increasing age.

– parasympathetic activity predominates in younger people

– sympathetic and parasympathetic tone becomes more equal in older

people.

42
Q

causes of sinus node dysfunction

A

– Inflammatory cardiac disease

– Cardiomyopathy

– Sclerodegenerative processes (replacement of normal organ-specific tissue with connective tissue)

– Coronary artery disease – poor blood supply to SA node

43
Q

cause of AV node diseases

A

– Coronary artery disease

– Rheumatic heart disease

– Inflammatory diseases

– Connective tissue disorders

– Calcification

44
Q

explain poor conduction = poor preload

A

Preload is the volume of blood that fills the ventricles during diastole

–Influenced by ‘atrial kick’ (is there a P wave?)
–Influenced by AV synchrony (Are P waves followed closely by QRS waves?)

The greater the venous return, the more the myocardial fibres will stretch (Frank Starlings Law)

–Loss of atrial kick and poor AV synchrony can mean poor cardiac output !

45
Q

The Patient’s underlying Cardiac Issues

Ventricular dysfunction

– Inability to compensate for fast or slow rhythms Ischaemic heart disease

– May cause arrhythmias due to lack of blood supply to conduction system Tachycardias

– May increase oxygen need due to increased workload of the heart Scar tissue from old infarcts may predispose to ventricular arrhythmias

A

T

46
Q

what makes an arrhythmia dangerous

A

rhythm too slow- inadequate O2

too fast, inadequete filling

serious ventricular irritability

47
Q

cause of slow rhythms

A

– Some medications e.g. digoxin, Beta Blockers

– Natural degeneration of the SA or AV nodes

– Surgery or disease of the aortic or mitral valves (very close to AV node)

– Threatened blood supply to the SA or AV nodes

48
Q

sinus bradycardia

A
49
Q

Sinus Pauses & Asystole

A
50
Q

heart blocks

A
51
Q

causes of fast rhythm

A

– Re-entry circuits

– Myocardial irritability - poor blood supply - poor oxygen supply - potassium and magnesium imbalances

– Acute infections
- Especially new atrial fibrillation from pneumonia, UTI etc

– Myocardial scarring

52
Q

atrial fibrillation

A
53
Q

atrial flutter and supraventricular tachycardia

A
54
Q

ventricular tachycardia

A
55
Q

ventricular fibrillation

A
56
Q

summary

A

5043 (5 decks)

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