Overview of cardiac diseases

Dr Aseel Aburub

NB Images from Tortora and Derrickson (2017) are

reproduced with permission for educational use Not
for reproduction.
Session Aims (Oveíview of caídiac diseases and
Evidence foí Caídiac Rehabilitation)

1. Build on knowledge gained in Anatomy and physiology

2. Provide an overview of cardiac diseases/disorders for which cardiac
rehabilitation may recommended.
3. Review the evidence (and guidelines) for cardiac rehabilitation.
4. Consider the pathway of care.
Caídiac diseases/disoídeís foí which
caídiac íehabilitation is íecommended.
Patient gíoups foí CPRP
Priority patient groups:
● acute coronary syndrome
● coronary revascularisation
● heart failure
Other patient groups known to
benefit:
● stable angina, peripheral arterial disease,
post-cerebrovascular event
● post-implantation of cardiac defibrillators
and resynchronisation devices
● post-heart valve repair/replacement
● post-heart transplantation and ventricular
assist devices
● Adult Congenital Heart Disease (ACHD)
Caídiovasculaí diseases (WHO, 2017)
Cardiovascular diseases (CVDs) kill 17.7 million people every year. This
represents 31% of all global deaths.

Primary presentations: myocardial infarctions and strokes.

Triggers: smoking, unhealthy diet, physical inactivity, alcohol misuse.

Modifiable risk factors: hypertension, elevated blood glucose,

overweight and
obesity

Our focus? Coronary heart disease and heart failure.

ľhe
heaít
Acute Coíonaíy Syndíomes
Acute Coíonaíy Syndíomes
...high íisk, medical emeígencies:

● Myocaídial infaíction
○ SľEMI oí Sľ-elevation myocaídial infaíction: caused by a sudden complete blockage of a
coíonaíy aíteíy.
○ Non-SľEMI: usually caused by a seveíely naííowed aíteíy (incomplete blockage).
○ ľ h e diagnosis is initially made by an electíocaídiogíam (ECG).
● Unstable angina (unexpected, seveíe chest pain).

NB: unstable angina contía-indicates exeícise...patients must be medically

stable befoíe being accepted foí CPRPs.

Definitions fíom NICE QS68 https://www.nice.oíg.uk/guidance/qs68

ACS: Myocaídial Infaíction

Univeísal definition of myocaídial infaíction

‘A íise in caídiac biomaíkeís (píefeíably caídiac tíoponin) with at least 1 value above the 99th peícentile
of the uppeí íefeíence limit and/oí a fall in caídiac biomaíkeís, togetheí with at least 1 of the following:

● symptoms of ischaemia
● new oí píesumed new significant Sľ-segment-ľ wave changes oí new left bundle bíanch block
● pathological Q wave changes in the ECG
● imaging evidence of new loss of viable myocaídium oí new íegional wall motion abnoímality
● identification of an intíacoíonaíy thíombus by angiogíaphy.’ (NICE, 2014)
Pathophysiology of ACS (Kumaí and Cannon, 2009)
Atheíoscleíosis: ľ h e píocess of plaque foímation in the intima of laíge and medium-sized aíteíies.

Risk factoís (hypeítension, diabetes, smoking and hypeícholesteíolemia) cause damage to the
endothelium of the blood vessel which can píecipitate the initiation of the atheíoscleíotic píocess.

Once the endothelium has been damaged, the inflammatoíy cells migíate into the subendothelium and
diffeíentiate to become macíophages. ľhese macíophages digest oxidized low-density lipopíotein
(LDL), (also píesent in the aíteíial wall), tíansfoím into foam cells and cause the foímation of fatty
stíeaks. ľhese macíophages íelease chemoattíactants and cytokines which peípetuate the píocess.

Moíe often than not, the píocess occuís without demonstíable symptoms, but in some cases plaques
may íuptuíe causing ACS.

ľ h e íate of píogíession of atheíoscleíotic lesions is vaíiable, nonlineaí, and unpíedicīable.

ľypes of
plaque

https://cardiology.medicinematters.in/image_gallery/morphologic-variants-of-the-thin-cap-atheroma/
ľhíombus foímation (Kumaí and Cannon, 2009)

ľhíombosis occuís at the íuptuíe site.

ľ h e degíee of thíombus foímation may deteímine whetheí the íuptuíe of a plaque íesults in ACS.
Factoís include the makeup of the plaque itself, the seveíity of the íuptuíe, the degíee of inflammation,
and blood flow, togetheí with the individual’s tendency towaíds thíombus foímation. Studies using
intíavasculaí ultíasonogíaphy have shown that at least 80% of patients with ACS exhibit multiple plaque
íuptuíes distinct fíom the culpíit lesion.
Plaque íuptuíe accounts foí 75% of deaths fíom MI
Supeíficial endothelial eíosion accounts foí the íemaining 25%.
Read about ‘white clots’ and ‘íed clots’ in this íefeíence.
ľheíapeutic inteíventions (NICE, 2014)
Unstable angina and NSľEMI (white clots):
‘Adults...who have an inteímediate oí higheí íisk of futuíe adveíse caídiovasculaí events aíe offeíed
coíonaíy angiogíaphy (with follow-on peícutaneous coíonaíy inteívention [PCI] if indicated) within 72
houís of fiíst admission to hospital.’

SľEMI (íed clots):

‘Adults...who píesent within 12 houís of onset of symptoms have PCI as the píefeííed coíonaíy
íepeífusion stíategy, as soon as possible but within 120 minutes of the time when fibíinolysis could have
been given.’

Conseívative tíeatment and Coíonaíy Aíteíy Bypass Gíafting aíe also used in the tíeatment of ACOs and
CHD.
Revasculaíisation - PCI and CABG
Peícutaneous Coíonaíy Inteívention

● PCI is caííied out via caídiac catheteíization (the inseítion of a catheteí tube and injection
of contíast medium, into the coíonaíy aíteíies).

● ľ h e tíeated aíteíy may be suppoíted by the inseítion of a stent.

Coíonaíy Aíteíy Bypass
Gíafting
If needed, the coronary arteries can be ‘bypassed’
using blood vessel harvested from elsewhere in the
body:

● Left or right internal mammary artery (LIMA/RIMA)

● Radial artery
● Long saphenous vein
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Heaít Ïailuíe
Heaít Ïailuíe
Heart failure describes a condition where
the heart fails to maintain adequate
circulation to the tissues for normal
metabolism.

The heart is a double pump; heart

failure can affect the left side of the
heart, the right side of the heart, or
both.
Chíonic and Acute Heaít Ïailuíe
‘Heaít failuíe is a complex clinical syndíome of symptoms and signs that suggest
the efficiency of the heaít as a pump is impaiíed’ NICE (2010) CG108.

• It is caused by stíuctuíal oí functional abnoímalities of the heaít.

• HF íesults fíom ‘stíuctuíal oí functional impaiíment of ventíiculaí filling oí ejection of
blood’ (AHA, 2013).

‘Acute heaít failuíe íefeís to the íapid onset of a clinical syndíome wheíe the
heaít is unable to pump sufficient blood to píovide foí the needs of the body’ NICE
(2015) QS103

• ‘Acute HF can píesent as new-onset heaít failuíe in people without known caídiac
dysfunction, oí as acute decompensation of chíonic heaít failuíe.’ NICE (2014) CG187
Left-sided (oí left ventíiculaí heaít failuíe)
Heart failure most commonly involves the LV:

Heart failure with reduced ejection fraction (HFrEF)

Also called ‘systolic’ failure as it affects the ability of the left ventricle to
contract normally and force sufficient blood into the systemic
circulation.

Heart failure with preserved ejection fraction (HFpEF)

Also called ‘diastolic’ failure (or diastolic dysfunction) - in this case, the
left ventricle loses its ability to stretch (it becomes stiffened) or relax
normally which affects ventricular filling.
Right-sided heaít failuíe
RV failure is less common:

Affects the right side of the heart and the pulmonary

circulation.
● Right sided heart failure can follow left sided heart failure as
pressure ‘backs up’ in the system (most common) OR
● Occur in isolation OR
● Occur as a result of chronic lung disease (typically Chronic
Obstructive Pulmonary Disease (COPD)).
Congestive Caídiac Ïailuíe

...is so called because of the ‘congestion’ in the tissues which occurs as a

result of a slowing of the circulation. Oedema +/- shortness of breath
is the common clinical manifestation.

It is a somewhat outdated term...

Causes of Heaít Ïailuíe
Factors originating
from the heart:

CHD - reduced blood flow and

oxygen delivery to the External factors:
myocardium causing impaired
function. Increased afterload (pressure)
- uncontrolled hypertension.
MI - infarcted tissues does not
HEARľ Increased stroke volume
recover, the remaining muscle
must compensate. (volume) - aterio-venous
ÏAILURE shunts.
Valve disease.
Increased body demands.
Congenital defects.

Cardiomyopathies - known
(bacterial/viral; alcohol
induced) or idiopathic.

Myocarditis.
Clinical Ïeatuíes of Heaít Ïailuíe
● Shortness of breath (dyspnea), fatigue
● Reduced exercise tolerance
● Fluid retention (which may cause pulmonary and/or
splanchnic congestion and/or peripheral edema).

Symptoms vary - not all patients will present with symptoms of

fluid overload.
ľ h e addition of detail and typical M E ľ values aíe
helpful
*MET (metabolic equivalent) is defined as the resting VO2 for a 40-year-old 70kg man.1 MET = 3.5mL O2 /min/kg body weight. Reproduced
from: National Heart Foundation of Australia and the Cardiac Society of Australia and New Zealand (Chronic Heart Failure Guidelines Expert Writing Panel).
Guidelines for the prevention, detection and management of chronic heart failure in Australia. Updated October 2011

NYHA grading MET*

Class I No limitations. Ordinary physical activity does not cause undue fatigue, >7
dyspnoea or palpitations (asymptomatic LV dysfunction).

Class II Slight limitation of physical activity. Ordinary physical activity results in 5

fatigue, palpitation, dyspnoea or angina pectoris (mild CHF).

Class III Marked limitation of physical activity. Less than ordinary physical 2-3
activity leads to symptoms (moderate CHF).

Class IV Unable to carry on any physical activity without discomfort. Symptoms of 1.6
CHF present at rest (severe CHF).
Measuíement of Heaít Ïailuíe (Objective)
Objective assessment class (can be added to NYHA subjective
assessment grading)
A No objective evidence of cardiovascular disease. No symptoms and no
limitation in ordinary physical activity. (asymptomatic LV dysfunction).

B Objective evidence of minimal cardiovascular disease. Mild symptoms and slight

limitation during ordinary activity. Comfortable at rest. (mild CHF).

C Objective evidence of moderately severe cardiovascular disease. Marked

limitation in activity due to symptoms, even during less-than-ordinary activity.
Comfortable only at rest. (moderate CHF).

D Objective evidence of severe cardiovascular disease. Severe limitations.

Experiences symptoms even while at rest. (severe CHF).
Measuíement of Heaít Ïailuíe (Objective)
In heaít failuíe theíe is a íeduced foíce foí each filling píessuíe
ľhis íesults in abnoímal ejection fíaction
● ľhe volume of blood pumped fíom ventíicle compaíed to
volume of
blood in ventíicle

An echocaídiogíam measuíes the diffeíence (see lateí).

Pathophysiology...
In heart failure is the heart having problems...

...beating harder or
...beating faster or
...both?

What is the heart unable to maintain?

Caídiac Output
What is it?
L per
min Q
• Volume of blood ejected by the heaít in 1 40
minute (left and íight sides)
What is it compíised of?
30
• Stíoke volume x heaít íate
• SV = blood pumped each beat
• HR = heaít beats peí minute 20
Volume
• Incíeases by 5x when active 10
CO in caídiac population At Rest
• Maintained by incíeased HR 5
• Incíeases by 2x when active
0
N HF N HF
Caídiac Output
What is it?
L per
min Q
• Volume of blood ejected by the heaít in 1 40
minute (left and íight sides) During
What is it compíised of? Activit
30 y
• Stíoke volume x heaít íate
• SV = blood pumped each beat
• HR = heaít beats peí minute 20
Volume
• Incíeases by 5x when active 10
CO in caídiac population At Rest
• Maintained by incíeased HR 5
• Incíeases by 2x when active
0
N HF N HF
Caídiac Output
What is it?
L per
min Q
• Volume of blood ejected by the heaít in 1 40
minute (left and íight sides) During
What is it compíised of? Activit
30 y
• Stíoke volume x heaít íate
• SV = blood pumped each beat
• HR = heaít beats peí minute 20
Volume
• Incíeases by 5x when active 10
CO in caídiac population At Rest
• Maintained by incíeased HR 5
• Incíeases by 2x when active
0
N HF N HF
Caídiac Output
What is it?
L per
min Q
• Volume of blood ejected by the heaít in 1 40
minute (left and íight sides) During
What is it compíised of? Activit
30 y
• Stíoke volume x heaít íate
• SV = blood pumped each beat
• HR = heaít beats peí minute 20
Volume
• Incíeases by 5x when active 10
CO in caídiac population At Rest
• Maintained by incíeased HR 5
• Incíeases by 2x when active
0
N HF N HF
Ïactoís influencing SľROKE VOLUME 1
1. End Diastolic Volume (píe-load)
• ľ h e amount of blood in the ventíicles at the end of diastole, just befoíe
ejection
2. Contíactility (inotíopy)
• Incíeased foíce of contíaction not due to incíeased end diastolic
volume
3. Peíipheíal Resistance (afteíload)
• Resistance needed to be oveícome to eject blood fíom left ventíicle
into systemic ciículation
Ïactoís influencing SľROKE VOLUME 2
END DIASTOLIC CONTRACTILITY PERIPHERAL
VOLUME INOTROPIC RESISTANCE
Ïactoís influencing SľROKE VOLUME 3
END DIASTOLIC CONTRACTILITY PERIPHERAL
VOLUME INOTROPIC RESISTANCE

INCREASED VASODILATION /
GREATER EDV
ADRENALINE VASOCONSTRICTION

INCREASED CROSS
GREATER MUSCLE CALCIUM SECTIONAL
FIBRES STRETCH RELEASE AREA / LENGTH

STRONGER STRONGER NEGATIVE / POSITIVE

CONTRACTION CONTRACTION IMPACT
Ïactoís influencing HEARľ R AľE
1
1. Incíease in sympathetic neuíal activity
• Contíolled by the bíain’s Caídiovasculaí Centíe (Medulla Oblongata)
acting on SA node
2. Incíease in sympathetic hoímonal activity
• Noíadíenaline / adíenaline act on SA node
3. Decíease in paíasympathetic activity
• ľhought to be initiated fiíst to allow the above to occuí
Ïactoís influencing HEARľ R AľE
2 HORMONE PARASYMPATHETIC
NEURAL
ACTIVITY ACTIVITY
ACTIVITY
Valve disoídeís as a cause of heaít failuíe
Valve disoídeís as a cause of heaít failuíe
Stenosis will obstíuct oí íestíict the flow of blood, the heaít theíefoíe has
to pump haídeí to foíce the blood thíough the valve.
Incompetence oí íeguígitation (when the valve fails to close píopeíly)
allows blood to leak backwaíds. Registíation íeduces píessuíe - íequiíed
foí the passive filling of the atíia and ventíicles. Moíe active contíaction
is needed which incíeases myocaídial woíkload.