Angina Pectoris -mismatch between oxygen demand and oxygen supply

Angina Pectoris

-‘strangling feeling in the chest’

Chest pain resulting from low blood supply to cardiac muscle

Main cause of Angina: Coronary Artery Disease (CAD)

-Imbalance between heart’s oxygen demand and supply.  Either an increase in myocardial  oxygen demand or decrease in myocardial oxygen supply.

Factors that would increase myocardial oxygen demand or decrease myocardial oxygen supply: 

Age, Smoking, Diabetes Mellitus (DM), Dyslipidemia (abnormal amount of lipids in blood-usually hyperlipidemia), Family history of cardiovascular disease, Hypertension, Kidney Disease (esp. microalbuminuria  or GFR<60ml/min), Obesity, Physical inactivity and prolonged psychosocial stress.

-Symptoms: Chest Discomfort (a pressure,heaviness or tightness, choking sensation). Separately, discomfort may also be experienced in the back, neck, jaw or shoulders (referred pain)  and shortness of breath (dypsnea).

*Pain may/may not be accompanied with breathlessness, sweating and nausea.

-Myocardial ischemia occurs when heart muscles receive inadequate supply of blood and oxygen to function normally either because of increased oxygen demand or decreased supply to myocardia (tissue hypoxia occurs)

-This inadequate perfusion of blood could be due to blocked or narrowed arteries (artherosclerosis).

1) Inadequate oxygen delivery

Inadequate oxygen transfer from lungs to blood.

-Inadequate delivery of oxygenated blood to cells (ischemia) due to low cardiac output (CO) which is determined by :

CARDIAC OUTPUT (CO)=HEART RATE (HR) X STROKE VOLUME (SV)

                                                                       and

by the back pressure against the aortic valve (diastolic blood pressure-preload)

which the heart must push against the valve to deliver the blood

Thus,

Increased Heart Rate (HR)=Increased Workload=Increased CO=Increased oxygen demand

Increased stroke volume (SV)=Increased Workload=Increased oxygen demand

Increased Stroke volume (SV)=Increased stretch of heart muscle which increases contractility or how hard the muscle contracts=Increased Workload=Increased oxygen demand

Increased diastolic BP=Increased workload to open aortic valve=Increased oxygen demand

The treatment of angina should then:

(a) Increase supplemental oxygen to the heart, deliver oxygen enriched blood via an adequate perfusion pressure (Increases oxygen supply)

(b) Dilate coronary arteries to increase flow of oxygen-enriched blood around any blockage to reach hypoxic cardiac muscle. (Increases oxygen supply)

(c) Decrease the workload of the heart to reduce oxygen demand

-Decrease preload by dilating the large veins, which decreases blood return to the atria and ventricles. This decreases stroke volume, which decreases cardiac output and thus decreases cardiac workload.

-Decrease afterload by dilating the large arteries, which decreases the diastolic BP, decreasing the amount of pressure the heart has to generate to open the aortic valve, which decreases cardiac workload.

-Decrease heart rate and contractility which will decrease Cardiac output, which will decrease cardiac workload.

Conditions that increases Oxygen supply

1.Stress
2.Exercise
3.During increased heart rate

Conditions that decrease Oxygen supply 

1.Coronary arteries diseases
—Accumulation of plaques
—Platelets aggregation
—Stenosis or spasm or constriction or narrowing
2.Reduction in blood flow to heart
—Due to constriction of blood vessels
3.Reduction in o2carrying capacity of blood
—Decrease Hb levels (in anemic conditions)
—Normal blood flow  and supply but decrease in o2 carrying capacity

Types of Angina:

1) Stable Angina (Effort angina)- Chest pain due to ischemia of the heart muscle (generally due to obstruction/spasm of the coronary arteries-Decreases oxygen supply)

Therapeutic treatment outcome: Improves balance of myocardial oxygen supply and demand (Decrease workload of heart)

(a) By increasing supply by dilating the coronary vasculature

(b) Decreasing demand by reducing cardiac work (Reducing CO)

*Most Drugs target (b) by decreasing heart rate, decreasing myocardial contractility (increase ESV, decreases SV), decreasing ventricular wall stress (decreasing preload, EDV by reducing the stretch of myocytes)

2) Prinzmetal Angina (Invariant)-Cornary artery spasm /Non-Exertional Angina

Due to: Spasms in the arteries that supply blood to the heart. Temporary constriction in one or more of the coronary arteries leads to lack of oxygen supply and nutrients (i.e. Reduced blood flow–>Reduced blood supply)

-Coronary vasoconstriction results in reduced blood flow and ischemic pain.

-Occurs in people aged 50 or younger

Severe and lasts more than 15 mins (DOES NOT GO AWAY!)

-Discomfort or pain usually in the early hours of the morning. Occurs more often during rest or extreme motion rather than physical activity.

Root cause: Unknown but females with a family history of coronary heart disease or aggressive behaviour (Type A) personality would increase risk. Drugs such as antibiotics, medicines and chemotherapy medications could precipitate CAS.

Recreational Drugs such as cocaine, Amphetamine, alcohol can also cause CAS.

Therapeutic treatment outcome: Prevent coronary vasospasm

Note: Calcium channel blockers, but not nitrates influence mortality and the incidence of Myocardial infarction favourably in variant angina.

Why? Ans: Calcium channel blockers (e.g. Verapamil or Diltiazemmay reverse coronary spasm refractory (Symptoms reoccur despite therapy) to intracoronary nitroglycerin.

In addition to relaxation of vascular smooth muscle, Calcium channel blockers also produce negative inotropic effects (decreases force) and chronotropic effects in the heart (decreases heart rate).

NO, on the other hand, has effects on vascular smooth muscle. The use of high doses of organic nitrates may reduce blood pressure  to an extent that coronary flow is compromised, thus reflex tachycardia occurs (overrides benefical effect on oxygen demand–>aggrevate ischemia) 

3) Unstable Angina-Acute coronary syndrome

-Pathophysiology: Due to the reduction of coronary blood flow due to the transient platelet aggregation on apparently normal endothelium, coronary artery spasms or coronary thrombosis.

-Process usually starts with artherosclerosis (building up of plaque which undergoes thrombosis and results in ischemia, resulting in cell necrosis)

-Occurs at rest (minimal exertion) and last for more than 10 mins

-Severe and/or occurs with a crescendo pattern (i.e. intensifies over time)

Indication of an impending heart attack

Therapeutic treatment outcome: Increase myocardial blood flow

(a) Use of anti-platelet agents and heparin to remove blood clot in coronary arteries

(b) Coronary by pass surgery to restore blood flow via mechanial means

(c) Use of coronary stents (balloons) to artificially dilate the coronary arteries so as to restore blood flow

Coronary Artery Bypass Graft

***Definition of key terms:

  • Stroke Volume: The volume of blood pumped from one ventricle of the heart with each beat.

SV= EDV-ESV

  • End-Diastolic Volume (EDV): Refers to the volume of blood in the right/left ventricle at the end load or filling in (Diastole). For an average man EDV approx 120 ml

Main factors affecting EDV are due to venous compliance. Increasing venous compliance means that the veins can be stretched more which implies more blood can be held in the periphery. Thus, venous return DECREASES and reduces EDV.

  • End-Systolic Volume (ESV): Refers to the volume of blood in a ventricle at the end of contraction or systole (beginning of diastole). For an average man ESV approx 50 ml, represented by the end of a T wave.

Main factors affecting ESV are afterload and contractility of the heart (Increase in contractility of the heart means lower End-Systolic Volume). 

  • Afterload: (aorta) The resistance to ejection during systole (the force opposing ventricular ejection). The ventricle must overcome aortic pressure in order to eject blood.

Increased afterload = increased workload and decreased cardiac output and slower contraction (More resistance)

Main factors affecting afterload: Aortic pressure and systemic vascular resistance

–>When afterload increases, there is an increase in end-systolic volume and a decrease in stroke volume.

  • Preload: End volumetric pressure that stretches the left or right ventricle of the heart to its greatest dimensions under physiological demands (i.e. the initial stretching of cardiomyocytes prior to contraction)

–>The pressure at the end of diastole (filling of ventricles)…aka left ventricular end diastolic pressure. Partial reflection of volume present in ventricles. 

Factors affecting preload: Influenced by venous return. Increased preload (to a point) = Increased cardiac output (More blood pumped out)

  • Ejection volume: Represents the volumetric fraction of EDV pumped out of the ventricle (heart) with each heart beat

Ef= (SV/EDV)= (EDV-ESV)/EDV

  • Cardiac Workload: The amount of work the heart has to do to pump blood throughout the body.

-Main factors: Amount of blood pumped from left ventricle to the rest of the body + Arterial resistance + Strength and frequency of muscle contractions

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