CARDIOVASCULA

R
DISORDERS
GROUP 2
Heart
Anatomy
The heart functions as a muscular
pump, circulating blood
throughout the pulmonary and
systemic circuits. It is located in
the mediastinum, enclosed within
the pericardial cavity or
pericardium.
Pericardium: A double-
walled sac containing the
heart, consisting of the
fibrous and serous layers.
 Structure and
Functions
Chambers:
• Atria (right and left): Receive blood returning to the heart.
• Ventricles (right and left): Pump blood out of the heart.

Valves:
• Atrioventricular (AV) valves (tricuspid and mitral): Prevent
backflow from ventricles to atria.
• Semilunar valves (pulmonary and aortic): Prevent backflow
from arteries to ventricles.

Wall layers of the Heart:

• Myocardium: The muscular wall of the heart, responsible for
contraction.
• Endocardium: Lines the heart chambers, ensuring smooth
blood flow.

Septa:
• Interatrial septum: Separates the atria.
• Interventricular septum: Separates the ventricles.
 Conduction
System (Electrical
Control):
The conduction system initiates and
Component
coordinates heart contractions.
s:
• Sinoatrial (SA) node: The heart's pacemaker,
located in the right atrium. Generates
impulses at a basal rate of approximately 70
beats per minute.
• Atrioventricular (AV) node: Delays impulse
transmission, allowing atrial contraction.
• Bundle of His: Conducts impulses from the
AV node to the ventricles.
• Purkinje fibers: Distribute impulses
throughout the ventricular myocardium,
causing contraction.

Impulse Pathway: SA node → atria → AV node →

bundle of His → Purkinje fibers → ventricles.
 Control of the
Heart
Regulation:
Autonomic nervous system (sympathetic and
parasympathetic) modulates heart rate.
• Sympathetic -
• Parasympathetic -
Hormones (e.g., epinephrine) influence heart
rate and contractility.
Intercalated discs: Specialized junctions
between cardiac muscle cells, facilitating rapid
impulse transmission.
 Coronary Circulation: Blood
Supply to the Heart
Importance of Coronary Circulation:
Allows the oxygenated blood flow and
circulate through all body systems.

Cardiac muscle requires a constant supply

of oxygen and nutrients to function.
Coronary arteries provide oxygen and
nutrients to the heart muscle.
Limited oxygen storage capacity in the
heart muscle makes continuous blood
supply crucial.
 Major Coronary
Arteries:
Two main arteries: the right and left coronary arteries.

Originate from the aorta, just above the aortic valve.

Left Coronary Artery:

• Divides into the left anterior descending (LAD) artery.
• Supplies the anterior interventricular septum and left
ventricle.
• Also branches into the circumflex artery, supplying the
left atrium and left ventricle.

Right Coronary Artery:

• Supplies the right atrium and ventricle.
• Branches into the marginal artery and posterior
interventricular artery.
Collateral Develops when a coronary artery is partially
obstructed, providing alternate pathways.

Circulation • Provides alternate pathways for blood

flow.
• Artery B dilates (widens) to compensate
for reduced flow in Artery A.
• Capillaries from Artery B open and
extend to supply the affected area.
• Helps maintain blood flow to the heart
muscle, reducing the risk of ischemia
(lack of blood supply).

Anastomoses:
• Connections between branches of
coronary arteries and blood vessels.
• Facilitate collateral circulation by
providing alternative routes for blood.
• Clinically significant for surgical
procedures such as coronary artery
bypass grafting (CABG).
The Cardiac
Cycle
The cardiac cycle
refers to the
alternating sequence
of events in one
heartbeat: diastole
(relaxation) and
systole (contraction)
of the heart. This
coordinated cycle
ensures efficient blood
pumping.
Events in 1. Atria Relaxed, Ventricles Relaxed (Diastole): Blood
flows from the superior and inferior venae cavae into
the Cardiac the right atrium, and from the pulmonary veins into the
Cycle left atrium.
2. AV Valves Open: Pressure in the atria exceeds
ventricular pressure, opening the AV valves.
3. Blood Flows into Ventricles: The atria empty into the
ventricles.
4. Atrial Systole: The atria contract, pushing any
remaining blood into the ventricles.
5. Atria Relax.
6. Ventricular Systole Begins: Ventricles contract, and
pressure increases.
7. AV Valves Close: Prevent backflow of blood into the
atria.
8. Isovolumetric Contraction: For a brief moment, all
valves are closed, and ventricular pressure continues to
build without volume change.
9. Semilunar Valves Open: When ventricular pressure
exceeds atrial pressure, the semilunar valves open, and
blood is ejected into the pulmonary artery and aorta.
Note: Left ventricular pressure must be higher than
aortic pressure for blood ejection.
10. End of Systole: The atria begin to fill again as the
ventricles relax, the aortic and pulmonary valves close
Equal Volumes of Blood:
The same volume of blood is pumped from the right and left
sides of the heart during each cycle.
This ensures balanced systemic and pulmonary circulation.

Additional Points:
Anastomoses: Direct connections between small branches of
arteries, providing alternate blood flow routes.
Collateral Circulation: The development of new blood vessels
to bypass obstructed arteries, crucial for maintaining blood
flow during coronary artery disease.
Factors Affecting Coronary Blood Flow:

Myocardial Contraction: Compresses arteries, reducing

blood flow.
Atherosclerosis: Narrowing of arteries, reducing blood
flow.
Impaired Diastole: Reduces coronary filling time.

Right Coronary Artery Dominance:

In most individuals, the right coronary artery supplies the
SA node.
Venous Drainage: Coronary veins drain into the right
atrium.
Cardiac Cycle: The sequence of events in a single
heartbeat.

Diastole: Relaxation of the heart muscle.

Systole: Contraction of the heart muscle.
Atria: The upper chambers of the heart.
Ventricles: The lower chambers of the heart.
AV Valves (Atrioventricular Valves): Valves between the atria and
ventricles.
Semilunar Valves: Valves between the ventricles and the pulmonary
artery/aorta.
Isovolumetric Contraction: A brief period of ventricular contraction
with no change in volume.
Anastomoses: Connections between blood vessels.

Collateral Circulation: Alternate blood flow pathways.

Atherosclerosis: Plaque buildup in arteries.
The Cardiac Cycle: Sounds,
Pulse, and Output
Diastole (Stages 1, 2, Systole (Stages 3, 4, 5):
6): Stage 3: Systole begins,
Stage 1: All valves closed, ventricles are full.
atria and ventricles relax. Stage 4: Ventricles begin
Stage 2: Increased atrial contraction, atria relax.
pressure opens AV valves, Stage 5: Ventricles contract,
ventricles fill. increased pressure opens
Stage 6: Ventricles relax, aortic and pulmonary
atria and pulmonary veins valves, blood ejected.
fill, pulmonary valves close.
The Cardiac Cycle: Sounds,
Pulse, and Output
Heart Sounds (Lub-Dub) Pulse
"Lub" (S1): Closure of the AV • Indicates heart rate.
valves at the beginning of • Palpable in peripheral arteries
ventricular systole. (e.g., radial artery in the wrist).
"Dub" (S2): Closure of the • During ventricular systole, the
semilunar valves at the end of surge of blood expands the
ventricular systole. arteries.
Murmurs: Abnormal heart sounds • Characteristics of the pulse
due to turbulent blood flow, often (weakness, irregularity) can
caused by defective valves (leak indicate problems.
or incomplete closure). • Apical Pulse: Heart rate
Septal Defects: Abnormal holes in measured directly over the
the heart septum can also cause heart.
murmurs.
Cardiac
Output (CO)
Volume of blood ejected by a ventricle in one minute.
CO = Heart Rate (HR) x Stroke Volume (SV).

Stroke Volume: Volume pumped from one ventricle in one

contraction.

Total blood volume circulates through the system every minute.

Cardiac output can increase with exercise due to increased heart

rate and venous return.

Starling's Law: The heart contracts more forcefully when it is

stretched, increasing stroke volume.
 Pulse Points
Pulse points indicate arterial locations where
pulsations can be felt.
Common points include:
• Temporal artery (forehead)
• Facial artery (jaw)
• Carotid artery (neck)
• Apical pulse (heart)
• Brachial artery (elbow)
• Radial artery (wrist)
• Femoral artery (groin)
• Popliteal artery (behind knee Dorsalis
pedis (foot)
Pulse reflects heart rate and rhythm, used to
assess cardiovascular function.
Cardiac Definition: The amount of blood

Output (CO)
pumped by each ventricle in one
minute.
Formula: CO = Heart Rate (HR) x Stroke
Volume (SV)
HR: Number of ventricular
contractions per minute.
SV: Volume of blood ejected per
ventricle per contraction.
Average CO: 4900-5000 mL/min.
Factors Affecting CO:
Sympathetic nervous system
stimulation
Epinephrine (adrenaline)
Venous return (preload)
Myocardial contractility
Peripheral resistance (afterload)
Cardiac reserve: ability of the heart to
increase output in response to
increased demand.
Blood
Vessels
Arteries, capillaries, and veins form a closed system for blood distribution.

Arteries: Carry blood away from the heart.

Capillaries: Facilitate exchange of oxygen and carbon dioxide between
blood and tissues.
Veins: Return blood to the heart.

Pulmonary and systemic circulations allow for gas exchange in the lungs
and nutrient delivery throughout the body.

Preload refers to the amount of blood delivered to the heart by venous

return.
Afterload is the force required to eject blood from the ventricles.
 Blood Vessel
Arterioles:
• Characteristics:
Smaller branches of arteries.
• Control blood flow into capillaries.
• Smooth muscle in walls regulates diameter (vasoconstriction/vasodilation).

Capillaries:
• Very small vessels forming networks.
• Slow blood flow for exchange of nutrients and wastes.
• Precapillary sphincters control blood flow into capillaries.

Veins:
• Carry blood back to the heart.
• Larger veins collect blood from venules.
• Majority of blood (approximately 70%) is located in veins at any time.
• Capacitance vessels (storage of blood).
• Valves prevent backflow.
• Skeletal muscle action and respiratory movements assist venous return.

Vein Structure:
Walls made of three layers: tunica intima (endothelial layer), tunica media (smooth
muscle), tunica adventitia (connective tissue).
 Anatomy of Major Arteries
and Blood Vessel
Arteries highlighted:
Characteristics
Head & Neck: Anterior Cerebral, Middle Cerebral,
Basilar, Internal Carotid, External Carotid,
Vertebral, Common Carotid.
Upper Extremities: Subclavian, Axillary, Brachial,
Radial, Ulnar.
Thorax: Innominate (Brachiocephalic trunk).
Abdomen: Celiac, Splenic, Renal, Superior
Mesenteric, Aorta, Inferior Mesenteric.
Lower Extremities: Common Iliac, External Iliac,
Internal Iliac, Common Femoral, Deep Femoral
(Profunda Femoris), Superficial Femoral, Popliteal,
Anterior Tibial, Posterior Tibial, Peroneal, Dorsalis
Pedis.
Function: Arteries transport blood away from the
heart to body tissues.
 Anatomy of Major Veins
and their Characteristics
Veins Highlighted:

Head & Neck: Internal Jugular, External Jugular.

• Upper Extremities: Subclavian, Axillary, Brachial, Radial
(Paired), Ulnar (Paired), Cephalic, Basilic, Median
Cubital.
• Thorax: Right Innominate (Brachiocephalic), Left
Innominate (Brachiocephalic), Superior
Vena Cava, Hepatic, Renal, Inferior Vena Cava.
• Abdomen: Common Iliac, Internal Iliac (Hypogastric),
External Iliac.
• Lower Extremities: Common Femoral, Profunda
Femoris, Superficial Femoral, Popliteal,
• Anterior Tibial (Paired), Posterior Tibial (Paired),
Peroneal (Paired), Great Saphenous,
Lesser Saphenous.
• Deep Arm Veins & Superficial Arm Veins
• Deep Leg Veins & Superficial Leg Veins
 Veins Characteristics
Structure:
Chemical Mediators:
• Tunica Intima: Endothelial layer (innermost).
• Tunica Media: Layer of smooth muscle (thinner than
• Histamine and
in arteries).
• Tunica Adventitia: Outer connective tissue layer temperature increase
(contains elastic and collagen fibers). can cause vasodilation.
• Vasa Vasorum: Tiny blood vessels that supply blood
• Norepinephrine and
to the vessel walls.
• Compliance: Veins are highly elastic, allowing them epinephrine stimulate
to adjust to changes in blood volume. alpha-adrenergic
• Blood Reservoir: Veins hold a large percentage of
blood volume. receptors, causing
• Valves: Prevent backflow of blood, especially vasoconstriction.
important in limbs. • Angiotensin is a potent
• Smooth Muscle: Less smooth muscle than arteries.
• Autoregulation: localized
systemic vasoconstrictor.
vasodilation/vasoconstriction in response to tissue • Vasomotor tone is
needs. maintained by the
Example: Decreased pH, increased CO2, or decreased sympathetic nervous
O2 leads to vasodilation. system.
Blood
Pressure
Blood Pressure (BP): Pressure of blood against systemic
arterial walls.
Normal Range: 120/70 mmHg (approximate).
Systolic Pressure: Higher number, pressure during
ventricular contraction.
Diastolic Pressure: Lower number, pressure during
ventricular relaxation.
Measurement: Brachial artery using a sphygmomanometer
and inflatable cuff.
Pulse Pressure: Difference between systolic and diastolic
pressure.
Equation: BP = CO x PR
CO: Cardiac Output (volume of blood pumped per minute).
PR: Peripheral Resistance (resistance to blood flow in
arteries).
Factors Affecting Blood
Pressure
Cardiac Output (CO): Increased CO leads to increased BP. Decreased CO leads to
decreased BP.
Peripheral Resistance (PR): Increased PR leads to increased BP. Decreased PR
leads to decreased BP.
Factors Affecting Blood
Pressure Examples (Figure 18-8): No change
in CO, no change in PR = No
change in BP. Increased CO,
decreased PR = Elevated BP.
Increased Heart Rate (CO),
systemic vasoconstriction (PR) =
Increased BP. Decreased Stroke
Volume (CO), systemic
vasodilation (PR) = Decreased BP.
Viscosity: Blood thickness affects BP.
Elasticity: Arterial wall elasticity affects BP.
Venous Return: Amount of blood returning to the
heart affects CO.
 Regulation of Blood
Pressure
Autonomic Nervous System (ANS):
Sympathetic Nervous System (SNS) increases BP via
vasoconstriction and increased heart rate.
Parasympathetic Nervous System decreases BP via
vasodilation and decreased heart rate.
Baroreceptors: Detect changes in blood pressure.
Signal the vasomotor control center in the medulla.
Adjust blood distribution to maintain normal BP.
Example: Adjusting for postural changes.
Hormones
Hormonal Control of Blood Pressure

Antidiuretic Hormone (ADH) increases water reabsorption by

the kidneys, leading to higher blood volume and blood pressure.
Also acts as a vasoconstrictor (vasopressin).

Aldosterone increases blood volume by promoting sodium

reabsorption in the kidneys.

Renin-Angiotensin-Aldosterone System (RAAS) is initiated

by a decrease in renal blood flow. Renin activates
angiotensinogen, leading to angiotensin II, which is a potent
vasoconstrictor and stimulates aldosterone release.
 HEART DISORDERS
Heart Disorders - Cardiovascular disorders are a major cause of illness and
death in North America. These disorders include conditions like:

• Congenital Heart Defects: These are heart abnormalities present from birth.
• Hypertensive Heart Disease: This heart condition arises from high blood
pressure, which puts extra strain on the heart.
• Angina: It's chest pain that occurs when the heart muscle doesn't get
enough oxygen. This is often due to reduced blood flow, commonly from
conditions like atherosclerosis or coronary artery spasms.
• Heart Attacks (Myocardial Infarction): This happens when a coronary artery
gets completely blocked, leading to prolonged lack of oxygen and the death
of heart muscle cells.
• Arrhythmias: These are irregular heartbeats or abnormal heart rhythms.
• Congestive Heart Failure: It's a condition where the heart can't pump
enough blood to meet the body's needs.
 Diagnostic Tests for Cardiovascular
Function
• Electrocardiogram (ECG): Used for • Auscultation: Stethoscope is used
diagnosing arrhythmias, to detect murmurs from valve
myocardial infarction, infection, abnormalities.
and pericarditis; it's noninvasive
and shows heart conduction
activity. Holter monitors record
ECG changes during daily
activities.
 Diagnostic Tests for Cardiovascular
• Echocardiography: Function
Ultrasound • Exercise Stress Tests: Assess
creates heart and valve images, cardiovascular function and check
showing valvular abnormalities, for exercise-induced problems.
congenital defects, and changes in
heart structure/function.
 Diagnostic Tests for Cardiovascular
• Chest X-ray: Shows Function
heart • Nuclear Imaging: Uses radioactive
size/shape and pulmonary substances to assess infarct size,
congestion. myocardial perfusion, and
ventricle function.
 Diagnostic Tests for Cardiovascular
Function
• Cardiac Catheterization: Catheter • Blood Tests: Assess serum
is inserted into a blood vessel to triglyceride and cholesterol
visualize the heart, measure levels, electrolytes, and blood
pressures, and assess valve/heart cell counts. Arterial blood gas
function. Coronary angiography determination is essential in
visualizes coronary artery blood patients with shock or myocardial
flow. infarction.
 Diagnostic Tests for Cardiovascular
Function
Coronary angiography: is
a medical procedure used
to visualize the blood flow
within the coronary
arteries. These are the
arteries that supply
oxygen-rich blood to the
heart muscle.
General Treatment Measures for Cardiac
Disorders
• Dietary Modifications: Reducing total fat, saturated
fat, "trans" fats, and sodium intake.

• Regular Exercise: Improves cardiovascular

function, lowers lipid levels, increases HDL, and
reduces stress.
• Cessation of Smoking: Decreases coronary disease
risk by reducing vasoconstriction, heart rate,
platelet adhesion, and increasing oxygen
availability.
General Treatment Measures for Cardiac
• Drug Therapy: Disorders
⚬ Vasodilators (e.g., nitroglycerin): Reduce workload and
act as coronary vasodilators.
⚬ Beta-blockers (e.g., metoprolol): Treat hypertension,
dysrhythmias, and angina by blocking SNS effects on the
heart.
⚬ Calcium Channel Blockers: Decrease cardiac
contractility, act as antiarrhythmics, antihypertensives,
and vasodilators.
⚬ Digoxin: Treats heart failure and atrial dysrhythmias by
slowing conduction and increasing heart contractility.
⚬ Antihypertensive Drugs: Include adrenergic-blocking
agents, calcium blockers, diuretics, ACE inhibitors, and
angiotensin II receptor blocking agents.
General Treatment Measures for Cardiac
Disorders
• Drug Therapy:
.
⚬ Diuretics: Remove excess sodium and water to
reduce blood volume and edema.
⚬ Anticoagulants: Reduce blood clot formation risk;
aspirin is commonly used.
⚬ Cholesterol/Lipid-Lowering Drugs (Statins):
Reduce LDL and cholesterol by blocking liver
synthesis.
 CORONARY ARTERY DISEASE (CAD)
Coronary Artery Disease (CAD), also known as Ischemic Heart
Disease (IHD), and Acute Coronary Syndrome, are terms that
describe a spectrum of conditions resulting from insufficient
blood supply to the heart muscle.

• Coronary Artery Disease (CAD): This is a general term that

includes conditions where the heart muscle doesn't get
enough blood.

• Ischemic Heart Disease (IHD): This is another term for CAD,

emphasizing the ischemia (lack of oxygen) to the heart
muscle.

• Acute Coronary Syndrome: This refers to a sudden reduction

in blood flow to the heart. It includes conditions like unstable
 Arteriosclerosis Atherosclerosis
• Arteriosclerosis is a general • Atherosclerosis is a specific
term describing the hardening type of arteriosclerosis.
and thickening of arterial • It's characterized by the
walls. buildup of atheromas (plaques)
• It mainly affects small arteries within the walls of large
and arterioles. arteries.
• This process reduces the • Atheromas consist of lipids
elasticity of arteries, making (fats), cells, fibrin, and cell
them thick and hard, which can debris.
narrow the lumen (the inside • These plaques can obstruct
space of the artery). blood flow.
• Arteriosclerosis can lead to
ischemia (reduced blood flow)
and necrosis (tissue death).
 Key Differences
• Arteriosclerosis is a broader term for the
general hardening and loss of elasticity in
arteries, especially smaller ones.

• Atherosclerosis is a specific condition

involving plaque buildup within the walls
of larger arteries.
 Composition of Lipoproteins

Lipoproteins are essential substances that transport

lipids (fats), including cholesterol and triglycerides, in
the blood.
Cholesterol + Triglycerides + Proteins +
Phospholipids
=
LIPOPROTEI
N
Transport of Lipoproteins in Blood
1.Dietary cholesterol and triglycerides are taken in.
2.Chylomicrons, which are lipoprotein particles, are
absorbed into the blood and lymph.
3.Lipids are taken up by adipose (fat) and skeletal muscle
cells.
4.Remnants are sent to the liver.
5.The liver synthesizes lipoproteins.
6.LDL (low-density lipoprotein) transports cholesterol to
cells.
7.LDL attaches to LDL receptors in smooth muscle and
endothelial tissue.
8.HDL (high-density lipoprotein) transports cholesterol
from cells to the liver.
Transport of Lipoproteins in Blood

In essence, lipoproteins are like little packages

that carry fats through the bloodstream,
delivering them to where they're needed and
removing excess cholesterol.
 Development of an Atheroma Leading to
Arterial Occlusion
The development of an atheroma, which can lead to arterial occlusion
(blockage), is a complex process:
1.It starts with damage to the endothelium, the inner lining of the
artery.
2.This damage causes inflammation.
3.White blood cells (monocytes and macrophages) and lipids
accumulate in the artery's inner lining.
4.Smooth muscle cells multiply.
5.A plaque (atheroma) forms and inflammation continues.
6.Platelets stick to the damaged area, forming a thrombus (blood
clot) and partially obstructing the artery.
7.Lipids continue to build up, and fibrous tissue develops.
8.This process narrows the artery, reducing blood flow.
9.The plaque can rupture, leading to a thrombus that causes a total
obstruction.
Development of an Atheroma Leading to
Arterial Occlusion
 Possible Consequences of
Atherosclerosis
Atherosclerosis can lead to a range of serious
cardiovascular complications:
• As atheromas (plaques) grow, they can
partially obstruct arteries, leading to angina
pectoris (chest pain due to lack of oxygen to
the heart muscle).
• If an atheroma causes a total obstruction, it
can result in a myocardial infarction (heart
attack), where part of the heart muscle dies.
 Possible Consequences of
Atherosclerosis
• Atherosclerosis can also affect arteries in other
parts of the body, leading to:
⚬ Strokes (cerebrovascular accidents) if it occurs in
carotid or cerebral arteries.
⚬ Peripheral vascular disease, causing damage to
blood flow in the legs and feet.
⚬ Aneurysms (bulges in the artery wall) or rupture
and hemorrhage of the vessel.
Possible Consequences of
Atherosclerosis
 Etiology of Atherosclerosis
• The etiology of atherosclerosis is
multifactorial, meaning it develops from
a combination of factors. These factors
can be categorized into those that can
be changed (modifiable) and those that
cannot (non-modifiable).
 Etiology of Atherosclerosis
Non-modifiable risk factors (cannot be changed):

• Age: The risk of atherosclerosis increases with age,

especially after 40 years, and is more common in
men.
• Gender: Women have some protection due to higher
HDL levels until after menopause, when estrogen
levels decrease.
• Genetic/Familial Factors: These factors influence
lipid levels, metabolism, and cell receptors for
lipids; some conditions, like familial
hypercholesterolemia, are inherited.
 Etiology of Atherosclerosis
Modifiable risk factors (can be changed):

• Obesity and Diet: Diets high in cholesterol and animal fat

contribute to higher serum lipid levels, particularly LDL.
Obesity, especially in children, is a growing concern.
• Cigarette Smoking: Smoking lowers HDL, increases LDL,
promotes platelet adhesion, and increases fibrinogen and
clot formation, as well as vasoconstriction.
• Sedentary Lifestyle: Lack of physical activity contributes to
sluggish blood flow and obesity. Exercise is beneficial as it
reduces blood pressure and stress and increases HDL while
lowering LDL and cholesterol.
 Etiology of Atherosclerosis
Modifiable risk factors (can be changed):

• Diabetes Mellitus: Individuals with diabetes,

especially if poorly controlled, tend to have
increased serum lipid levels and endothelial
degeneration.
• Poorly Controlled Hypertension: High blood
pressure causes damage to the endothelium.
• Oral Contraceptives and Smoking: The
combination of some oral contraceptives and
smoking increases risk
 Diagnostic Tests for
Atherosclerosis
1.Serum Lipid Levels
2.C-Reactive Protein (CRP)
Levels
3.Exercise Stress Testing
4.Nuclear Medicine Studies
Treatments for Atherosclerosis
• Weight Management
• Dietary Changes
• Medications: Lipid-reducing
drugs
• Sodium Intake Restriction
• Management of Primary
Disorders
• Smoking Cessation
• Regular Exercise
• Anticoagulant Therapy
 Coronary Artery Bypass Grafting
(CABG)
Coronary artery bypass grafting (CABG) is a surgical
procedure used to improve blood flow to the heart in people
with severe coronary artery disease.

• During CABG, a healthy blood vessel is taken from another

part of the body (often a vein from the leg or an artery
from the chest).
• This vessel is then used to "bypass" the blocked portion of
a coronary artery, creating a new route for blood to flow to
the heart muscle.

In essence, CABG reroutes blood flow around the obstruction,

ensuring the heart receives the oxygen and nutrients it needs
Coronary Artery Bypass Grafting
(CABG)
 Angina Pectoris
Angina pectoris is chest pain due to a
temporary oxygen deficit in the heart muscle.
It is often triggered by physical or emotional
stress. Myocardial infarction (MI), or heart
attack, occurs when a coronary artery is
completely blocked, leading to prolonged
ischemia and death of heart tissue.
Angina
Pectoris
 Etiology
Angina occurs when the heart muscle's demand for oxygen
exceeds the supply. This mismatch can result from:
• Reduced blood supply due to partial obstruction by
atherosclerosis.
• Coronary artery spasm.
• Arteriosclerosis.
• Myocardial hypertrophy (heart enlargement).
• Severe anemias.
• Respiratory disease.
• Increased oxygen demands, such as from tachycardia or
hypertension.
Factors that can precipitate
angina attacks
• Physical or emotional stress.
• Running upstairs.
• Getting angry.
• Respiratory infection with fever.
• Exposure to weather extremes or
pollution.
• Eating a large meal.
 Signs and Symptoms
• Recurrent, intermittent brief episodes of
substernal chest pain.
• Pain triggered by physical or emotional
stress.
• Pain described as tightness or pressure in the
chest.
• Pain may radiate to the neck and left arm.
• Possible pallor, diaphoresis (excessive
sweating), and nausea.
• Attacks vary in severity and last a few
seconds or minutes.
 Treatment
• Emergency Treatment for Angina Attack
⚬ Let the patient rest and stop activity.
⚬ Seat the patient in an upright position.
⚬ Administer nitroglycerin sublingually.
⚬ Check pulse and respiration.
⚬ Administer oxygen if necessary.
⚬ If pain persists after 5 minutes, a second dose of
nitroglycerin can be given.
⚬ If pain persists after three doses in a 10-minute period,
treat as a heart attack and call for assistance.
⚬ For a patient without a history of angina, seek emergency
medical aid if pain persists after 2 minutes.
 Treatment
• Anginal pain is usually quickly relieved by rest and coronary
vasodilators, such as nitroglycerin.

Long-term management may include:

• Avoiding sudden physical exertion, especially in cold or hot
weather.
• Avoiding marked fatigue or strong emotional incidents.
• Antianxiety and stress reduction techniques.
• Regular use of nitroglycerin in various forms (ointment,
patch, spray, oral tablets) to reduce the number of attacks.
 Heart Attack
-is the blockage of a coronary artery cuts off blood
supply to part of the heart muscle. This leads to
tissue death (necrosis) in the affected area.
Damage and Healing:
• The size of the blockage determines the severity of
the heart attack.
• Inflammation occurs around the damaged area.
• Scar tissue forms over time, replacing the dead
muscle.
• Collateral circulation (new blood vessels) can
develop to compensate, but it's not always
effective.
 These signs may be
WARNING intermittent at first

SIGNS OF • Chest pain (pressure,

heaviness, burning)

HEART especially with increased

activity.
• Shortness of breath,
ATTACK sweating, weakness,
fatigue.
• Nausea, indigestion.
• Anxiety and fear.
MANIFESTATIONS:
• PAIN- sudden, severe chest pain
radiating to the left arm, shoulder, jaw,
or neck is the hallmark of myocardial
infarction.
• Pallor and diaphoresis, nausea, dizziness
and weakness, and dyspnea.
• Marked anxiety and fear
• Hypotension: pulse is rapid and weak as
cardiac output decreases and shock
develops.
TREATMENT
:
• Thrombolytic therapy (clot-dissolving drugs)
is crucial within the first 30 minutes.
• Paramedics administer medications and
defibrillation.
• Automated defibrillators are available in
public places.
SYMPTOMS OF HEART ATTACK:

• Severe chest pain: Described as crushing or

heavy, not always present.
• Other symptoms: Indigestion, nausea,
dizziness, weakness, anxiety, rapid pulse, low
blood pressure.
DIAGNOSTIC TESTS:

• ECG (Electrocardiogram): Detects changes in heart

rhythm and electrical activity.
• Blood tests: Measures levels of cardiac enzymes
(troponins, CK-MB, AST, LDH) released when heart
muscle is damaged.
• Other tests: Electrolyte levels, white blood cell count,
and inflammatory markers may be checked.
 COMPLICATIONS:
• Sudden death: Often due to arrhythmias (irregular
heart rhythms).
• Arrhythmias: Can be caused by damage to the
heart's electrical system.
• Cardiogenic shock: Heart can't pump enough blood,
leading to organ damage.
• Congestive heart failure (CHF): Heart's pumping
ability is weakened.
• Rupture of the necrotic area: Weakened heart
muscle can tear, especially in those with ventricular
aneurysms.
• Thromboembolism: Blood clots can form in the
damaged area and travel to other parts of the body,
causing complications like pulmonary embolism or
stroke.
 TREATMENT:
• Paramedics provide immediate care, including life-saving
medications.
• Hospitals offer oxygen therapy, pain relief, and medications
to dissolve clots (thrombolytics).
• Pacemakers may be used if the heart's electrical system is
affected.
• Surgery (like bypass surgery) may be needed for severe
cases.
• Cardiac rehabilitation programs help with recovery through
diet, exercise, and stress reduction.
• Aspirin is often recommended to prevent further clotting.
 Cardiac Dysrhythmias
(Arrhythmias)
• Abnormal heart rhythms caused by damage to the
heart's electrical system or other factors like electrolyte
imbalances or stress.
• Symptoms: Palpitations, dizziness, lightheadedness,
chest pain, fainting.
• Diagnosis: ECG (electrocardiogram) is used to monitor
heart rhythm.
• Treatment: Depends on the type of arrhythmia and its
cause.
 Types of Arrhythmias
• Sinus Node • Atrial Conduction
Abnormalities: Abnormalities:
⚬ Sinus bradycardia: ⚬ Atrial Conduction
regular but slow heart Abnormalities are the
rate, less than 60 beats most common
per minute dysrhythmias.
⚬ Sinus tachycardia: ⚬ Atrial fibrillation:
Rapid and irregular
regular rapid heart rate, contractions of the atria.
100-160 beats per ⚬ Premature atrial
minute. contractions (PACs):
⚬ Sick sinus syndrome: Extra heartbeats
is a heart condition originating in the atria.
marked by alternating
bradycardia (slow) and
tachycardia (fast) heart
• Heart's Electrical • ECG: A test that records the
System: The heart has a heart's electrical activity. The
natural pacemaker (SA image shows how different parts
node) that sends signals of the ECG wave (P, QRS, T)
through pathways (AV correspond to different electrical
events in the heart.
node, bundle branches)
to make it contract.
• Atrioventricular Node • Ventricular Conduction
Abnormalities (Heart Abnormalities: Problems with
Blocks): Problems with electrical signals in the
electrical signals passing from ventricles.
the atria to the ventricles.
⚬ Bundle Branch Block:
• First-degree: Slowed Delayed conduction in one
conduction, prolongs the PR ventricle, usually no major
interval. The time between atrial effect.
and ventricular contractions. ⚬ Ventricular Tachycardia:
• Second-degree: Some signals Rapid heart rate, reduces
blocked, leading to a missed blood output.
ventricular conduction. ⚬ Ventricular Fibrillation:
• Third-degree (Complete): No Uncoordinated contractions,
transmission of impulses from ineffective pumping, can
the atria to the ventricles, cause cardiac arrest.
ventricles contract ⚬ Premature Ventricular
spontaneously at a slow rate of Contractions (PVCs): Extra
30-45 beats per minute. beats from the ventricle,
usually harmless unless
frequent.
Treatment: Pacemakers:
• Small device implanted to
• Identify and treat regulate heartbeat.
the cause: Drugs, • Uses electrical signals to
electrolyte stimulate the heart.
• Helps when the heart's
imbalances, heart natural pacemaker isn't
disease. working properly.
• Antiarrhythmic
drugs: To control
abnormal rhythms.
• Pacemaker: To
regulate heart rhythm
if other treatments
fail.
Cardiac Arrest: KEY TAKEAWAYS:
A heart attack is a serious medical emergency
caused by a blocked artery, leading to heart
• Sudden stop of heart function. muscle damage. Recognizing the warning signs
and seeking immediate treatment is crucial to
• No blood flow, leading to minimize damage and improve survival.
unconsciousness and breathing A heart attack causes significant damage to the
cessation. heart muscle, leading to a range of symptoms
and potential complications. Early diagnosis and
• Caused by heart problems, drug treatment are crucial to minimizing damage and
overdose, etc. preventing life-threatening consequences.
Treatment for heart attacks focuses on restoring
blood flow and preventing further damage, while
treatment for arrhythmias aims to correct
Emergency Treatment (AED): abnormal heart rhythms and manage symptoms.
Both conditions require prompt medical attention
and ongoing care.
• AED (Automated External
Pacemakers help hearts beat regularly, while
Defibrillator): Device that delivers AEDs are crucial for restarting a heart during
an electric shock to restart the heart. cardiac arrest. CPR is vital until an AED is
available.
• Used in cardiac arrest caused by
ventricular fibrillation.
• Simple to use: Follow voice
prompts.
• CPR (Cardiopulmonary
Resuscitation): Chest
compressions and rescue breaths to
maintain blood flow until AED arrives.
 Congestive Heart Failure (CHF)
and its progression.
• CHF occurs when the heart can't
pump enough blood to meet the
body's needs. It can be acute
(sudden) or chronic (long-term)
and results from various heart
problems or other conditions.

Causes include:

Heart problems: Heart attack,

valve defects.
Other conditions: Hypertension
(high blood pressure).
The page focuses on left-sided CHF:
• Heart muscle weakens (often the left ventricle).
• Ventricle doesn't empty fully.
• Cardiac output (blood pumped) decreases.
• Blood backs up in the lungs (pulmonary congestion).
• This back-up increases resistance for the right ventricle, potentially
leading to right-sided CHF:
• Right ventricle weakens and can't empty fully.
• Blood backs up in the body (systemic circulation).
• Edema (swelling) occurs in the legs and digestive system.

The body tries to compensate through:

Sympathetic Nervous System (SNS) activation: Increases heart rate
and force, constricts blood vessels.
Renin-Angiotensin System activation: Leads to fluid retention.
Treatment for CHF includes
medications that:
• Reduce heart workload: Alpha-
adrenergic blockers, Beta blockers,
Calcium blockers.
• Improve heart function: Digoxin.
• Help the body get rid of excess
fluid: Diuretics.
• Block the renin-angiotensin
system: ACE inhibitors.

In short, CHF is when the heart fails to

pump adequately, leading to fluid
buildup in the lungs and body. The
body tries to compensate, and
medications are used to manage the
condition.
Left-Sided CHF: Right-Sided CHF:
• Left ventricle weakens and • Right ventricle weakens and
can't empty properly. can't empty properly.
• Decreased cardiac output • Decreased cardiac output (blood
(blood pumped) to the pumped) to the body.
body. • Reduced blood flow to the
• Reduced blood flow to the kidneys, triggering the renin-
kidneys, triggering the angiotensin system, leading to
renin-angiotensin system, fluid retention.
• Blood backs up into the systemic
leading to fluid retention. circulation (vena cava).
• Blood backs up into the • Increased venous pressure causes
lungs (pulmonary vein). edema (swelling) in legs and liver,
• High pressure in lung and other abdominal organs.
capillaries causes • Very high venous pressure leads
pulmonary congestion or to distended neck veins and
edema (fluid in the lungs). cerebral edema (fluid in the
brain).
The body's compensatory mechanisms (renin-angiotensin, SNS)
can worsen the condition:
* Increased heart rate and peripheral resistance strain the heart.
* Increased fluid retention adds to the heart's workload.
* The heart chambers dilate (enlarge), and the heart muscle thickens
(cardiomegaly), further compromising function.
In short, this page visually explains how left-sided CHF leads to lung
problems and right-sided CHF leads to body-wide fluid retention,
both ultimately harming the heart.
Causes:
Left-Sided CHF: Infarction (heart attack), valve stenosis (narrowing),
hypertension, hyperthyroidism.
Right-Sided CHF: Infarction of the right ventricle, pulmonary valve
stenosis, pulmonary disease (lung problems).
Basic Effects:
• Both: Decreased cardiac output (less blood pumped).
• Left-Sided: Pulmonary congestion (fluid in lungs).
• Right-Sided: Systemic congestion (fluid in body), edema (swelling) in
legs and abdomen.
Signs and Symptoms:
• Forward Effects (due to decreased output): Fatigue, weakness,
dyspnea (shortness of breath), exercise intolerance, cold intolerance
(both types of CHF).
• Compensations (body trying to adapt): Tachycardia (fast heart
rate), pallor (pale skin), secondary polycythemia (increased red blood
cells), daytime oliguria (reduced urine).
• Backup Effects (due to fluid buildup):
• Left-Sided: Orthopnea (difficulty breathing lying down), cough,
shortness of breath, paroxysmal nocturnal dyspnea (sudden nighttime
breathlessness), hemoptysis (coughing up blood), rales (crackling lung
sounds).
• Right-Sided: Dependent edema (swelling in legs), hepatomegaly
(enlarged liver), splenomegaly (enlarged spleen), ascites (fluid in
abdomen), distended neck veins, headache, flushed face.
Etiology (Causes): Signs and Symptoms
(General):
• Impaired pumping ability
or electrical conduction • Progress as the condition
problems. worsens.
• Congenital heart • Sudden death can occur.
defects. • Reduced blood supply to
• Coronary artery disease. tissues.
• Hypertension. • Shortness of breath,
• Valve problems. especially with exertion.
• Lung diseases (for right- • Exercise intolerance.
sided CHF). • Dizziness.
This page contrasts the causes, effects, and symptoms of left-sided and
right-sided CHF, highlighting how left-sided CHF primarily impacts the
lungs while right-sided CHF leads to fluid buildup throughout the body.
Figure 18-24: Shows a heart with hypertensive heart disease, including
a thickened left ventricle and a dilated right ventricle.
 Young Children with CHF:
Key Points:
• Infants and children present
• Pulmonary Edema: Fluid accumulation
in the lungs, often occurring at night, differently than adults.
leading to breathing difficulties, coughing, • Congenital heart defects are a
and frothy, blood-tinged sputum.
• Rales: Bubbling sounds in the lungs due
common cause.
to fluid. • Feeding difficulties, failure to
• Right-Sided CHF Symptoms: Fluid thrive, and delayed growth are
buildup in the body, including dependent
edema (swelling in legs/buttocks), often the first signs.
hepatomegaly (enlarged liver), • Babies may fall asleep while
splenomegaly (enlarged spleen), abdominal
distension (ascites), and jugular venous feeding and be irritable when
•
distension. awake.
Ascites: Fluid accumulation in the
abdominal cavity, leading to abdominal • Rapid breathing, grunting, flared
distension. nostrils, and wheezing are
• Impact on Breathing: Fluid in the lungs
impairs gas exchange, causing shortness of common.
breath and difficulty breathing when lying • Right-sided CHF may lead to
down (orthopnea).
• Cough: Irritation from fluid in the lungs hepatomegaly and ascites.
leads to coughing. • A third heart sound (gallop
rhythm) is often heard.
Diagnostic Tests:
• Radiographs: Show heart enlargement and fluid in the lungs.
• Cardiac Catheterization: Measures pressures in the heart.
• Arterial Blood Gases: Assess oxygen levels.

Treatment of Congestive Heart Failure

(CHF).
• Treat the underlying cause: Address the root problem if possible.
• Reduce heart workload: Avoid excessive fatigue, stress, and sudden exertion.
• Prevent respiratory infections: Get flu shots (prophylactic measures).
• Maintain a healthy diet: Low sodium, low cholesterol, adequate protein and iron, and sufficient
fluids.
• Manage anxiety: Use anti-anxiety drugs or sedatives if needed.
• Medications are crucial:
• ACE inhibitors Reduce renin secretion and vasoconstriction.
• Digoxin: Improves heart pumping efficiency.
• Antihypertensives and vasodilators: Lower blood pressure.
• Diuretics: Reduce fluid buildup.
• Long-term medication management is essential: Check for effectiveness, toxicity, and drug
interactions.

In essence, CHF treatment focuses on addressing the cause, reducing stress on the heart,
managing symptoms with medications, and maintaining a healthy lifestyle.
 Congenital Heart Defects
(CHDs):
.
• Structural defects present at birth.
• Occur during the first 8 weeks of
embryonic life.
• Can involve valves, septa (walls), or
major vessels.
• Relatively common (8 in 1000 births).
• Major cause of death in the first year of
life.
• Require surgical intervention.
• Genetic and environmental factors
contribute.
• Often occur with other developmental
problems
Pathophysiology:
• Valvular defects: Interfere with normal blood flow.
• Septal defects: Allow mixing of oxygenated and
deoxygenated blood.
• Results: Decreased oxygen supply to tissues, potential
for heart failure.

Heart Valve Defects

A. Normal Valve: Blood flows freely forward, no backflow
.
B. Stenosis: Narrowed opening, less blood flow, no backflow.

C. Incompetent Valve: Leaky valve, blood flows forward but

also regurgitates backwards.

D. Effect of Aortic Stenosis:

• * Narrowing limits blood flow from the ventricle.
• * Left ventricular hypertrophy (thickening).
• * Decreased cardiac output.
• * Incomplete atrial emptying.

Overall, this explains the causes and effects of birth defects

in the heart, how lung disease can lead to right heart failure,
and it visually reviews the impact of different heart valve
problems on blood flow.
Congenital Heart Defects (CHDs), focusing on
acyanotic and cyanotic conditions, and Tetralogy of
Fallot as a specific example.
Acyanotic Defects:
• Blood shunts from left to right (e.g., Ventricular
Septal Defect - VSD).
• Oxygenated blood mixes with deoxygenated
blood in the lungs.
• Increased blood volume in the lungs leads to
pulmonary congestion.
• Right-sided heart failure can occur.
• Symptoms: May be asymptomatic or include
murmur, pallor, rapid pulse, dyspnea (shortness of
breath), squatting position, clubbed fingers.
Cyanotic Defects:
• Blood shunts from right to left (e.g., Tetralogy of
Fallot).
• Deoxygenated blood enters systemic circulation.
• Reduced oxygen in the blood leads to cyanosis
(bluish skin).
• Symptoms: Similar to acyanotic, but with
cyanosis.
Tetralogy of Fallot (Cyanotic):
Four defects:
• Pulmonary stenosis (narrowing of pulmonary valve).
• Ventricular septal defect (VSD).
• Right ventricular hypertrophy (thickening of right ventricle).
• Dextroposition (overriding) of the aorta.
• Leads to right-to-left shunt and cyanosis.

General Information:
• Etiology (Causes): Multifactorial, including genetics and environmental factors
(rubella, alcohol, diabetes).
• Compensation: Increased heart rate, contraction force, and peripheral
resistance to improve oxygen delivery.
• Diagnosis: Echocardiography, radiography, cardiac catheterization.
• Treatment: Surgical repair is often needed.

In essence, this explains how congenital heart defects can lead to either
increased blood flow to the lungs (acyanotic) or decreased oxygen
delivery to the body (cyanotic), using Tetralogy of Fallot as a key example. It
also covers the causes, symptoms, diagnosis, and treatment of these conditions.
Echocardiography, a diagnostic tool for
heart conditions, and Ventricular
Septal Defect (VSD), a common
congenital heart defect.
Echocardiography (Echo):Uses
ultrasound to visualize the heart.
• Figure 18-27 shows different views
obtained during an echo.
• A: Position of the transducer on the
chest.
• B: 2D image of a normal heart
showing the four chambers (left
atrium, left ventricle, right atrium,
right ventricle).
• C: Echo of a patient with mitral
stenosis (narrowing of the mitral
valve). Shows thickening of the
mitral valve leaflets, hypertrophy of
the atrial wall, and enlargement of
the atrial chambers.
• ECG: Electrocardiogram is recorded
simultaneously.
Ventricular Septal Defect (VSD):
• Most common congenital heart defect.
• "Hole in the heart" between the ventricles.
• Size varies.
• Small defects may close spontaneously.
• Large openings cause a left-to-right shunt (blood flows from left to right
ventricle).
• Left ventricle has higher pressure, so blood flows to the right ventricle and into
the lungs.
• This reduces blood flow to the body.
• Over time, it can lead to pulmonary hypertension (high blood pressure in the
lungs).
• Untreated VSD can lead to right heart failure and Eisenmenger syndrome
(reversal of shunt and cyanosis).
• Prophylactic antibiotics may be given before certain procedures to prevent
endocarditis (infection of the heart lining).
In short, this explains how echocardiography provides detailed images of the heart
and how VSD, a hole between the ventricles, can cause blood flow problems and
potentially serious complications if untreated.
Ventricular Septal Defects (VSDs), Valvular
Defects, and Tetralogy of Fallot

Ventricular Septal Defect (VSD):

• Abnormal opening between ventricles.

• Causes altered blood flow.

• Type and amount of blood flow depend on the size of the

opening.
• Patent Ductus Arteriosus (PDA): Ductus arteriosus (vessel
between aorta and pulmonary artery) fails to close after
birth.
• Sketching the abnormal blood flow pattern helps
understand the murmur.
Valvular Defects:
• Malformations of heart valves (aortic, mitral, pulmonary,
tricuspid).
• Stenosis: Narrowing of the valve, restricting blood flow.
• Incompetence (Regurgitation): Valve fails to close properly,
causing backflow.
• Mitral valve prolapse: Common occurrence where valve
leaflets balloon backward.

Effects:
• Reduced efficiency of heart pumping.
• Increased workload on the heart.
• Potential for heart chamber enlargement and failure.
Figure 18-28: Shows normal
and enlarged heart with mitral
stenosis.
• Surgical replacement with
mechanical or tissue valves
may be necessary.
• Patients may need
anticoagulants (ASA) to
prevent blood clots.
• Antibiotics may be needed
before procedures to
prevent bacterial
endocarditis.
Tetralogy of Fallot:
• Most common cyanotic congenital heart defect.
• Complex defect with four abnormalities:
• Pulmonary stenosis (narrowed pulmonary valve).
• Ventricular septal defect (VSD).
• Dextroposition (overriding) of the aorta.
• Right ventricular hypertrophy (thickening).
• Causes cyanosis ("blue babies").
• Alters pressures and blood flow in the heart.
In short, this explains how holes between the heart ventricles
(VSDs) and malfunctioning heart valves can disrupt normal
blood flow, and describes Tetralogy of Fallot, a complex birth
defect that causes cyanosis.
Blood flow problems in Tetralogy of Fallot, a congenital
heart defect:
• Pulmonary valve stenosis: Narrowing of the valve restricts blood
flow from the right ventricle.
• Right ventricular hypertrophy: The right ventricle works harder,
leading to thickening and high pressure.
• Right-to-left shunt: High pressure in the right ventricle forces
deoxygenated blood through the ventricular septal defect (VSD) into the
left ventricle.
• Aorta position: The aorta's position over the VSD further directs
deoxygenated blood into systemic circulation.
• Result: Lungs get less blood, body gets a mix of oxygenated and
deoxygenated blood.
• Oxygen deficit: Significant lack of oxygen in the body leads to
cyanosis (blue skin) and other systemic effects.
In short, Tetralogy of Fallot causes deoxygenated blood to bypass the lungs
and enter the body, resulting in low oxygen levels and cyanosis.
 INFLAMMATION AND INFECTION IN THE
HEART
Rheumatic Fever & Rheumatic Heart Disease
Definition
• Rheumatic Fever (RF): A systemic inflammatory
disease that occurs after an untreated or poorly
treated streptococcal throat infection (Group A beta-
hemolytic Streptococcus, GAS).
• Rheumatic Heart Disease (RHD): The chronic cardiac
complication of rheumatic fever, causing permanent
damage to the heart valves due to repeated
inflammation and scarring.
Cause:
• Untreated strep throat (pharyngitis) caused by GAS
bacteria.
• The body's immune system mistakenly attacks its own
 Pathophysiology
1. Strep infection triggers an abnormal immune response, where
antibodies attack connective tissues in the heart, joints, skin, and
nervous system.
2. Pancarditis develops (inflammation of all heart layers):
⚬ Endocarditis (valve inflammation) → Valve scarring and stenosis.
⚬ Myocarditis (heart muscle inflammation) → Arrhythmias and
heart failure.
⚬ Pericarditis (outer layer inflammation) → Pericardial effusion and
chest pain.
3. Chronic damage leads to valvular fibrosis and dysfunction → Risk
of heart failure.
Signs & Symptoms
• Fever, malaise, and fatigue.
• Migratory polyarthritis (painful swelling of large joints).
• Carditis (inflammation of heart tissue) → Causes chest pain,
murmurs, and arrhythmias.
• Skin manifestations: Erythema marginatum (pink skin rash) &
subcutaneous nodules.
COMPLICATIONS: TREATMENT:
• Chronic rheumatic heart disease • Antibiotics (Penicillin)
(permanent valve damage). to eliminate strep
• Mitral and aortic valve stenosis → infection.
Leading to heart failure. • Anti-inflammatory
• Increased risk of infective medications (Aspirin,
endocarditis. Corticosteroids) for
joint and heart
DIAGNOSIS: inflammation.
• Long-term
• ASO (Antistreptolysin O) titer prophylactic
(detects past strep infection). antibiotics to prevent
• Echocardiogram (assesses heart recurrence.
valve damage). • Valve repair or
• ECG (detects arrhythmias and replacement surgery
conduction abnormalities). if severe damage
occurs.
 INFECTIVE ENDOCARDITIS
Definition
• A bacterial or fungal infection of the heart's inner lining
(endocardium) and valves, leading to vegetation formation and
valve destruction.

Cause & Risk Factors

• Bacteria enter the bloodstream (bacteremia) from:
⚬ Dental procedures
⚬ IV drug use
⚬ Prosthetic heart valves
⚬ Rheumatic heart disease
⚬ Congenital heart defects
 Pathophysiology
1.Bacteria adhere to the heart valves, forming vegetations
(clumps of bacteria, fibrin, and platelets).
2.Vegetations damage valves, causing stenosis or regurgitation.
3.Pieces of vegetation embolize other organs (brain, kidneys,
lungs).

Signs & Symptoms

• Fever, chills, night sweats.
• Heart murmurs (new or worsening).
• Petechiae (tiny red spots on skin/mucosa).
• Splinter hemorrhages (thin red lines under nails).
• Osler’s nodes (painful red lesions on fingers/toes).
• Janeway lesions (painless red spots on palms/soles).
Complications
• Septic emboli → Can cause stroke, organ infarcts, or
pulmonary embolism.
• Valve perforation → Leads to heart failure.

Diagnosis
• Blood cultures (identify bacteria).
• Echocardiography (TEE) (detects vegetations).

Treatment
• IV antibiotics for 4-6 weeks.
• Surgical valve replacement if severe.
 Signs & Symptoms
PERICARDITIS
• Sharp chest pain (worse when lying
down, better when sitting up).
Definition • Pericardial friction rub (heard on
auscultation).
• Pericardial effusion (fluid
• Inflammation of the pericardium accumulation).
(outer sac around the heart).
Complications
Causes
• Cardiac tamponade (fluid
• Viral infections (most common). compresses heart, causing shock).
• Bacterial infections (TB, Staph, Diagnosis & Treatment
Strep).
• Post-myocardial infarction • ECG, echocardiogram,
(Dressler’s Syndrome). pericardiocentesis.
• Autoimmune diseases (Lupus, • NSAIDs, steroids, pericardial
Rheumatoid Arthritis). drainage if severe.
 Vascular
Disorders
Arterial Disorders
• A bacterial or fungal infection of the heart's inner lining
(endocardium) and valves, leading to vegetation formation and
valve destruction.
1.Hypertension (High Blood Pressure)
• Primary hypertension (no known cause).
• Secondary hypertension (caused by kidney disease,
hormonal imbalance).
• Complications: Stroke, heart failure, aneurysms.
• Treatment: Lifestyle changes, antihypertensive medications.
 Vascular Disorders
2. Peripheral Vascular Disease (PVD) & Atherosclerosis
• PVD: Narrowed arteries reduce blood flow to limbs.
• Atherosclerosis: Plaque buildup in arteries.
• Symptoms: Leg pain, ulcers, gangrene.
• Treatment: Exercise, medication, surgery (bypass or
angioplasty).

3. Aortic Aneurysms
• Abnormal dilation of the aorta due to weakened artery
walls.
• Risk factors: Hypertension, atherosclerosis.
• Symptoms: Often asymptomatic until rupture.
• Treatment: Surgery if large or at risk of rupture.
 Venous
Disorders
Varicose Veins
• Enlarged, twisted veins due to valve dysfunction.
• Symptoms: Leg pain, swelling.
• Treatment: Compression stockings, lifestyle changes,
surgery.

Thrombophlebitis & Phlebothrombosis

• Thrombophlebitis: Vein inflammation with clot formation.
• Phlebothrombosis: Clot forms without major
inflammation.
• Complication: Pulmonary embolism (life-threatening).
• Treatment: Blood thinners, movement, compression
 Shock
• Definition: Life-threatening condition where the body's
tissues don't get enough oxygen due to poor blood flow.
• Causes: Low blood volume (hypovolemic), heart problems
(cardiogenic), blockage of blood flow (obstructive), or blood
vessel dilation (distributive – septic, anaphylactic, etc.).
• Effects: Decreased blood pressure, reduced blood flow to
organs, leading to oxygen and nutrient deficiency.
• Body's Response: Compensatory mechanisms like
increased heart rate, constricted blood vessels, and fluid
retention try to maintain blood pressure.
• Treatment: Depends on the cause and focuses on restoring
blood volume and improving circulation.
 Shock

In essence, both conditions disrupt normal blood flow, but in

different ways. Thrombophlebitis/phlebothrombosis involves
localized clots in veins, while shock is a systemic issue of
inadequate blood flow to the entire body.
 Shock
1. Trigger: Decreased Blood Pressure
2. Body's Initial Response (Compensations):
• Sympathetic Nervous System: Triggers anxiety,
restlessness, rapid heart rate, constricted blood vessels (to
raise pressure), and pale skin.
• Renin-Angiotensin-Aldosterone System: Constricts
blood vessels and retains sodium/water to increase blood
volume.
• ADH (Antidiuretic Hormone): Retains water to increase
blood volume.
3. Direct Effects of Low Blood Pressure (if
compensations fail):
• Lethargy, weakness
• Anaerobic metabolism (cells work without oxygen) leading to
metabolic acidosis (acid buildup)
 Shock
4. Worsening Circulation and Cell Damage:
• Slow blood flow in tiny vessels (microcirculation)
• Ischemia (lack of oxygen) in organs
• Thrombus formation (blood clots)
• Decreased organ function
• Necrosis (tissue death), e.g., in kidneys
5. Reduced Blood Return to the Heart (Venous Return):
6. Further Decrease in Heart Output:
• Severe acidosis
• Disseminated Intravascular Coagulation (DIC - widespread
clotting)
• Organ damage (e.g., acute renal failure, lung damage)
 Shock
7. Decompensation (Body Can't Keep Up):
• Shock worsens quickly as compensations fail.
• Vasoconstriction in organs worsens ischemia.
• Fluid shifts from blood to tissues.
• Organ damage and failure.

In simple terms, shock starts with low blood pressure. The body
tries to fix it by speeding up the heart, squeezing blood vessels,
and retaining fluid. If these fail, blood flow slows, organs get
damaged, and the condition worsens rapidly, leading to organ
failure and death.
 Complications of Shock
• Acute Renal Failure: Kidney damage due to poor blood
flow.
• Acute Respiratory Distress Syndrome (ARDS): Lung
damage due to fluid buildup.
• Hepatic Failure: Liver damage.
• Paralytic Ileus: Intestinal paralysis.
• Infection/Sepsis: From gut bacteria entering the
bloodstream.
• Disseminated Intravascular Coagulation (DIC):
Widespread clotting leading to bleeding problems.
• Decreased Heart Function: Due to oxygen deprivation.
• Multi-organ Failure: Failure of multiple organs, leading to
death.
 Causes of Shock
• Hypovolemic: Loss of blood or fluids (e.g., bleeding, burns,
dehydration).
• Cardiogenic: Heart's inability to pump (e.g., heart attack,
arrhythmia).
• Distributive (Vasogenic): Blood vessels widen too much,
causing low blood pressure. Includes:
⚬ Neurogenic: Nervous system damage (e.g., spinal cord
injury).
⚬ Anaphylactic: Severe allergic reaction.
⚬ Septic: Severe infection.
 Symptoms of Shock

• Agitation/Restlessness (first sign)

• Low blood pressure (hypotension)
• Rapid heart rate (tachycardia)
• Pale, cool, clammy skin
• Rapid, shallow breathing
• Lethargy, weakness, dizziness
• Decreased urine output
 Treatment of Shock (Emergency)
• Position: Place patient on their back with legs elevated.
• Airway: Ensure a clear airway.
• Call for Assistance: Get help immediately.
• Oxygen: Administer oxygen.
• Identify Cause: Determine the underlying cause and
treat it (e.g., epinephrine for anaphylaxis).
• Fluids: Administer fluids to increase blood volume.
• Monitor: Closely monitor vital signs and urine output.

In essence, shock is a medical emergency caused by various

factors, leading to poor tissue oxygenation and potentially
fatal complications. Prompt treatment focuses on addressing
the underlying cause and supporting the body's circulation.
 Stages of Shock:
• Early (Compensated):
• Symptoms: Anxiety, restlessness, thirst, rapid heart rate
(tachycardia).
• Body's Response: Tries to compensate by increasing heart rate and
constricting blood vessels.
• Progressive:
• Symptoms: Lethargy, weakness, cool/moist skin, low blood
pressure, rapid/shallow breathing, decreased urine (oliguria),
metabolic acidosis.
• Body's Response: Compensatory mechanisms start to fail.
• Decompensated (Irreversible):
• Symptoms: Stupor, confusion, abnormal heart rhythm (arrhythmia),
slow/weak pulse, metabolic acidosis, acute respiratory distress
syndrome (ARDS), multiple blood clots, liver failure, kidney failure,
intestinal paralysis, gastrointestinal bleeding.
• Body's Response: Organ systems begin to fail, leading to death.
 Key Points:

• Early signs are the body's attempts to

compensate.
• Progressive signs show the body's failure to
maintain blood pressure and oxygen
• Decompensated shock is the final stage where
organs fail, and recovery is unlikely.
 Treatment Focus
• Early intervention to prevent progression to
decompensation.
• Addressing the underlying cause (e.g., fluids for blood
loss, epinephrine for anaphylaxis).
• Supporting vital functions (e.g., oxygen, medications
to increase blood pressure).
In short, shock progresses through stages, starting with
compensatory mechanisms and ending in organ failure. Early
recognition and treatment are crucial to prevent irreversible
damage and death.
THANK YOU!