Topic 5.
1 Cardiovascular Pathophysiology and Treatment
Learning Outcomes
Describe some diagnostic tests and
tools for assessing cardiovascular
function
Describe the relevant aspects of
diet and lifestyle to cardiac
Notes
Electrocardiogram: useful in initial Dx and monitoring of arrhythmias, myocardial infarction, infection, and
pericarditis
 Holter monitor allows an individual to pursue daily activities while an ECG is recorded
Auscultation: valvular abnormalities or abnormal shunts of blood cause murmurs, which can be detected by
auscultation
Phonocardiograph: recording of heart sounds
Echocardiography: ultrasound (reflected sound waves) used to record image of the heart and valve movements –
useful for Dx valvular abnormalities, congenital defects and changes in heart structure or function
Exercise stress test: assess general cardiovascular function and for exercise-induced problems
Chest x-ray films: show the shape and size of the heart as well as any pulmonary congestion associated with heart
failure
Nuclear imaging: thallium can be used to assess the size of a MI, the extent of cardiac perfusion and function of
the ventricles
 Tomographic studies: illustrate various levels of a tissue mass
 Nuclear medicine studies: identify dead or damaged area of myocardial tissue
Single-photon emission compute tomography (SPECT): specialized CAT scan tat assesses cardiac ischemia at rest
Cardiac catheterization: a catheter is passed through a large vein in the leg to the ventricle to visualize the inside
of the heart, measure pressures, and assess valve and heart function
Angiography: used to assess blood flow in the coronary circulation and obstructions can be assessed and then
treated
 Injection of thrombolytic agents
 Laser therapy to break clots
 Balloon angioplasty to open arteries
Troponin blood test: measure serum troponin that are released been cardiac muscle has been damaged – the
more damage, the higher the levels of troponin
Doppler: assess blood flow in the peripheral vessels, records the sounds of blood flow or obstruction
Blood tests: serum triglyceride and cholesterol levels, sodium levels, potassium, calcium, and other electrolytes
Arterial blood gas determination: check the current oxygen level and acid-base balance in patients with shock or
MI
Healthy diet - reducing total fat intake and intake of saturated and “trans” fat
Regular exercise – lowers serum lipid levels, increasing HDL levels, reduces stress levels
function
Describe cardiac anatomy and the
cardiac cycle
Describe the electrical conduction
system of the heart including
depolarization and repolarization
Moderation in alcohol intake
Cessation of smoking
Safe sexual practices
Immunizations
Monitoring body weight and blood pressure
Basic screening tests of cholesterol levels and the presence of cancer
Cardiac Cycle
Refers to the alternating sequences of diastole, the relaxation phase of cardiac activity, and systole, or cardiac
contraction
1. Diastole
 Atria fill
 All valves close
2. Diastole
 Increased atrial pressure opens AV valves
 Ventricles fill
3. Systole begins
 Atria contract and empty
 Ventricles are full
4. Systole
 Ventricles begin contraction
 Pressure closes AV valve
 Atria relax
5. Systole
 Ventricles contract
 Increased pressure in ventricles
 Aortic and pulmonary valves open
 Blood ejected into aorta and pulmonary artery
6. Diastole
 Ventricles empty
 Ventricles relax
 Aortic and pulmonary valves close
Impulses to initiate cardiac contractions are conducted along specialized myocardial fibers
 No nerves are present within the cardiac muscle
 Intercalated discs: between fibers contain desmosomes, which prevent cells from separating during

Describe the role of the nervous
system and endocrine system in
regulating the heart
contraction
 Gap junctions: permit ions to pass from cell to cell, facilitating the impulse
Pathway of Conduction
1. Sinoatrial (SA) node – located in the wall of the right atrium
 “pacemaker”
 Basic rate, sinus rhythm, 70 bpm
 Can be altered by autonomic nervous system and by circulating hormones
2. Atrial conduction pathways
 Results in contraction of both atria
3. Atrioventricular (AV) node – floor of the right atrium near the septum
 Only anatomic connection between atrial and ventricle portions of the conduction system
 Slight delay at AV node to allow for ventricular filling
4. Bundle of His
5. Right and left bundle branch
6. Purkinje fibers
 Stimulates contraction of two ventricles
Electrocardiogram
Atrial contraction is represented by depolarization in the P wave, and ventricle contraction is shown by the QRS
wave of depolarization. The QRS masks the wave of repolarization of the atria, but the T wave represents the
repolarization of the ventricles
Nervous Control
Cardiac control center
 In the medulla of the brain
 Controls the heart rate and force of contraction
Baroreceptors: in walls of the aorta and internal carotid arteries and detect changes in blood pressure and the
cardiac center then responds through innervation of the nervous system
 Sympathetic innervation increases heart rate and contractility
o Beta1-adrenergic receptors in the heart are important site of action for some medications
 Parasympathetic stimulation by the vagus nerve slows the heart rate
Blood Pressure
Depends on cardiac output and peripheral resistance. Specific variables include:
 Blood volume and viscosity
 Venous return
 Rate and force of heart contractions

Explain how atheromas develop
State some factors that predispose
to atherosclerosis
 Elasticity of the arteries
Dilation of the blood vessels that leads to decreased peripheral blood pressure usually results form reduced SNS
stimulation, where systemic vasoconstriction occurs in response to increased SNS stimulation.
1. SNS and epinephrine act at the B1-adrenergic receptors, increasing the rate and force of contraction
2. SNS, epinephrine and norepinephrine increase vasoconstriction by stimulating A1 receptors in the
arterioles of skin and viscera
Hormonal Control
ADH: increases water reabsorption through the kidneys – increasing blood volume (ADH is also called
vasopresssin); also causes vasoconstriction
Aldosterone: increases blood volume by increasing reabsorption of sodium ions and water
Renin-angiotensin-aldosterone system: initiated when there is a decreased in renal blood flow. Stimulates the
release of renin, which activated angiotensin (vasoconstrictor) and stimulates aldosterone secretion
Arteriosclerosis is degenerative changes in the small arteries and arterioles. Elasticity is lost, and the walls become
thick and hard, and the lumen gradually narrows and becomes obstructed.
Atherosclerosis is differentiated by the prescience of atheromas, plaque consisting of lipids, cells, fibrin, and cell
debris which form inside the walls of large arteries.
 LDLs have a high lipid concentration and transport cholesterol from the liver to cells and is the major
contributive factor to atheromas
 HDLs are “good” lipoprotein, with a low lipid content and used to transport cholesterol away from the
peripheral cells to the liver where the undergo catabolism and excretion
Steps in atheroma development
1. Endothelial injury in the artery
2. Injury causes inflammation leading to elevated C-reactive protein (CRP) levels
3. WBCs and lipids accumulate in the inner lining of the artery or in the muscle layer
4. Smooth muscle cells proliferate or multiply
5. Plaque forms and inflammation persists
6. Platelets adhere to the rough surface, forming a thrombus
7. Lipids continue to build up, along with fibrous tissue – platelets release prostaglandins, further increasing
inflammation
8. More platelets aggregate to the site, enlarging the thrombus
Atheroma damages the arterial wall, weakens the structure, decreases the elasticity. They can calcify, causing
further rigidity of the wall.
Non-modifiable: age, gender, genetic or familial factors
Modifiable: obesity, diets, smoking, sedentary lifestyle, diabetes mellitus, poorly controlled hypertension
Compare angina and myocardial
infarction and describe the
treatment for each
Angina
Pathophysiology Occurs with deficient of O2 to the
heart: impaired blood flow, higher
demand on heart
Exertion also angina, vasospasm at
rest
Unstable angina is prolonged pain at
rest and of recent onset
Usually no permanent damage to
heart
Etiology Associated with atherosclerosis,
arteriosclerosis, vasospasm, and
myocardial hypertrophy
Precipitating factors are related to
activities that increase the demands
on the heart
Signs and Symptoms Reoccurring, intermittent brief
episodes of substernal chest pain
usually triggered by stress
Pallor, diaphoresis, nausea
Myocardial infarction
Occurs when a coronary artery is
totally obstructed, leading to
prolonged ischemia and cell death of
the heart wall. Infarction can develop
in 3 ways...
1. Thrombus may obstruct the
artery
2. Vasospasm may occur in the
presence of a partial
occlusion leading to a full
obstruction
3. Emboli breaks off and travels
to a smaller artery where it
occludes blood flow
-Point of obstruction becomes
necrotic and area of ischemia
surrounds it. Enzymes are released in
the blood (A rise in Troponin levels is
considered the most specific from
myocardial tissue damage)
-If blood supply can be restored
within 20-30mins, irreversible
damage may be prevented.
Most common cause is
atherosclerosis, with thrombus
attached.
Signs may be intermittent initially...
1. Feeling of pressure,
heaviness, or burning in the
chest, especially with

Describe the common arrhythmias
leading to cardiac arrest
Treatment Usually relieved by rest and coronary
vasodilators
Name Conduction Change
Bradycardia Rate regular, <60BPM
Tachycardia Rate Regular, 100-160 BPM
Atrial Flutter Rate 160-250 BPM
Fibrillation (atrial or ventricular) Rate over 300 BPM; uncoordinated
muscle contractions
Premature Ventricular Contractions Additional Ectopic Beats
(PVC)
Bundle Branch Block Delayed conduction in one bundle
branch, wide QRS wav
1st Degree Heart Block Delays conduction in AV node,
prolongs PR interval
2nd Degree Heart Block Delays conduction in AV node,
gradually increasing PR until one
contraction is missed
increased activity
2. Sudden shortness of breath,
sweating, weakness, fatigue
3. Nausea, indigestion
4. Anxiety and fear
Other signs include Pallor,
diaphoresis, hypotension, and low-
grade fever
-Keep patient calm, 02, and
analgesics such as morphine for pain
relief
-Anticoagulants such as heparin or
warfarin
-meds to reduce dysrhythmias
-defibrillation or pacemaker
-digoxin supports heart function
-Prophylactic ASA
Effect
-Stroke volume decreases
-Possibly reduced cardiac output
Possibly reduced cardiac output
-Less filling time
-Often reduced cardiac output
No filling, no output-cardiac standstill
May induce fibrillation
No effect
No effect
Periodic decrease in output

Discuss the causes of congestive
heart failure
Explain the outcomes of left and
right heart failure and the
treatment for each
Total (3rd Deg) Heart Block No conduction in AV node, ventricles Marked decrease in output, causing
slowly contract independent of atrial syncope
contraction
Left Sided CHF:
-Infarction of left ventricle, aortic valve stenosis, hypertension, hyperthyroidism
Right Sides CHF:
-Infarction of right ventricle, pulmonary valve stenosis, pulmonary disease (cor pulmonale)
Stenosis- less blood can flow through the valve opening due to “hardening” of the valve. This causes back
pressure.
Left-Sided CHF Right-Sides CHF
Basic Effects -Decreased cardiac output -Decreased cardiac output
-Pulmonary Congestion -systemic congestion
-edema of legs and abdomen
Signs and Symptoms
Forward Effects (less blood reaching Decreased blood supply to the tissues Decreased blood supply to the tissues
tissues ) and general hypoxia, Fatigue, and general hypoxia, Fatigue,
weakness, dyspnea, exercise weakness, dyspnea, exercise
intolerance, cold intolerance intolerance, cold intolerance
Compensations Tachycardia and pallor, secondary Tachycardia and pallor, secondary
polycythemia (increased polycythemia (increased
RBCs=increased hematocrit), daytime RBCs=increased hematocrit), daytime
oliguria (decreased production of oliguria (decreased production of
urine) urine)
Backup Effects (congestion behind -Orthopnea (difficulty breathing while -Dependent edema in feet
the affected ventricle) lying down) -hepatomegaly (enlarged liver) and
-Cough producing white or pink- splenomegaly (enlarged spleen)
tinged phlegm -ascites (accumulation of fluid in
-SOB abdominal cavity)
-Paroxysmal nocturnal dyspnea (SOB -distended neck veins
and coughing at night) -headache
-hemoptysis (coughing up blood) -flushed face
-Rales (crackles on inspiration)

Discuss the pathology of
Rheumatic fever
Describe the pathology of
endocarditis and pericarditis
Explain the development and
effects of hypertension
Treatment
 Alpha-Adrenergic Blockers- cause vasodilation by blocking vasodilatory (A1) response
 Vasodilators- cause vasodilation (reducing blood pressure and reducing force required to pump)
 Calcium channel blockers, beta blockers, and digoxin- decrease the work of the heart by decreasing rate
or force
 ACE Inhibitors- block angiotensin 1 from being converted to angiotensin 2, reducing vasoconstriction
 Diuretics- decrease aldosterone secretion which decreases water retention an reduces blood pressure and
resistance from edema
Results from an abnormal immune reaction occurring a few weeks after an untreated infection, usually caused by
strains of Streptococcus. Antibodies react with connective tissue (collagen) in the skin, joints, brain and heart
which causes inflammation. The heart is the only site where scar tissue occurs, causing rheumatic heart disease.
Can cause pericarditis, myocarditis, or endocarditis (most common).
Inflammation in the heart by Streptococcus or Staphylococcus aureus may involve one or more layers of the
heart:
1. Pericarditis- inflammation of the outer layer, may include effusion (excessive fluid accumulation), which
may impair filling (cardiac tamponade). Effusion can be serous (normal inflammation), fibrinous or
purulent (infection) or may contain blood (AKA hemopericardium- from trauma or cancer). Inflammation
of pericardium may also cause chest pain and a friction rub (grating sound heart with auscultation). The
right side of the heart is commonly affected first as it has lower internal pressure, causing systemic effects
like edema and JVD. Chronic pericarditis can result in adhesions between pericardial membranes, limiting
movement of the heart
2. Myocarditis- localized lesions in heart muscle, called Aschoff Bodies, that may interfere with conduction
3. Endocarditis- Most common problem. Affects the heart valves. Valves become edematous or grow
Verrucae (wart-like vegetations along valve cusps). The mitral valve is most frequently effected. These
both effect the flow of blood to the left ventricle. Pieces may also break off, causing infarction or infection
in other tissues. Eventually the valve can become scarred, leading to stenosis or valve incompetence.
Chordae tendineae can also be affected causing them to shorten and create valve malfunction.
Hypertension is classified in Three major categories:
1. Primary or Essential Hypertension: is idiopathic. Develops when the BP is consistently above 140/90.
Diastolic pressure is important as it indicates the degree of peripheral resistance, and increased workload
 of the left ventricle. Generally caused by an increase in arterial vasoconstriction (from increased
stimulation, atherosclerosis, etc). Vasoconstriction can lead to decrease blood flow to kidneys, leading to
increased renin, angiotensin, and aldosterone secretion. These substances lead to further
vasoconstriction and increased blood volume, further increasing blood pressure. Chronic high blood
pressure can cause damage to arterial walls. Arteries become hard and thick (sclerotic), with narrowed
lumens. Walls may also dilate or tear, forming an aneurysm. Blood supply to the area can be reduced
leading to ischemia, and necrosis. Areas most frequently damaged are kidneys, brain, and retina. This can
lead to chronic renal failure, hemorrhagic stroke, loss of vision, or CHF.
2. Secondary Hypertension: results from renal or endocrine disease, or pheochromocytoma (benign tumor
of adrenal medulla)
3. Malignant or Resistant Hypertension: hypertensive emergency with extremely high BP. Usually results in
organ damage, including the CNS and renal system. Ex: Head injury
Describe the pathology of Is a dilatation and weakening of the arterial wall, most commonly in the thoracic or abdominal aortas. Most often
aneurysms develop from a defect in medial layer, often associated with turbulent blood flow at the site. Trauma can result in
tearing tissues. Syphilis may also damage the tissues in the arterial wall. Dilatation can enlarge and eventually
create a thrombus that can obstruct branching arteries or become a source of embolus. Many aneurysms
eventually rupture, causing massive hemorrhage.
 Saccular: bulging on one side
Fusiform: circumferential dilatation
Dissection: tear in intima, allowing blood to flow along the length of the vessel between the layers of the arterial
wall
Describe varicose veins, Varicose Veins: most common in the legs but also found in the esophagus (esophageal varices) and the rectum
phlebothrombosis, and (hemorrhoids). May develop from a defect or weakness in the vein walls or in the valves. Superficial veins lack
thrombophlebitis the muscle support of the deep veins. Increased hydrostatic pressure from standing can cause the wall of the vein
to stretch or dilate. The weight of the blood then damages the valve below, leading to backflow distal to the
starting point. Varicosities can predispose thrombus formation.

Thrombophlebitis: Refers to the development of a thrombus in a vein in which inflammation is present. Platelets
adhere to the inflamed site, and thrombus develops.
Phlebothrombosis: Development of thrombus without prior inflammation. Inflammation can occur secondary to
thrombus formation. Clot is less firmly attached than thrombophlebitis.
-Both types of thrombosis have the same predisposing factors such as:

Discuss the types of shock, the
effects of shock, and treatments
for shock
Effects of Shock
1. Immobilization or constriction by clothing for long periods of time causing blood stasis
2. Endothelial injury from trauma, chemical injury, intravenous injection, or inflammation
3. Increased blood coagulation which may result from dehydration, cancer, pregnancy, or increased platelet
adhesion.
Type Mechanism Specific Causes
Hypovolemic Loss of blood or plasma Hemorrhage, burns, dehydration,
peritonitis, pancreatitis
Cardiogenic Decreased pumping capability of the Myocardial Infarction of left ventricle,
heart cardiac arrythmia, pulmonary
-Obstructive shock is a subcategory: embolus, cardiac tamponade
interfering with blood flow through (pulmonary embolus and cardiac
the heart tamponade are obstructive)
Vasogenic (neurogenic or Vasodilation owing to loss of Pain and fear, spinal cord injury,
distributive) sympathetic and vasomotor tone hypoglycemia (insulin shock)
Anaphylactic Systemic vasodilation and increased Insect stings, drugs, nuts, shellfish,
permeability owing to severe allergic allergens
reaction
Septic (Endotoxic) Vasodilation owing to severe Virulent microorganisms (gram-
infection, often with gram-negative negative bacteria) or multiple
bacteria infections
1) Compensation signs
a) Cool, moist, pale skin
b) Tachycardia
c) Oliguria; vasoconstriction shunts blood from the viscera and the skin to the vital areas
2) Septic Shock (“Warm Shock”) signs
a) Fever
b) Warm, dry, flushed skin
c) Rapid, strong pulse
d) Hyperventilation

Describe the pathophysiology of
cardiac tamponade, aortic
dissection, and hypertension and
the treatments for each
Describe and identify four lead
e) Evidence of infection
3) Decompensation Signs (drop in BP and blood flow)
a) Lethargy
b) Weakness
c) Dizziness
d) Weak, thready pulse
e) Initial hypoxemia and respiratory alkalosis as respirations increase
f) Acidosis or low serum pH due to anaerobic metabolism is compensated for by increased
respirations
g) As shock progresses, metabolic acidosis dominates
Treatment of Shock
 Place patient in supine position
 Cover and keep warm
 Administer 02
 IV fluids
 Drugs/treat underlying condition (epi for anaphylaxis, vasopressors, stop bleeding)
Pathophysiology of ailments listed are answered in questions above.
Treatment
1) Cardiac Tamponade: Fluid aspirated from the pericardial sac (paracentesis) and analyzed to determine the
cause (infection vs structural problem)
2) Aortic Dissection: Surgical repair with resection and replacement with a synthetic graft can prevent
rupture.
3) Hypertension: Treated in a sequence of steps, beginning with lifestyle changes (reduce salt, weight, stress,
and improve cardiovascular fitness). Second step is mild diuretics such as thiazide diuretics. Third step (or
maybe the first depending on condition) is an ACE inhibitor (drugs ending in “pril). Other conditions such
as high serum sodium may require stronger diuretics such a furosemide (lasix). Other antihypertensives
are alpha1 blockers, calcium channel blockers (reducing heart action and peripheral resistance) or beta
blockers (reducing heart action and decreases renin release)
ECG rhythms
Describe and list the indications,
contraindications, dosages of the
basic EMS cardiac drugs as outline
in the AHS medical protocols
Vasodilators (e.g. nitroglycerin or long-acting isosorbide)
 Reduce peripheral resistance systemically and therefor the workload for the heart and act as coronary
vasodilators
 May decrease blood pressure, resulting in flushing or dizziness
Beta blockers (e.g. metoprolol or atenolol)
 Treat hypertension and dysrhythmias as well as reduce number of angina attacks
 Block the B1-adrenergic receptors to the heart, preventing the SNS from increasing heart activity
Calcium channel blockers
 Bock movement of calcium ions into the cardiac and smooth muscle fiber
 Decreased cardiac contractility (e.g. diltiazem reduces contractility and conductivity)
 An antidysthythmic particularity for excessive atrial activity (e.g. Verapamil slows HR by depressing action
of AV and SA nodes)
 Antihypertensive and vasodilator (e.g. nifedipine and Amlodipine)
 Prophylactics purpose for angina
 These drugs do not affect skeletal muscles as more calcium is stored in skeletal muscle cells
Digoxin
 Cardiac glycoside that has been used for a treatment for heart failure and atrial dysrhythmias
 Slows conduction of impulses and HR – improves efficiency of the heart as it is inotropic (increased
contractility)
 Contractions are less frequent but stronger
 Very narrow therapeutic range, and can easily cause toxicity
Antihypertensives (including adrenergic or sympathetic-blocking agents, calcium blockers, diuretics, ACE
inhibitors, and angiotensin II receptor blocking agents)
 Some cause orthostatic hypertension
 Used for essential hypertension or congestive heart failure or after MI
Adrenergic-blocking drugs
 Act on SNS centrally (brain), may block peripheral (arteriolar) A1-adrenergic receptors, or may act as
direct vasodilators
Angiotensin-converting enzyme inhibitors
 Currently preferred in Tx of patients with HTN and CHF
 Block the conversion of angiotensin I to angiotensin II (stimulated by the release of renin from the kidney
and is a powerful vasoconstrictor)
 Enalaril (Vasotec), ramipril (Altace), captopril (Capoten), and perindopril (Coversyl)
 o Reduce peripheral vascular resistance (vasoconstriction) and aldosterone secretion (thus
decreasing NA+ and H20 retention)
o Results in decrease in preload and after load
o Angiotensin II receptor blocking agents prevent angiotensin from acting on blood vessels and thus
lower blood pressure
 E.g. isosartan (Cozaar) and irbesartan (Avapro)
Diuretics (e.g. hydrochlorothiazide or furosemide)
 Remove excess NA+ and H20 from the body through the kidneys by blocking the reabsorption of NA+ or
H20
 Useful for Tx of HTN and CHF as they increase urine output and reduce blood volume and edema
 Some also remove to much potassium
o Sprionolactone is a “potassium-sparing” diuretic
Anticoagulants
 “Blood thinners” are used to reduce the risk of blood clot formation
 In many cases, ASA is recommended to decrease platelet adhesion
 Oral anticoagulants may be taken in high risk individuals, and block the coagulation process
o Warfarin (Coumadin)
 Must monitor vitamin K levels
o Newer medications like apixaban (Eliquis), dabigatran (Pradaxa), edoxaban (Savaysa) and
Rivaroxaban (Xarelto)
 Not affected by vitamin K levels
 These new drugs act higher on the coagulation cascade and cannot be fixed with TXA!
 Imperative to measure prothrombin time or activated partial thromboplastin time to prevent hemorrhage
Cholesterol or lipid-lowering drugs (e.g. statins: simvastatin (Zocor) and atorvastatin (Lipitor))
 Reduce LDL and cholesterol content of the blood by blocking synthesis in the liver
 Looking to assess their role in atheroma formation