disorders of :blood pressure regulation, pericardium , infectious disorder, CAD, valvular heart disease

What is blood pressure?

• Rhythmic ejection of blood from the left ventricle into the aorta 

• GOAL: Maintain consistent blood flow to vital organs to prevent organ damage 

• Decreases in blood pressure decrease blood supply to tissues of the body and may result in cell death, likewise increases in blood pressure can have devastating effects on the tissues of the body  

What are the Determinants of Blood Pressure: 

• Cardiac output 

• Peripheral vascular resistance [Afterload] 

• Systolic Blood Pressure 

  • Reflects an increase in aortic pressure as a result of ejection of blood from left ventricle

  • Dependent upon:

    • (1) amount of blood ejected

    • (2) velocity of ejection &

    • (3) elasticity of aorta 

What is the…

• Pressure in the arterial system during the relaxation period of the heart 

• Dependent upon

  • (1) elasticity of aorta

  • (2) resistance of arterioles that control blood flow into the microcirculation

  • (3) functional ability of the aortic valve 

Diastolic Blood Pressure 

What is the..

• The difference between systolic and diastolic pressure (SBP – DBP = pulse pressure) 

• Example: 120/80       120-80 = 40 pulse pressure 

pulse pressure

What is the..

• Average blood pressure in the systemic circulation  

• Good indicator of tissue perfusion 

• Normal: ____70-100 mmHg_________ 

• MAP = 1 systolic +2 diastolic ÷3 (greater fraction of the cardiac cycle is spent in diastole) 

• Example 120/80  MAP =  120 (1 systolic) + 160 (2 diastolic) / 3 

  •   MAP = 280/ 3   

    • MAP = 93 

 

Mean Arterial Pressure

KNOW HOW TO CALCULATE MEAN ARTERIAL PRESSURE (MAP)!!!!!!!

Example:

• MAP = 120 (1 systolic) +160 (2 diastolic)/ 3                

  •   MAP = 280/ 3   

    • MAP = 93 

Mechanisms of Blood Pressure Regulation 

• Arterial blood pressure must remain somewhat consistent in order to maintain tissue perfusion 

1. Short-Term Regulation:

2. Long-Term Regulation

What is short-term regulation? (Mechanisms of Blood Pressure Regulation)

Corrects imbalances in blood pressure that occur within minutes or hours: neural, humoral, baroreceptors, chemoreceptors

What is long-term regulation? (Mechanisms of Blood Pressure Regulation)

• (daily, weekly, monthly)  

• Mechanism of blood pressure control that take over once the short-term effects are exhausted 

• Kidneys are the backbone of long-term regulation by controlling fluid and electrolyte balances 

• Neural mechanisms

• Humoral mechanisms

What are the backbone of long-term regulation by controlling fluid and electrolyte balances 

kidneys

Long term regulation, NEURAL MECHANISMS

• Autonomic nervous system

  • parasympathetic nervous system

  • sympathetic nervous system

• baroreceptors

• chemorecptors

Autonomic nervous system

• Parasympathetic Nervous System;

  • Transmitted via vagus nerve

  • Decreases heart rate 

• Sympathetic Nervous System 

  • Vasoconstriction

  • Increases heart rate 

  • Increaes cardiac contractility 

Parasympathetic Nervous System;

• Transmitted via vagus nerve

• Decreases heart rate 

Sympathetic nervous system

• Vasoconstriction

• Increases heart rate 

• Increaes cardiac contractility 

What are barorecptors?

Pressure sensitive receptors located in the wall of certain blood vessels (i.e. carotid & aortic arteries) and the heart that sense changes in the stretch of the vessel wall and send impulses to cardiovascular control center in the brain to correct the problem 

What are chemoreceptors?

• Receptors in arteries (carotid & aorta), that sense changes in O2, CO2, H+ ion concentrations in the blood 

• Regulate ____ventilation____________  

• Assist in producing vasoconstriction in response to decreases in O2 

What is humoral mechanisms?

Hormones that affect blood pressure 

• RAAS: renin, angiotensin, aldosterone system 

• ADH (vasopressin): PP hormone; released in response to decrease in blood volume/BP or increase in osmolality (dehydration) [hint: increase osmolality=thirst] 

• Epinephrine: released from adrenal gland when SNS is activated: induces vasoconstriciton________ & _____increased______HR 

Hormones that affect blood pressure 

• RAAS:

• renin, angiotensin, aldosterone system 

Hormones that affect blood pressure 

ADH (vasopressin):

• PP hormone; released in response to decrease in blood volume/BP or increase in osmolality (dehydration) [hint: increase osmolality=thirst] 

Hormones that affect blood pressure 

Epinephrine:

• released from adrenal gland when SNS is activated: induces vasoconstriction & increased HR 

Hypertension chart

	Systolic	Diastolic
Normal	<120	<80
Prehypertension	120-139	80-89
Stage I HTN	140-159	90-99
Stage II HTN	> 160	>100

Normal systolic and diastolic

<120 systolic , <80 diastolic

Prehypertension systolic and diastolic

systolic: 120-139 

diastolic: 80-89

Stage I HTN systolic and diastolic

systolic: 140-159 

diastolic: 90-99

Stage II HTN systolic and diastolic:

systolic: > 160

diastolic: > 100

hypertension contributing factors

Non-modifiable 

• Gender 

• Age 

• Race 

• Co –morbidities? (DM, CKD) 

Modifiable 

• Diet 

• Sedentary lifestyle 

• Obesity 

• Smoking 

• Alcohol 

• Oral contraceptives 

• Obstructive sleep apnea 

• Stress 

• Co-morbidities (DM, CKD, secondary HTN) 

What are non-modifiable Contributing Factors of hypertension?

• Gender 

• Age 

• Race 

• Co –morbidities? (DM, CKD) 

What are modifiable Contributing Factors of hypertension?

• Diet 

• Sedentary lifestyle 

• Obesity 

• Smoking 

• Alcohol 

• Oral contraceptives 

• Obstructive sleep apnea 

• Stress 

• Co-morbidities (DM, CKD, secondary HTN) 

Pathophysiology of hypertension

• Overactivity of SNS–

  • vasoconstriction

  • increased HR,

  • Systemic Vascular Resistance (SVR)

  • INCREASED cardiac output (CO) 

• Overactivity of renin-angiotensin-aldosterone system

  • increased vasomotor tone and salt & water retention

• Problem with Atrial Natriuretic Peptide (vasodilator) 

• Diabetics :

  • insulin resistance decreases the release of endogenous vasodilators, affects renal function, and increases SNS activity 

• Chronic Hypertension damages vessel walls, particularly arteries and arterioles 

  • The vessels thicken & strengthen in order to withstand the increase in pressure 

  • Then they hypertrophy and eventually the lumen permanently narrows 

  • Injury to the vessel wall stimulates the inflammatory process and increases capillary permeability – Na, H20, plasma proteins, etc. seep into the vascular compartment and cause further thickening 

 

Chronic Hypertension damages vessel walls, particularly arteries and arterioles 

• The vessels thicken & strengthen in order to withstand the increase in pressure 

• Then they hypertrophy and eventually the lumen permanently narrows 

• Injury to the vessel wall stimulates the inflammatory process and increases capillary permeability – Na, H20, plasma proteins, etc. seep into the vascular compartment and cause further thickening 

Manefestations of Hypertenstion:

• “Silent killer” 

  • initially asymptomatic 

• Headache   

• Vision problems 

• Dizziness 

• Chest pain 

• Tinnitus 

• Flushed face 

• Epistaxis  

Hypertenstion:

****GOAL: REDUCE B/P AND PREVENT OR LESSEN ORGAN DAMAGE*****

• Heart: increased workload of left ventricle leading to heart failure, accelerates plaque formation (atherosclerosis) & rupture 

• Brain: risk for brain attack, dementias, and cognitive impairments 

• Kidney: may lead to chronic kidney disease (CKD) secondary to renal artery stenosis and arhterosclerosis

 

• Eyes: hypertensive retinopathy 

• Peripheral vascular disease & atherosclerosis 

How does hypertension damage the heart?

increased workload of left ventricle leading to heart failure, accelerates plaque formation (atherosclerosis) & rupture 

How does hypertension damage the brain?

risk for:

• brain attack

• dementias

• cognitive impairments 

How does hypertension damage the kidney?

may lead to chronic kidney disease (CKD) secondary to renal artery stenosis and arhterosclerosis

How does hypertension damage the eyes?

hypertensive retinopathy 

What is  

SYSTOLIC HTN/ ISOLATED SYSTOLIC HYPERTENSION 

• Systolic pressure ____>140 mmHg____________ mmHg

• diastolic pressure ___<90 mmHg____________ mmHg 

• Rise in SBP: left ventricular hypertrophy & increased myocardial oxygen demand 

• Increased pulse pressure: limits coronary artery perfusion 

• Predisposition to aneurysms & atherosclerosis & thrombosis 

Age related factors of SYSTOLIC HTN/ ISOLATED SYSTOLIC HYPERTENSION 

• Prevalence of HTN in children increasing 

• BP increases from infancy to late adolescence 

• 50% of adults age 60-69 years and 75% of adults 70> have HTN 

  • Stiffening of large arteries: elastin gradually replaced with collagen 

  • Decrease baroreceptor sensitivity 

  • Increased peripheral vascular resistance 

  • Decreased renal blood flow 

What is…

• An abnormal drop in blood pressure upon changing positions 

• Change in SBP(systolic blood pressure) > 20mmgHg 

• Change in DBP(diastolic blood pressure) > 10mmHg 

ORTHOSTATIC HYPOTENSION 

Patho of ORTHOSTATIC HYPOTENSION 

• 500-700 mL of blood shifted to lower part of body when changing from supine to upright—decrease of central blood volume and arterial pressure 

• Absence of normal circulatory reflexes or blood volume, blood pools in lower parts of the body, cardiac output falls, BP drops, and blood flow to the brain is inadequate 

What are causes of ORTHOSTATIC HYPOTENSION

• Altered baroreceptor response 

• Disorders of ANS 

• Increase in age 

• Medications 

• Prolonged bedrest 

• Reduced blood volume 

What are manefestations of ORTHOSTATIC HYPOTENSION 

• Asymptomatic 

• Dizziness (i.e. falls) 

• Diaphoresis (sweating) 

• Nausea 

• Vomiting 

What is ..

• Inflammation of the pericardium of less than 2 weeks 

• Increased capillary permeability of the pericardium allows plasma proteins and fibrinogen to escape into the pericardial space & Exudate forms in the pericardial space 

• May be from an isolated disease or a systemic process 

 

ACUTE PERICARDITIS  

What are causes of ACUTE PERICARDITIS  

• Bacterial, viral or fungal infections 

• Connective tissue diseases: SLE or RA 

• Uremia/azotemia (nitrogenous buildup) 

• MI / Cardiac surgery 

• Cancer 

• Trauma 

• Radiation 

• Drug toxicity 

Acute pericarditis:

  Manifestations [TRIAD]: vary based on cause 

• ____Chest pain_________:  

  • Abrupt onset of sharp pain in the  

  • precordial area, may radiate, &  worsens with

    •   deep breating,

    • coughing,

    • swallowing (changes in venous return)

  • Often relieved by sitting up and leaning forward 

• Pericardial ___friction rub______: high-pitched, scratchy sound 

• electrocardiograph_changes 

ACUTE PERICARDITIS :

What is Pericardial friction rub?

high-pitched, scratchy sound 

What is…

• Accumulation of fluid in the pericardial cavity typically from inflammation or infection 

• Normal: 10-50 ml of thin clear, straw-colored fluid in pericardial sac 

• Small, slow fluid increases usually asymptomatic 

• Rapid fluid increases may produce cardiac tamponade with LIFE THREATENING symptoms 

PERICARDIAL EFFUSION 

What are causes of PERICARDIAL EFFUSION 

• Cancer/Neoplasms 

• Cardiac surgery 

• Trauma 

• Inflammation 

• Myocardial infarction with cardiac rupture 

• Dissecting aortic aneurysm 

What is the patho of PERICARDIAL EFFUSION 

• Effect varies based on amount of fluid, how fast fluid accumulates, & elasticity of heart muscle tissue 

• Can lead to CARDIAC TAMPONADE: compression of heart due to accumulation of fluid, pus, or blood in pericardial sac. LIFE THREATENING 

What is the compression of heart due to accumulation of fluid, pus, or blood in pericardial sac. LIFE THREATENING

CARDIAC TAMPONADE

What are the manefestations of cardiac tamponade

• Decreased Stroke Volume (SV), (amount of blood pumped with each beat) 

• Decreased Cardiac Output (CO) (how much blood ejected over the minute) 

• Decreased Venous Return 

• Decreased blood pressure (Hypotension) 

• Increased heart rate (tachycardia) 

• Increased contractility 

• Jugular Vein Distension (JVD) 

• Narrowed pulse pressure 

• Muffled heart sounds 

• Pulsus Paradoxus: fall of BP during inspiration 

• Signs of circulatory shock 

What is ..

• Life-threatening infection on the inner lining of the myocardium (endocardium) and valves; leads to formation of bulky friable(easily tearbale, thin) vegetation(growth) and destruction of cardiac tissue 

• Cardiac tissue is destroyed and vegetative lesions form on heart valves 

• Aortic and mitral valves most susceptible 

infective endocarditis

What are the Risk Factors of endocarditis  

• Mitral valve prolapse 

• Congenital heart disease (CHD) 

• Cardiac prosthesis  

• Host factors: Immunocompromised individuals, cancer, diabetes, alcohol or IV drug abusers, neutropenia 

 

Manifestations of infective endocarditis 

• S/S Systemic Infection 

• Anorexia 

•  Chills 

• Fever 

•  Lethargy 

•  Malaise 

• Petechial hemorrhages 

What disease is being described?

• Acute ___Immune mediated ________ multi system inflammatory disease that follows a Group-A Beta hemolytic streptococcus  

• Onset is _______2-3 weeks after ____________ infection 

• May cause chronic valvular disorders—fibrotic valvular disorders, has serious complication 

• Major health issue in underdeveloped countries  

• Most common cardiovascular disease in children and youth 

1. Uncured strep throat eventually damages the heart valves  

rheumatic heart disease

What are manifestations of rheumatic heart disease 

• Carditis  

• Erythema Marginatum  

• History of sore throat and subsequent signs and symptoms strep throat 

• Polyarthritis  

• Subcutaneous nodules  

• Sydenham Chorea (neurological disorder, rapid irregular movement of arms, legs, and face) 

Coronary artery disease

Myocardial Oxygen Supply and demand 

Supply determined by oxygen supply 

• coronary arteries

• capillary inflow

• Ability of hemoglobin (Hgb) to deliver oxygen 

 

Demand determined by workload 

• _heart rate__

• __left ventricular contractility__ 

• systolic pressure

What is..

• Heart disease that is caused by impaired blood flow to the myocardium, usually from atherosclerosis  

• CAD may lead to ischemia, angina, myocardial infarction (MI), dysrhythmias, heart failure, sudden death  

Coronary Artery Disease (CAD) = Atherosclerosis 

What are the Risk Factors of

Coronary Artery Disease (CAD) = Atherosclerosis

modifiable vs nonmodifiable

1. Cigarette smoking 

2. Elevated BP 

3. Elevated LDL 

4. Decreased HDL 

5. Diabetes 

6. Increasing age 

7. Abdominal obesity 

8. Physical inactivity 

Coronary Circulation: [Hint: Coronary anatomy will not be on exam, know that the farther up the blockage occurs, the greater the infarcted area] 

• Left Coronary Artery (Left Main) 

  • Anterior Descending (LAD) 

    • Supplies: Left anterior ventricle & anterior interventricular septum 

  • Circumflex (CIRC) 

    • Supplies: Lateral wall of left ventricle 

• Right Coronary Artery (RCA), Supplies: Rt side of the heart 

  • Posterior Descending Artery 

    • Supplies: Posterior interventricular septum

    • SA node / AV node 

    • Posterior heart 

Pathogenesis of CAD 

• Atherosclerosis can affect one or all thee of the major coronary arteries and their branches  

• REMEMBER: platelets play a major role in CAD 

What plays a major role in CAD 

platelets

Type Types of CAD

1. Acute Coronary Syndrome  

• Unstable Angina 

• Myocardial Infarction 

unstable plaque: ruputures— platelet adhesion— thrombus formation obstructs blood flow

2. Chronic Ischemic Heart Disease 

• Stable Angina 

• Silent Myocardial Ischemia 

• Variant Angina 

fixed plaque: obstucts blood flow

What is acute coronary syndrom?

• Unstable Angina 

• Myocardial Infarction 

unstable plaque: ruputures— platelet adhesion— thrombus formation obstructs blood flow

What is Chronic Ischemic Heart Disease 

• Stable Angina 

• Silent Myocardial Ischemia 

• Variant Angina 

fixed plaque: obstucts blood flow

What is…

• Diminished oxygen delivery (perfusion) to myocardium 

• Ischemia begins (hypoxic injury) and may progress to infarction (death) of myocardial tissue 

• Myocardial Infarction is known as “heart attack”  

 

Acute Coronary Syndromes (ACS) 

 

Acute Coronary Syndromes (ACS) :

The area of infarction (death) is determined by many factors, what are they?

• Amount of collateral circulation present 

• Amount of the myocardium that is deprived of O2 

• BP, HR and cardiac rhythm 

• Coronary artery that is blocked 

• Duration of the occlusion 

• Metabolic demands of the myocardium 

ischemia

injury

infarction

death

What are the Pathophysiologic Changes OF Acute Coronary Syndromes (ACS) 

• Hypoxic cellular injury (ischemia) 

• Irreversible myocardial cell death (infarction) may occur after 20-40 minutes of severe ischemia – directly related to hypoxia 

• Local response to hypoxia

  • Localized vasodilation 

  • Acidosis  

  • Electrolyte shifts 

• SNS is activated secondary to hypoxia and pain  

• Necrotic myocardial cells will undergo healing process 

  • Inflammatory response begins 2-3 days after infarction 

  • Necrotic cells are replaced with scar tissue 

  • Scar tissue is incapable of contraction, conduction, and lacks elasticity  

 

What types of Myocardial infarctions are there?

• transmural infarct

• Subendocardial Infarct 

What kind of infarct is being descibed?

• Most common type of infarct 

• Full thickness of the ventricular wall 

• Also known as STEMI (ST segment elevated myocardial infarction) 

transmural infarction

What kind of infarction is being described?

• Inner ⅓ to ½ of ventricular wall 

• Also known as NSTEMI (non-ST segment elevated myocardial infarction) 

subendocardial infarct

(myocardial infarction) GOAL: 

Restore oxygen to the myocardium 

• Known as reperfusion– re-establish blood flow to the myocardium 

• Timely restoration of oxygen may prevent infarction (necrosis) of myocardial tissue 

 

What is reperfusion?

re-establish blood flow to the myocardium 

Myocardial infarction:

Laboratory Findings (Serum Biomarkers) 

• **Troponin: highly specific for myocardial tissue 

  • Begin to rise withing 3 hrs and stay elevated 7-10 days 

• Creatine kinase (CK-MB): muscle cells 

• Myoglobin: intracellular storage site of O2 in muscle cells 

What is the highly specific serum biomarker for myocardial tissue 

troponin

What are the manifestations of Myocardial Infarction (MI)

• May occur as abrupt onset or as an extension of UA/NSTEMI 

• Severe, crushing substernal chest pain 

• May radiate to jaw, neck or left arm 

• Unrelieved with Nitroglycerine(vasodilator) 

• GI distress: nausea and vomiting (N/V): may be mistaken for indigestion 

• Fatigue and weakness especially of arms and legs 

• SNS stimulation– tachycardia, restlessness, feelings of impending doom 

• May have productive cough with pink frothy sputum(pleural edema) 

• Skin pale and moist (diaphoretic) 

• Women: atypical ischemic-type chest discomfort 

• Elderly: often c/o SOB more frequently than chest pain 

 

What are complications of myocardial infarction (MI)

• Size and location of damaged myocardial tissue determine the prognosis 

• **Life-threatening dysrhythmias 

• Heart failure 

• Pericarditis: large infactis with low ejection fraction (EF) 

• Cardiogenic shock 

• Rupture of the heart muscle or valves  

• Sudden death 

What is being described?

• Stable Angina“fixed plaque” 

  • Early symptom of CAD 

  • Episodes of angina  

    • Precipitated by physical exercise, exposure to cold, emotional stress

    • Angina is relieved with rest and/or medications 

 

• Silent Myocardial Infarction 

  • Painless episodes of myocardial oxygen deprivation 

 

• Variant (Vasospastic/Printzmetal Angina) 

  • Pain related to myocardial oxygen deprivation that occurs at rest, during sleep, or with minimal physical exertion 

Chronic Ischemic Heart Disease 

What is ..

“fixed plaque” 

• Early symptom of CAD 

• Episodes of angina  

  • Precipitated by physical exercise, exposure to cold, emotional stress

  • Angina is relieved with rest and/or medications 

Stable Angina

What is a Painless episodes of myocardial oxygen deprivation 

 

Silent Myocardial Infarction 

What is..

Pain related to myocardial oxygen deprivation that occurs at rest, during sleep, or with minimal physical exertion 

 

Variant (Vasospastic/Printzmetal Angina) 

Hemodynamics of Valves 

• Promotes unidirectional flow through the 4 heart chambers 

• aortic_ & mitral_ most affected because ____higher pressure on left side of heart_

• Causes of valvular disease: 

  • Congenital defects 

  • Degenerative changes 

  • Inflammation/infection 

  • Ischemia 

  • Trauma 

What are causes of valvular disease?

• Congenital defects 

• Degenerative changes 

• Inflammation/infection 

• Ischemia 

• Trauma 

Two primary problems occur with valvular disease 

1. Opening 

2. Closing

Stenosis   (opening)	Regurgitation   (closing)
Narrowing of valve or failure of leaflets to open properly– opening problem	Incompetent valve or incomplete closure of a valve – closing problem
Constricted and narrow	Insufficient and fails to close
Impaired forward flow; resistance to blood flow through the valve	Allows backward flow (“leak”)
Blood volume and workload increases in the chamber “behind” diseased valve	Blood volume and workload increases in the chamber “behind” diseased valve
Increased volume leads to chamber dilation, increased workload leads to hypertrophy	Increased volume leads to chamber dilation, increased workload leads to hypertrophy

is this stenosis or regurgitation?

Narrowing of valve or failure of leaflets to open properly– opening problem

Constricted and narrow

Impaired forward flow; resistance to blood flow through the valve

Blood volume and workload increases in the chamber “behind” diseased valve

Increased volume leads to chamber dilation, increased workload leads to hypertrophy

Stenosis (opening)

Is this stenosis or regurgitation?

Incompetent valve or incomplete closure of a valve – closing problem

Insufficient and fails to close

Allows backward flow (“leak”)

Blood volume and workload increases in the chamber “behind” diseased valve

Increased volume leads to chamber dilation, increased workload leads to hypertrophy

Regurgitation (closing) 

What is the…

Narrowing of the valve orifice &/or failure of leaflets to open properly  

• Causes a resistance of blood through the valves 

• Increases volume & workload of the chamber attempting to empty through the narrow valve 

stenosis

Mitral Valve Disorders 

• mitral stenosis

• mitral regurgitation

What is the….

• Incomplete opening of mitral valve with left atrial distention and impaired filling of the left ventricle 

• Replacement of valvular tissue along with stiffness of the valve 

• Most commonly the result of rheumatic fever

• Continuous, progressive, life-long disorder 

Mitral Valve Stenosis 

Manefestations of Mitral Valve Stenosis 

• depend on severity of obstruction & are related to elevation in left atrial pressure & pulmonary vascular congestion, decreased_ cardiac output & left atria enlargement

  • Pulmonary congestion

  • Nocturnal paroxysmal dyspnea

    • nocturnal(night) paroxysmal(comes and goes) dyspnea(shortness of breath), & orthopnea  

  • Palpitations, chest pain, weakness, fatigue 

  • PAC's, A-fib & paroxysmal atrial tachycardia 

  • Risk for thrombus & stroke 

    • Because blood is flowing it can cause clots, if it breaks through it can get into your brain  

What is the…

Incomplete closure of a valve allowing the backflow of blood 

Mitral valve regurgitation

What are causes of mitral valve regurgitaiton?

• Rheumatic heart disease 

• MI 

• Papillary muscle dysfunction or rupture 

• Papillary Controls mitral valve 

• Stretching of valve structures due to dilation of left ventricle 

• Mitral valve prolapse:  “flappy mitral valve syndrome” 

  • Degeneration of valve leaflets that cause them to be enlarged and floppy so they ballon back 

  • More frequently in women than men; Familial tendency 

  • Associated with Marfan's syndrome, osteogenesis imperfecta, cardiac, hematological, neuroendocrine, metabolic & psychological disorders 

Mitral valve prolapse:  “flappy mitral valve syndrome” 

• Degeneration of valve leaflets that cause them to be enlarged and floppy so they ballon back 

• More frequently in women than men; Familial tendency 

• Associated with Marfan's syndrome, osteogenesis imperfecta, cardiac, hematological, neuroendocrine, metabolic & psychological disorders 

What is

Increased resistance to ejection of blood from left ventricle into the aorta 

• Causes: Congenital malformation or acquired calcification(from atherosclerosis) 

 

• Patho: slow and varies widely; process similar to CAD; progresses from base of cusps to the leaflets which reduces leaflet motion 

 

• Left ventricle wall becomes thicker (hypertrophy) but normal chamber volume maintained 

 

• More common in men 

 

• More common with HLD (hyperlipidemia) 

Aortic valve stenosis

What are causes of Aortic valve stenosis

Congenital malformation or acquired calcification(from atherosclerosis) 

what is the patho of Aortic valve stenosis

• slow and varies widely; process similar to CAD; progresses from base of cusps to the leaflets which reduces leaflet motion 

What are the symptoms of Aortic valve stenosis

• Murmur 

• Angina 

• Syncope 

• Heart failure 

• Exertional dyspnea (SOB with activity) 

What is …

• Incompetent valve that allows blood flow back into LV during diastole 

• LV increase stroke volume to include blood leaking back 

• Causes:

  • rheumatic fever

  • , idiopathic dilation of aorta,

  • congenital defects

  • , HTN,

  • trauma 

• Patho:

  • develops from conditions that cause scarring of leaflets or enlargement of orifice 

Aortic valve Regurgitation