Cardiovascular Pathophysiology Flashcards
Atherosclerosis
Hardening / lesions of arteries due to accumulation along intima in lumen of vessels of:
- smooth muscle cells
- connective tissue
- macrophages
- lipids
- -> Calcification
- -> Impairs blood flow
- -> Calcification
Stages:
- Initiation/Formation
- Adaptation
- Clinical
- Could lead to:
- MI
- Cerebral infarct
- Gangrene
- Aneurysm
- Occlusion / Ischemia
- Thromboembolism
Lesion
Abnormality in tissue – Atherosclerotic:
- Plaque - Atheromas - Fibrous plaques - Fibro-fatty lesions
Contributing factors:
- Cytokines - T lymphocytes - Endothelium - Thrombosis
Atheroma
Arterial wall remodeling
–> area of thickened intima
*Can break off / rupture
Stages:
- Initiation/Formation
- Adaptation
- Clinical
Hyperplasia
Excessive cell growth
Regression
Body fixes itself
Infarct
Cell death caused by restricted blood supply to area
Angiogenesis
New vascular formation / regeneration
Risk Factors for Development of Atherosclerosis / CAD
- Smoking
- HTN
- Family Hx
- Sedentary lifestyle
- Obesity
- Diabetes
- Dyslipidemia (high LDL, low HDL)
- Age / Sex / Race
- Hot reactor
- High Homocysteine
- High C-Reactive protein
CAD
(Coronary Artery Disease) - Ischemic Heart Disease
Deficit in O2 blood to myocardium
*Leading cause of death
Could lead to:
- Angina
- MI
- CHF
- Death
HTN
(Hypertension)
Persistent elevation of blood pressure
*Risk factor for CAD
Stage I:
Systolic BP > 140mmHg
Diastolic BP > 90mmHg
Obesity
BMI > 30kg/m2
*Risk factor for CAD
Diabetes
DM
Impaired fasting glucose > 100mg/dL
*Risk factor for CAD
Hypercholesterolemia
High blood cholesterol > 200mg/dL
LDL > 130mg/dL
HDL < 40mg/dL
*Risk factor for CAD
Lipid Metabolism
Cholesterol is insoluble, so must be transported in blood bound to lipoproteins
Normal < 200mg/dL
VLDL
LDL - target of therapeutic treatment
HDL
HDL
(High Density Lipoproteins) = Good cholesterol
Remove cholesterol from blood
–>liver for removal from body
Normal > 40mg/dL
LDL
(Low Density Lipoproteins) = Bad cholesterol
Oxidized and taken up by macrophages to lesions
Normal < 130mg/dL
Framingham Heart Study
Study to ID common factors contributing to CVD
Raynaud Phenomenon
Intermittent, bilateral attacks of ischemia caused by cold and emotions
Aneurysm
Weakening / bulge in wall of vessel
DVT
(Deep Venous Thrombosis) *ACUTE
Blood clot formed in vessel of lower extremity
-Inflammatory response
-Constant pain
PAD / PVD
(Peripheral Artery / Vascular Disease) *CHRONIC
Complication of atherosclerosis
-Pain with exertion, goes away with rest
Coronary Arteries
Right: off anterior aorta
-In right AV sulcus
Left: off posterior aorta
- LAD
- Circumflex
Angina
- Most common symptom of CAD
- Caused by ischemia (75-90% occlusion)
Symptoms:
- Substernal pressure (feels like indigestion)
- Pain in L arm, jaw (toothache), scapula
- Ltd duration
- Worse with exertion, better with rest
ACS
(Acute Coronary Syndrome)
Umbrella term for CAD symptoms
MI
(Myocardial Infarction)
Death of tissue due to prolonged ischemia, commonly from advanced atherosclerosis
--> Decreased effectiveness and efficiency of the pump
-Dec ventricular function (EF)
-Dec contractility
-Abnormal wall motion
-Inc ESV / EDV
-Inc LV ED pressure
Symptoms:
- Prolonged angina
- Cyanosis
- Dyspnea (SOB)
- Nausea
- Diaphoresis
- EKG changes
*40% females - no angina
Diaphoresis
Excessive sweating / perspiration
MI: Immediate Mgmt
Dial 911, Chew aspirin
In ER:
-EKG
-Meds:
Nitrates
Morphine
Antiarrhythmics
Anticoagulants = bleed
-Thrombolytics
-Blood Labs
-O2
Ischemic Heart Disease
Coronary Artery Disease (CAD)
Alphabet Approach to Patient Management
A -antiplatelet
- anticoagulant - ACE Inhibitor - Angiotensin receptor blocker
B -beta blocker
-BP control
C -Cholesterol tx
-Cig smoking cessation
D -Diabetes mgmt
-Diet
E -Exercise
ACE
(Angiotensin Converting Enzyme)
Arrhythmia
Irregular heartbeat
Physiological Controls of SV
(Stroke Volume)
- Preload
- Contractility
- Afterload
mVO2
Myocardial oxygen uptake (WORKLOAD of heart)
= How much O2 needs to be delivered to myocardium for
adequate function at any given time
Preload
Physiological control of SV
Degree of stretch of myocardial fibers prior to contraction
-Dependent on venous return
^preload = ^mVO2 = ^SV
Contractility
Physiological control of SV
Increased interaxns of myofilaments at cross-bridges
Increased Ca
Increased SNS input
^Contractility = ^mVO2 = ^SV
Afterload
Physiological control of SV
Amount of pressure ventricles must overcome during systole to open semilunar valves and eject blood
-If arterial pressure increases, so does afterload
^Afterload = ^mVO2 = Dec SV
CHF
(Congestive Heart Failure)
Heart unable to maintain adequate output to meet metabolic needs
*Abnormally high atrial filling pressures
- CO maintained by compensatory mech:
- ^LV EDP
- ^EDV
- ^SNS stimulation
Hypertensive Heart Disease
Cardiac hypertrophy secondary to prolonged systemic pressure overload
Endocardial / Valvular Disease
Damage to valves, impairing their function
–> Regurgitation (retrograde blood flow)
Ex: MVP
MVP
(Mitral Valve Prolapse)
Most common valvular disease
Infective Endocarditis
Inflammation of the endocarditis with vegetations on valves
–> Erosion –> Valvular Impotence
*Bacterial or viral, IV drugs, catheters
Cardiomyopathy
Primary noninflammatory myocardial disease
*NOT attributable to pressure or volume overload
- Dilated / Congestive –> CHF
- Hypertrophic / ASH / IHSS –> thickened myocardium
- Restrictive / Infiltrative –> ltd EDV –> CHF
ASH
(Asymmetric Septal Hypertrophy)
IHSS
(Idiopathic Hypertrophic Subaortic Stenosis)
Congenital Heart Disease
Major heart disease within first decades
- Acyanotic Group (No sys/pulm mixing)
- Cyanotic Tardive Group (Sys/pulm shunt reversal
- Cyanotic Group (Mixing of sys/pulm)
