Chapter 26 & 27: Cardiovascular System Flashcards
Causes of Secondary Hyperlipidemia (4)
Results from systemic disturbance
1) Obesity with high-caloric intake
2) DM
3) Hypothyroidism
4) Liver disease
Thromboangiitis Obliterans is the inflammation of _______ arteries that can extend to involved adjacent veins and nerves.
medium-sized
Risk Factors for Atherosclerosis
Hypercholesterolemia Hyperlipidemia HTN Smoking DM
______ has to occur for atherosclerosis to begin
Endothelial damage
Most common cause of Thromboangiitis Obliterans (Buerger’s Disease)
Most common in young men who smoke heavily (tobacco allergy)
Buerger’s Diseases affect ______ extremities
Lower extremities
Clinical Manifestations of Thromboangiitis Obliterans
#1 = PAIN color/temperature changes paresthesia weak pulses in feet loss of hair/thin, shiny skin edema in legs can lead to GANGRENE
Raynaud’s Syndrome
SMALL arteries and arterioles spasm and constrict in response to stimuli such as cold, exercise, and emotional stress
Part of the body most commonly affected by Raynaud’s
fingers more often than toes
Clinical Manifestations of Raynaud’s
COLOR CHANGES (W - B - R)
throbbing pain
paresthesia
fingertips thickened and nails become brittle
Main Cause of Chronic Arterial Disease
atherosclerosis
Main Cause of Chronic Venous Insufficiency
increased venous hydrostatic pressure
prolonged standing, obstruction, incompetent valves, sedentary lifestyle
Risk Factors for CAD
same as atherosclerosis
HTN, DM, smoking, hypercholesterolemia
Risk Factors For CVI
prolonged standing obstruction sedentary lifestyle DM obesity
Varicose Veins
dilated torturous veins of the lower extremities
Etiology of Varicose Veins
Incompetent valves
Increased venous pressure
Increased intra-abdominal pressure (obesity, pregnancy, heavy lifting)
Pathogenesis of Varicose Veins
walls of the vessel stretch = incompetent valves = venous congestion = vein walls bulge out
Risk Factors for DVT
VIRCHOW’S TRIAD
Venous Stasis
Hypercoagulability
injury to Venous Wall
Most Common Clinical Manifestation of DVT
Edema in affected leg
pain
possible redness or warmth
Causes of Primary Hypertension
Essential/Idiopathic
May not have known causes Lifestyle factors Family history Age Race (black)
Risk Factors of Primary HTN
age, gender, race, family hx DM dyslipidemia high sodium sedentary lifestyle abdominal obesity excess alcohol smoking OSA
Causes of Secondary Hypertension
Renal disease
Adrena Cortex D/O (excess aldosterone, cortisol)
Pheochromocytoma
Oral contraceptives
Pheochromocytoma
tumor of tissue in the adrenal medulla
controls release of norepinephrine/epi
Target Organ Damage of HTN (5)
Heart Peripheral Arteries Kidneys Brain Retina
Changes in Retina r/t HTN
Drusen Cotton-wool spots Microaneurysms A-V nicking Superficial retinal hemorrhages
Most Common Viral Causes of Acute Pericarditis (4)
1) Influenza
2) Epstein-Barr
3) Varicella
4) Coxsackie
Triad of Manifestations for Acute Pericarditis
Chest pain (worse w/ deep breathing, coughing - relieved sitting up/leaning forward) Pericardial Friction Rub ECG changes
Cardiac Tamponade
Compression of the heart due to accumulation of fluid, pus, or blood in the pericardial sac
Clinical Manifestations of Cardiac Tamponade
BECK’S TRIAD
Hypotension
Jugular vein distention (JVD)
Muffled heart sounds
Key Diagnostic Finding for Cardiac Tamponade
Pulsus Paradoxus
Pulsus Paradoxus
Pulse is diminished or absent during inspiration and stronger in expiration
Myocardial oxygen supply is determined by:
capillary flow along with the ability of hemoglobin to deliver O2 to muscle
Factors that decrease coronary blood flow:
vasospasm
stenosis
thromobosis
Factors that increase myocardial oxygen demand
increased HR
increased LV contractility
SBP or myocardial wall stress
Angina
chest pain caused by myocardial ischemia
occurs when there is decreased blood flow to myocardium and/or increased demand for oxygen that cannot be met
Stable Angina
CP associated with stable atherosclerotic pain = occurs with exertion, emotional stress, or exposure to cold
Characteristics of Stable Angina
Precordial or substernal pain
constricting, squeezing, suffocating
Should resolve with rest/NTG
Treatment for Stable Angina
Beta-blockers
Nitroglycerin
Variant (Prinzmetal) Angina
Pain caused by coronary spasm - usually occurs during rest (nocturnal)
can cause arrhythmias
___________ is the initial manifestation of ischemic heart disease
Stable angina
Potential Causes of Variant Angina
Hyperactive SNS response
Imbalance of endothelium-derived factors
Defects in Ca handling from VSM
Alteratio in NO production
Treatment for Variant Angina
Calcium-channel blockers
Nitrates
Dilated Cardiomyopathy
Genetic and Nongenetic
SYSTOLIC dysfunction
ventricular enlargement = impaired contractility
blood builds up after systole
______ cardiomyopathy is one of the most common causes of heart failure.
Dilated cardiomyopathy
Hypertrophic Cardiomyopathy
Genetic
DIASTOLIC dysfunction
Left ventricular hypertrophy = decreased ventricle size
ventricular filling is inadequate
atrial kick is needed = LA hypertrophy
_________ cardiomyopathy is the most common cause of sudden death in young athletes.
Hypertrophic
Restrictive Cardiomyopathy
Genetic and Nongenetic
DIASTOLIC dysfunction
decreased ventricular compliance/filliing due to stiff, rigid ventricular walls
Restrictive cardiomyopathy can be caused by ______ or _________
sarcoidosis or cancer
Most common cause of Infective Endocarditis
Staphylococcus aureus
Pathogenesis of Infective Endocarditis
Vegetations attach loosely to heart valves
Can break off, travel, and become emboli
Bacteremia initiates immune response
Growth causes valve destruction
Clinical Manifestations of Infective Endocarditis (FROM-JANE)
Fever Roth Spots Osler nodes Murmur Janeway lesions Anemia Nailbed hemorrhages (splinter) Emboli
Valvular Heart Disease
STENOSIS
Inability of leaflets to open and close properly
blood flow is impeded
Stenosis results in decreased ____, ____, ____ and impaired ____________.
decreased CO
decreased EF and SV
impaired ventricular filling
Valvular Heart Disease
REGURGITATION
Backflow of blood through a valve that cannot close properly due to damage or disease
Etiologies of Mitral Stenosis
Acute rheumatic fever
Bacterial endocarditis
You would hear a low-pitch diastolic murmur and an opening snap in:
MITRAL STENOSIS
Mitral Stenosis results in:
Pulmonary HTH and R heart failure
Mitral Regurgiation leads to
dilation of both chambers
pulmonary congestion
RV failure
Etiologies of Mitral Regurgitation
Endocarditis Rheumatic fever MVP or mitral stenosis Papillary muscle rupture Chordae tendinae rupture
You would hear a pansystolic murmur in:
MITRAL REGURGITATION
In mitral regurgitation, the PMI is:
displaced left and downward
with a palpable thrill
Risk Factors for Aortic Stenosis
Congenital bicuspid aortic valve
Calcification/Hypercholesterolemia
Hx of rheumatic valve disease
Triad of Symptoms of Aortic Stenosis
Angina
Dyspnea
Syncope
You would feel a thrill in the aortic area (2nd ICS RSB) and hear a loud systolic ejection murmur in:
AORTIC STENOSIS
Aortic Regurgitation leads to:
LV dilation and hypertrophy
Pressure and volume overlaod
Pulmonary edema
Early changes in Aortic Stenosis leads to:
diastolic dysfunction
decreased compliance and unchanged contractility
Late changes in Aortic Stenosis lead to:
systolic dysfunction
myocardial ischemia
abnormal wall motion
decreased contractility = decreased SV
Risk Factors for Aortic Regurgitation
Rheumatic heart disease
Infective endocarditis
Marfan’s Syndrome
Hypertension
You would see a Water-Hammer (Corrigan’s) pulse in:
AORTIC REGURGITATION
this is prominent carotid pulsations - head bobbing with each heartbeat
You would hear a decrescendo diastolic murmur at Erb’s point (LSB) in:
AORTIC REGURGITATION
Cardiac Reserve
ability of the heart to increase its CO during increased activity
Heart failure occurs when any type of cardiac dysfunction causes:
Failure to empty
Reduction of cardiac output
Decrease in cardiac reserve
HIGH OUTPUT Heart Failure
heart cannot pump sufficient amounts of blood to meet the increased circulatory needs of tissues
heart weakens = LV fails
LOW OUTPUT Heart Failure
LV is unable to fill with adequate blood to pump out to the tissues
Occurs with impaired venous return
Inadequate O2 is delivered
SYSTOLIC FAILURE Heart Failure
Reduced EF failure (<40%)
Decreased contractility
Preload increases and afterload decreases
Leads to pulmonary and peripheral edema
DIASTOLIC FAILURE Heart Failure
Preserved EF failure
Relaxation of the ventricle in impaired and cannot fill properly
Common in adults with HTN
Ventricle cannot stretch but CAN contract
Left-Sided Heart Failure leads to
Pulmonary fluid overload
Main Complication of Left-Sided Heart Failure
Pulmonary Edema
Clinical Manifestations of L-sided Heart Failure
DOE PND Orthopnea S3 or S4 gallop Tachypnea and tachycardia Fine crackles Cough - may produce pink, frothy sputum
Right-Sided Heart Failure leads to:
systemic fluid overload
Signs of Systemic Fluid Overload
R-sided HF
Peripheral edema Weight gain JVD Hepatomegaly and ascites Kidney enlargement
Clinical Manifestations of R-Sided Heart Failure
Dependent edema (early sign) RUQ discomfort Weight gain Decreased UO or nocturia JVD, hepatomegaly, ascites
Compensatory Mechanisms in Heart Failure
attempt to maintain CO and cardiac reserve Frank-Starling Mechanisms SNS Activity RAAS Natriuretic Peptides
Frank-Starling Mechanisms
SV increased through increase in EDV
increased filling = increased stretching = increased contractile force
stretch is limited and this mechanism fails over time
SNS Activity
compensatory activity in HF
helps maintain perfusion to heart and brain
stimulates HR and contractility
vasoconstricion = increased afterload
heart has to work harder but cannot do so
RAAS
compensatory action in HF
activated d/t decrease in renal blood flow secondary to low CO
increases preload and afterload
Natriuretic Peptides (ANP and BNP)
promote rapid natriuresis and diuresis
decrease preload and afterload
can inhibit the SNS, RAAS, and ADH
Atrial Natriuretic Peptide (ANP)
released by the atria d/t increased atrial stretch/pressure
produces rapid, temporary loss of Na, water, and potassium
acts as an antagonist to renin and aldosterone
Brain Natriuretic Peptide (BNP)
released by the ventricles due to ventricular volume expansion and pressure overload
acts as a vasodilator and diuretic
3 Specific Mechanisms in Treating HF
Slowing HF
Increasing contractility
Reducing cardiac workload (reduce preload and/or afterload)
Shock is defined as:
the acute failure of the circulatory system to maintain adequate blood flow (and therefore oxygen delivery) to body tissues and vital organs
Compensatory Mechanisms in Shock (that eventually fail and become detrimental)
SNS activation
Alpha1 and Beta1 = increased HR and contractility
Beta2 = bronchodilation
Hypovolemic Shock
Most common type of shock
Caused by a large reduction in circulating blood volume = unavailable for the transport of oxygen and nutrients to tissues
Causes of Hypovolemic Shock
Hemorrhage
Burns
Dehydration
Third-spacing
Treatment of Hypovolemic Shock
Fluid volume replacement first = crystalloids, colloids, blood prodcuts
Vasoconstricting drugs
Supplemental O2
Cardiogenic Shock
Decreased CO as a result of decreased myocardial contractility, increased afterload, and excess preload
Preload and afterload is increased in _____ shock
CARDIOGENIC
Causes of Cardiogenic Shock
MI = most common cause
Mechanical obstructions
Obstructive Causes of Cardiogenic Shock
Cardiac tamponade
Tension pneumothorax
Large pulmonary embolism
Treatment of Cardiogenic Shock
Vasoactive medications first
nitroglycerin and nitroprusside
Positive inotropics = dobutamine
Distributive Shock
Normovolemic shock caused by MASSIVE VASODILATION
Includes: neurogenic, anaphylactic, and septic shock
Neurogenic Shock
occurs when there is a disturbance in the nervous system that interrupts sympathetic outflow = vasodilation
Causes of Neurogenic Shock
Upper spinal cord injury/disease Spinal anesthesia TBI Extreme emotional distress/fear/anxiety Hypoxia Hypoglycemia
Pathogenesis of Anaphylactic Shock
IgE attaches to mast cells
Mast cells release histamine and prostaglandins
Causes vasodilation, laryngeal edema, bronchial constriction, cardiovascular collapse, respiratory failure
Clinical Manifestations of Anaphylactic Shock
Hypotension Urticaria and hives Angioedema = hoarseness/stridor Chest tightness Abdominal cramps Decreased CO, SVR, PA readings
Septic Shock
Most common type of distributive shock
Due to massive infectious process - bacteria multiple faster than body can kill them and release endotoxins and exotoxins
________ is the key mediator of septic shock
Nitric oxide (released by activated endothelial cells)
Causes of Septic Shock
Nosocomial infections
Gram negative bacteria: E. coli, Klebsiella, Pseudomonas
Early Stages of Septic Shock
Bounding pulses Hypotension Tachypnea Increasd UO Hyperthermia Increased CO
Late Stages of Septic Shock
Weak, rapid pulse Hypotension Bradypnea Oliguria Hypothermia AMS Decreased CO
