Chapter 26 & 27: Cardiovascular System Flashcards
1
Q
Causes of Secondary Hyperlipidemia (4)
A
Results from systemic disturbance
1) Obesity with high-caloric intake
2) DM
3) Hypothyroidism
4) Liver disease
2
Q
Thromboangiitis Obliterans is the inflammation of _______ arteries that can extend to involved adjacent veins and nerves.
A
medium-sized
3
Q
Risk Factors for Atherosclerosis
A
Hypercholesterolemia Hyperlipidemia HTN Smoking DM
4
Q
______ has to occur for atherosclerosis to begin
A
Endothelial damage
5
Q
Most common cause of Thromboangiitis Obliterans (Buerger’s Disease)
A
Most common in young men who smoke heavily (tobacco allergy)
6
Q
Buerger’s Diseases affect ______ extremities
A
Lower extremities
7
Q
Clinical Manifestations of Thromboangiitis Obliterans
A
#1 = PAIN color/temperature changes paresthesia weak pulses in feet loss of hair/thin, shiny skin edema in legs can lead to GANGRENE
8
Q
Raynaud’s Syndrome
A
SMALL arteries and arterioles spasm and constrict in response to stimuli such as cold, exercise, and emotional stress
9
Q
Part of the body most commonly affected by Raynaud’s
A
fingers more often than toes
10
Q
Clinical Manifestations of Raynaud’s
A
COLOR CHANGES (W - B - R)
throbbing pain
paresthesia
fingertips thickened and nails become brittle
11
Q
Main Cause of Chronic Arterial Disease
A
atherosclerosis
12
Q
Main Cause of Chronic Venous Insufficiency
A
increased venous hydrostatic pressure
prolonged standing, obstruction, incompetent valves, sedentary lifestyle
13
Q
Risk Factors for CAD
A
same as atherosclerosis
HTN, DM, smoking, hypercholesterolemia
14
Q
Risk Factors For CVI
A
prolonged standing obstruction sedentary lifestyle DM obesity
15
Q
Varicose Veins
A
dilated torturous veins of the lower extremities
16
Q
Etiology of Varicose Veins
A
Incompetent valves
Increased venous pressure
Increased intra-abdominal pressure (obesity, pregnancy, heavy lifting)
17
Q
Pathogenesis of Varicose Veins
A
walls of the vessel stretch = incompetent valves = venous congestion = vein walls bulge out
18
Q
Risk Factors for DVT
VIRCHOW’S TRIAD
A
Venous Stasis
Hypercoagulability
injury to Venous Wall
19
Q
Most Common Clinical Manifestation of DVT
A
Edema in affected leg
pain
possible redness or warmth
20
Q
Causes of Primary Hypertension
Essential/Idiopathic
A
May not have known causes Lifestyle factors Family history Age Race (black)
21
Q
Risk Factors of Primary HTN
A
age, gender, race, family hx DM dyslipidemia high sodium sedentary lifestyle abdominal obesity excess alcohol smoking OSA
22
Q
Causes of Secondary Hypertension
A
Renal disease
Adrena Cortex D/O (excess aldosterone, cortisol)
Pheochromocytoma
Oral contraceptives
23
Q
Pheochromocytoma
A
tumor of tissue in the adrenal medulla
controls release of norepinephrine/epi
24
Q
Target Organ Damage of HTN (5)
A
Heart Peripheral Arteries Kidneys Brain Retina
25
Changes in Retina r/t HTN
```
Drusen
Cotton-wool spots
Microaneurysms
A-V nicking
Superficial retinal hemorrhages
```
26
Most Common Viral Causes of Acute Pericarditis (4)
1) Influenza
2) Epstein-Barr
3) Varicella
4) Coxsackie
27
Triad of Manifestations for Acute Pericarditis
```
Chest pain (worse w/ deep breathing, coughing - relieved sitting up/leaning forward)
Pericardial Friction Rub
ECG changes
```
28
Cardiac Tamponade
Compression of the heart due to accumulation of fluid, pus, or blood in the pericardial sac
29
Clinical Manifestations of Cardiac Tamponade
| BECK'S TRIAD
Hypotension
Jugular vein distention (JVD)
Muffled heart sounds
30
Key Diagnostic Finding for Cardiac Tamponade
Pulsus Paradoxus
31
Pulsus Paradoxus
Pulse is diminished or absent during inspiration and stronger in expiration
32
Myocardial oxygen supply is determined by:
capillary flow along with the ability of hemoglobin to deliver O2 to muscle
33
Factors that decrease coronary blood flow:
vasospasm
stenosis
thromobosis
34
Factors that increase myocardial oxygen demand
increased HR
increased LV contractility
SBP or myocardial wall stress
35
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
36
Stable Angina
CP associated with stable atherosclerotic pain = occurs with exertion, emotional stress, or exposure to cold
37
Characteristics of Stable Angina
Precordial or substernal pain
constricting, squeezing, suffocating
Should resolve with rest/NTG
38
Treatment for Stable Angina
Beta-blockers
| Nitroglycerin
39
Variant (Prinzmetal) Angina
Pain caused by coronary spasm - usually occurs during rest (nocturnal)
can cause arrhythmias
40
___________ is the initial manifestation of ischemic heart disease
Stable angina
41
Potential Causes of Variant Angina
Hyperactive SNS response
Imbalance of endothelium-derived factors
Defects in Ca handling from VSM
Alteratio in NO production
42
Treatment for Variant Angina
Calcium-channel blockers
| Nitrates
43
Dilated Cardiomyopathy
| Genetic and Nongenetic
SYSTOLIC dysfunction
ventricular enlargement = impaired contractility
blood builds up after systole
44
______ cardiomyopathy is one of the most common causes of heart failure.
Dilated cardiomyopathy
45
Hypertrophic Cardiomyopathy
| Genetic
DIASTOLIC dysfunction
Left ventricular hypertrophy = decreased ventricle size
ventricular filling is inadequate
atrial kick is needed = LA hypertrophy
46
_________ cardiomyopathy is the most common cause of sudden death in young athletes.
Hypertrophic
47
Restrictive Cardiomyopathy
| Genetic and Nongenetic
DIASTOLIC dysfunction
| decreased ventricular compliance/filliing due to stiff, rigid ventricular walls
48
Restrictive cardiomyopathy can be caused by ______ or _________
sarcoidosis or cancer
49
Most common cause of Infective Endocarditis
Staphylococcus aureus
50
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
51
Clinical Manifestations of Infective Endocarditis (FROM-JANE)
```
Fever
Roth Spots
Osler nodes
Murmur
Janeway lesions
Anemia
Nailbed hemorrhages (splinter)
Emboli
```
52
Valvular Heart Disease
| STENOSIS
Inability of leaflets to open and close properly
| blood flow is impeded
53
Stenosis results in decreased ____, ____, ____ and impaired ____________.
decreased CO
decreased EF and SV
impaired ventricular filling
54
Valvular Heart Disease
| REGURGITATION
Backflow of blood through a valve that cannot close properly due to damage or disease
55
Etiologies of Mitral Stenosis
Acute rheumatic fever
| Bacterial endocarditis
56
You would hear a low-pitch diastolic murmur and an opening snap in:
MITRAL STENOSIS
57
Mitral Stenosis results in:
Pulmonary HTH and R heart failure
58
Mitral Regurgiation leads to
dilation of both chambers
pulmonary congestion
RV failure
59
Etiologies of Mitral Regurgitation
```
Endocarditis
Rheumatic fever
MVP or mitral stenosis
Papillary muscle rupture
Chordae tendinae rupture
```
60
You would hear a pansystolic murmur in:
MITRAL REGURGITATION
61
In mitral regurgitation, the PMI is:
displaced left and downward
| with a palpable thrill
62
Risk Factors for Aortic Stenosis
Congenital bicuspid aortic valve
Calcification/Hypercholesterolemia
Hx of rheumatic valve disease
63
Triad of Symptoms of Aortic Stenosis
Angina
Dyspnea
Syncope
64
You would feel a thrill in the aortic area (2nd ICS RSB) and hear a loud systolic ejection murmur in:
AORTIC STENOSIS
65
Aortic Regurgitation leads to:
LV dilation and hypertrophy
Pressure and volume overlaod
Pulmonary edema
66
Early changes in Aortic Stenosis leads to:
diastolic dysfunction
| decreased compliance and unchanged contractility
67
Late changes in Aortic Stenosis lead to:
systolic dysfunction
myocardial ischemia
abnormal wall motion
decreased contractility = decreased SV
68
Risk Factors for Aortic Regurgitation
Rheumatic heart disease
Infective endocarditis
Marfan's Syndrome
Hypertension
69
You would see a Water-Hammer (Corrigan's) pulse in:
AORTIC REGURGITATION
| this is prominent carotid pulsations - head bobbing with each heartbeat
70
You would hear a decrescendo diastolic murmur at Erb's point (LSB) in:
AORTIC REGURGITATION
71
Cardiac Reserve
ability of the heart to increase its CO during increased activity
72
Heart failure occurs when any type of cardiac dysfunction causes:
Failure to empty
Reduction of cardiac output
Decrease in cardiac reserve
73
HIGH OUTPUT Heart Failure
heart cannot pump sufficient amounts of blood to meet the increased circulatory needs of tissues
heart weakens = LV fails
74
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
75
SYSTOLIC FAILURE Heart Failure
Reduced EF failure (<40%)
Decreased contractility
Preload increases and afterload decreases
Leads to pulmonary and peripheral edema
76
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
77
Left-Sided Heart Failure leads to
Pulmonary fluid overload
78
Main Complication of Left-Sided Heart Failure
Pulmonary Edema
79
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
```
80
Right-Sided Heart Failure leads to:
systemic fluid overload
81
Signs of Systemic Fluid Overload
| R-sided HF
```
Peripheral edema
Weight gain
JVD
Hepatomegaly and ascites
Kidney enlargement
```
82
Clinical Manifestations of R-Sided Heart Failure
```
Dependent edema (early sign)
RUQ discomfort
Weight gain
Decreased UO or nocturia
JVD, hepatomegaly, ascites
```
83
Compensatory Mechanisms in Heart Failure
```
attempt to maintain CO and cardiac reserve
Frank-Starling Mechanisms
SNS Activity
RAAS
Natriuretic Peptides
```
84
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
85
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
86
RAAS
| compensatory action in HF
activated d/t decrease in renal blood flow secondary to low CO
increases preload and afterload
87
Natriuretic Peptides (ANP and BNP)
promote rapid natriuresis and diuresis
decrease preload and afterload
can inhibit the SNS, RAAS, and ADH
88
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
89
Brain Natriuretic Peptide (BNP)
released by the ventricles due to ventricular volume expansion and pressure overload
acts as a vasodilator and diuretic
90
3 Specific Mechanisms in Treating HF
Slowing HF
Increasing contractility
Reducing cardiac workload (reduce preload and/or afterload)
91
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
92
Compensatory Mechanisms in Shock (that eventually fail and become detrimental)
SNS activation
Alpha1 and Beta1 = increased HR and contractility
Beta2 = bronchodilation
93
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
94
Causes of Hypovolemic Shock
Hemorrhage
Burns
Dehydration
Third-spacing
95
Treatment of Hypovolemic Shock
Fluid volume replacement first = crystalloids, colloids, blood prodcuts
Vasoconstricting drugs
Supplemental O2
96
Cardiogenic Shock
Decreased CO as a result of decreased myocardial contractility, increased afterload, and excess preload
97
Preload and afterload is increased in _____ shock
CARDIOGENIC
98
Causes of Cardiogenic Shock
MI = most common cause
| Mechanical obstructions
99
Obstructive Causes of Cardiogenic Shock
Cardiac tamponade
Tension pneumothorax
Large pulmonary embolism
100
Treatment of Cardiogenic Shock
Vasoactive medications first
nitroglycerin and nitroprusside
Positive inotropics = dobutamine
101
Distributive Shock
Normovolemic shock caused by MASSIVE VASODILATION
| Includes: neurogenic, anaphylactic, and septic shock
102
Neurogenic Shock
occurs when there is a disturbance in the nervous system that interrupts sympathetic outflow = vasodilation
103
Causes of Neurogenic Shock
```
Upper spinal cord injury/disease
Spinal anesthesia
TBI
Extreme emotional distress/fear/anxiety
Hypoxia
Hypoglycemia
```
104
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
105
Clinical Manifestations of Anaphylactic Shock
```
Hypotension
Urticaria and hives
Angioedema = hoarseness/stridor
Chest tightness
Abdominal cramps
Decreased CO, SVR, PA readings
```
106
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
107
________ is the key mediator of septic shock
Nitric oxide (released by activated endothelial cells)
108
Causes of Septic Shock
Nosocomial infections
| Gram negative bacteria: E. coli, Klebsiella, Pseudomonas
109
Early Stages of Septic Shock
```
Bounding pulses
Hypotension
Tachypnea
Increasd UO
Hyperthermia
Increased CO
```
110
Late Stages of Septic Shock
```
Weak, rapid pulse
Hypotension
Bradypnea
Oliguria
Hypothermia
AMS
Decreased CO
```
