CV Flashcards
1
Q
General causes of edema
A
Increased hydrostatic pressure (impaired venous drainage, CHF)
Decreased oncotic pressure (nephrotic syndrome, cirrhosis, and protein malnutrition)
2
Q
Generalized edema is called
A
Anasarca
3
Q
Pulmonary edema is usually caused by
A
LV failure or ARDS
4
Q
Edema has this effect on the inflammatory process
A
It diminishes it, causing impaired wound healing and ability to fight infection
5
Q
When blood accumulates within a tissue, it is referred to as a
A
hematoma
6
Q
Classification of hemorrhages
A
1-2mm = petechiae 2-5mm = purporas 1-2cm = bruises (SQ hematoma with RBC deposition which are then phagocytosed by macrophages)
7
Q
Resolution of a bruise
A
RBCs are phagocytosed by macrophages. The hemoglobin is metabolized into bilirubin, which is then converted to hemosiderin (golden-brown)
8
Q
Examples of cardiac dysfunction that can cause thrombus formation
A
1) MI- irregular contraction of the myocardium and damage to endocardium cause mural thrombus formation
2) Rheumatic heart disease- mitral valve stenosis, causes atrial dilation with a-fib-> stasis of blood->mural thrombus
3) Atherosclerosis (causes EC injury and abnormal BF)
9
Q
What is a mural thrombus?
A
A thrombus in a large vessel that will decrease blood flow through that vessel
10
Q
Septic shock has a mortality rate of ______% and is associated with _______failure
A
25-50%
multi-organ
11
Q
Layers of the BV wall and their components
A
Tunica intima
- Endothelium
- Basement membrane
- Internal elastic membrane
Tunica Media
- Smooth muscle cells
- Elastic fibers
Tunica adventitia
- Areolar connective tissue (thin layer of connective tissue that runs lengthwise down the vessel).
12
Q
Characteristics of vascular smooth muscle cells
A
1) Contractile
2) Secretory (formation of matrix, growth factors, and proteases)
3) Plasticity (can hypertrophy, proliferate, and change phenotype)
13
Q
Vascular tone is regulated by
A
Myogenic tone (intrinsic tone) and neurohormonal tone (extrinsic factors in the blood)
14
Q
Vasodilators secreted by the endothelium
A
NO and prostacyclin (PGI2)
prostacyclin also inhibits platelet aggregation
15
Q
Vasoconstrictor released by the endothelium
A
Endothelin
16
Q
Factors released by the endothelium
A
Vasodilators (NO and PGI2)
Vasoconstrictors (endothelin)
Anti-aggregatory for platelets
Anti-mitogenic for vascular smooth muscle
17
Q
5 Roles of the endothelium
A
1) Acts as a barrier
2) Secretory (vasodilators and constrictors)
3) Modulatory (on platelets and vascular smooth muscle)
4) Metabolic (ACE produces angiotensin II and breaks down bradykinin)
5) Plasticity (angiogenesis in response to injury and ischemia)
18
Q
What controls blood flow into a region?
A
Resistance of the microcirculation. Arterioles are the main factor responsible for the SVR. Precapillary sphincters also help maintain BP and selectively regulate flow through vascular beds.
19
Q
What is the equation for Poiseuille’s Law?
A
P = (8nLQ)/(pi r^4)
20
Q
3 ways local blood flow is controlled
A
1) Metabolic regulation (local metabolites produce vasodilation)
2) Autoregulation (increase in transmural pressure causes vasoconstriction)
3) Shear stress (causes vasodilation). Constant “scratching” from shear stress can cause endothelial damage
21
Q
What is lymph composed up?
A
Mostly water and some small amounts of protein (mostly albumin) that are too large to be absorbed by the capillary.
22
Q
Capillary outflow exceeds venous absorption by about _____L/day
A
3 L/day
This is why we need our lymphatics!
23
Q
Pathway of the lymphatics and how the fluid moves
A
Valves ensure unidirectional flow, and the lymphatic vessels are occasionally compressed by contraction of skeletal muscle, pulsatile expansion of arteries within the same sheath, and by contraction of the smooth muscle of the lymphatic vessel. Lymph returns to the circulation via the thoracic duct and the right lymphatic duct.
24
Q
Oncotic pressure in the interstitium should be
A
0
25
How does fluid enter the lymphatic system?
Pressure gradients. As fluid escapes the capillary, the interstitial pressure rises and enters the lymphatic vasculature.
26
Five most common causes of edema
1) Increased capillary permeability
- Inflammation
2) Increased capillary hydrostatic pressure
- CHF, ascites/liver cirrhosis, venous obstruction
3) Decreased plasma oncotic pressure
- Malnutrition, protein loss via urine, liver disease
4) Lymphatic obstruction
- Node removal, neoplasm, post-irradiation
5) Sodium retention
- Excessive salt intake with renal insufficiency, increased reabsorption of Na, renal hypoperfusion, RAAS activation
27
Why is edema a problem?
Edema increases the distance required for nutrients, oxygen, and wastes to move between the capillaries and tissues. Increased tissue pressure may also decrease capillary blood flow.
Both of these factors make it difficult to heal wounds and fight infections, and can result in the development of ulcerations.
28
Treatment of edema
Compression stockings, salt restriction, diuretics, reduce standing for long periods of time
29
What is the basic definition of shock?
Failure of the cardiovascular system to adequately perfuse tissues, resulting in widespread impairment in cellular metabolism. Untreated, it will lead to organ failure and death.
30
Cardiogenic shock
Results from the inability of the heart to pump enough blood to the tissues. Most commonly due to an acute MI or severe myocardial ischemia. Three general causes of this type of shock:
1) Reduced contractility (MI, cardiomyopathy, papillary muscle rupture)
2) Impaired diastolic filling (ventricular dysrhythmias & cardiac tamponade)
3) Outflow obstruction (PE & valvular disorders)
31
Hypovolemic shock
Caused by a loss of body fluids:
1) Bood (hemorrhage)
2) Plasma (burns)
3) Other: sweat, emesis, diarrhea, diabetes insipidus, etc
Shock develops once intravascular volume has decreased by about 15%
Body will increase SVR in an attempt to maintain BP
32
Neurogenic shock
MASSIVE vasodilation due to imbalance between SNS and PSNS activity. Decreased SNS activity causes vasodilation, and because of this, there is not enough pressure to drive nutrients across capillary membranes, and delivery to cells is diminished.
Causes: Trauma to spinal cord or medulla
Hallmarks: decreased SVR and HR (due to unimpeded PSNS activity)
33
Anaphylactic shock
Due to a widespread allergic (IgE mediated) reaction. This causes systemic vasodilation and capillary leakiness, causing venous pooling, edema, and decreased nutrient delivery.
34
This type of shock is first among deaths in the ICU
Septic shock
35
Septic shock
The spread of a localized infection into the bloodstream. Release of endotoxins (LPS) from gram (-) bacteria upon their death.
These endotoxins trigger the release of inflammatory mediators such as TNF, IL-1, and IL-6/8, causing a systemic inflammatory response.
This inflammatory response causes low SVR, low BP, tachycardia, and temperature instability. Also causes endothelial damage, activating the coagulation cascade and possibly set of DIC.
36
Nonprogressive stage of shock
Compensatory mechanisms activated*, perfusion maintained, primarily affecting cardiac, cerebral, pulmonary (whatever that means).
* = Baroreceptor reflex, CAs, activation of RAAS, ADH, and SNS
37
Progressive stage of chock
Damage is occurring, but it is reversible.
Worsening O2 supply/demand (causes anaerobic metabolism and acidosis, pH induced vasodilation, and decreased venous return), endothelial cell injury and DIC. At this stage, vital organs are affected--patient may be confused and have low UO.
38
Irreversible stage of shock
Irreversible damage has occurred (cell death)
Necrosis, lysosomal leakage (which is damaging to the heart), and decreased myocardial contractility. Bowel becomes ischemic and leaks flora into the circulation. Kidneys fail due to acute tubular necrosis.
39
Characteristics of central venous thrombi in superficial veins
Cause local congestion, pain, swelling, and rarely embolize.
Swelling and impaired venous drainage predispose the skin to infection and development of venous stasis ulcers.
40
Characteristics of deep thrombi
Tend to be in large veins above the knee and are asymptomatic. These tend to embolize.
41
A PE can cause these complications if >60% of pulmonary circulation is obstructed
Sudden death, cor pulmonale, or CV collapse
42
Effect of small, medium, and multiple PEs
Small- infarct usually occurs
Medium- no infarct due to collateral flow, but can cause LV failure
Multiple- pulm HTN and RV failure
43
Virchow's Triad
Hypercoagulability
Abnormal blood flow
Endothelial injury
44
Patho of atherosclerosis
Starts with endothelial Injury! May be due to smoking, autoimmune, virus, HTN, DM, high LDL, low HDL, etc).
1) Endothelial injury
2) Damaged endothelial cells become inflamed and unable to produce normal antithrombotic, vasodilatory, and anti-mitogenic substances
3) Macrophages adhere to the damaged endothelium
4) Macrophages then release ROS that oxidize LDL and further damage the vessel wall
5) Oxidized LDL enters the intima and is engulfed by resident macrophages (turning them into foam cells). Once enough of these foam cells accumulate, the lesion is called a fatty streak.
6) Once formed, the fatty streak continues to release more ROS, causing further vessel damage
7) Due to loss of anti-mitogenic effects of the endothelium, smooth muscle cells (SMCs) proliferate and migrate into the intima over the fatty streak. The SMCs also change their phenotype to a secretory cell, and what they secrete is extracellular matrix and other growth factors. Release collagen and form a fibrous plaque.
8) This fibrous plaque may calcify and protrude into the vessel, obstructing flow into distal tissues.
45
What is the barrier between the intima and the media?
Internal elastic lamina
46
Platelet activation and athersclerosis
The whole event is a giant inflammatory signal. Can cause platelets to activate and build upon the plaque (atheroma).
47
What is the purpose of the fibrous plaque?
To create a shield from the inflammation. The blood should be able to flow over it and be ok. If the cap doesn't form quick enough or isn't stabile enough, then the stuff underneath it is stimulation for inflammation and platelet activation.
48
Common place in plaques to develop clots
The "shoulder" of the plaque (the corners of the plaque)
49
What is a vulnerable plaque?
One that doesn't have the stabilizing fibrous plaque
50
Cause of essential hypertension
Idiopathic
51
Common cause of aneurysms
Atherosclerosis
Other causes: Traumatic injury to the aorta and marfan's syndrome.
52
Where do most aneurysms occur?
Abdominal and thoracic aorta
53
What can aneurysms result in?
Rupture, obstruction, embolism, impingement, and formation of a mass.
54
What is the difference between a true and false aneurysm?
A true aneurysm involves all three layers of the vessel wall.
A false aneurysm is where blood leaks through the vessel wall, but is contained by the adventitia.The risk of rupture is higher in a false aneurysm.
55
Increased pressure load causes this type of hypertrophy
Concentric hypertrophy- sarcomeres are added in parallel, increasing the thickness of the myocardium. This allows the heart to generate higher pressures. This leads to a stiff ventricle and impaired filling.
56
Increased volume load causes this type of hypertrophy
Eccentric hypertrophy- lengthening of the sarcomeres, resulting in dilation. This allows the heart to expand to receive a greater volume of blood.
57
Angina pectoris will develop once the coronary lumen has decreased by ____%
75%
58
Types of angina
Stable (occurs during exertion)
Variable (occurs at rest or during sleep)
Unstable (increasing frequency of pain)
59
Definition and causes of sudden cardiac death
Sudden, unexpected death caused by a loss of heart function. Can be caused by PE, ruptured aortic aneurysm, and ventricular arrhythmias (V-fib).
60
This part of the myocardium is the most vulnerable to ischemia
The subendocardium (furthest away from the coronaries). Damage to this area can be caused by a transient ischemic event.
If ischemia continues, the entire myocardium will infarct (transmural infarct).
61
Examples of the CK-dimers and their location
CK-MM (heart and skeletal muscle)
CK-BB (brain and lung)
CK-MB (mostly from the myocardium)
62
CK-MB levels
Appear within 2-4 hours, peaks at 18, and returns to baseline by 48.
63
Troponin Levels
Tropinins T and I appear within 2-4 hours, peak at 18, and remain elevated for 4-7 days. Troponins are the most specific indicators of an MI.
64
Three types of cardiomyopathy
Dilated, hypertrophic, and restrictive
65
General definition of cardiomyopathy
Disease of the myocardium
66
Dilated cardiomyopathy
Progressive dilation (eccentric hypertrophy) of all chambers of the heart. This causes systolic dysfunction due to ineffective contraction, decreased EF, and eventually HF.
67
Causes of dilated cardiomyopathy
1) Idiopathic (2/3 of cases)
2) Environmental factors (CAD, valve disease, ETOH, drugs, infections, etc)
3) Genetic disorder (defective gene coding for dystrophin, a protein needed for muscle contractility)
68
Hypertrophic cardiomyopathy
Concentric hypertrophy causes impaired diastolic filling (due to stiff ventricle) and outflow obstruction (septum obstructing the LV outflow tract). Outflow obstruction is worse when HR increases during exertion.
69
Will increasing preload assist CO for someone with dilated cardiomyopathy?
No. In this condition, the heart keeps stretching, but it is not able to contract. Increasing preload will not help.
70
Restrictive cardiomyopathy
Here, the myocardium has become rigid and noncompliant. This results in impaired filling and a weak systole (contractility is reduced).
71
Causes of restrictive cardiomyopathy
Endomyocardial fibrosis (endpoint of an inflammatory process) and cardiac amyloidosis (proteins that were once soluble become insoluble and deposit themselves into the interstitial space)
72
What is cor pulmonale?
Pulmonary HTN leads to RV hypertrophy and dilation
73
Aortic stenosis becomes hemodynamically significant when the transvalvular pressure gradient is > ____ an the valve orifice is less than _____
50mmHg
| 1cm2 (normal area is 2.5-3.5cm2)
74
Classic triad of aortic stenosis symptoms
1) Angina (often even without CAD)
2) Dyspnea on exertion
3) Syncope (fainting)
Outflow obstruction causes LV hypertrophy to compensate for the increased workload. Eventually the hypertrophy increases O2 demand so much that the coronaries (even healthy ones) are unable to provide enough O2. This causes ischemic attacks and angina.
75
Basic problem with rheumatic fever
Causes an autoimmune reaction that leads to scarring and fibrosis of the valve leaflets, leading to stenosis and regurgitation.
76
Patho of mitral stenosis
Fusion of leaflets of the mitral valve due to rheumatic fever. This causes increased LA pressures and LA dilation. LA dilation places someone at high risk for developing A-fib, which predisposes to clots. Severe stenosis will back pressures into the pulmonary system and cause CHF.
77
In mitral stenosis, the valve area is < _____cm2 and a mean LA pressure of ____mmHg is needed to maintain adequate CO
1cm2
| 25mmHg
78
Two causes of aortic stenosis
1) Non-rheumatic (progressive calcification and stenosis of a congenitally abnormal aortic valve)
2) Rheumatic (due to rheumatic fever)
79
Structural effects of rheumatic fever on the heart
1) Schoff bodies within the myocardium (nodule from inflammation)
2) Vegetations on the valves
3) Thickening of the chordae tendinae
4) Fibrinous pericarditis
80
Most common causes of mitral regurgitation
MVP and rheumatic heart disease
81
Patho of mitral regurgitation
LA overload due to retrograde flow during systole. This causes LA dilation (and resultant a-fib). Valve structures will stretch due to the dilation as well, resulting in even more regurgitation.
82
Mitral regurgitation will result in an enlarged ___ wave on PAC tracing
V wave. The magnitude of the V wave correlates with the magnitude of regurgitation.
83
Mitral valve prolapse (MVP) patho
Weak connective tissue causes billowing of the mitral valve into the LA during systole. This billowing also causes the leaflets to part slightly, causing regurgitation into the LA.
84
Cause of MVP
Inherited connective tissue disorders (Marfan's, etc.)
85
Most common complication of MVP
Infective endocarditis
86
Causes of aortic regurgitation
1) Acute (infective endocarditis, trauma, dissection of thoracic aneurysm)
2) Chronic (rheumatic fever, chronic HTN)
87
Patho of Aortic Regurgitation
LV volume overload due to receiving blood from both the LA and aorta during diastole. The LV dilates and hypertrophies. Due to the hypertrophy, SBP will increase, and due to regurgitation, DBP will decrease. Eventually, the dilation and hypertrophy will cease to compensate for the aortic incompetence and failure will occur.
88
Angiogenesis stems from ___ cells
Endothelial
89
Angina is associated with ____% lumen occlusion
75%
90
Cardiac infarction begins within _____min of an occlusion
20-30 minutes
91
This type of cardiomyopathy is also known as congestive cardiomyopathy
Dilated cardiomyopathy
92
Causes of dilated cardiomyopathy
1) Idiopathic (2/3 of cases)
2) Environmental (viruses, ETOH, chemo, DM, drug toxicity, many others)
3) Genetic (abnormal gene coding for dystrophin)
93
This type of heart failure occurs with dilated cardiomyopathy
Biventricular failure
94
Problems with hypertrophic cardiomyopathy
1) Ineffective diastole (impaired relaxation)
2) Powerful systole
3) Obstruction of LV outflow tract
4) Collagen deposition
5) Altered contractile proteins in the myocytes
95
Basic problems with restrictive cardiomyopathy
Impaired ventricular filling and weak systole
96
When does the RV tend to fail in cor pulmonale?
When the PA pressure equals the systemic pressure
97
When does angiogenesis occur?
In response to low oxygen supply in the tissues
98
Arterial thrombi usually originate from
The heart
Also my come from ulcerated athersclerotic plaques or aneurysms.
99
Consequences of systemic thromboembolism depend on
Collateral blood flow and the caliber of the occluded vessel
100
Infarction may occur due to
1) Occlusion of arterial supply
2) Blockage of venous drainage
3) Swelling of an atheroma (hemorrhage within a plaque)
4) Local vasospasm
5) Compression of a vessel (tumor)
101
What factors may cause an atherosclerotic plaque with a thin fibrous cap to rupture?
Shear forces
Inflammation
Apoptosis
Degradative enzymes released by macrophages
102
What occurs in response to plaque rupture?
Inflammation and cytokine release
Platelet adherence and activation
Production of thrombin and vasoconstrictors
Basically, inflammation, vasospasm, and both clotting cascades activate, causing an acute decrease in arterial blood flow.
103
Shock is also known as
CV collapse
104
The most common cause of HTN is
Idiopathic (95% of cases)
| Probably some combo of genetic and environmental risk factors
105
What is malignant HTN?
Rapidly increasing HTN that if unattended can result in death within 2 years. Presents with a DBP >120 and can cause renal failure and retinal damage.
106
Why are people with AAAs at higher risk of stroke/MI?
Because the aneurysm vas most likely initiated by an atherosclerotic plaque, meaning there are other plaques within the body that could rupture and lead to infarction.
107
What is forward heart failure?
Inadequate CO (patients present with weakness, fatigue, hypotension)
108
Why is ventricular hypertrophy only a short-term solution?
Because over time, it increases the myocardial O2 demands, predisposing the heart to ischemic injury
109
What is the difference between compensated and decompensated HF?
In compensated, the heart is able to meet the O2 requirements of the body, and in decompensated, it cannot.
110
When is dyspnea most noticeable in CHF?
On exertion and when lying down (orthopnea)
111
An MI may result in cardiogenic shock if ____% of the ventricle is involved
40%
112
Silent infarcts are more common in
those with HTN and DM and the elderly
