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Cardiovascular Diseases (*BP and BP Control (*Baroreceptors
note that…
Cardiovascular Diseases
*BP and BP Control
*Baroreceptors
- note that baroreceptors of the carotids sense high and low pressures
- massaging the carotids
--> they sense high pressure and tell efferent vagus to slow the heart at the SA and AV nodes
Baroreceptors example
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Notes:
- note that for regulation of BP you have 2 basic baro receptors
--> carotid sinus baroreceptors
--> aortic arch baroreceptors
- note also that attached to each of these are chemoreptors at the carotid sinus and the aortic arch
- the carotid sinus is NOT in the common carotid, but in the internal carotid just above the bifurcation
--> think it needs to be monitered internally!!!
- carotid sinus BR = afferent nerve = glossopharyngeal = CN 9
--> GLOSSY CARROTS ARE good in VAGUS = CN 10
- arotic arch BR = afferent nerve = vagus
- note that CN 9 / 10 go together often for reflexes
--> CN 9 / 10 = afferent and efferent for gag reflex
--> both for separate BP baroreceptors here
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Isolate Systolic HTN = Aging Ateriosclerosis
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*DVT and PE
Clinical Cases
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DVT
- unilateral swelling of calves
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Heparin vs LMWHs
pregnancy is a case where you want to use LMWHs
--> enoxaparin, daltaparin
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*Infective Heart Diseases
- Infective Endocarditis
- Rheumatic Heart Disease
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*Rheumatic Heart Disease / Acute Rheumatic Fever
- from group a strep (trep pyogenees and strep throat) antibodies
Acute Rheamatic Fever
- antibodies to strep. pyogenes M proteins
- crossreact with endocardium and heart valves
Acute Rheumatic fever = acute RF ARTHRITIC RHEUMITRAL REGURGE FEVER
- ARTHRITIC = RF causes migrating arthritis
- RHEUMITRAL = RF causes mitral valve reguurge in the short run and stenosis in the long run
- FEVER = RF causes fever due to infection and antibodies
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PathoPhys
- Aschoff bodies = granulomas in the endocardium
- collection of B / T cells, macrophages, giant cells
- cause inflammation and secondary fibrosis
--> leads to MAT valve regurge, then stenosis later
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Sequeae of rheumatic Heart Disease
Isolated MV Regurge / Stenosis
- higher pressures proximal to the MV
- lower pressures distal to the MV
Mitral Valve Stenosis / Regurgitation from RHD
- develops into left atrium enlargement
- this infringes on 2 things
--> compression of the esophagus and dysphagia
--> compression of the recurrent laryngeal nerve
--> causing hoarseness in the voise
left atrium enlargement for MV stenosis and RHD
- Mitral Valve Stenosis develops into left atrium enlargement
- this infringes on 2 things
--> compression of the esophagus and dysphagia
--> compression of the recurrent laryngeal nerve
--> causing hoarseness in the voise
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Notes:
- recall that the esophagus sits right atop the spine and the aorta and vena cavas are on the right
- the left atrium makes up the posterior part of the heart
Combine AV and MV Regurge / Stenosis
- higher pressures proximal to the MV
- lower pressures distal to the MV
Clinical Cases
Clinical Case
- 3 more items...
Heart *Valve Diseases
- Aortic Stenosis most common HV disease
- M >> A > T rule for Rheumatic fever
Mitral Valve
Mitral Valve Prolpase
- leads to Mitral Valve Regurgitation = worse
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Mitral Valve Prolpase
- leads to Mitral Valve Regurgitation = worse
Aortic Valve
Aortic Valve Stenosis
- most common vavlular disease
- normal in aging due to necrosis of cells and celcification
Aortic Valve Calcification following Necrosis of the cells case
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Aortic Regurgitation
- WIDE PULSE PRESSURE
--> this is the biggest thing seen with aortic regurgitation
Clinical Signs
- wide pulse pressure
--> water hammer pulse
--> can see it in the curve of the aorta
- loss of the dicrotic notch
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*Shock
4 Types of SHOCK = SHOC
- Septic Shock
- Hypovolemic Shock
- Obstructive Shock
- Cardiogenic Shock
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Reading the table for SHOC:
- look at CVP = central venous pressure first
- low CVP --> S or H
- high CVP --> O or C
SH Difference
- look at SVR
- Septic shock
--> primary problem is resistance and trying to kill pathogen
--> low SVR
- Hypovolemic shock
--> primary problem is low blood volume
--> HIGH SVR
OC Difference
- look at PCWP
- Obstructive shock
--> obstruction before the lungs causes the blood to back up in the right side of the heart
--> low PCWP
- Cardiogenic shock
--> problem is in the heart
--> thus the PCWP = before the heart is fine and increased
--> high PCWP
Septic Shock
- primary thing = peripheral vasodilation
--> lowered TPR
Pathophys
- primary thing = peripheral vasodilation
--> lowered TPR
- ONLY type of shock with LOW SVR = systemic vascular resisance = afterload
- also ONLY type of shock with HIGH MvO2 = mixed venous O2 pressure
- high MvO2 means there is high O2 in the venous blood
--> since in septic there is low SVR, and so much blood being pumped quickly that tissues can't take the O2
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Hypovolemic Shock
Pathophys
- primary thing in hypovolemic shock = low blood volume gives low preload for right side of heart
--> everything alse is low after this
--> EXCEPT for peripheral resistance
- peripheral resistance remains high as it wants to maintain the BP higher since it has NO VOLUME
- recognize first two kinds of SHOCK through SHOC
= Septic / distributive + hypovolemic
- they both have low CVP = central venous pressure and PCWP
--> hypovolemic due to low volume
--> septic due to vasodilation everywhere to kill pathogens
- difference between SH of SHOC is
= septic has low TPR / SVR = systemic vasc resistance
= hypovolemic has high SVR
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Obstructive Shock
Pathophys
- primary thing in obstructive shock = low PCWP = wedge pressure
- note Obstructive shock = means obstructive cardio pulmonary
--> PE or tension pneumothorax
--> where backpressure from the lungs causes obstruction for right side of heart
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Cardiogenic Shock
Pathophys
- primary thing in cardiogenic shock = ventricle not working
--> everything including the PCWP is fine, just the LV is down
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*Pericarditis
Common Presentation of Pericarditis
- PLEURITIC chest pain --> always have to rule this out along with respiratory disease
- BETTER on leaning forward
--> think Peri = outside layer of the heart
--> thus affected by rubbing on other things
- pericardial FRICTION RUB
--> most unique physical finding for pericarditis
- pericarditis can have pulsus parodixus
--> but this is not specific to pericarditis
- ST Elevation in all leads
--> think the pericardium surrounds the entire heart so inflammation everywhere in all leads on ECG
Pericarditis Mimics an MI STEMI
- at first seems like a STEMI
- but the STEMI happns in all leads due to inflammation of all myocardium of the ventricles
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Pulses Paradoxis
- sine wave of varying amplitude of ventricle tachycarida
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Pericardial *Effusion
- fluid in the pericardial sac
Cardiac *Tamponade
- fluid in the pericardial sac is preventing the heart from pumping
A TOAST to Pulsus Paradoxus
--> A TOST gives the causes of pulsus paradoxus
- A = asthma
- T = tamponade
- OAS = Obstructive Sleep Apnea
- A = asthma
- T = tamponade
Clinical Cases
Clinical Case
- 3 more items...
BECK Triad for Cardiac TAMPONADE
- hypotension
--> since the heart can't pump against the pressure
- JVD = distended neck veins and raised JVP
--> blood not pumping so backs up
- distant heart sounds
--> since the fluid around the heart muffles the sound
Pulsus Paradoxus
- A TOAST to Pulsus Paradoxus
--> A TOST gives the causes of pulsus paradoxus
- inspiration increases the preload to the heart
- the right side of the heart is so compressed by the cardiac tamponade already and from the beating LV
- the RV actually has such a high pressure it pushes the intraventricular septum to bulge into the LV
- this causes the LV pressure to rise by 10 mm Hg
- get an upstroke of 10 on systolic BP during inspiration
- = pulsus paradoxus
Causes of Pericarditis
- most common is viral infection
--> this can NEVER be confirmed so often called idiopathic pericarditis
--> resolves on own with supportive care?
Viral Pericarditis
- most common cause of acute pericarditis
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Notes:
- note that in acute pericarditis, unless you absolutely have Uremia or eveidence of an autoimmune disease present
--> you assume it is viral cause
Constrictive Pericarditis = Calcification of pericardium
- special type of pericarditis, often secodnary to TB infection
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PAthophys of Acute Pericarditis
- fibrinous (laying down of fibrin) is the most common way that pericarditis occurs
- regardless of the underlying cause
- note it is the fibrous layers that cause roughening of the visceral and parietal layers of pericardium
--> causes the friction rub heard in pericarditis
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Internal Bleeding
- important for internal bleeding to identify the compartment of the body that the blood is in
- since many parts of the body are sealed into different compartments, think of it like a ship trying to contain blood
Intrapelvic Bleeding
- common site for femoral catheders that are inserted too deep and go through back of the artery
Femoral Catheders and Intrapelvic Bleeding
- common site for femoral catheders that are inserted too deep and go through back of the artery
- note that femoral catheders are inserted just above the inguinal ligament
- above the femoral triangle
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*Pulmonary Hypertension
- Either PAH = Pulmonary Arterial HTN
- Pulmonary HTN (default is secondary to another disease)
*PAH = Pulmonary Arterial HTN
- NOT from another underlying condition (except RA and systemis sclerosis)
- usually hereditary
- death is NOT from MI, from right HF and respiratory failure
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Chemical signallers from endothelium to tunica media SM layerPro vasoconstriction and proliferation of SM cells
- endothelin-1
- target with bosentan
- think of for PAH you need to relax and going to the beach with a stereo to tan
--> BOSE N' TAN
Pro vasodilation and anti proliferation of SM cells
- NO --> cGMP pathway
--> nitrates
--> ANP BNP cGMP Sidenafil PDE inhibiotr
- PGI2 = prostacyclin = Gs cAMP pathway
--> prostacyclin analogs = esoprestonol
--> think of Esomeprazole as PPI, eseprestonol is synergistic with it for the stomach, can be used for artery vasodilation too
PAH Physiology
- local vasconstiction mediators and growth of endothelium cells incrreased
- local vasodilators mediators and antiproliferation of endothelial cells are decreased
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PAH and Sequalae
- RV HYpertrophy
- most common cause of death = HF and respiratory failure
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Pulmonary HTN
- Pulmonary HTN has an underlying condition like Left sided HF that precedes it
Left Sided HF and Pulmonary HTN
- LHF of ANY causes gives higher LV pressure
--> backpressure to left atrium
--> backpressure to pulmonary veins
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*AAA = Abdominal Aortic Aneurism
- 75-90% fatality with AAA rupture
- presents with ACUTE abdominal pain and hypoTN
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More likely to get AAA AS a MALE
- order of risks for AAA
- A = age > 65
- S = smoking
- MALE
*Aortic Dissection
- EXTREMELY fast onset with aortic dissection
- Stanford Class A vs Stanford Class B
- STANFORDDD = DISSECTION
--> not for coarctation
--> coarc has adult vs. child
Stanford Class A vs B Aortic Dissection
A = before the right brachiocephalic artery branch from aorta
B = right after the left subclavian artery branch
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Risk Factors for Aortic Dissection
- HTN by far the biggest
- Marfans Syndrome
- note all other risk factors like smoking, diabetes, hyperchol etc.
--> more related to atherosclerosis and aneurisms
--> aortic dissection is different and strictly pressure related
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Presentation of Aortic dissection
- EXTREMELY fast onset chest pain with aortic dissection
--> pain radiates to the back
- biggest risk factors for Aortic dissection
--> chronic uncontrolled HTN
- Marfan's syndrome
Xray of aortic dissection
- showing enlarged mediastinum
- there is a also an enlarged heart here
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*Atherosclerosis
- formation of plaques from inflammation underneath endothelial cells
- caused by FFAs and cholesterol deposited by LDLs and eaten by macrophages --> foam cells
- accumulation of foam cells = atherosclerotic plaques
- note it is the SM muscle cells in arteries that make the collage of the fibrous cap (NOT fibroblasts)
- the lipid and foam cells are in the interstitium, just above the muscle cells
--> think the muscle cells get aggitated by the foam cells above and make collagen for protection so they can keep working
Slow growing Atheromas - Collateral artery growth response
- it is the smaller plaques that rupture that are more dangerous
- NOT the large slow growing plaques
- VEG factor = vascular endothelial growth factor
--> released by ischemic cardiac cells to make collateral blood vessels
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Atherosclerosis catches up with ACPC rock band in the long run
- Atherosclerotic ROCK band sing the song ANGINA
Atherosclerosis ANGINA = ACPC
--> think of the worst and most common areas of atherosclerosis sequelae
- A = ischemic colitis
- CP = most common then are angina of the chest, then calves = PAD
- C = then CVA from carotid arteries
- A = Abdominal Aorta
- C = Coronary arteries
- P = popliteal artery
- C = carotid artery
"3 Anginas of the Body"
- 1 = cardiac Angina
- 2 = Calf muscle Angina (caludication)
- 3 = Abdominal Angina
--> Ischemic colitis
--> RAS = renal artery Stenosis
"3 Anginas of the Body"
- 1 = cardiac Angina
- 2 = Calf muscle Angina (caludication)
- 3 = Abdominal Angina
--> Ischemic colitis
--> RAS = renal artery Stenosis
*RAS = renal artery Stenosis
- one of the 3 Anginas of the Body = ACPA
- aorta and renal artery are the most common site in abdomen aorta for atherosclerosis
- low O2 and blood flow to ONE kidney
--> constant and refractory releaase of EPO and RAAS system
--> RAS = MOST COMMON cause of refractory HTN
- you other kidney compensates by getting huge to take over the filtration load
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Pathophys - Atheroma and plaque formation with Fibrous cap
- 3 types of cells make an important contribution to forming atheromas in the arteries
- first there needs to be inflammatory, turbulent HTN blood flow and hyperlipidemia and hypercholesteremia
--> perfect storm to begin the formation
- endothelium = are the first affected (damaged walls)
--> they release cytokines to recruit leukocytes (mainly macrophages and T lymphocytes)
--> main cytokines = IL-1 and endotheli-1
- Macrophages and T lymphocytes
- extravate into the blood vessel intima
--> release more cytokines
--> phagocytose the lipids and make foam cells
- Smooth muscle cells
--> endothelin-1 makes the SM cells proliferate, get thicker and release Extracellular matrix materials
--> main thing SM release is collagen
--> collagen then forms the fibrous cap
--> this constant ECM production (collagen) from the SM is a vicious cycle though since it kills the same SM that make it and leads to hardenning of the arteries over time
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*Angiodemia
- angio = blood vessels
--> swelling of the blood vessels
- occurs in the lips, eyes and tongue
- either mast cell degranulation
--> IgE type 1 reaction
--> IgE independent mast cell (drugs = oppioids)
- ACEIs / bradykinin excess
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*CAD = Coronary Artery Disease
- note that angina symptoms from CAD don't happen until 70% blockage of vessels
--> up until this point the local metabolites Adenosine and NO are able to compensate
Coronary Steal from Drugs
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*Watershed Zones
- located at the distal ends of 2 different artery supplies
- protection against local infarction
--> since have an extra blood supply in case
- worse off for global hypotension (shock)
--> because they are a combination of many distal arteries they have a low pressure
--> get ischemia in low BP
Watershed Areas of the Brain
- between the major arteries
- ACA and MCA
- MCA and PCA :
- the hippocampi are big watershed areas of the brain
--> think hippos NEED water bad
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Watershed Areas of the Colon
- think the most distal areas of he colon
- splenic flexure
- sigmocolonic junction
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*Vasculitides
- inherited blood vessel disorders
- see other notes
Large Vessel Arteritis
- 2 sets, both affect women
- Takayasu in young Asian women
- Polymyalgia / Giant Cell arteritis in older women
Takayasu Arteritis
- young Asian women < 40
- IYA ATTACKA ya AORTA!!
IYA ATTACKA ya AORTA!!
- Takayasu affects the aorta and its branches
Notes:
- main difference between Takayasu arteritis and Giant Cell Arteritis /PMR = polymyalgia rheumatica
- Takayasu is in younger Asian females
--> GCA is in older people, ALL over 50
- Takayasu affects the aorta and its branches
--> GCA the temporal artery
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Medium / Small Vessel Arteritis
- Osler-Weber- Rendu Syndrome
- PAN = Polyarteritis Nodosa
Osler-Weber-Rendu Syndrome
- recurrent epistaxis = nosebleeds
- telangiectasias = spider veins
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*PAN = Polyarteritis Nodosa
- Mainly small to medium arteries involved
- sporadic
- PAN acronym for Poly Arteritis Nodosa
- PA = PAN ALL small/medium arteries of the body
--> renal artery most common
- PA = PAlpable Purpura common
- N = Nodosa NOT the LUNGS
--> no lung involvement
Palpable Purpura
- non-blanching (pressing on it does not change the colour)
--> indicates it is a hemorrage
- cause by mini hemorrages in the cutaneous capillaries
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Children's *Kawasaki Arteritis
- medium-small arteritis that effects kids < 5 years old
- 5 5 and 5 rules for Kawasaki Arteritis
--> age < 5
--> fever > 5 days
--> 5 things wrong with their extremities
A burn from a Kawasaki motorcycle gives you a rash...put on some Warm CREAMWarm = > 5 day fever (5 letters)
- C = cervical lymphadenopathy (unilateral) and conjunctivitis (bilateral)
--> not wearing glasses and 1 bee to the eye
--> 1 bee goes down your throat and straight to the lymph node
- R = rash over entire body
--> from the hot fuel tank
- E = erythema on palms and soles
--> from the handle bars and foot pegs
- A = ASA (spirin) is the treatment
--> only indiction when you are allowed to give aspirin
--> otherwise can cause Reyes syndrome
- M = mucus membranes
--> dry, red strawberry tongue
--> 2nd bee gt you twice
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*Varicose Veins
- incompetent vein valves
- leads to venous stasis dermatitis
--> RBC's extravate into the tissue and through macrophage breakdown release their Iron into the tissues
- poor wound healing
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*Pulsus Paradoxus
- normal for systolic BP to drop on inspiration, due to lower intrathoracic pressure
--> increase venous return through vena cava
--> increased pooling of blood in the pulmonary system
- normal = 10 mmHg drop in systolic
- Pulsus paradoxus > 10 drop in systolic BP on inspiration
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*Berry Aneurisms
- congenital disorder
- many are assymptomatic and may never rupture
Berry Aneurisms with Coarctation of the aorta
- coarctation increases HTN and possibility of rupture of Berry aneurism
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*Superior Vena Cava Syndrome
- most common causes are Non-Hodgekin Lymphoma
- lung cancer
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