5 Cardiac part 2 Flashcards
Heart failure definition
Function/structural changes with decrease CO or pulmonary/systemic congestion
CHF
Left sided heart failure, which will cause right sided
Cor pulmonale
Right sided heart failure ONLY
Causes of CHF (left sided) in order
HTN CAD LV MI Aortic stenosis Bicuspid stenosis Cor pulmonale Cardiomyopathy Congenital defects
Right sided heart failure causes in order
Left sided failure CAD RV MI Pulmonary/tricuspid stenosis Pulmonary disease Cardiomyopathy Congenital defects
CO = HR X SV
HR is regulated by SNS and PNS
SV is regualted by pre/after load and contractility
Preload determinants
Venous return and length of diastole
Two types of increased afterload
Systemic and pulmonary
Myocardial contractility
Inotropy = contractility
Myocardial cells have less SR (less Ca2+ stores)
Myocardial cells need calcium from two sources for depol
Release from SR AND
Influx of extracellular across sarcolemma into sarcoplasm
cAMP
Myocardial cells have large number of calcium channels, opening mediated by cAMP and B1 innervation directly stimulates production of cAMP
How dig works
Increased intracellular Na+ disrupts Na+/Ca2+ pump resulting in increase in intracellular Ca2+
Two types of dysfunction
Systolic and diastolic
Systolic dysfunction
Decrease myocardial contractility decreases ejection fraction which retains blood in ventricles.
This increases EDV and blood begins to back up
Causes of systolic dysfunction
Decreased contractility from CAD and cardiomyopathy
Volume overload from valve insufficiency and anemia
Pressure overload from valve stenosis and HTN
Diastolic dysfunction
Normal heart contractions, but relaxation is abnormal.
Creates less blood in ventricles which decreases CO and lack of filling causes backwards congestion
Causes of diastolic dysfunction
Impedance of expansion from pericardial effusion, pericarditis
Increased thickness from hypertrophy
Delayed relaxation from aging or ischemic heart disease
Left ventricular dysfunction
L failure leads to backup of oxygenated blood in pulmonary circulation which causes edema and decreased CO from RV Pulmonary edema (especially at night) and general decreased perfusion are common manifestations
RV dysfunction
Backup of deoxygenated blood into systemic and decreases preload so decreased CO
Commonly presents as peripheral edema, portal vein HTN and ascites, JVD
Compensatory mechanisms for heart failure
SNS
RAAS
Frank starling
Cardiac remodelling
SNS activity
Increased catechols increase ino, dromo, and chrontropy as well as PVR which leads to increased CO but also increased MVO2
Preload and contractility drop from increased rate and PVE leads to increased afterload, furthering the condition
RAAS
Decreased renal perfusion releases renin
Renin increases angiotension I which is converted to II in the lungs by ACE
Angio II causes PVR increase and ADH from pituitary and aldosterone from adrenals
which cause fluid retention (ADH is vasopressin, solute free)
How does RAAS negatively effect HF
Fluid retention increases preload and afterload, further exacerbating the condition
Frank starling and HF
Increase preload cannot be utilized by failing heart, but the MVO2 is still increased from it
Cardiac remodeling HF
Myocytes respond to an increase in pressure and volume by undergoing hypertrophy (increased wall thickness should decrease MVO2) but is often replaced with connective tissue
Wall tension formula
RadiusXIVP/Thickness
Positive feedback loops which exacerbate HF
A1 and B@
RAAS
Increased myocardial contractility (inotropy)
Cardiac remodeling
Clinical manifestations of HF
SOB Orthopnea Paroxysmal nocturnal dyspnea Cardiac asthma Cheyne-strokes resps Pulmonary edema Fatigue, weakness, altered LOC JVD Ascites Oliguria
What is Acute Arterial Occlusion and where does it happen
From the heart, atherosclerotic plaques within an artery, fat from a fracture or amniotic fluid create an embolic occlusion
Seven P’s of acute arterial occlusion
Pain Pallor Pulselessness Paresthesia Paralysis Pistol shot Polar (line of demarcation?)
Atherosclerotic occlusive disease
Narrowing of arterial lumen for atherosclerotic plaque resulting in ischemia, same risk/patho as coronary
Most common in lower legs
S&S of atherosclerotic occlusive disease
Claudication
Blanched legs when elevating
Skin breakdown, ulceration, gangrene
Thromboangiitis obliterans
Beurger disease
Inflammatory arterial disorder leading to thrombosis of medium sized arteries of foot/lower leg (arms/hands too)
Inflammation can extend to adjacent nerves and veins
Thromboangiitis Obliterans most likely to effect
Smokers/ chewing tobacco users
Tobacco causes immune response in susceptible pts
Men 25-40 and most common in middle east/ far east
Raynauds
Primary type from SNS hyperactivity (unknown reason) and can be set off by emotional stress/cooling
Secondary is due to frostbite, vibrating tools, collagen disease, neuro disorder, chronic artery occlusive disorders (anything known to cause vasospasm)
4 in 10,000, more common in females
Presents as discoloured/numb fingers
Aneurysm definition
Localized dilation of blood vessel (usually an artery)
True aneurysm
Bounded by complete vessel wall with at least 50% increase in diameter
Blood is contained inside complete vessel (berry, saccular, fusiform)
False aneurysm
Rupture of part of the vascular wall causing formation of extravascular hematoma
Blood is contained within segments of vascular wall or CT
(dissecting)
Berry Aneurysm
Small, spherical dilation at bifurcation communicating with the main vessel by a small opening
Involves all 3 layers
Saccular aneuysm
Weakness on one side of vessel and attached to main vessel via a small stem which appears like a sac
Involves all 3 layers
Fusiform
Tapering at both ends (aka circumferential) and involves all 3 layers
Dissecting aneurysm
Tear in intimal lining of vessel creating a blood filled cavity
Etiology of aneurysms
Atherosclerosis is most common (plaque erodes vessel wall)
Can also be caused by trauma, syphilis, infections, congenital defects
Patho of aneurysms
Atheroma with central soft core (lipid and cell debris) covered by fibrous cap can be ruptured by pressure which can cause intimal ulceration
Irregular blood flow by aneurysm (whorls and eddies) predispose individual to thrombosis
Aortic aneurysm
Is most common, linked to HTN and inheritance, atherosclerosis and has high mortality rates
Where can aortic aneursym hit
Ascending aorta, aortic arch, descending, thoracoabdiomainal or abdominal
Types of aneurysms associated with aortic aneurysms
Commonly fusiform but can be saccular
Abdominal most commonly at bifurcation
Bifurcation is normally 2cm, so 3cm means aneurysm
Merk aneurysms
Type A is confined to ascending aorta
Type B confined to descending aorta
Clinical manifestations of aneurysms
Palpable at 4cm
Pulsating mass
Mid-abdominal and lumbar pain
Rupture will cause hypovolemic shock and profound hypotension
Aortic dissection patho
Usually ascending aorta, linked to HTN and degenerative smooth muscle disorders, intimal tear causes hemorrhage into vessel wall with resultant longitudinal tearing
Clinical manifestations of aortic dissection
Tearing pain in chest (ascending) back (descending)
Unilateral BP
Neuro symptoms from disruption of blood flow to CNS
Overview of varicose veins
Blood pooled creating tortous and dilated veins (varicosities)
Most commonly involving saphenous veins
Pain and edema
Primary varicose veins
Valve dysfunctions in superficial saphenous veins of legs from recurrent or prolonged increases in pressure (standing still, being preggo)
Secondary varicose veins
Dysfunction within deep venous channels of legs (DVT, fistula’s, congenital malformations)
Causes of varicose veins
Genes, standing too long, preggos
Complications of varicose veins
Chronic venous insufficiency (inadequate venous return over long period of time)
Chronic pooling causes edema, sluggish circulation, cellular exchange is impaired, venous stasis ulcers
EMS concerns of varicose veins
Blood flow in varicose veins is turbulent and slow, favors clotting and thrombi, thrombi can dislodge as emboli (PE)
Virchows Triad
Stasis of blood, increased coagulability, endothelial injury
immobility, oral contraceptives, trauma
High risk for venous thrombosis
Post partum Long hospital stays Orthopedic surg Leg casts Dehydration Varicose veins
Homan’s sign
Passively dorsiflex foot with knee extended (squeeze calf)
