Cardiovascular System & Patients Flashcards
Embryonic Development
Heart starts out as single ventricle and single atrium
- Truncus arteriosus
- Sinus Venous
- Umbilical Vein (OXYGENATED blood from placenta)
Foramen Secundum
- “Foramen ovale” after birth
- May form Patent Foramen Ovale or atrial-septal defect (ASD) if open after birth
Inter-ventricular Foramen
- May form Interventricular Septal Defect (VSD) if not closed after 7th week of fetal development
Week 4 of Heart Development
- Partitioning of aorta-ventricular canals
- Interventricular foramen closes at 7th week IVF (or Ventricular septal defect VSD)
Heart Development at Birth
- Final separation between systemic and pulmonary circulations
- Septum secundum forms the foramen ovale
- patient foramen ovale allows oxygenated blood to go to the systemic circulation before birth
- closes at birth (or ASD)
- Ductus arteriosus- connects aorta to L pulmonary artery (patent ductus arteriosus PDA)
Congenital CV Defects: Right-Left Shunt
- cyanotic congenital heart disease
- Examples: Tetralogy of Fallot
What is the Tetralogy of Fallot
transposition of great arteries, persistent truncus arteriosus, tricuspid artesia, anomalous pulmonary venous connection
Congenital CV Defects: Left- Right Shunts
- No Cyanosis but pulmonary HTN and pulmonary artery changes
- Ex: ASD, VSD, PDA
Obstruction
- Stenosis: narrowing
- Artesia: obstruction
- Increased resistance causes chamber hypertrophy/dilation
- Ex: Coarctation of aorta (common), pulmonary stenosis or artesia
Function of heart and blood vessels
- transport nutrients and oxygen
- endocrine function –> regulation of fluid balance and growth
Elastic Arteries
- “distribution arteries”
- function: aid in conduction and flow and smooth flow
Muscular Arteries
- Branches of the elastic arteries
- “resistance” arteries
- function: regulation of flow, alter resistance
Capillaries (and venules)
- Exchange vessels
- Function: nutrient and waste exchange between tissues and blood
Veins
Capacitance vessels
Structure of Veins
- assist in moving blood by one way valves that prevent back flow
- located in beds where compression by muscles forces blood toward heart (especially effective in beds in calf and dorsum of foot)
- negative pressure in thoracic cavity during inhalation assists in venous return
Exchange within the capillary
a gradient forms along the length of the capillary, such that
at the beginning, net filtration occurs, and at the end,
absorption. The result is an equilibrium and fluid balance
over the whole length of the capillary
Pericardium
– Fibrous outer layer of pericardium
– Inner, smooth layer (parietal and visceral)
– at base, pericardium attaches heart to diaphragm
Myocardium
– Cardiomyocytes, fascicles and bundles of fascicles are invested in connective tissue
– Layers of muscle are woven in a complex pattern with a
swirling twist, allowing for a wringing motion during
contraction.
Excitation- Contraction Coupling
- AP causes Ca2+ channels to open
- Extracellular Ca2+ triggers SR release of Ca2+ (Ca-induced Ca-release)
- Ca2+ binds to troponin, triggering actin-myosin interaction
- Tension develops
- Relaxation occurs when Ca sequestered by SR
Innervation of the Heart- Sympathetics
– pre-ganglionic cells in lateral gray of upper cervical segments
– post ganglionic cells in cervical, 3rd &4th Thoracic ganglia
– increase strength, rate of contraction, increase rate and extent of
relaxation
Innervation of the Heart- Parasympathetics
– pre-ganglionic cells in medulla (N ambiguous, etc…)
– travel in vagus nerve
– decrease rate of contraction, slow conduction, decrease strength
of contraction and slow rate of relaxation
Effects of Aging on CV System
- Decreased vascular elasticity –> increased blood pressure
- Left ventricular hypertrophy –> decreased ventricular compliance
- decreased adrenergic responsiveness –> decreased exercise heart rate
- diastolic dysfunction –> impaired ventricular filling with potential to increase cardiac preload and CHF
- decreased lean body mass –> decreased muscle strength and peak oxygen consumption
What is arterial blood pressure
pressure that results from the rate of flow of blood through and against the resistance of the peripheral arteries
Mean arterial pressure
driving force & tissue perfusion P
MAP = [SBP + (2x DBP)] / 3
Pulse Pressure
SBP - DP
reflects adaptation to exercise
Orthostatic Hypotension
• Delay/ insensitivity in baroreceptor reflex, dehydration or
pooling of blood leads to decreased blood pressure and flow to brain
• Defined as decrease in blood pressure when going from
supine →sitting or sitting →standing
When does orthostatic hypotension occur?
after prolonged bed rest, in patients with generalized hypotension, and in Heart failure
What is orthostatic hypotension associated with?
• Strongly associated w/ Ca2+-channel blockers (procardia)
Guidelines of orthostatic hypotension
- decrease is SBP of 20 mmHg or DBP of 10 mmHg
Jugular Venous Distension
- Examine pt with head up at 45 degree angle
- Compress SCM muscle with note if the vein is distended above the level of the clavicle
What does jugular venous dissension indicate?
elevated venous pressure and R heart failure
Risk factors of peripheral artery disease
smoking, HTN, atherosclerosis, DM, high cholesterol, greater than 60 yo
Signs and symptoms of peripheral artery disease
– Intermittent claudication (leg pain with walking gets better with rest)
– Other pain, aches, or cramps with walking
– Muscle atrophy (weakness),
– Hair loss,
– Smooth, shiny skin or skin that is cool,
– Decreased or absent pulses in feet
– Cold or numb toes
– Sores or ulcers in the legs or feet that don’t heal
Medical management of peripheral artery disease
– Aspirin or similar antiplatelet, statins and other medications to
reduce atherosclerosis and medication to treat HTN
• Quit smoking
• Surgery may be required (angioplasty, stent or bypass graft)
* PT: Exercise, exercise, exercise!*
– Walking is optimal, but also cycling, other aerobic Ex, HIIT
Radial peripheral pulse
compress radial artery under index fingers at distal radius
brachial peripheral pulse
compress brachial artery medial to insertion of biceps
Carotid Pulse
- slide index and middle fingers lateral from cricoid cartilage on the trachea to jugular groove on either side
- Feel for pulse and listen with stethoscope for murmur
Carotid Bruit
“whooshing” or murmur sound heard over
the carotid artery. In most cases, it occurs above the clavicle and indicates a carotid blockage
Pedal Pulse
anterior surface of foot, between maleoli, just lateral to the extensor Hallicus longus tendon
What to feel for when examining pulses
texture of artery wall, rhythm, regularity, force:
weak or thready, strong or bounding
Pulse Grading
0 - Absent - No perceptible pulse
1+ - Thread - Barely perceptible, easily obliterated with slight pressure
2+ - Weak - Difficult to palpate, slightly stronger than thread, can be obliterated with light pressure
3+ - Normal - Easy to palpate, requires moderate pressure to obliterate
4+ - Bounding - Very Strong, hyperactive
Arterial Insufficiency
Associated with painful Ulcers, cramps, gangrene, exercise intolerance, CAD,
CVA, etc
Venous Insufficiency
Associated with infection, Ulcers, VTE, DVT, cramps, leg pain
Doppler Assessment of ABI
- Apply US gel and hold Doppler probe 45-70° angel on arm skin as BP
cuff is deflated –> note first point flow is detected and point where max flow is detected - Apply US gel and hold Doppler probe 45-70° angel on posterior tibial
artery as BP cuff above ankle is deflated –> note first point flow is detected and point where max flow is detected
What position should the patient be for the Doppler Assessment of ABI
lying flat to decrease the effect of gravity
ABI ration
LE systolic pressure (ankle) / UE systolic pressure (brachial)
ABI 1.0 - 1.2
Normal
ABI 0.8- 1.0
- Minimal peripheral arterial disease
- compression for edema is safe
ABI 0.5- 0.8
- Moderate peripheral arterial disease
- possible intermittent claudication
- Refer to vascular specialist
- Compression therapy contraindicated if < 0.6
ABI < 5.0
- Severe ischemia with resting pain
- compression therapy contraindicated
ABI < 0.2
Ischemia and necrosis
ABI 1.0-1.3
May occur with venous hypertension
ABI >1.3
Non-reliable in patients with diabetes due to calcification of arteries
Peripheral Edema
- Common finding
- Variable depending on body position (dependent vs. independent)
- May indicate elevated venous pressure and R HR
Pitting Edema Measurement
- Patient in supine with leg/foot in dependent position and then independent position
- Push down on dorsum of foot for 10 seconds
- Palpate for depression (30 sec)
- Compress over medial malleolus
- keep moving up to determine height of edema
Pitting Edema Levels
- 1+ Barely perceptible
- 2+ easily identified depression (EID) but rebounds < 15 seconds
- 3+ EID, rebounds 15-30 sec
- 4+ EID, rebounds in > 30 sec
Volume measurements of edema
- Simplest is to use a volumetric tank
- Fill tank to designated limit, then place the involved extremity in up to an established, reproducible landmark
Girth Measurements for edema
– Use tape measure around the diameter of the limb crossing designated landmarks
- Compare to previous measurements (tibial tuberosity, medial and lateral malleoli or figure 8 of foot)
- Compare to uninvolved limb (if possible)
What does Rubor- Dependency Test indicate?
arterial insufficiency
Rubor Dependency Test Instructions
- Patient supine- note the color of plantar aspect of foot
- Elevate leg to 45-60° x 1 minute - then note the color of the foot (observe for pallor)
- Lower leg to dependent position (back to plinth)
What is the normal response of Rubor Dependency Test
normal, expected skin color in approximately 15 seconds
During Rubor Dependency Test, what does reperfusion in > 30 sec AND dark-red or rubor appearance mean?
The test is positive for severe ischemic disease
(rumor results from reactive hyperemia/vasodilation)
How to determine how severe PAD is based on Rubor Dependency Test
The faster pallor appears in elevated position or longer it takes for
the rubor to appear in the dependent position, the more severe PAD.
What activates the coagulation cascade that causes VTE or DVT
Coagulation cascade is activated with surgery or trauma and remains active x 5-6 weeks
45 - 80% of symptomatic VTE events occur when?
after hospital discharge
Factors that predispose to VTE/DVT
– Cancer
– Bed rest
– Muscle wasting
– Immobilization
– Burn or other wounds
– Edema
– Heart failure
How can diagnosis of VTE or DVT be made?
Doppler ultrasound,
venogram or D-Dimer test
Best results of VTE
- The best results are found when medication is combined with mobility
- In a study that examined the combination of ambulation and prophylactic enoxaparin, those who were ambulatory and given medication had a significantly lower rate of VTE
Non-Pharmacological Rx for DVT
mobilization, exercise, ROM, ambulating, anti-coagulants and anti-thrombosis devices (TED hose, and compression
Study the Wells Clinical Decision Rule to Diagnose DVT
Study Constans Criteria for Risk of UE DVT
Padua Prediction Score for VTE/DVT
recommended for hospitalized patients based on Am Coll of Chest Physicians guidelines
– Useful for patient with cancer, trauma, other serious conditions
Khorana Score for VTE/DVT
- recommended for patients with cancer
- Allocates points based on 5 clinical and pre-chemo Rx lab values: primary tumor site, platelet count, hemoglobin, leukocyte count, BMI
Key Phrases VTE/DVT Guidelines
- Advocate for culture of mobility and physical activity
- Assess for risk of VTW with reduced moility
- Assess for additional risk factors of VTE in all high-risk patients
- Establish likelihood of LE DVT when patient presents with symptoms
- Mobilize patients with LE DVT when therapeutic level of anticoagulation achieved
- Mobilize individuals with IVC filter
- Consult medical team to initiate mobility with distal LE DVT not treated with IVC filter or anticoagulant
- Mobilize pt’s with non-massive PE when therapeutic level of anticoagulation achieved
You should not mobilize massive PEs or submissive/intermediate high-risk PEs until what?
until they are low risk and hemodynamically stable
Auscultation of Aortic Area
2nd IC space
R sternum
Aortic value
Auscultation of Pulmonic Area
2nd IC space
L sternum
Pulmonic valve
Auscultation Tricuspid area
4-5th IC space
R sternum
tricuspid vavle
sidelying on L
Auscultation of Mitral Area
5th IC space
L MCL
Mitral valve
sidelying on L
S1 Lub
closure of mitral and tricuspid valves
S2 Dub
closure of aortic and pulmonic valves
S3 Lub Dub Dub
- low pitched, also called a gallop
- Normal in young & athletes
- in > 40: heart failure and cardiac hypertrophy
- SLOSHing in
S4 La Lub Dub
- low pitched, also called atrial gallop
- abnormal, indicates chronic HTN, cardiomyopathy, hypertrophy
- “Stiff” wall
Murmurs
- Whooshing
- systolic
- Lush Dub, valve regurgitation or aortic/pulmonary stenosis (leaky valve)
Mitral or tricuspid murmur
S1 may be obscured or it occurs between S1 and S2 (systole)
Aortic or pulmonic murmur
S2 is obscured or it occurs between S2 and S1 (diastole)
Parasympathetic Cranial Nerves
CN X to SA note, AV node, and ventricles
What does sbp reflect
Contractility and compliance of arteries
What does dbp reflect
Total peripheral resistance and heart rate
