Cardiac Flashcards
1
Q
Layers of the heart
A
Epicardium: outer layer directly covering heart
Myocardium: middle, thick mucosal layer, resoinsoble for relaxation and contraction of heart
Endocardium: inner, lies internal chamber of heart, houses capillaries, nerve fibres and heart conduction cells
2
Q
Serous pericardium
A
- Parietal layer: outer layer attached to fibrous pericardium
- Visceral layer: inner most, directly covers heart and roots of great vessels, blends with epicardium
Between the two = pericardial cavity
3
Q
Control of the heart
A
Heart rate and force is controlled by cardiac control center in the medulla
Baroreceptors in walls of aorta and internal carotid arteries detect changes in BP –> cardiac center responds through stimulation of sympathetic nervous system or parasympathetic nervous system
- SNS increases HR and contractility
PNS decreases HR and contractility
4
Q
What makes the lub dub sound
A
- Closure of AV = lub
○Right side= tricuspid
○ Left side = bicuspid - Closure of semi lunar = dubb
○ Right side = pulmonary valve
Left side = aortic valve
5
Q
Blood vessel layers
A
Tunica intima: inner layer made up pf endothelial cells
Tunica media: middle layer, made up of smooth muscle that controls diameter and lumen size
6
Q
Coronary circulation
A
Right and left coronary arteries - branch off aorta above aortic valve
L coronary A. divides into left ant descending and L circumflex A
Right coronary A divides into right marginal A and posterior inter ventricular A
7
Q
Non modifiable CVD risk factors
A
- Gender
- Race
- Family history
Age
8
Q
modifiable CVD risk factors
A
- Hypertension
- Hyperlipidemia
- Diabetes
- Obesity
- Smoking
- Poor diet
9
Q
Artherosclerosis patho
A
- Fatty streak formation
i. Endothelial cells damaged –> LDL penetrate damaged epithelium and accumulate in artery wall –> inflammation
ii. WBC activated and enter to engulf LDL and become foam cells
iii. Foam cells cluster together and form fatty streaks
2. Atheroma/plaque formation
i. Fatty streak grows as more cholesterol, lips and inflamatory cells accumulate
ii. Smooth muscle cells migrate from deeper levels to repair fatty streak–> form fibrous cap over the lipids
3. Plaque rupture and complications
i. Continued inflammation weakens the cap, if it ruptures the contents are exposed to the blood stream forming a blood clot (thrombus) at the site
ii. Clot can partially or fully obstruct the artery –> myocardial Infarction, stroke or peripheral artery
Can break off and travel within the body (when thrombus breaks off it is called an embolus)
10
Q
Atherosclerosis etiology
A
○ Modifiable and non modifiable
- Smoking, sedentary lifestyle, diabetes, Obesity, high fat diet elevate serum lipid
11
Q
Atherosclerosis clinical features
A
○ Initially asymptomatic
○ Ischemia in affected tissue
○ Depends on location
§ Coronary artery - angina, MI
§ Carotid artery - TIA or stroke
Peripheral artery - aneurysm, peripheral artery diseas
12
Q
Atherosclerosis treatment
A
○ Slow disease progression
○ Diet changes, 150m exercise, smoking cessation
○ Weight and stress management
○ Pharmacological
§ Lipid lowering therapy
§ Antiplatelet to reduce clot formation
○ Control primary disorder
○ Surgical intervention if there is advanced obstruction
§ Ballon angioplasty
Enterectomy
13
Q
Complications of atherosclerosis
A
Angina, MI, aneurysm, peripheral vascular disease, transient ischemic attack
14
Q
Peripheral artery disease
A
narrowed peripheral arteries reduce blood flow to arms or legs
15
Q
PAD patho and risk factors
A
as per atherosclerosis (obstruction in peripheral artery)
16
Q
PAD clinical features
A
Lower extremity pain due to ischemia
○ Claudication: leg pain associated with exertion due to muscle ischemia, initally resolves with rest but may not once advanced
- Non healing wounds/ulcers: due to blood supply (often in foot)
- Skin discoloration/gangrene
○ Initially color discoloration and can progress to necrosis
○ Dry shiny hairless skin
○ Skin temp reduced due to reduced blood flow
- Decreased pulses
- Sensory loss (generally distal or proximal, “glove and stocking distribution”)
- Fatigue and weakness
17
Q
PAD diagnosis
A
- Ankle brachial measure
Doppler (reduced blood flow and pulses)
18
Q
PAD treatment
A
- Prevention (smoking cessation, BP control, activity)
- Goals: slow progression of atherosclerosis, maintain lower limb circulation, treat complications
- Education to avoid skin trauma, regular exam to avoid pressure areas
- Medication to improve peripheral vasodilation and improve perfusion to limbs
- Surgery
○ Bypass reduction
○ Debride ulcers
Amputation if dangerous
19
Q
Hypertension stage 1 and 2
A
- Stage 1: 130-139/80-85
Stage 2: 140/90 or above
20
Q
Hypertension patho
A
- 3 major categories
○ Primary: idiopathic (BP> 140/90)
○ Secondary: from other pathology (renal or endocrine disease)
○ Malignant/resistant HTN: difficult to control (needs over 3 antihypertension drugs)- Increased arteriole vasoconstriction due to increased peripheral resistance, reduces system capacity and increases afterload
- Decreased blood flow through kidney, secrete renin, angiotensin and aldosterone which causes more vasoconstriction –> further BP increase
- Increased BP will cause damage to blood vessels
thickened walls, narrowing lumen, dilation or tea
21
Q
Hypertension etiology
A
- Age
- Men more
- Genetics (African American, family)
- High sodium
- Obesity
Prolonged or recurrent stress
22
Q
Hypertension clinical features
A
- Asymptomatic early on and vague symptoms
Fatigue, malaise, morning headache
23
Q
Hypertension diagnosis
A
at least 2 of the following
○ 24hr mean BP SBP ≥ 125 or DBP ≥ 75
○ Daytime mean SBP ≥ 130 or DBP ≥80
Nighttime mean SBP ≥ 110 or DBP ≥80
24
Q
Hypertension treatment
A
- Non pharmacological
○ Salt restriction, potassium supplementation, weight loss, DASH diet, limit alcohol
○ Exercise 3-4x weekly
○ Stress management - Pharmacological
Antihypertensive (usually in stage 2)
25
Hypertension complications
○ Left ventricular hypertrophy
○ Heart failure
○ Ischemic stroke
○ MI
Chronic kidney failure
26
Aortic Aneurysm patho
- Most common in thoracic or abdominal aorta
- Multifactorial systemic process caused by alterations in vascular wall --> loss of wall strength and defect in middle layer of vessel
○ Due to inflammation, protein breakdown and genetics
- Dilation can enlarge overtime
- Thrombus may also form in the dilated area and become an embolus
- Can rupture and cause a hemorrhage
- Different shapes
○ Fusiform - circumferential dilation
○ Saccular - bulging wall on 1 side
Dissecting - tear in intima, allow blood to flow along length of vessel between layers of arterial wall
27
Aneurysm etiology
- Risk: atherosclerosis, smoke, age, male, family, HTN
- Trauma
- Infection (e.g. syphilis, HIV)
Congenital (e.g. connective tissue disease)
28
Aortic aneurysm clinical features
- Asymptomatic until rupture
- Symptomatic but not ruptured
○ Abdominal, back or flank pain
○ Fever or malaise
○ Pulsatile abdominal mass
○ Can compress other structures (e.g. esophagus)
- Symptomatic and ruptured
○ Severe pain, hypotension, pulsatile abdominal mass (~50% of cases)
Critical to see immediate medical attention
29
Aortic aneurysm diagnosis
- Asymptomatic via incidental finding
Symptomatic (US, CT, MRI)
30
Aortic aneurysm treatment
- Manage based on diameter and presence of symptoms
○ Asymptomatic and small (<5.5cm) --> conservative management
○ Asymptotic and large (>5.5cm) elective surgical repair via AAA repair
- Surgery
○ Open graft
Endovascular repair
31
Acute coronary syndrome
Umbrella term for a range of conditions related to sudden, reduced blood flow to the heart
- Angina pectoris
Myocardial infarction
32
Angina patho
- Myocardial oxygen demands exceed O2 supply
○ Most often when there is a sudden O2 demand increase (e.g. exertion)
- Vessels are damaged so cannot vasodilate to meet blood supply demand
- Reduced supply can be due to:
○ Partial obstruction of a coronary artery
○ Spasm in coronary artery
- May lead to myocardial infarction
No damage unless they are frequent, prolonged or severe
33
Angina etiology
- Insufficient myocardial blood flow is associated with atherosclerosis, arteriosclerosis, vasospasm and myocardial hypertrophy
- Severe anemia and respiratory disease can cause oxygen deficit
Exertion
34
Angina clinical features
- Chest pain
- Pressure or heaviness
- Tightness, squeezing, constriction in center or left of chest
Caused by exertion and made better my rest
35
Angina diagnosis and treatment
Diagnosis: based on symptoms
Treatment
- Goal: relieve symptoms, prevent future cardiac events
- Prevention: beta blockers, calcium channel blockers, long acting nitrates
- Acute symptom management
○ Nitroglycerin (reduces systemic resistance and vasospasms)
○ Antiplatelet
○ Reduce exasperating factors (e.g. underlying disease or rest)
Regular follow up every 6-12 months
36
Myocardial infarction patho
- MI (heart attack) occurs when blood flow is fully obstructed due to atherosclerosis in one or more arteries leading to ischemia and cell death in the heart wall
- Most involve all layers of the heart
- Most often involve left ventricles (contracts against higher resistance)
- At location of obstruction, heart becomes necrotic and area of injury, inflammation and ischemia develop around it and cardiac enzymes are released
- Myocardial contractility and conduction are lost once O2 is depleted
- If blood supply can be restored in 20-30min, may prevent damage
- Myocardial fibres do not regenerate and fibrous tissue develops around the area of necrosis creating a scar
Collateral circulation may reduce size of infarct
37
MI etiology
- Most common cause is atherosclerosis, usually with thrombus
- Infarction can develop 3 ways
○ Thrombus can build and obstruct and block artery
○ Vasospasm can occur in presence of partial obstruction by atheroma/plaque leading to total obstruction
Part of thrombus can break free and the emboli can flow through the coronary artery blocking i
38
MI diagnosis
- ECG changes
○ STEMI - ST elevation (generally full occlusion)
○ NSTEMI - non ST elevation (often smaller artery)
- Nuclear imaging
- Presence of enzymes, factors and electrolytes in blood test
○ Increase in myosin and troponin
○ Increased serum levels
○ Abnormal potassium and sodium
Increased inflammatory markers
39
MI clinical features
- Pain
- Men
○ Sudden substernal chest pain radiating into left arm, shoulder, jaw, neck or back
- Women
○ Jaw, neck or upper back pain
○ Pain or pressure in lower chest or upper abdomen (often interpreted as indigestion)
○ Extreme fatigue, fainting
- Pallor, diaphoresis (sweating), nausea, weakness, dyspnea
- Anxiety/fear
- Hypotension
- Rapid, weak pule as CO decreases
Low grade fever
40
MI treatment
- Goals: reduce risk of death and extent of permanent injury
- Symptom management
○ Angina: nitroglycerin and antihypertensives +/- diuretics to reduce BP and O2 demand
○ Pain relief
- Reperfusion
○ Antithrombotic therapy
○ Angioplasty to restore blood flow + stent
○ Coronary artery bypass surgery
- Lifestyle modification
Smoking cessation, exercise, nutrition, weight management, managing chronic disease
41
Heart failure patho
- Any structural or functional cardiac disorders that impair the ability of ventricles to fill with or eject blood
- Left and right HF can occur together or separately
○ Left HR often causes right HF
○ E.g. pulmonary valve stenosis affects right side first vs MI in left ventricle affects right ventricle first
- CO decreases initially --> compensatory Mx
○ Increased SN drive --> increased vasoconstriction and increased resistance of left ventricle --> increased HR and force
○ Decreased blood flow to kidney--> renin secretion --> vasoconstriction --> aldosterone stimulation --> Na and H2O retention --> increased blood volume
- While CO is maintained, peripheral resistance and afterload are increased --> increased workload for the heart
- Increased HR --> decreased filling
- Heart remodels to adapt but reaches a limit with time --> heart failure
Inability to maintain pumping capacity --> CO or SV decrease --> less blood reaches organs/tissues --> decreased cell function --> fatigue, lethargy, mild acidosis and increased RR
42
RHF vs LHF
Left side heart failure:
Left ventricle cannot pump all blood into systemic circulation (decreased CO) so normal blood volume returning from lungs cant enter the left heart --> backup of fluid into the lungs --> pulmonary congestion and increased capillary pressure --> pulmonary edema
Right side HF:
Right ventricle cannot maintain output (decreased CO) so less blood is getting into circulation --> systemic circulation back up--> systemic congestion returning to heart --> increased blood volume in legs, feet and abdomen
43
HF etiology
- LHF cause: LV infarct, aortic valve stenosis, HTN
RHF: RV infarct, pulmonary valve stenosis, pulmonary disease
44
HF clinical features
- Either side
○ Hypoxia, fatigue, weakness, dyspnea, decreased exercise tolerance, cold intolerance, dizziness
- LHF
○ Dyspnea, orthopnea as pulmonary edema develops, frothy sputum
○ Coughing due to fluid irritating respiratory passages
○ Paroxysmal nocturnal dyspnea due to acute pulmonary edema
○ Decreased exercise tolerance
- RHF
○ Edema in feet or legs, increases JVO
○ Hepatomegaly and splenomegaly --> digestive issues
○ Ascites - fluid in peritoneal cavity as fluid accumulates, can cause abdominal distension and impair lung expansion
Flushed face, distended neck, headache, visual disturbance
45
HF classification
- Ejection fraction
○ HF with LV ejection fraction <40% = HF with reduced ejection fraction
○ HF with LVEF 41%-49% = HF with mid range ejection fraction
HF with LVEF >50% = HF with preserved ejection fraction
46
HF classes
1 = no limitation in PA
2 = slight limitation with PA, fine at rest
3 = marked limitation with PA, fine at rest. Less than ordinary intesity causes fatigue, SOB
4 = symptoms at rest
47
HF diagnosis
- Based on history, physical exam, labs and imagining
- Gold standard: identifying elevated pulmonary capillary wedge pressure at rest with left pulmonary artery catheter
Results can indicate whether a patient can mobilize or not
48
HF treatment
- Treat underlying problem
- Reduce workload on heart by avoiding excessive fatigue, stress, sudden exertion
- Meds
○ ACE inhibitors for vasodilation
○ Digoxin - improves cardiac efficiency
○ Antihypertensives and vasodilators to reduced BP
Diuretics to reduce fluid accumulation
49
CVD and stroke
- Overlapping risk factors
- Likely have blockages in arteries including carotid
- Can lead to 2 kinds of ischemic stroke
○ Atherothrombotic: plaque reduces blood flow to brain (major stroke)
Embolic - plaque breaks from primary site and travels to brain where it lodges in artery
50
CVD and osteoporosis
- Shared risk factors
○ Smoking, reduced activity, alcohol, hypertension (all which can promote atherosclerosis and bone demineralization)
- Common pathophysiological mechanisms
○ Inflamatory markers and cytokines
○ Endogenous sex hormones (estrogen deficiency) - estrogen has protective effect on CV system
- Common genetic factors
○ Some genes are associated with both BMD loss and atherogenesis
- Causal association
Atherosclerosis --> decreased blood flow to lower extremities --> decreased intraosseous blood circulation --> altered metabolism
51
Type 2 diabetes and stroke
- CVD is most. Prevalent cause of mortality in diabetes patients
- Diabetes patients often have many risk factors for developing CVD
○ HTN
○ Abnormal cholesterol and high tryglycerides
○ Obesity
○ Poorly controlled sugars
Lack of activty
52
COPD and HF
- COPD --> hypoxia --> pulmonary arteries constrict --> increased pulmonary vascular resistance
- Increased resistance --> pulmonary hypertension --> Right ventricle must pump against higher pressure and overtime will hypertrophy --> dilation and failure due to reduced contractile efficiency
- RHF develops -->
○ Peripheral edema
○ Jugular venous distension
○ Hepatomegaly
○ Ascites
HF impact on COPD
- LHF -->pulmonary congestion --> worse dyspnea
Reduced CO --> less O2 to respiratory muscle -->. Respiratory fatigue
53
Physio management
General goals
- Improve CV endurance and functional capacity
- Reduce dyspnea and fatigue
- Lifestyle modifications
- Self monitoring and symptom recognition
- Improve QOL
Acute
- Mobility and function
- Education (lifestyle, smoking, exercise)
Sub acute
- Outpatient cardiac rehab
Transition to maintenance and self monitoring
54
Cardiac rehab
Structured multidisciplinary approach to support patient with MI, heart failure or cardiac surgery
Goal: improve cardiac health, reduce risk of future cardiac events, enhance QOL
Includes
- Initial evaluation
○ Cardiac assessment
○ Functional capacity testing (6MWT)
○ Medical history and risk factor assessment
- Supervised exercise
○ Aerobic
○ Resistance
○ Intervals (later)
○ Flexibility and balance
- FITT: 5x week, 50-70% Max HR, 20-60min, aerobic
- Education and lifestyle modification
