Cardiac Flashcards
Layers of the heart
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
Serous pericardium
- 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
Control of the heart
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
What makes the lub dub sound
- Closure of AV = lub
○Right side= tricuspid
○ Left side = bicuspid - Closure of semi lunar = dubb
○ Right side = pulmonary valve
Left side = aortic valve
Blood vessel layers
Tunica intima: inner layer made up pf endothelial cells
Tunica media: middle layer, made up of smooth muscle that controls diameter and lumen size
Coronary circulation
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
Non modifiable CVD risk factors
- Gender
- Race
- Family history
Age
modifiable CVD risk factors
- Hypertension
- Hyperlipidemia
- Diabetes
- Obesity
- Smoking
- Poor diet
Artherosclerosis patho
- 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)
Atherosclerosis etiology
○ Modifiable and non modifiable
- Smoking, sedentary lifestyle, diabetes, Obesity, high fat diet elevate serum lipid
Atherosclerosis clinical features
○ Initially asymptomatic
○ Ischemia in affected tissue
○ Depends on location
§ Coronary artery - angina, MI
§ Carotid artery - TIA or stroke
Peripheral artery - aneurysm, peripheral artery diseas
Atherosclerosis treatment
○ 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
Complications of atherosclerosis
Angina, MI, aneurysm, peripheral vascular disease, transient ischemic attack
Peripheral artery disease
narrowed peripheral arteries reduce blood flow to arms or legs
PAD patho and risk factors
as per atherosclerosis (obstruction in peripheral artery)
PAD clinical features
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
PAD diagnosis
- Ankle brachial measure
Doppler (reduced blood flow and pulses)
PAD treatment
- 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
Hypertension stage 1 and 2
- Stage 1: 130-139/80-85
Stage 2: 140/90 or above
Hypertension patho
- 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
Hypertension etiology
- Age
- Men more
- Genetics (African American, family)
- High sodium
- Obesity
Prolonged or recurrent stress
Hypertension clinical features
- Asymptomatic early on and vague symptoms
Fatigue, malaise, morning headache
Hypertension diagnosis
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
Hypertension treatment
- Non pharmacological
○ Salt restriction, potassium supplementation, weight loss, DASH diet, limit alcohol
○ Exercise 3-4x weekly
○ Stress management - Pharmacological
Antihypertensive (usually in stage 2)
Hypertension complications
○ Left ventricular hypertrophy
○ Heart failure
○ Ischemic stroke
○ MI
Chronic kidney failure
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
- Multifactorial systemic process caused by alterations in vascular wall –> loss of wall strength and defect in middle layer of vessel
Aneurysm etiology
- Risk: atherosclerosis, smoke, age, male, family, HTN
- Trauma
- Infection (e.g. syphilis, HIV)
Congenital (e.g. connective tissue disease)
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
- Symptomatic but not ruptured
Aortic aneurysm diagnosis
- Asymptomatic via incidental finding
Symptomatic (US, CT, MRI)
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
- Surgery
Acute coronary syndrome
Umbrella term for a range of conditions related to sudden, reduced blood flow to the heart
- Angina pectoris
Myocardial infarction
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
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
- Severe anemia and respiratory disease can cause oxygen deficit
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
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
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
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
- Infarction can develop 3 ways
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
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
- Men
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
- Symptom management
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
- Left and right HF can occur together or separately
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
HF etiology
- LHF cause: LV infarct, aortic valve stenosis, HTN
RHF: RV infarct, pulmonary valve stenosis, pulmonary disease
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
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
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
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
- Gold standard: identifying elevated pulmonary capillary wedge pressure at rest with left pulmonary artery catheter
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
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
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
- Common pathophysiological mechanisms
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
- Diabetes patients often have many risk factors for developing CVD
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
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
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
